MONTHLY

By Chris Beardsley

NOV 2020
EDITION
November 2020 Edition
Editorial by Chris Beardsley
In this strength training section of this edi-
tion, I reviewed two new studies that affect
our understanding of the psychobiological
model of fatigue during exercise. This mod-
el has great explanatory power for central
nervous system (CNS) fatigue, but some
aspects of it remain unclear. These new
studies help to shed light on exactly how
motivation and perception of effort each
might influence the level of central motor
command during exercise, and thereby
affect the level of CNS fatigue.

In the hypertrophy section of the edition, I

reviewed two studies that affect our under-
standing of strength training as a stressor

W elcome to the November 2020 edi-

tion! The lead article this month
reviews a study that measured the force
within the definition used by the general
adaptation syndrome (GAS). Traditionally,
it has been assumed that strength train-
and cross-sectional areas of type I and
ing workouts can always be considered as
type II muscle fibers in bodybuilders and
stressors, and yet recent work by research-
in untrained controls. As in some previous
ers into stress as a more general concept
studies, the researchers found that the
suggests that this may only be possible
bodybuilders displayed larger type II mus-
when the workouts [A] involve certain spe-
cle fibers but lower muscle fiber force rela-
cific elements and [B] produce certain spe-
tive to cross-sectional area in these fibers.
cific physiological responses. Consequently,
Yet, this difference between the bodybuild-
while some strength training programs
ers and the untrained controls disappeared
probably can be modeled within the GAS,
after correcting for swelling that occurred
others almost certainly cannot. Read on to
during the experimental processes, sug-
learn more! See you next month.
gesting that bodybuilding likely does not
cause more sarcoplasmic hypertrophy.

Published by Strength
and Conditioning
Research Limited
 November 2020 Edition
Contents

Strength training
Single fiber specific tension in bodybuilders and untrained controls
1
Does bodybuilding reduce the myofibrillar density of individual muscle fibers?

Why does training closer to failure cause a larger fiber type shift?
2
During velocity-based training, a greater velocity loss produces a greater shift from type IIX to type IIA

Motivational self-talk can improve exercise performance

3
What is the role of motivation in the psychobiological model of central nervous system fatigue?

Measuring central nervous system fatigue during low-intensity exercise

4
Does the perception of effort act as the ultimate limiting factor during long-duration exercise?

Athletic performance
Reducing the force-velocity imbalance enhances gains in maximum strength
5
How might reducing the force-velocity imbalance affect maximum strength?

Effects of wearable resistance on sprinting biomechanics

6
Does wearable resistance require the hip extensors and hip flexors to produce more work done?

Hypertrophy
Can we model strength training workouts as stressors?
7
Is it appropriate to consider strength training as a stressor and use the general adaptation syndrome?

Effects of training to failure on the rate of recovery from a workout

8
Does training to failure increase the time it takes to recover from a strength training workout?

Effects of strength training at long and short maximum muscle lengths

9
Does the seated leg curl produce greater hypertrophy than the lying leg curl in all regions of all of the knee flexors?

Why do muscles have a memory of previous training?

10
Do muscle fibers retain myonuclei during detraining?

Published by Strength
and Conditioning
Research Limited
 Single fiber specific tension in body-
builders and untrained controls

I t is well-known that bodybuilders typically display

a lower level of maximum strength for a given
muscle size compared to strength athletes such as
powerlifters. While this difference is commonly at-
tributed to neural adaptations, there are also indi-
cations that larger muscle fibers may not always
produce the same force per unit cross-sectional
area as smaller muscle fibers. However, it is unclear
whether this finding is the result of real differences
in myofibrillar density or whether it is an artefact of
the experimental process.

Key findings
When comparing bodybuilders with recreationally-active controls, the bodybuilders dis-
played non-significantly larger type I muscle fibers and significantly larger type II muscle
fibers. Specific tension (single fiber force relative to cross-sectional area) of the type II
muscle fibers appeared to be smaller in bodybuilders, but this difference disappeared af-
ter correcting for swelling induced by the experimental process.

Practical implications
Bodybuilding training is unlikely to have negative effects on maximum strength by pro-
ducing muscle fibers with a lower myofibrillar density (and therefore lower specific ten-
sion). The differences in maximum strength between bodybuilders and powerlifters are
likely to arise from differences in neural adaptations (coordination, agonist voluntary acti-
vation, and antagonist coactivation), lateral force transmission, and tendon stiffness.

Are muscle fibres of body builders intrinsically weaker? A comparison with

single fibres of aged-matched controls. Monti, E., Toniolo, L., Marcucci, L.,
Bondì, M., Martellato, I., Šimunič, B., & Reggiani, C. Acta Physiologica, e13557.
(PubMed)
Background
OBJECTIVE To compare the specific tension of single muscle fibers taken from
bodybuilders and age-matched control subjects.

INTERVENTION
POPULATION
Subjects attended two testing sessions. In one testing session, a
vastus lateralis muscle biopsy was provided. In another testing 12 subjects (6 body-
session, subjects performed a maximal isometric knee extension builders and 6 age-
test and their quadriceps muscles were scanned with ultrasound matched, untrained but
for measurements of size and architecture. recreationally-active
controls)

MEASUREMENTS
Whole muscle size: By quad-
riceps and vastus lateralis
cross-sectional area (CSA) using
ultrasound.
RESULTS
Bodybuilders displayed non-significantly greater quadri-
ceps CSA and significantly greater vastus lateralis CSA
than the age-matched controls.

Maximum strength, and Bodybuilders displayed significantly greater knee exten-

strength relative to muscle sion MVIC force as well as non-significantly greater knee
size: By knee extension maxi- extension MVIC force relative to quadriceps CSA than
mum voluntary isometric con- the age-matched controls.
traction (MVIC) force.

Muscle fiber CSA: From vastus Bodybuilders displayed non-significantly greater type I
lateralis biopsies and immuno- muscle fiber CSA, as well as significantly greater type II
histochemical staining. muscle fiber CSA than the age-matched controls.

Single muscle fiber specific
tension: By placing single mus-
cle fiber segments into an appa-
ratus fitted with a force trans-
ducer.
Specific tension of type I fibers did not differ signifi-
cantly between groups. Specific tension of type II fibers
was significantly lower in bodybuilders than in controls.
This difference disappeared after correcting fiber size for
swelling caused by the experimental treatment.

Myonuclear domain (MND): There was a non-significant tendency for the MND to be
Of single muscle fibers. smaller in bodybuilders than in controls.

Myosin content: Using electro- There was no significant difference in myosin content
phoretic separation and densi- between the muscle fibers of bodybuilders and controls.
tometry to assess the ratio be-
tween myosin content and fiber
volume.

SUMMARY
When comparing bodybuilders with recreationally-active controls, the
bodybuilders displayed non-significantly larger type I muscle fibers and significantly larger
type II muscle fibers. Specific tension (single fiber force relative to cross-sectional area) of
the type II muscle fibers appeared to be smaller in bodybuilders, but this difference disap-
peared after correcting for swelling induced by the experimental process.

T his study compared bodybuilders with
recreationally-active controls, and
found that the bodybuilders displayed
non-significantly larger type I fibers and
significantly larger type II fibers. This was
largely in accordance with expectations,
since previous research has shown that
fast twitch (type II) muscle fibers tend to
grow to a greater extent after strength
training than slow twitch (type I) muscle
fibers (1–6), likely because slow twitch
fibers are already somewhat developed by
the activities of daily life.
Analysis
Additionally, this study found that the spe-
cific tension of type II fibers appeared to
be smaller in bodybuilders, but this differ-
ence disappeared after correcting for swell-
ing induced by the experimental process.
While this may appear unexpected, it was
actually in agreement with the literature,
because of the mechanisms that underpin
strength gains after training. To under-
stand why this is the case, it is helpful to
consider the various ways in which ratios
of strength relative to size are measured in
exercise science.

1. Exercise strength relative to
whole muscle size
One common measurement of strength
relative to size is the expression of exercise
1RM or a maximum level of isometric force
relative to the size of a whole muscle. The
measurement of muscle size can be either
its volume or its cross-sectional area. In
this situation, the factors that determine
muscle force include: [A] coordination in
the exercise (7,8), [B] the level of volun-
tary activation of the muscle (the number
of high-threshold motor units that can be
recruited) (9,10), [C] the level of antago-
nist coactivation (the extent to which the
antagonist muscle opposes the agonist
muscle) (11), [D] the total size of the mus-
cle fibers that are working to produce force
in the exercise (12), [E] the proportion of
force that is transmitted efficiently (later-
ally) between fibers through costameres
(13), [F] myofibrillar density (14), and [G]
tendon stiffness (during isometric or con-
centric-only contractions) (15).
It is clear that when we assess strength
and muscle size in this way, a large num-
ber of factors can alter the ratio between
strength and size, some of which are locat-
ed in the central nervous system and some
of which are located within the muscle. We
cannot therefore draw conclusions about
the strength of individual muscle fibers
within a muscle based on the ratio of exer-
cise strength relative to whole muscle size.
Analysis
2. Involuntary muscle force relative
to whole muscle size
A very uncommon (but very informative)
measurement of strength relative to mus-
cle size can be calculated by recording
involuntary force during assessments of
voluntary activation using the interpolated
twitch technique (13). This measurement
can be further refined to remove the influ-
ence of antagonist muscle coactivation by
measuring the activation of the antagonist
and calculating its force production relative
to its activation during a maximal contrac-
tion of that muscle. Additionally, by mea-
suring the internal moment arm lengths of
the muscle using imaging scans, the actual
agonist muscle force can be calculated, and
not merely the joint torque.
Ultimately, this process therefore allows
the calculation of muscle force relative to
whole muscle size (either cross-sectional
area or volume) after removing the effects
of [A] coordination, [B] the level of ago-
nist muscle voluntary activation, and [C]
the level of antagonist muscle coactivation.
Consequently, the remaining factors that
can influence muscle force are: [D] the
total size of the muscle, [E] the propor-
tion of force that is transmitted efficiently
(laterally) between muscle fibers through
costameres, [F] the myofibrillar density of
muscle fibers, and [G] tendon stiffness (in
isometric or concentric-only contractions).

3. Muscle fiber force relative to
muscle fiber size
Another common measurement of strength
relative to size is the expression of single
muscle fiber force relative to single mus-
cle fiber cross-sectional area. This is often
called “specific tension” in the literature
(although the same term is confusing-
ly also sometimes used to refer to other
measurements of strength relative to size).
As in this study, researchers calculate this
measurement by taking muscle biopsies
and then isolating single muscle fibers.
The cross-sectional areas of these single
muscle fibers are then measured and their
ability to produce force is assessed by plac-
ing them in a solution that causes them to
be activated, while recording the isometric
force that is produced with a transducer.
When we assess muscle fiber strength and
size in this way, only a small number of
factors can alter the ratio between strength
and size. Obviously, none of the factors
that involve the central nervous system
can have any effect. Similarly, neither the
antagonist muscle or the tendon can have
an effect, since these are not connected to
the muscle fiber when it is producing force.
Also, the amount of lateral force transmis-
sion is also unable to contribute, because
the external collagen layer around each
muscle fiber (the endomysium) is removed
as part of the experimental process.
Analysis
Ultimately, this process therefore allows
the calculation of single muscle fiber force
relative to its size, and the only factors
that can contribute are those that affect
the number of actin-myosin crossbridges
that can form at a given contraction veloc-
ity. When studying muscle fibers of specific
types (slow twitch or fast twitch), the only
factor that can influence muscle fiber force
relative to its size is therefore the density
of the myofibrils inside the fiber.
What does this mean?
This study found that the specific tension
(muscle fiber force relative to its cross-sec-
tional area) of single muscle fibers was
the same in untrained individuals and in
bodybuilders. This suggests that myofibril-
lar density does not change substantial-
ly with long-term strength training. This
agrees largely with the existing literature.
Older studies found that myofibrillar den-
sity remained unchanged after strength
training (16,17), and more recent work has
suggested that short periods of strength
training might reduce myofibrillar density
regardless of the volume or relative loads
that are used during training (18,19), while
very long exposure to strength training
might cause it to increase slightly (14).
This suggests that differences in strength
between bodybuilders and powerlifters with
similar levels of muscle mass are likely to
result from one of the many other factors.

Conclusions
When comparing bodybuilders with rec-
reationally-active controls, the body-
builders displayed non-significantly larger
type I muscle fibers and significantly
larger type II muscle fibers. Specif-
ic tension (single fiber force relative to
cross-sectional area) of the type II mus-
cle fibers appeared to be smaller in body-
builders, but this difference disappeared
after correcting for swelling induced by
the experimental process.
Analysis
Practical implications
Bodybuilding training is unlikely to have
negative effects on maximum strength
by producing muscle fibers with a lower
myofibrillar density (and therefore low-
er specific tension). The differences in
maximum strength between bodybuilders
and powerlifters are likely to arise from
differences in neural adaptations (coor-
dination, agonist voluntary activation,
and antagonist coactivation), lateral force
transmission, and tendon stiffness.

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 Why does training closer to failure
cause a larger fiber type shift?

M any studies that have examined velocity-based

training have found that maximal effort strength
training with a greater velocity loss on each set (and
therefore training closer to failure) causes smaller
increases in measures of high-velocity strength and
speed (such as jumping and sprinting). This has
been attributed to the greater velocity loss involving
greater fatigue and therefore greater signaling that
causes a shift away from the very fast (type IIX)
fiber type. These very fast fibers are critical for the
performance of very fast movements.

Key findings
In strength-trained males, strength training with a larger velocity loss on each set caused
greater hypertrophy and greater fiber type shifts away from the IIX isoform. These great-
er fiber type shifts away from the type IIX isoform (and to a lesser extent the hypertro-
phy) were associated with an increase in the expression of a phosphorylated isoform of
CaMKII, which has previously been implicated in fiber type shifts.

Practical implications
When training athletes to perform in fast movements (such as throwing, jumping, and
sprinting), it is likely optimal to avoid training close to failure, because this causes a shift
away from the fastest fiber type that is key to the production of force at fast speeds.

Role of CaMKII and sarcolipin in muscle adaptations to strength training with

different levels of fatigue in the set. Martinez-Canton, M., Gallego-Selles, A.,
Gelabert-Rebato, M., Martin-Rincon, M., Pareja-Blanco, F., Rodriguez-Rosell, D.
& Calbet, J. A. (2020). Scandinavian Journal of Medicine & Science in Sports.
(PubMed)
Background
OBJECTIVE To explore the effects of strength training with a smaller (20%) or a
larger (40%) velocity loss on each set on hypertrophy and fiber type
shifts, in strength-trained males.

INTERVENTION
POPULATION
All subjects trained 2 times per week for 8 weeks, with 3 sets of
the Smith machine full squat, using the same percentage of 1RM 24 males, aged 23 ± 2
in each group (70 – 85% of 1RM). The V20 group stopped each years, with >1.5 years of
set when bar speed fell by 20% from the bar speed in the fastest strength training expe-
(first) rep, while the V40 group stopped when bar speed fell by rience, allocated to 20%
40% from the bar speed in the fastest (first) rep. Bar speed was and 40% velocity loss
tracked constantly by mean propulsive velocity (MPV), which is groups (V20 and V40)
the speed recorded in the concentric phase during which barbell
acceleration is greater than acceleration due to gravity.

MEASUREMENTS RESULTS
Muscle fiber type: By vastus Type IIX fiber proportion reduced significantly only in V40.
lateralis biopsies and myosin
heavy chain (MHC) isoforms.

Muscle size: By quadriceps Vastus lateralis CSA and vastus intermedius CSA both in-
muscle cross-sectional area creased significantly in V40 but not in V20.
(CSA) by magnetic resonance
imaging (MRI) scans.

Protein analysis: By vastus CaMKII isoform and phosphorylated (Thr287) CaMKII

lateralis muscle fiber biopsies
and subsequent Western blot-
ting to examine changes in
Ca2+-calmodulin-dependent
protein kinase II (CaMKII).
expression each increased significantly and similarly after
training in both groups. The expression of phosphorylated
(Thr287) CaMKII δD isoform increased significantly after
training only in V40 (and this was moderately associated
with the number of reps done in training (r = 0.59), the
vastus lateralis and intermedius hypertrophy (r = 0.48),
and the reduction in type IIX proportion (r = 0.72).

SUMMARY
In strength-trained males, strength training with a larger velocity loss
on each set caused greater hypertrophy and greater fiber type shifts away from the IIX
isoform. These greater fiber type shifts away from the type IIX isoform (and to a lesser
extent the hypertrophy) were associated with an increase in the expression of a phosphor-
ylated isoform of CaMKII, which has previously been implicated in fiber type shifts.
 Analysis

T his study reported that in strength-

trained males, strength training with
a larger velocity loss on each set caused
Additionally, previous research into the
mechanisms of fiber type shifts has impli-
cated CaMKII signaling events in moving
greater hypertrophy and greater fiber type fibers away from less oxidative isoforms
shifts away from the IIX isoform. These (4). Importantly, this research has shown
greater fiber type shifts away from the that CaMKII signaling events appear to
type IIX isoform (and to a lesser extent the respond to the nature of the muscle acti-
hypertrophy) were associated with an in- vation that is used during training, because
crease in the expression of a phosphorylat- of the way in which this muscle activation
ed isoform of Ca2+-calmodulin-dependent affects the calcium ions that are released
protein kinase II (CaMKII), which has pre- into the muscle fiber cytoplasm by means
viously been implicated in fiber type shifts. of the excitation-contraction coupling pro-
cess. Specifically, since CaMKII is activated
Clearly, there are two key findings of this and deactivated relatively slowly by the
study. Firstly, this study showed that CaM- presence or absence of calcium ions, it is
KII signaling mediates the shifts in fiber therefore most strongly stimulated to pro-
type after strength training, such that duce a signaling response when calcium
when sets involve more reps and are taken ions are produced constantly (for a pro-
closer to failure, this causes a greater fiber longed period of time) or in intermittent
type shift compared to when sets involve contractions with short rests. Brief periods
fewer reps and are stopped short of failure. of muscle activation are too short in length
Secondly, this study appeared to show that to stimulate CaMKII signaling, but longer
CaMKII signaling may also be involved in periods of muscle activation can produce a
stimulating hypertrophy, albeit to a lesser stimulus, and (importantly), the signaling
extent than in the fiber type shifts. magnitude increases cumulatively when
this stimulation is applied for increasingly
1. Muscle fiber type shifts long periods of time with either no rest or
Previous strength training research has with only short rests between contractions
shown that fiber type shifts away from the (4). This would predict that CaMKII signal-
very fast type IIX isoform are greater when ing would be more pronounced as a result
a larger volume of training is performed of performing more total reps (and there-
(1,2) and also when sets are taken closer fore a higher total volume), but only when
to failure (3). Yet, no previous research has those reps were performed with short rests
explored the underlying molecular signal- between them.
ing mechanisms of these effects.

I t is believed that the reduction in type
IIX fiber proportion contributes to a
change in the gradient of the force-velocity
profile. Indeed, fast twitch muscle fibers
are actually the only ones that are capable
of contributing to force production at high
speeds (5). This suggests that when the
fastest (type IIX) muscle fibers experience
reductions in their maximal shortening
speeds because of shifts in their fiber type,
the overall force production of the muscle
at fast speeds will reduce substantially.
This will cause a reduction in the maximum
theoretical velocity of the force-velocity
profile, even as maximum theoretical force
is increased due to other adaptations.
Indeed, blocks of heavy strength training
often do shift the force-velocity profile such
that maximum theoretical force increases
while maximum theoretical velocity reduc-
es (6–9). Yet, this shift does not always
occur when the strength training sets are
structured as clusters (10), which involve
taking short rests within each set. Taking
short rests within the set likely reduces
CaMKII signaling, which reduces the mag-
nitude of the fiber type shift, which pre-
vents a large reduction in maximum the-
oretical velocity from occurring. Similarly,
there is evidence that training with lower
volumes (in terms of the number of sets)
also reduces the magnitude of the fiber
type shift and maximizes gains in force
production at fast speeds (2).
Analysis
2. Hypertrophy
To date, the only well-established mech-
anism that produces hypertrophy is me-
chanical tension. This mechanical tension
can be produced either by a muscle fiber
itself (by the creation of actin-myosin
crossbridges) or by an external stretch.
Nevertheless, researchers have investi-
gated the possibility of other mechanisms
in order to explain situations in which the
amount of hypertrophy is greater than
might be expected for the estimated level
of mechanical tension.
For example, it has been suggested that
muscle damage might be a mechanism
that produces hypertrophy. This was pro-
posed on the basis that eccentric training
produces more muscle growth than con-
centric training (and also causes more
muscle damage), and because full range of
motion (ROM) training often causes more
muscle growth than partial ROM training
(and also causes more muscle damage).
Yet, in both cases, the amount of mechan-
ical tension that is experienced by each
working muscle fiber is actually greater
when performing eccentric contractions
(compared to concentric contractions) and
when doing full ROM training (compared to
partial ROM training) because of the in-
volvement of passive elements inside the
muscle fibers that contribute to force pro-
duction when the muscle is stretched.

S imilarly, it has been suggested that the
accumulation of metabolites during
fatiguing contractions (called “metabolic
stress”) might be a mechanism that pro-
duces hypertrophy. This was initially pro-
posed because isometric training caused
more hypertrophy when contractions were
performed with short rests compared to
with long rests, while also causing a larger
amount of metabolite accumulation (11).
Even so, the accumulation of metabolites
is a marker of fatigue. When working mus-
cle fibers are fatigued, this requires other
muscle fibers to be activated through an
increase in effort leading to an increase
in motor unit recruitment levels (12,13).
Isometric training with short rests would
have involved the recruitment of more
high-threshold motor units than isometric
training with long rests. Importantly, be-
cause of the force-velocity relationship, the
muscle fibers that belong to low-threshold
motor units experience very high levels of
mechanical tension on a daily basis and
therefore are not capable of growing af-
ter additional training (14). Thus, only by
recruiting high-threshold motor units is it
possible to produce muscle growth. Con-
sequently, the accumuation of metabolites
was never necessary to explain the results
of these early studies, since the greater
hypertrophy was caused by the application
of mechanical tension to a more responsive
group of muscle fibers.
Analysis
More recently, researchers have suggested
that muscle activation may be a key fac-
tor that determines hypertrophy, through
its effects on the release of calcium ions
into the cytoplasm (15). Indeed, several
studies have identified potential roles for
calcium ion-related signaling processes in
causing hypertrophy (4). However, there is
also evidence from studies involving pas-
sive static stretching of muscles that mus-
cle activation (and the subsequent calcium
ion release) is not necessary for hyper-
trophy to occur (16). Also, some research
has shown that muscle activation may not
enhance the hypertrophy that occurs so
long as the amount of mechanical tension
is kept at the same level (17). Conversely,
changing the level of mechanical tension
while keeping the level of muscle activation
the same has a very marked impact on the
resulting hypertrophy, with greater levels
of mechanical tension causing much great-
er muscle growth (18,19). Moreover, when
studies have identified greater transient
increases in myofibrillar protein synthesis
(MYOPS) rates as a result of muscle acti-
vation combined with mechanical tension
(compared to mechanical tension alone),
this could very easily be explained by the
need to repair the muscle damage that
is caused by the muscle activation, since
calcium ions are the main cause of damage
after exercise (20), and since muscle dam-
age repair is known to require a transitory
increase in MYOPS rates (21).

T his study reported that there was an
association between the calcium ion–
related signaling events and the amount
of hypertrophy that resulted. Given that
the number of reps in this context reflects
an increasing amount of reps performed
in sequence (and therefore an increasing
stimulus for calcium ion-related signaling),
this might be presented as further (albeit
indirect) evidence to link muscle activation
with muscle growth. However, this link may
actually be purely coincidental, in the same
way as the link between lactate and muscle
growth has been shown to be coincidental.
Previous studies have found that lactate
increases in proportion to the proximity to
muscular failure (21,22) and many rodent
studies have presented evidence that links
lactate with hypertrophy (23–28).
Conclusions
In strength-trained males, strength train-
ing with a larger velocity loss on each set
caused greater hypertrophy and great-
er fiber type shifts away from the IIX
isoform. These greater fiber type shifts
away from the type IIX isoform (and to
a lesser extent the hypertrophy) were as-
sociated with an increase in the expres-
sion of a phosphorylated isoform of CaM-
KII, which has previously been implicated
in fiber type shifts.
Analysis
However, recent research in humans has
shown that the addition of exogenous lac-
tate during a strength training workout has
no effect on the post-workout increase in
muscle protein synthesis rates (29).This
shows that lactate itself is not involved in
the signaling processes causing muscle
growth. This demonstrates that metabolic
accumulation can occur in a dose-response
way with increasing proximity to failure
and yet be totally unrelated to the process
that causes muscle growth. Similarly, it is
possible that calcium ion-related signaling
can also occur in a dose-response way with
increasing proximity to failure, and yet
may well be totally unrelated to the pro-
cess that causes muscle growth, although
it is very likely involved in triggering similar
processes that lead to muscle fiber repair.
Practical implications
When training athletes to perform in fast
movements (such as throwing, jumping,
and sprinting), it is likely optimal to avoid
training close to failure, because this
causes a shift away from the fastest fiber
type that is key to the production of force
at fast speeds.

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 Motivational self-talk can improve
exercise performance

D uring sustained exercise, performance is strongly

limited by the central nervous system (CNS).
A popular explanation of how the CNS regulates
exercise performance is the psychobiological model,
which integrates inputs from the brain and from
the body to produce a certain level of voluntary
command to the working muscles, thereby producing
motor unit recruitment. Yet, it is unclear how this
model balances motivation and afferent feedback
from muscles to determine the maximum level of
voluntary command that can be produced.

Key findings
In amateur triathletes, practicing motivational self-talk reduced 750m swimming time
while increasing outcome expectancy and leaving the perceived level of effort unchanged.
It seems likely that the motivational self-talk was effective at increasing motivation, which
allowed a higher level of central motor command to be achieved for a given level of per-
ceived effort, thereby increasing exercise performance.

Practical implications
Techniques that increase motivation during exercise (such as using self-talk, increasing
autonomy, obtaining feedback, and others) can improve performance and this likely oc-
curs through an increase in the level of motor unit recruitment that can be achieved for a
given perceived level of effort. Increases in maximum strength and muscle size will likely
be improved by using such techniques, since the recruitment of more motor units allows
more muscle fibers to be trained.

Motivational self-talk improves time-trial swimming endurance performance in

amateur triathletes. De Matos, L. F., Bertollo, M., Stefanello, J. M. F., Pires, F.
O., da Silva, C. K., Nakamura, F. Y., & Pereira, G. (2020). International Journal
of Sport and Exercise Psychology, 1-14. (Link)
Background
OBJECTIVE To assess the effects of motivational self-talk on swimming times in
amateur triathletes.

INTERVENTION
POPULATION
Subjects performed two 750m swimming tests in a 50m pool as fast
as possible. Each test was performed after a standardized warm-up. 21 amateur triathletes
After the first test, subjects wrote down thoughts that occurred to (15 males, 6 females),
them while swimming. According to their group allocation, these aged 21 – 47 years,
thoughts were converted to four statements that had either an in- allocated into a control
structional purpose (e.g. “I will focus on technique”) or a motivation- group or a motivational
al purpose (e.g. “I believe I can swim faster”). Subjects memorized
group
these thoughts and repeated them during training sessions for the
following 12 days and also during the second test.

MEASUREMENTS RESULTS
Exercise performance: By Subjects in the motivational group achieved a significant
750m test time. reduction in 750m swimming time from the first to the
second test (by 2.8%), while the subjects in the control
group did not.

Perception of effort: By
self-reported rating of perceived
exertion (RPE) on the (6–20
point) Borg scale immediately
after the 750m tests.
Both the motivational and control groups reported the
same RPE in the first test (17.2 and 17.3 points, respec-
tively) and in the second test (17.1 and 17.4 points,
respectively), without any change between tests.

Psychological measures: By Mood

the Brunel Mood Scale (BRUMS)
to assess mood (since this can
affect motivation) and by out-
come expectancy (self-predicted
time to swim 750m in the test).
Subjects in both groups displayed similar BRUMS scores
on the days of both tests, indicating that it was unlikely
that mood affected the results.
Outcome expectancy
Subjects in the motivational group achieved a significant
increase in their outcome expectancy from the first to
the second test (by 6%), while the subjects in the con-
trol group did not.

SUMMARY
In amateur triathletes, practicing motivational self-talk reduced 750m
swimming time while increasing outcome expectancy and leaving the perceived level of
effort unchanged. It seems likely that the motivational self-talk was effective at increasing
motivation, which allowed a higher level of central motor command to be achieved for a
given level of perceived effort, thereby increasing exercise performance.

T his study reported that in amateur
triathletes, practicing motivational self-
talk reduced 750m swimming time while
increasing outcome expectancy and leaving
the perceived level of effort unchanged. It
seems likely that the motivational self-talk
was effective at increasing motivation, and
that this allowed a higher level of central
motor command to be achieved for a given
level of perceived effort, thereby increasing
exercise performance.
Currently, there are two popular models
for explaining how endurance performance
is limited by the brain. One of these is
the central governor model (1–3), and its
successor the integrative governor model
(4), while the other is the psychobiologi-
cal model (5–7). The key advantage of the
psychobiological model is that it combines
existing physiology and psychology togeth-
er without proposing any new components.
The psychobiological model identifies that
exercise performance can be limited by the
brain, and that performance is reduced by
a reduction in the size of the signal from
the central nervous system (CNS) to the
muscles. This signal, which is often called
the “central motor command” is what caus-
es the recruitment of motor units. Reduc-
ing the size of this signal therefore brings
about a reduction in the number of motor
units that are recruited and producing force
during an exercise task.
Analysis
The psychobiological model then identifies
that the size of the central motor command
that is sent by the CNS to the muscle is
affected by two factors: [A] the level of
motivation to perform the exercise task,
and [B] the perceived level of effort during
the task.
Indeed, the effects of motivation on ex-
ercise performance can be observed in
strength training as well as during endur-
ance exercise, since interventions such
as increasing autonomy (8) and providing
feedback (9) are known to improve the
level of motivation in an exercise task, and
also improve performance. Similarly, the
perceived level of effort during the task
is known to affect the size of the central
motor command, since increased affer-
ent feedback from muscles (in the form of
burning and aching sensations) has been
shown to reduce exercise performance
during high-intensity exercise (10–14).
Also, the perceived level of effort during
the task is determined by the size of the
central motor command itself (15). Thus,
as the size of the central motor command
increases in order to achieve higher lev-
els of motor unit recruitment, it becomes
progressively more and more difficult to
achieve incremental increases in neural
drive to the muscle. This essentially cre-
ates a negative feedback loop for motor
unit recruitment.

I nterestingly, this study reported that in-
creasing the level of motivation reduced
swimming time while leaving the perceived
level of effort unchanged. When using the
psychobiological model, this suggests that
increased motivation did not permit a high-
er level of perceived effort to be experi-
enced, but rather that it reduced the level
of perceived effort that was experienced
for a certain level of central motor com-
mand. This fits with other research show-
ing that interventions that increase motiva-
tion (such as listening to fast tempo music)
increase exercise performance but either
do not affect the self-reported level of
perceived effort (16–18) or reduce it (19).
This is the exact opposite of what would be
expected if motivation permitted a higher
level of perceived effort to be experienced.
Conclusions
In amateur triathletes, practicing motiva-
tional self-talk reduced 750m swimming
time while increasing outcome expec-
tancy and leaving the perceived level of
effort unchanged. It seems likely that
the motivational self-talk was effective at
increasing motivation, which allowed a
higher level of central motor command to
be achieved for a given level of perceived
effort, thereby increasing exercise perfor-
mance.
Analysis
Consequently, although the psychobiolog-
ical model is often presented as showing
[A] motivation and [B] perceived level of
effort as having independent effects on
the level of central motor command that
can be achieved during an exercise task,
it seems more likely that the level of mo-
tivation alters the perception of effort in
much the same way as afferent feedback
and the current size of the central motor
command do. Thus, a revised presentation
of the model might involve all factors first
affecting the perception of effort before
they influence the size of the central motor
command to the muscle, which essentially
suggests that the ultimate limiting factor
for exercise performance is always the per-
ception of effort (albeit this can be altered
through several mechanisms).
Practical implications
Techniques that increase motivation
during exercise (such as using self-talk,
increasing autonomy, obtaining feedback,
and others) can improve performance
and this likely occurs through an increase
in the level of motor unit recruitment that
can be achieved for a given perceived
level of effort. Increases in maximum
strength and muscle size will likely be
improved by using such techniques, since
the recruitment of more motor units al-
lows more muscle fibers to be trained.

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humans. British Journal of Sports Medicine, 38(6), 797-
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2. Noakes, T., St, C., & Lambert, E. (2005). From ca-
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 Measuring central nervous system
fatigue during low-intensity exercise

C entral nervous system (CNS) fatigue occurs during

all forms of exercise, but more so in low-intensity
exercise than during high-intensity exercise (contrary
to popular belief). A popular model of CNS fatigue is the
psychobiological model, in which inputs from the brain
(motivation) and from the body (afferent feedback)
both influence the central motor command to muscles
(which is what causes the recruitment of motor units).
Yet, it is unclear how these effects of these inputs from
the brain and body differ during exercise and during the
testing of fatigue after exercise.

Key findings
When untrained males performed a very low-intensity (10% of MVIC) isometric contrac-
tion to task failure, strength reduced to approximately 50% of the time to task failure,
while central nervous system fatigue increased to approximately 90% of the time to task
failure, and corticospinal excitability and inhibition were mostly unaffected. Rating of per-
ceived exertion increased linearly all the way through to task failure.

Practical implications
Central nervous system (CNS) fatigue arises during long-duration exercise, as measured
by changes in voluntary activation during short-duration, maximal effort contractions. The
accumulation of CNS fatigue seems to be closely related to the increasing perception of
effort, which probably arises due to increasing afferent feedback and progressively de-
creasing motivation to continue the exercise.

Task failure during sustained low-intensity contraction is not associated with

a critical amount of central fatigue. Souron, R., Voirin, A. C., Kennouche, D.,
Espeit, L., Millet, G. Y., Rupp, T., & Lapole, T. (2020). Scandinavian Journal of
Medicine & Science in Sports. (PubMed)
Background
Background
OBJECTIVE To examine the progression of central nervous system (CNS) fatigue
during a very low-intensity isometric contraction performed to task fail-
ure, in untrained males.

INTERVENTION
POPULATION
Subjects performed a sustained isometric contraction of the quad-
riceps muscles at 90o knee flexion at 10% of maximum voluntary 11 physically active
isometric contraction (MVIC) force to task failure (defined as being males, aged 24 ± 5
unable to maintain the required level of force for 3 seconds). Mea- years
surements of strength, CNS fatigue, and peripheral fatigue were
taken every 3 minutes during the contraction to assess their de-
velopment over time.

MEASUREMENTS RESULTS
Exercise duration The average duration of the contraction was 33 minutes,
with considerable individual variation (13 – 91 minutes).

Maximum strength: By MVIC
knee extension force.
MVIC force reduced significantly from 20 – 50% of the
time to task failure, but not thereafter. Thus, it appeared
to reduce non-linearly (it reduced more rapidly earlier in
the contraction) At the point of task failure, MVIC force
was reduced by 49%.

Voluntary activation: By stim- Voluntary activation reduced significantly from 40 – 90%

ulation of the motor cortex using of the time to task failure, but not thereafter. Thus, it ap-
transcranial magnetic stimula- peared to reduce largely linearly over time. At the point
tion (TMS) during MVICs. of task failure, voluntary activation had reduced by 21%.

Corticospinal excitability and MEP area and silent period duration reduced significantly
inhibition: By motor-evoked from 20% of the time to task failure, but not thereafter.
potential (MEP) area and cortical They reduced only slightly at the start of the contraction,
silent period duration, by TMS. and then remained constant thereafter.

Rating of perceived exertion: RPE increased almost linearly from 10% of the time to
By a visual analog scale. task failure through to 100% of the time to task failure.

Peripheral fatigue: By electri-
cal stimulation of the muscle to
produce twitches at 10Hz and
100Hz.
Twitch force was significantly decreased at task failure
(by 34%), indicating peripheral fatigue. Also, the ratio of
low-to-high frequency force was significantly decreased
at task failure (by 35%), indicating that there was some
excitation-contraction coupling failure.

SUMMARY
When untrained males performed a very low-intensity (10% of MVIC)
isometric contraction to task failure, strength reduced to approximately 50% of the time
to task failure, while central nervous system fatigue increased to approximately 90% of
the time to task failure, and corticospinal excitability and inhibition were mostly unaffect-
ed. Rating of perceived exertion increased linearly all the way through to task failure.
 Analysis

T his study reported that when untrained

males did a very low-intensity isometric
contraction (equivalent to 10% of maxi-
Importantly, voluntary activation only uses
measurements of force to identify the pres-
ence of CNS fatigue. It does not record
mum voluntary isometric contraction force) the electrical signals transmitted to and
to task failure, maximum strength reduced through the muscle by electromyography.
through to 50% of the time to reach task Therefore, the calculation is not subject to
failure before reaching a plateau. In con- the substantial limitations that are involved
trast, voluntary activation reduced more in recording muscle activation (2).
progressively and linearly through to 90%
of the time to reach task failure. This Additionally, as this study clearly shows,
steady, linear increase in the amount of voluntary activation is a very different
central nervous system (CNS) fatigue was measurement from corticospinal excitabil-
matched by a steady, linear increase in the ity and corticospinal inhibition. Measure-
self-reported rating of perceived exertion ments of these properties are often taken
(RPE) over the course of the contraction. after strength training workouts (3), and
after strength training programs (4), but
Voluntary activation is the gold standard there is a lack of agreement regarding
measurement for CNS fatigue during and what they signify. Theoretically, temporary
after exercise (1). It is calculated by com- changes in corticospinal excitability and in-
paring the amount of force that is produced hibition might indicate potentiation or CNS
during maximal, voluntary contractions fatigue, while long-term changes might
(usually isometric contractions) with the reflect adaptations. However, as demon-
amount of force that is produced during strated in this study, corticospinal excitabil-
maximal, voluntary contractions during ity and corticospinal inhibition often display
which an electrical stimulus is provided to very different changes during and after a
the motor point for the muscle or a tran- workout from the gold standard measure-
scranial magnetic stimulus is provided to ment of voluntary activation, suggesting
the motor cortex to produce an involuntary that other factors probably influence them.
contraction. If this stimulus can increase Indeed, there is evidence to suggest that
the force produced during the maximal, changes in corticospinal excitability and
voluntary contraction, then this indicates corticospinal inhibition are greatest when
an inability to recruit high-threshold motor the workouts involve more motor learning
units fully. This inability can reflect CNS (5,6), suggesting that these measurements
fatigue if it has occurred in response to a may also indicate that improvements in
bout of exercise. coordination are occurring.
 Analysis

I n the psychobiological model of exercise,

the brain produces a signal that creates
movement. This signal is called the “central
Increases in perceived effort during low–
intensity exercise seem to result from two
totally different sources.
motor command” and it is sent to the mus-
cles to stimulate motor unit recruitment. Firstly, they occur when peripheral fa-
Large signals create a high level of motor tigue reduces the force produced by the
unit recruitment, while smaller signals cre- working muscle fibers. This necessitates
ate a low level of motor unit recruitment. an increase in the level of motor unit re-
The central motor command also produces cruitment, which is produced voluntarily
a secondary signal, which is our perceived by increasing the level of central motor
level of effort. This perceived level of effort command. Since the level of central motor
therefore increases progressively as the command is a key input into the perceived
size of the central motor command (and level of effort, the perception of effort in-
the level of motor unit recruitment) both creases accordingly.
increase. However, we can only tolerate a
certain level of perceived effort for a given Secondly, increases in perceived effort
bout of exercise (but the exact level might occur because of afferent feedback from
vary according to our level of motivation). working muscles. During high-intensity
Therefore, there is a limit on how large the exercise, this afferent feedback proba-
central motor command can be, and how bly results from metabolite accumulation
many motor units can be recruited. (8). In low-intensity exercise, the afferent
feedback probably arises from other sourc-
In the psychobiological model of exercise es, including inflammation (9). When this
(7), central nervous system (CNS) fatigue afferent feedback contributes to increased
arises when either [A] the level of per- perception of effort, it does so without
ceived effort is increased by other factors altering the size of the central motor com-
(which do not simultaneously increase the mand and the level of motor unit recruit-
size of the central motor command), or [B] ment. Therefore, it creates CNS fatigue.
the level of motivation is reduced (although Interestingly, research has often shown
it is not clear whether motivation acts inde- that CNS fatigue accumulates steadily over
pendently of the level of perceived effort). time during long-distance exercise (10)
To the extent that perceived effort is the (a finding that was noted in this current
primary factor, CNS fatigue should increase study). Other research has similarly found
very closely in tandem with increases in that inflammation builds up gradually over
the rating of perceived exertion (RPE). time in much the same way (11).

I nterestingly, although the isometric
contraction was performed with 10% of
maximum voluntary isometric contraction
(MVIC) force, the reduction in maximum
strength at task failure was only 49%. The
reduction in voluntary activation contrib-
uted approximately 40% of this reduc-
tion, while peripheral fatigue contributed
the remaining 60%. This suggests that
when the subjects tested their maximum
strength and voluntary activation during
and then immediately after exercise, their
central nervous system (CNS) fatigue was
lower than during the exercise bout itself.
This discrepancy between the CNS fatigue
that is experienced during the long-dura-
tion, low-intensity exercise and during the
short-duration strength test might arise
from the influence of motivation on the
perceived level of effort.
Conclusions
When untrained males performed a very
low-intensity (10% of MVIC) isometric
contraction to task failure, strength re-
duced to approximately 50% of the time
to task failure, while central nervous
system fatigue increased to approximate-
ly 90% of the time to task failure, and
corticospinal excitability and inhibition
were mostly unaffected. Rating of per-
ceived exertion increased linearly all the
way through to task failure.
Analysis
Indeed, the psychological demands that
are involved in maintaining force levels
at a certain level indefinitely are different
from those that are involved in producing
a maximal amount of force for a very short
period of time. This difference might rea-
sonably be expected to affect the level of
motivation that is experienced during the
exercise bout, which in turn influences the
size of the central motor command (and
thus the level of motor unit recruitment).
This important finding demonstrates that
a certain amount of CNS fatigue during
long-duration, aerobic exercise may not be
apparent when measured using changes
in voluntary activation. However, whether
there are discrete elements of CNS fatigue
that can be identified and characterized as
caused by different mechanisms remains to
be established.
Practical implications
Central nervous system (CNS) fatigue
arises during long-duration exercise, as
measured by changes in voluntary activa-
tion during short-duration, maximal effort
contractions. The accumulation of CNS
fatigue seems to be closely related to
the increasing perception of effort, which
probably arises due to increasing afferent
feedback and progressively decreasing
motivation to continue the exercise.
 References
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 Reducing the force-velocity imbalance
enhances gains in maximum strength

T raditionally, strength coaches have programmed

heavy strength training, power exercises, and speed
exercises (such as plyometrics) for athletes, with a
view to enhancing the ability to produce force at various
different velocities. Even so, research has found that
each individual athlete likely has an optimal force-ve-
locity profile for any given athletic movement that
enables them to perform that movement most effective-
ly. Thus, altering a force-velocity profile can enhance
athletic performance in the same way as increasing the
ability to exert force at a fast or a slow velocity.

Key findings
In professional male rugby league players, a training program that was designed to re-
duce the force-velocity imbalance caused a greater improvement in maximum squat
strength and maximum theoretical force in a force-velocity profile test, as well as a great-
er improvement in vertical jump height, compared to a general strength training program
that incorporated both heavy strength training and power training exercises.

Practical implications
Testing athletes for their force-velocity profiles (and calculating force-velocity imbalances)
before starting a training program is a useful way of producing a greater improvement
in various athletic performance measures. However, the improvements are likely to be
greatest in those exercises or movements that are used to calculate the force-velocity
profile, so these should chosen carefully to reflect the demands of the sport.

Optimised force-velocity training during pre-season enhances physical perfor-

mance in professional rugby league players. Simpson, A., Waldron, M., Cushion,
E., & Tallent, J. (2020). Journal of Sports Sciences, 1-10. (PubMed)
Background
OBJECTIVE To compare the effects of general strength and power training with an
individualized training program intended to reduce the force-velocity
profile imbalance, in male rugby athletes.

INTERVENTION
POPULATION
Subjects did 3 workouts per week for 8 weeks, including 2 lower body
exercises in each workout. GEN did a balanced routine involving heavy 29 professional rugby
strength training exercises, power training exercises, and plyometrics. league athletes, aged 24
IND performed routines that varied between athletes, depending on ± 3 years, allocated into a
whether they were classified as having a low or high force deficit or a
general strength and pow-
low or high velocity deficit. Where athletes were classified as having a
er training group (GEN) or
force deficit, they trained with a greater proportion of heavy strength
individualized training to
training exercises and a smaller proportion of power training exercis-
reduce their force-velocity
es and plyometrics. Where athletes were classified as having a velocity
deficit, they used more power training exercises and plyometrics. profile imbalance (IND)

MEASUREMENTS RESULTS
Maximum strength: By 3RM IND achieved a significantly greater change in 3RM back
back squat. squat compared to GEN.

Sprint running performance: Sprint running performance did not change significantly
By 10m and 20m sprint times, in either group after training.
using timing gates.

Vertical jump height: By squat IND achieved a significantly greater improvement in

jump height using an iPhone squat jump height compared to GEN.
app.

Force-velocity profile: By Force-velocity profile

maximum theoretical force
(FMAX), maximum theoretical
velocity (VMAX), and the gradi-
ent of the force-velocity profile
(GRAD) during the squat jump
performed with a range of loads.
The force-velocity imbalance was
calculated as the difference be-
tween the optimal force-velocity
profile and the actual force-ve-
locity profile of each athlete.
IND achieved a significantly greater change in FMAX
and GRAD compared to GEN. However, GEN achieved
a significantly greater improvement in VMAX compared
to IND. This was probably because the subjects allocat-
ed to IND included a greater number of force-deficient
athletes than velocity-deficient athletes, and therefore
would have trained using a larger proportion of heavy
strength training exercises.
Force-velocity imbalance
IND achieved a significantly greater reduction in their
force-velocity imbalance compared to GEN.

SUMMARY
In professional male rugby league players, a training program that was
individualized to reduce the force-velocity imbalance caused a greater increase in maxi-
mum squat strength and maximum theoretical force in a force-velocity profile test, as well
as a greater improvement in vertical jump height, compared to a general strength training
program that incorporated both heavy strength training and power training exercises.

T his study reported that in professional
male rugby league players, a train-
ing program that was designed to reduce
the force-velocity imbalance caused a
greater improvement in maximum squat
strength and maximum theoretical force
during a force-velocity profile test, as well
as a greater improvement in vertical jump
height, compared to a general strength
training program that incorporated both
heavy strength training and power training
exercises in a standard volume allocation
for all athletes.
Analysis
Essentially, this study showed that when
athletes have force-velocity imbalances,
then training to remove these imbalances
is an effective way of improving athletic
ability. Previous studies have shown that
having a force-velocity imbalance has a
negative effect on performance in a move-
ment (1–3) and that reducing this imbal-
ance can improve performance (4–8). It
seems likely that testing the force-velocity
profile of athletes before embarking on a
training program is a relatively easy way to
maximize improvements from training.

V arious adaptations result from heavy
strength training that enhance the
maximum strength in a movement. These
include improvements in coordination (9),
reductions in antagonist muscle coactiva-
tion (10), increases in agonist motor unit
recruitment (11,12), increases in muscle
fiber size (13) and potentially also myo-
fibrillar density (14), increases in lateral
force transmission through an addition of
costameres (15,16), and increases in ten-
don stiffness (17,18). These adaptations
can be categorized into those that alter
the force-velocity gradient (by increasing
maximum theoretical force to a greater
extent than maximum theoretical velocity)
and those that do not (since they increase
maximum theoretical force and velocity to
the same extent).
Several adaptations that occur after heavy
strength training have a large effect on
maximum theoretical force, but do not
affect maximum theoretical velocity to the
same extent. These include improvements
in coordination, reductions in antagonist
coactivation, hypertrophy, and increases in
lateral force transmission. In contrast, oth-
er adaptations occur after heavy strength
training that improve maximum theoreti-
cal force and velocity to the same extent.
These include an increase in the recruit-
ment of the agonist muscle motor units,
and an improvement in myofibrillar density
(to the extent that this occurs).
Analysis
Various adaptations occur after fast move-
ment training that enhance maximum
velocity in a movement. These include im-
provements in exercise coordination (19),
reductions in antagonist muscle coactiva-
tion (20,21), increases in agonist motor
unit recruitment (22), increases in motor
unit firing rate (23), and increases in sin-
gle fiber contraction velocity (24). These
adaptations can be categorized into those
that alter the force-velocity gradient (by
increasing maximum theoretical velocity
more than maximum theoretical force) and
those that do not. Improvements in coor-
dination, reductions in antagonist coacti-
vation, increases in motor unit firing rate,
and increases in single fiber contraction
velocity all improve maximum theoretical
velocity, but do not enhance maximum
theoretical force to the same extent. In
contrast, increases in agonist motor unit
recruitment increase maximum theoretical
force and velocity to the same extent.
In addition to these specific adaptations
that occur after each type of training, one
other factor also influences the changes
in the force-velocity gradient. Since heavy
strength training tends to involve more
fatigue during each set compared to fast
movement training, it also tends to cause
a larger shift in muscle fiber type, which is
known to have a negative effect on max-
imum theoretical velocity, and thereby
shifts the force-velocity gradient (25).

I n this study, the primary exercise for
measuring the force-velocity imbalance
was the vertical jump. Most other simi-
lar studies have used the same exercise
(4–7) and only a small number have as-
sessed the force-velocity imbalance during
sprint running (8). In this study, reducing
the force-velocity imbalance was clearly
very beneficial for improving vertical jump
height, and yet had no similar positive ef-
fect on sprint running performance.
Importantly, the force-velocity imbalance
is probably movement-specific, and some
athletic movements are likely much more
velocity-dominant than others. Indeed,
given that the sprint involves a faster
movement speed and a shorter duration
of ground contact time in which to pro-
duce force, it is quite likely that individuals
who are velocity dominant (force deficient)
when measured by a vertical jump test
may not as velocity dominant (force defi-
cient) when measured in a sprinting test.
Indeed, several studies have shown that
sprinting speed tends to improve together
with either a constant force-velocity profile
or a shift towards a velocity dominant pro-
file (26–28). This has practical implications
for training athletes and for the selection of
force-velocity profile testing method that is
used prior to training. When athletes need
to prioritize sprinting performance, it may
be a better approach to use a sprint to
measure the force-velocity profile.
Analysis
In this study, the researchers found that
reducing the force-velocity imbalance had a
marked effect on maximum strength, such
that the group that trained with the indi-
vidualized (optimized) programs achieved
greater improvements in both maximum
theoretical force and 3RM back squat than
the group that used a general training
program. This might be taken to indicate
that reducing the force-velocity imbalance
during the vertical jump exercise was also
effective for enhancing maximum strength.
However, it is also important to note that
the group that trained with the individual-
ized (optimized) programs included a larg-
er number of athletes with a force deficit
(10 subjects) than with a velocity deficit
(5 subjects), and so the group on average
would have trained with a larger volume of
heavy strength training than was included
in the general training program (the way
in which force deficits are addressed is by
performing a larger proportion of heavy
strength training exercises and a smaller
proportion of power training exercises and
plyometrics). This may also explain why
the group that used the general training
program achieved a larger improvement in
maximum theoretical velocity compared to
the group that used optimized programs.
Indeed, it is unlikely that simply addressing
the force-velocity deficit itself was respon-
sible for reducing maximum theoretical
velocity.

Conclusions
In professional male rugby league play-
ers, a training program that was de-
signed to reduce the force-velocity deficit
caused a greater improvement in maxi-
mum squat strength and maximum the-
oretical force in a force-velocity profile
test, as well as a greater improvement
in vertical jump height, compared to a
general strength training program that
incorporated both heavy strength training
and power training exercises.
Analysis
Practical implications
Testing athletes for their force-veloci-
ty profiles (and then calculating their
force-velocity imbalances) before starting
a training program is a useful way of pro-
ducing a greater improvement in various
athletic performance measures. However,
the improvements are likely to be great-
est in those exercises or movements that
are used to calculate the force-velocity
profile, so these should chosen carefully
to reflect the demands of the sport.

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 Effects of wearable resistance on
sprinting biomechanics

S print running is an essential movement within

many team sports, and yet it has proven far
more difficult to improve through physical training
than other movements such as vertical jumping.
Various suggestions have been made for improving
the approach to physical training for sprinting, but
it remains a challenging area for development. Cur-
rently, many researchers are focusing on overload-
ing the sprinting movement itself by using resisted
sprinting in the form of either weighted sleds or
wearable resistance.

Key findings
In well-trained male track sprinters, using wearable resistance placed at the distal end
of the thigh equal to 2% of bodyweight (1% on each leg) during a sprint resulted in an
increase in sprint time but an increase in the angular work done at the hip joint. Howev-
er, there was no change to the hip joint angular range of motion during the sprinting gait
cycle, which suggests that movement patterns were not altered.

Practical implications
Using wearable resistance increases work done at the hip joint during sprinting. Since hip
work done is closely related to sprinting ability, it seems likely that this training method
will be effective for sprinters. Yet, by preferentially developing the hip musculature, it may
alter the relative contribution of the hip muscles during the sprinting movement. While
this is likely to be benefical for most athletes, it may not be ideal for all.

Thigh loaded wearable resistance increases sagittal plane rotational work of

the thigh resulting in slower 50-m sprint times. Macadam, P., Cronin, J. B.,
Uthoff, A. M., Nagahara, R., Zois, J., Diewald, S., & Neville, J. (2020). Sports
Biomechanics, 1-12. (Link)
Background
OBJECTIVE To find out whether adding wearable resistance to the thigh during
sprint running increases hip flexion and hip extension work done, in
male track sprinters.

INTERVENTION
POPULATION
Subjects did 2 sprints without wearable resistance and 2 sprints
with wearable resistance over a 50m distance from a block start, 15 male athletes, aged
with 10 minutes of rest between sprints. The wearable resistance 21.0 ± 2.5 years, with a
weighed 2% of bodyweight (1% on each leg) and was fitted to the 100m personal best time
distal end of the thigh to a pair of compression shorts using Velcro of 11.3 ± 0.5 seconds
attachments. Approximately two-thirds of each load was placed on
the anterior surface of the thigh, while the remaining one-third of
the load was placed on the posterior surface.

MEASUREMENTS RESULTS
Sprint time: By photocell tim- Sprint times when using wearable resistance were
ing gates positioned at 10m and non-significantly slower at 10m (by 1.4%), and signifi-
50m of the 50m sprint. cantly slower at 50m (by 1.9%).

Hip joint angle movements: Hip joint angular range of motion

By a wearable inertial measure-
ment unit fitted to the left thigh
of each athlete.
Hip joint angular range of motion did not differ signifi-
cantly between the wearable resistance and unresisted
sprints. This suggests that the movement patterns of the
sprints were not substantially affected by the addition of
the wearable resistance.

Hip joint angular velocities

N.B. For analysis, the sprint was With the exception of hip extension angular velocity in
divided into three acceleration the first phase of the sprint, hip extension and hip flexion
phases: (1) steps 1–2, (2) steps angular velocities was significantly reduced in all three
3–6, and (3) steps 7–10. phases of the sprint when using wearable resistance.

Hip work done: By a wearable Work done by the hip extensors and hip flexors was sig-
inertial measurement unit fitted nificantly greater when wearing wearable resistance in
to the left thigh of each athlete. each of the three acceleration phases of the sprint.

SUMMARY
In well-trained male track sprinters, using wearable resistance placed
at the distal end of the thigh equal to 2% of bodyweight (1% on each leg) during a sprint
resulted in an increase in sprint time but an increase in the angular work done at the hip
joint. However, there was no change to the hip joint angular range of motion during the
sprinting gait cycle, which suggests that movement patterns were not altered.

T his study reported that in well-trained
male track sprinters, using wearable
resistance placed at the distal end of the
thigh equal to 2% of bodyweight (1% on
each leg) during a sprint resulted in an
increase in sprint time but an increase in
the angular work done at the hip joint in
the sagittal plane (in both hip flexion and
also in hip extension). However, there was
no change to the hip joint angular range
of motion during the sprinting gait cycle,
which suggests that movement patterns
were not altered.
Analysis
Although several previous studies have
investigated the biomechanics of wearable
resistance during running both overground
and using treadmills (1–7), this is the first
study to show that wearable resistance
increases the work done by the hip flexors
and hip extensor during maximal effort,
overground sprint running. This is an im-
portant finding, because analyses of sprint
running biomechanics have shown that hip
flexor and hip extensor work done during
the sprint running gait cycle are closely
related to sprinting performance (8,9).

T he fact that using wearable resistance
resulted in higher hip extension and
hip flexion power outputs (work done over
time) suggests that maximal sprint running
does not involve optimal power output for
these muscle groups. Rather, it seems like-
ly that these muscle groups produce opti-
mal power outputs at slower velocities.
Several researchers have now shown that
athletes have specific force-velocity (FV)
profiles during vertical jumping (10) and
during sprint running (11), and that there
is an optimal FV profile for each athlete
during each of these movements that leads
to maximal power output being produced
by the overall system. Consequently, if an
athlete displays a FV profile that is sub-
stantially different from the optimal one,
they can improve their performance in a
movement by altering its gradient (and this
can change performance even without al-
tering either maximum force or maximum
velocity). Training that involves mainly fast
movements without load tends to shift the
FV profile to become more velocity-dom-
inant, while training that involves mainly
slow movements against heavy loads tends
to shift the FV profile to become more
force-dominant (12,13). By selecting the
appropriate type of training, an athlete
can maximize the effects of their training
programs by ensuring that maximal pow-
er is produced by the body in the targeted
movement at the right speed.
Analysis
Nevertheless, previous research has shown
that the FV profile of the body during verti-
cal jumps and squats does not necessarily
maximize power output at each joint (14–
16). Instead, it maximizes power output
of the whole system, which necessarily
requires compromises from each of the
joints to allow higher overal performance
from all joints working together. In fact,
power output can be maximized at specif-
ic joints by using loads that do not max-
imize power output of the whole system.
In this respect, it is very interesting that
power output of the hip joint is sometimes
maximized by using a heavier load than
maximizes the power output of the whole
system (16). This seems to fit well with the
findings of this study, assuming that the
majority of the athletes in this study dis-
played a FV profile for sprint running that
was reasonably close to the optimal one.
It is interesting to speculate about what
might happen as a result of training the hip
joint at a velocity that maximizes its pow-
er output (even though the power output
of the whole system may not be similar-
ly maximized). In considering this issue,
there are actually two completely different
questions: [A] what adaptations occur as
a result of training at a velocity that max-
imizes power output? And [B] how does
altering the maximum power output of one
joint affect the coordination of the system?

1. Adaptations at maximal power
Heavy strength training increases maxi-
mum strength through mechanisms inside
both the central nervous system (CNS) and
inside the muscle-tendon unit. These adap-
tations are reflected by increases in maxi-
mum theoretical force on the force-veloc-
ity (FV) profile. Fast movement training
increases maximum speed by means of
mechanisms inside both the CNS and in-
side the muscle. Such adaptations are re-
flected by increases in maximum theoreti-
cal velocity on the FV profile. Also, exercise
can alter the gradient of the FV profile by
performing a balance of strength training
and fast movement training, which alters
the point on the FV profile at which maxi-
mal power is produced. This third change
is caused by a larger or smaller change in
maximum theoretical force relative to the
change in maximum theoretical velocity.
Adaptations are stimulated by high tension
(in the case of maximal theoretical force),
a fast speed (in the case of maximal the-
oretical velocity), or a high effort (in both
cases). There are no adaptations that are
specifically stimuluated by producing a
high power output (which is a combination
of submaximal force and submaximal ve-
locity). Therefore, it is not clear how simply
achieving a high power output during an
exercise would produce superior adapta-
tions to producing either high mechanical
tension or high velocities.
Analysis
2. Impact on the whole system
There are indications that the relative con-
tributions of the muscle groups that con-
tribute to a movement can alter as a result
of training performed for one of the muscle
groups. For example, when single-joint hip
extension exercise is performed for the
gluteus maximus, this increases the contri-
bution of that muscle in multi-joint hip and
knee extension exercise, as shown by an
increase in corticospinal excitability and a
reduction in corticospinal inhibition, which
suggests that the motor unit recruitment
level of the muscle was increased (17).
Also, research has shown that muscles of
a group tend to be activated in proportion
to their size, with larger muscles receiving
proportionally higher levels of activation
and therefore contributing more to a move-
ment (18–20), likely because of the prin-
ciple of neuromechanical matching (21).
Thus, hypertrophy of a muscle group might
be expected to increase the contribution of
that muscle group to a movement.
This observation suggests that when mul-
tiple muscles are involved in a movement
(such as sprinting), then training one of
the major muscle groups (such as the hip
extensors) to a greater extent than the
others will likely increase the proportional
contribution of that muscle to the overall
movement. This is important, since that is
probably what happens after we train with
wearable resistance.

T herefore, wearable resistance train-
ing will likely increase the proportional
contribution of the hip extensors and flex-
ors to the sprinting movement. As with the
force-velocity (FV) profile of a movement,
athletes may also have joint contribution
profiles, since all movements necessari-
ly involve a compromise across all of the
joints that contribute. Yet, there may be
an optimal joint contribution profile that
can be attained, in which all joints produce
power close to their optimal level. Thus, it
seems likely that wearable resistance may
be very effective if it moves the joint con-
tribution profile towards the optimal one
(by increasing the relative contribution of
the hip extensors and flexors), but less
effective if it moves the joint contribution
profile away from the optimal one.
Conclusions
In well-trained male track sprinters,
using wearable resistance placed at the
distal end of the thigh equal to 2% of
bodyweight (1% on each leg) during a
sprint resulted in an increase in sprint
time but an increase in the angular work
done at the hip joint. However, there was
no change to the hip joint angular range
of motion during the sprinting gait cycle,
which suggests that movement patterns
were not altered.
Analysis
Nevertheless, given that the sprint running
movement is ultimately limited by the pos-
itive work done by the hip extensors and
flexors (8,9), it seems very likely that the
optimal joint contribution profile for sprint
running involves a large contribution from
the more proximal muscles of the body.
Consequently, to the extent that these
muscles increase their contributions, this is
likely to bring about an immediate increase
in sprint running performance in most
cases, with the end result that wearable
resistance may prove to be a very effective
training method for most athletes. Even so,
future research will need to compare this
form of training with conventional methods
such as heavy strength training, plyomet-
rics, and resisted, unresisted, and assisted
sprint running.
Practical implications
Using wearable resistance increases work
done at the hip joint during sprinting.
Since hip work done is closely related
to sprinting ability, it seems likely that
this training method will be effective for
sprinters. Yet, by preferentially develop-
ing the hip musculature, it may alter the
relative contribution of the hip muscles
during the sprinting movement. While
this is likely to be benefical for most ath-
letes, it may not be ideal for all.

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 Can we model strength training
workouts as stressors?

T raditionally, strength training workouts have been

treated as stressors in the context of the general
adaptation syndrome model, which proposes that all
stressors produce similar stress responses, which can
be acclimatized to over time, so long as they are not
excessive. Excessive stressors lead to weakening and
sickness. Stress responses can be categorized into two
pathways: the sympathetic adrenomedullary system
(which can be detected by changes in catecholamines),
and the hypothalamic-pituitary-adrenal (HPA) axis
(which can be detected by changes in cortisol).

Key findings
When strength-trained males perform a workout, they experience an increase in per-
ceived stress, an increase in sympathetic nervous system activity, and a reduction in
parasympathetic nervous system activity during the workout. Following the workout,
there is a rebound in parasympathetic nervous system activity. Yet, there is no sign of any
hypothalamic-pituitary-adrenal (HPA) axis stress response after exercise.

Practical implications
While strength training does display a stress response (and might therefore be modeled
as a stressor within the context of the general adaptation syndrome), it does not always
display stress responses in both of the key systems. The sustained fatigue that occurs af-
ter a strength training workout is likely better understood by reference to the mechanisms
of fatigue rather than by reference to the autonomic nervous system.

Resistance training as an acute stressor in healthy young men: associations

with heart rate variability, alpha-amylase, and cortisol levels. Becker, L., Sem-
mlinger, L., & Rohleder, N. (2020). Stress, 1-13. (PubMed)
Background
Background
OBJECTIVE To assess the stress responses in the sympathetic nervous system
(SNS) and in the hypothalamic-pituitary-adrenal (HPA) axis to a
strength training workout, in young, strength-trained males.

INTERVENTION
POPULATION
Subjects did a single workout involving 4 self-selected upper or
lower body strength training exercises that were each performed 45 strength-trained
for 4 sets of 10 reps to failure. The load was initially set as a males, aged 22.4 ± 2.0
10RM load, but this was adjusted downwards if 10 reps could not years (of whom 38 sub-
be achieved on any given set. Rest periods of 90 – 120 seconds jects chose to perform
were performed between sets. solely upper body exer-
cises)

MEASUREMENTS
Sympathetic nervous system
(SNS) activation: By salivary
markers of a-amylase.
RESULTS
Salivary markers of a-amylase increased significantly
from baseline to during the workout, indicating an in-
crease in SNS activation. Levels returned to baseline
immediately after the workout.

Hypothalamic-pituitary-adre- Salivary cortisol levels did not change from baseline to

nal (HPA) axis activation: By during the workout, but reduced from baseline to after
salivary markers of cortisol. the workout. Salivary cortisol levels after the workout
were significantly greater in those lifters who selected
lower body exercises.

Parasympathetic nervous RMSSD decreased significantly from baseline to during

system (PNS) activation: By
heart rate variability (HRV) root
mean square of successive dif-
ferences of successive R-R inter-
vals (RMSSD), with a heart rate
monitor.
the workout, which indicates a reduction in PNS activity.
Immediately after the workout, RMSSD increased sig-
nificantly compared to during the workout, indicating a
rebound in PNS activity.

Level of perceived stress: By Perceived stress increased significantly from baseline

a 10-point Likert scale ranging to during the workout. Levels returned to baseline after
between “not stressed at all” the workout.
and “extremely stressed.”

Level of affect: By the Positive Positive affect increased significantly immediately after
and Negative Affect Schedule the workout, while negative affect did not change.
(PANAS) questionnaire.

SUMMARY
When strength-trained males perform a workout, they experience an
increase in perceived stress, an increase in sympathetic nervous system activity, and a
reduction in parasympathetic nervous system activity during the workout. Following the
workout, there is a rebound in parasympathetic nervous system activity. Yet, there is no
sign of any hypothalamic-pituitary-adrenal (HPA) axis stress response after exercise.

T his study reported that when strength-
trained males perform a workout,
they experience an increase in perceived
stress, an increase in sympathetic nervous
system (SNS) activity, and a reduction in
parasympathetic nervous system (PNS)
activity during the workout. After the work-
out, there is a rebound in parasympathetic
nervous system activity. Yet, there is no
sign of any hypothalamic-pituitary-adrenal
(HPA) axis stress response after exercise.
Traditionally, strength training workouts
have been treated as acute stressors with-
in the general adaptation syndrome (GAS)
model (1,2). The GAS model proposes that
every stressor produces a similar stress re-
sponse, and that as an animal acclimatizes
to any particular stressor, the magnitude
of this stress response reduces. Failure to
acclimatize to the stressor can lead to a
potentially-damaging stress response that
weakens the animal, causing it to sicken
(3). There are two main stress response
systems: the sympathetic adrenomedullary
system (which involves the SNS and PNS),
and the HPA axis (4). The sympathet-
ic adrenomedullary system switches the
body between the “fight or flight” response
(which involves increased heart rate and
blood pressure as well as an elevated level
of systemic catecholamines) and the “rest
and digest” response (which involves re-
duced heart rate and blood pressure).
Analysis
The HPA axis manages cortisol release,
while is a secondary stress response that
occurs after an animal has been exposed
to a stressor. Psychologists have noted
that this stress response occurs in greater
magnitudes when a stressor is perceived to
be difficult to either control or predict. In
contrast to the sympathetic adrenomedul-
lary system, it is somewhat less involved in
preparing animals for exercise (4).
We might reasonably expect strength train-
ing workouts to produce increases in SNS
activity (and reductions in PNS activity) in
order to permit the body to function opti-
mally during exercise (which requires an
elevated heart rate and blood pressure).
Similarly, we might reasonably expect the
period immediately after strength train-
ing workouts to involve decreases in SNS
activity (and increases in PNS activity) as
the body returns to its resting state. Yet,
unless workouts were unaccustomed (and
therefore unpredictable) or prescribed (and
therefore not controllable), we might not
expect a strong HPA axis response.
Indeed, this study largely confirmed the
expected results. There were increases in
SNS activity (and reductions in PNS activi-
ty) during exercise, followed by decreases
in SNS activity (and increases in PNS ac-
tivity) immediately after the workout, but
there was no HPA axis upregulation.

N evertheless, while some studies simi-
larly show little change in cortisol after
a workout, other studies have found that
strength training workouts can elevate
cortisol levels (5–10). Since such respons-
es are more pronounced when workouts
are higher in volume or use larger muscle
mass, this may be because of the minor
role that cortisol does play in glucose me-
tabolism (11). Alternatively, it is possible
that some of the workouts may have been
perceived by the subjects as unaccustomed
(and therefore unfamiliar) or contrary to
their own choices for training (and so they
therefore lacked control). Indeed, a key
strength of this study was the use of a
self-selected workout by the subejcts.
Some researchers have suggested that
autonomic nervous system (ANS) recovery
(as indicated by an increase in SNS activity
and an increase in PNS activity) might be
a good way to monitor recovery from all
types of exercise. Strength training fatigue
is caused by excitation-contraction cou-
pling failure, myofibrillar damage, and cen-
tral nervous system fatigue that is in turn
caused by the myofibrillar damage. To the
extent that these fatigue mechanisms send
afferent feedback to the brain and spinal
cord, the strength losses should be reflect-
ed by changes in ANS activity. In contrast,
if any of these mechanisms do not provide
this feedback, then ANS recovery will occur
before strength recovery (12).
Analysis
On the one hand, it seems likely that there
is some feedback to the ANS as a result
of myofibrillar damage, because workouts
that use electrical stimulation cause very
pronounced myofibrillar damage (13) and
also cause an elevated SNS response (14).
Indeed, it is logical that myofibrillar dam-
age would provide some afferent feedback
that affects the ANS, since it likely causes
central nervous system fatigue through
similar afferent feedback pathways involv-
ing inflammatory mediators (15–17).
Nevertheless, there is evidence that ANS
recovery and strength recovery do not oc-
cur perfectly in parallel, and this suggests
that at least one mechanism of sustained
fatigue does not provide afferent feedback
to the ANS. Indeed, recent research has
shown that strength training with the same
number of total reps in a workout but with
each set taken closer to failure involves
slower strength recovery, but similar ANS
recovery (12). Given that full ANS recovery
can occur after two similar workouts and
yet one workout can display a more pro-
longed reduction in strength due to fatigue,
it seems likely that at least one mechanism
of fatigue does not provide feedback. This
is most likely to be excitation-contraction
coupling failure, since there is evidence
that myofibrillar damage causes afferent
feedback, and since excitation-contraction
coupling failure is known to be greater
when training closer to failure (18,19).
Illustration

Conclusions
When strength-trained males perform
a workout, they experience an increase
in perceived stress, an increase in sym-
pathetic nervous system activity, and a
reduction in parasympathetic nervous
system activity during the workout. Fol-
lowing the workout, there is a rebound in
parasympathetic nervous system activi-
ty. Yet, there is no sign of any hypotha-
lamic-pituitary-adrenal (HPA) axis stress
response after exercise.
Analysis
Practical implications
While strength training does display a
stress response (and might therefore be
modeled as a stressor within the context
of the general adaptation syndrome), it
does not always display stress responses
in both of the key systems. The sustained
fatigue that occurs after a strength train-
ing workout is likely better understood by
reference to the mechanisms of fatigue
rather than by reference to the autonom-
ic nervous system.

1. Cunanan, A. J., DeWeese, B. H., Wagle, J. P., Carroll, K.
M., Sausaman, R., Hornsby, W. G., & Stone, M. H. (2018).
The general adaptation syndrome: a foundation for the
concept of periodization. Sports Medicine, 48(4), 787-
797. (PubMed)
2. Buckner, S. L., Mouser, J. G., Dankel, S. J., Jessee, M.
B., Mattocks, K. T., & Loenneke, J. P. (2017). The general
adaptation syndrome: Potential misapplications to resis-
tance exercise. Journal of Science and Medicine in Sport,
20(11), 1015-1017. (PubMed)
3. Selye, H. (1950). Stress and the general adapta-
tion syndrome. British Medical Journal, 1(4667), 1383.
(PubMed)
4. Koolhaas, J. M., Bartolomucci, A., Buwalda, B., de
Boer, S. F., Flügge, G., Korte, S. M., & Richter-Levin, G.
(2011). Stress revisited: a critical evaluation of the stress
concept. Neuroscience & Biobehavioral Reviews, 35(5),
1291-1301. (Link)
5. Smilios, I., Pilianidis, T., Karamouzis, M., & Tokmakidis,
S. P. (2003). Hormonal responses after various resistance
exercise protocols. Medicine & Science in Sports & Exer-
cise, 35(4), 644. (PubMed)
6. Beaven, C. M., Gill, N. D., & Cook, C. J. (2008). Sali-
vary testosterone and cortisol responses in professional
rugby players after four resistance exercise protocols. The
Journal of Strength & Conditioning Research, 22(2), 426-
432. (PubMed)
7. Crewther, B., Cronin, J., Keogh, J., & Cook, C. (2008).
The salivary testosterone and cortisol response to three
loading schemes. The Journal of Strength & Conditioning
Research, 22(1), 250-255. (PubMed)
8. Uchida, M. C., Crewther, B. T., Ugrinowitsch, C., Ba-
curau, R. F., Moriscot, A. S., & Aoki, M. S. (2009). Hor-
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of similar total volume. The Journal of Strength & Condi-
tioning Research, 23(7), 2003. (PubMed)
9. McCaulley, G. O., McBride, J. M., Cormie, P., Hudson,
M. B., Nuzzo, J. L., Quindry, J. C., & Triplett, N. T. (2009).
Acute hormonal and neuromuscular responses to hy-
pertrophy, strength and power type resistance exercise.
European Journal of Applied Physiology, 105(5), 695-704.
(PubMed)
10. Villanueva, M. G., Villanueva, M. G., Lane, C. J., &
Schroeder, E. T. (2012). Influence of rest interval length
on acute testosterone and cortisol responses to vol-
ume-load-equated total body hypertrophic and strength
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search, 26(10), 2755. (PubMed)
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recovery in trained men: a randomized cross-over study.
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 Effects of training to failure on the
rate of recovery from a workout

S trength training workouts cause sustained

fatigue, which is the combined effect of three
fatigue mechanisms (excitation-contraction coupling
failure, myofibrillar damage, and central nervous
system fatigue). Additionally, to the extent that the
workout activates the sympathetic nervous system
(SNS) and the hypothalamic-pituitary-adrenal (HPA)
axis, it may result in a stress response that impacts
on the autonomic nervous system and affects sleep
quality and heart rate variability (HRV). However,
fatigue need not be related to stress responses.

Key findings
In strength-trained males, a strength training workout involving training to failure pro-
duced more long-lasting reductions in maximum strength compared to a workout involv-
ing the same total number of reps but stopping two reps before failure. However, there
were no differences between the two workouts in respect of (objective or subjective)
sleep quality or heart rate variability.

Practical implications
Stopping two reps before failure is a very effective way of reducing the amount of fatigue
that occurs from a strength training workout. However, differences in fatigue between
workouts that involve training to failure and workouts that involve stopping short of fail-
ure may not be observable in measures that assess the magnitude of the stress response,
such as heart rate variability and sleep quality.

Effects of resistance training intensity on the sleep quality and strength re-
covery in trained men: a randomized cross-over study. Ramos-Campo, D.,
Martínez-Aranda, L. M., Caravaca, L. A., Ávila-Gandí, V., & Rubio-Arias, J. Á.
Biology of Sport, 37(1), 81-88. (Link)
Background
OBJECTIVE To compare the effects of workouts involving training to failure and
training while stopping two reps before failure on maximum strength,
sleep quality, heart rate variability, in strength-trained males.

INTERVENTION
POPULATION
Subjects all performed two workouts involving 40 reps of the back
squat and bench press exercises on separate days. One workout 15 strength-trained
involved training to failure, while the other involved stopping short males, aged 23.4 ± 2.4
of failure. Training to failure involved 4 sets of 10 reps with ap- years
proximately 75% of 1RM and 90 seconds of rest between sets.
Training while stopping short of failure involved 5 sets of 8 reps
with approximately 75% of 1RM and 90 seconds of rest between
sets. Bar speed was measured during each set to ensure that the
intended proximity to failure was attained.

MEASUREMENTS
Maximum strength: By 1RM
back squat and 1RM bench
press.
RESULTS
The workout involving training to failure produced a
significant reduction in 1RM bench press and 1RM back
squat when measured 24 hours afterwards, while the
workout that involved the same number of reps but
without training to failure did not.

Sleep quality: By actigraphy,
which measures nocturnal activ-
ity using an accelerometer, and
by subjective sleep quality using
the Karolinska Sleep Diary (KSD)
questionnaire.
Sleep quality did not alter significantly as a result of ei-
ther workout, when measured by the accelerometer and
also when measured by the sleep diary. Also, there were
no differences between the workouts in respect of the
changes in sleep quality.

Heart rate variability (HRV): None of the HRV measures altered significantly as a
By a heart rate monitor worn result of either workout. Also, there were no differences
during sleep. between the workouts in respect of the changes in HRV
measures.

SUMMARY
In strength-trained males, a strength training workout involving train-
ing to failure produced more long-lasting reductions in maximum strength compared to
a workout involving the same total number of reps but stopping two reps before failure.
However, there were no differences between the two workouts in respect of (objective or
subjective) sleep quality or heart rate variability.

T his study reported that in strength-
trained males, a strength training
workout involving training to failure pro-
duced more long-lasting reductions in
maximum strength compared to a work-
out involving the same number of reps
but stopping two reps before failure. This
agrees with the small number of previous
studies comparing volume-matched work-
outs involving training to failure and stop-
ping short of failure (1), as well as with
other similar studies involving similar (but
not volume-matched) comparisons (2–6).
Analysis
The key finding of this study was that the
reduction in strength that was observed
at 24 hours after the workout was actu-
ally not mirrored by any changes in sleep
quality or heart rate variability (HRV). This
is important, because such measurements
are often taken by athletes to monitor their
rate of recovery after workouts. This study
suggests that while such measurements
may be helpful for monitoring autonomic
nervous system recovery from stress, but
they likely do not also capture sufficient
information about local muscular recovery.

D uring any bout of exercise, motor units
are recruited to activate their muscle
fibers. These muscle fibers then experience
excitation-contraction coupling, which puts
calcium ions into the cytoplasm to trigger
the binding of myosin heads to actin, which
produces the crossbridges that generate
force. The calcium ions that are sent into
the cytoplasm are usually immediately tak-
en back up into the sarcoplasmic reticulum.
However, this process is not perfect, and
some calcium ions escape, and drift further
into the muscle fiber. These calcium ions
trigger multiple fatigue mechanisms both
during and after exercise.
Two important fatigue mechanisms that
contribute to sustained strength loss after
exercise are excitation-contraction coupling
failure and myofibrillar damage. Long-last-
ing excitation-contraction coupling failure
and myofibrillar damage are likely caused
by proteases known as calpains (7–10).
These calpains are released by the muscle
fiber in response to the presence of the
calcium ions within the muscle fibers. Exci-
tation-contraction coupling failure is caused
when these proteases damage the minor
triadic proteins that hold the voltage sen-
sor of the transverse tubules near to the
calcium ion store of the sarcoplasmic re-
ticulum (11), causing the two structures to
move apart. Myofibrillar damage is caused
when calpains damage the myofilaments
and the cytoskeletal structures (7).
Analysis
The effect of calpains within muscle fibers
is essentially determined by how many
calcium ions are left to roam free inside
the cytoplasm once the fiber is deactivat-
ed and the excitation-contraction coupling
process has finished. This is affected by the
number of mitochondria inside the mus-
cle fibers, since one important action of
the mitochondria is to remove these free-
ly-moving calcium ions from the cytoplasm
(12). Consequently, since slow twitch
muscle fibers have many more mitochon-
dria for the same volume of muscle fiber,
they are far less likely to suffer from either
excitation-contraction coupling failure or
myofibrillar damage than fast twitch mus-
cle fibers. While the greater susceptibility
of fast twitch muscle fibers to sustained
fatigue after a workout has been known for
a long time (13,14), it is only recently that
researchers have identifed that this greater
fatigue involves a higher degree of exci-
tation-contraction coupling failure as well
as more myofibrillar damage (15)
Consequently, strength training workouts
have the potential to cause more sus-
tained fatigue after a workout than aero-
bic exercise bouts, since strength training
workouts involve the recruitment of more
high-threshold motor units (and therefore
the activation of a greater number of more
easily-fatigued fast twitch muscle fibers)
than aerobic exercise bouts.

C ontrary to popular belief, central ner-
vous system (CNS) fatigue does con-
tribute to sustained fatigue after a strength
training workout (16,17). However, this
CNS fatigue is not caused by reaching high
levels of motor unit recruitment during a
workout, as can be identified by looking
at the recovery of strength after a power
training workout (18). In fact, CNS fatigue
is most likely caused by an inflammatory
response to myofibrillar damage, in the
same way that CNS fatigue during bouts of
aerobic exercise is caused by the inflam-
matory response that occurs (19). There-
fore, CNS fatigue can be considered as a
secondary effect arising from muscle dam-
age, rather than as an effect that occurs
due to any other characteristic of a work-
out (such as training to failure). Put anoth-
er way, CNS fatigue is not triggered by us-
ing a high level of effort during a workout,
but is instead the result of triggering a high
level of myofibrillar damage. Since myo-
fibrillar damage is greater in fast twitch
muscle fibers, CNS fatigue will necessar-
ily be more pronounced after workouts
that involve a higher level of motor unit
recruitment, but this high level of motor
unit recruitment is not sufficient to trigger
the myofibrillar damage that causes CNS
fatigue. Rather, the activation of the mus-
cle fibers must continue during a set for a
sufficiently long time to trigger the calpain
release that causes excitation-contraction
coupling failure and myofibrillar damage.
Analysis
Indeed, previous research has shown that
excitation-contraction coupling failure takes
time to occur, and tends to be observed
towards the end of a task, close to task
failure (20,21). This probably happens be-
cause of the cumulative effects of calcium
ion accumulation, which can be terminated
once the muscle fiber is no longer being
activated.
This study confirms this model of sustained
fatigue after a workout, because it found
that fatigue lasted longer when training to
failure compared to when training while
stopping two reps before failure. It seems
likely that the levels of motor unit recruit-
ment would have been fairly similar in
both cases, which suggests that the num-
ber of fast twitch muscle fibers that were
trained in both cases would have been
similar. Therefore, how many fast twitch
fibers were activated cannot explain the
differences in the recovery rates after each
workout. Rather, it seems likely that it was
the duration of activation of the fast twitch
muscle fibers during each set that caused
the differences in fatigue. When training to
failure, the fast twitch fibers were activated
for longer during each set, and this pro-
vided a sufficient length of time for calci-
um overload to occur and thereby trigger
excitation-contraction coupling failure and
myofibrillar damage. In contrast, stopping
two reps before failure avoided the majori-
ty of these negative effects.

Conclusions
In strength-trained males, a strength
training workout involving training to
failure produced more long-lasting reduc-
tions in maximum strength compared to
a workout involving the same total num-
ber of reps but stopping two reps before
failure. However, there were no differenc-
es between the two workouts in respect
of (objective or subjective) sleep quality
or heart rate variability.
Analysis
Practical implications
Stopping two reps before failure is a very
effective way of reducing the amount
of fatigue that occurs from a strength
training workout. However, differences
in fatigue between workouts that involve
training to failure and workouts that in-
volve stopping short of failure may not be
observable in measures that assess the
magnitude of the stress response, such
as heart rate variability and sleep quality.

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(2020). Acute effects of equated volume-load resistance
training leading to muscular failure versus non-failure on
neuromuscular performance. Journal of Exercise Science
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5. Pareja-Blanco, F., Rodríguez-Rosell, D., Sánchez-Medi-
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 Effects of strength training at long
and short maximum muscle lengths

M uscle fibers increase in size after they are

exposed to mechanical tension. This tension can
be provided either by active forces generated by the
muscle fiber, or by passive forces imposed by the
external environment. When muscles reach longer
lengths during a strength training exercise, they typ-
ically experience higher passive forces. This is why
strength training with a larger range of motion (or
more accurately, a more stretched position during
an exercise range of motion) causes greater muscle
growth than a smaller range of motion.

Key findings
In untrained subjects, strength training which involves muscles reaching a long maximum
muscle length on each rep (as the hamstrings do during a seated leg curl) tends to cause
greater hypertrophy than strength training which involves muscles reaching a short max-
imum muscle length (as the hamstring do in a lying prone leg curl). Yet, the two types of
exercise cause similar protection against sustained post-workout fatigue.

Practical implications
Strength training exercises that involve reaching different maximum muscle lengths (ei-
ther because of a difference in a position of the neighboring joint or due to a difference in
the range of motion) are likely to produce differences in regional hypertrophy (both within
muscles and within muscle groups). Bodybuilders may therefore benefit from using a va-
reity of exercises and exercise ranges of motion.

Greater Hamstrings Muscle Hypertrophy but Similar Damage Protection after

Training at Long versus Short Muscle Lengths. Maeo, M., Meng, H., Yuhang, W.,
Sakurai, H., Kusagawa, Y., Sugiyama, T., Kanehisa, H., & Isaka, T. (2020).
Medicine & Science in Sports & Exercise.
Background
Background
OBJECTIVE To compare the effects of strength training in which muscles reach long
and short maximum muscle lengths on gains in muscle size and on the
magnitude of the repeated bout effect, in untrained individuals.

INTERVENTION
POPULATION
Study one: Subjects did 2 workouts per week for 12 weeks. Each
workout involved seated leg curls for one leg and lying prone leg curls 20 young, untrained sub-
for the other leg, for 5 sets of 10 reps with 70% of 1RM, with 2-second jects (study one and two)
lifting and lowering phases, and 2 minutes of rest between sets. and 12 young, untrained
subjects (study two only)
Study two: After the training program, the subjects did a single
workout involving seated eccentric-only leg curls for one leg and lying
prone eccentric-only leg curls for the other leg, for 3 sets of 10 reps
with 90% of 1RM, with 2-second lowering phases. An untrained group of
subjects did the same workout as a comparison group.

MEASUREMENTS
Muscle size: By muscle an-
atomical cross-sectional area
and volume of each hamstrings
muscle, using magnetic reso-
nance imaging (MRI) scans.
RESULTS
Anatomical cross-sectional area (ACSA)
Training to a longer maximum muscle length (with a seat-
ed leg curl) produced significantly greater increases in
biceps femoris and semitendinosus proximal region ACSA,
as well as biceps femoris distal region ACSA.

Muscle volume (MV)

Increases in semitendinosus, biceps femoris (long head),
and semimembranosus MV were significantly greater af-
ter training with a longer maximum muscle length (with a
seated leg curl) but the increase in sartorius MV was sig-
nificantly greater after training with a shorter maximum
muscle length (with a prone leg curl).

Sustained post-workout
fatigue: By 1RM of the exer-
cise used in training before the
workout and at 24, 48, and 72
hours afterwards.
1RM reduced significantly more after the test workout in
the untrained subjects than in the trained subjects. How-
ever, 1RM reduced similarly after the test workout in both
the seated leg curl and the prone leg curl.

Muscle damage: By the trans-
verse relaxation time (T2)
recorded using MRI scanning
before the workout and at 24,
48, and 72 hours afterwards.
T2 relaxation time increased significantly more in each
muscle after the test workout in the untrained subjects
than in the trained subjects. However, T2 relaxation time
increased similarly after the test workout in both the seat-
ed leg curl and the prone leg curl.

SUMMARY
In untrained subjects, strength training which involves muscles reach-
ing a long maximum muscle length on each rep (as the hamstrings do during a seated leg
curl) tends to cause greater hypertrophy than strength training which involves muscles
reaching a short maximum muscle length (as the hamstring do in a prone leg curl). Yet,
the two types of exercise cause similar protection against sustained post-workout fatigue.

T his study reported that in untrained
subjects, strength training which in-
volves muscles reaching a long maximum
muscle length on each rep (as the ham-
strings do during a seated leg curl) tends
to cause greater hypertrophy than strength
training which involves muscles reaching
a short maximum muscle length (as the
hamstring do in a prone leg curl). Even so,
there were differences in respect of the
muscle growth that occurred both within
regions of each muscle and also across all
of the muscles used during the exercise.
Analysis
While overall muscle growth was great-
er after training with a longer maximum
muscle length, this was only apparent for
the proximal regions of the biceps femoris
and the semitendinosus and for the distal
region of the biceps femoris. It was not
apparent for the distal region of the semi-
tendinosus, which was developed similarly
after training with long and short maxi-
mum muscle lengths. This suggests that
strength training at different maximum
muscle lengths can bring about differences
in regional hypertrophy.

S imilarly, while the increases in semiten-
dinosus, biceps femoris (long head),
and semimembranosus muscle volume
were significantly greater after training
with a longer maximum muscle length
(with a seated leg curl), the increase in
sartorius muscle volume was significantly
greater after training with a shorter maxi-
mum muscle length (with a prone leg curl).
This suggests that using different maxi-
mum muscle lengths altered which of the
knee flexors were most strongly involved in
producing force during each exercise.
Analysis
Differences in hypertrophy between regions
of muscles after training at long and short
maximum muscle lengths likely arise from
regional differences in sarcomere lengths,
which produce differences in the amount of
force that muscle fibers in each region can
produce at any given muscle length, due to
the length-tension relationship (1,2). Dif-
ferences in hypertrophy between muscles
likely arise because of the principle of neu-
romechanical matching (3), which causes
muscles to be activated according to how
much leverage they have for a movement.

M any previous studies have found that
muscle activation can differ between
regions of a muscle (4–9), and between
muscles of a group depending on the exer-
cise (10–13) or exercise variation (14–18)
that is used.
While the muscle fibers that are controlled
by single motor units are distributed ran-
domly within a muscle, they do tend to be
located in certain regions (19). This means
that the motor unit recruitment order can
affect the pattern of regional muscle ac-
tivation that occurs during a muscular
contraction. Nevertheless, if regional mus-
cle activation differs between tasks, this
necessarily means that motor unit recruit-
ment order must differ between tasks. This
appears to conflict with Henneman’s size
principle, which states that motor units are
always recruited in a size order (3). To rec-
oncile this inconsistency, researchers have
proposed the principle of neuromechani-
cal matching. This principle explains that
when a motor unit has many muscle fibers
in a certain area of a muscle, and that
area of the muscle has the ability to con-
tribute substantially to joint torque (either
because of a long internal moment arm
length or because of other features that al-
low the region to produce high forces, such
as the length-tension relationship), this
motor unit will be recruited preferentially
compared to motor unit of a similar size
with worse leverage (3).
Analysis
Essentially, this means that Henneman’s
size principle is still followed so long as
measurements of motor unit recruitment
order are made in the same movement
pattern each time. In contrast, when motor
unit recruitment is measured in two differ-
ent movement patterns, a different order
of motor units recruitment occurs. This is
important, since full motor unit recruitment
is rarely reached, even during maximal
voluntary isometric contractions (20,21).
And, given that central nervous system
(CNS) fatigue increases over the course
of a set (22,23), motor unit recruitment is
likely lower than this in the final reps of a
strength training set to failure. Thus, the
high-threshold motor units (and their mus-
cle fibers) that are left untrained by train-
ing to failure with one exercise will likely
be different from the high-threshold motor
units that are left untrained by training
to failure with a different exercise. This is
likely the main reason that muscle growth
occurs to a greater extent in some regions
than in others after strength training with
certain exercises (24–26).
Moreover, the same principle of neurome-
chanical matching that determines which
region of a muscle is more active during an
exercise (depending on their leverage) also
determines which muscles within a group
are more active, again according to how
much leverage each muscle has at a given
point in the exercise range of motion.

T his study showed that both exercises
(the seated and prone leg curls) had
similarly protective effects on post-work-
out fatigue. The protective effect of previ-
ous exercise on post-workout fatigue after
a subsequent bout of similar exercise is
termed the “repeated bout effect” (RBE).
The exact mechanisms underlying the RBE
are not known and many possibilities have
been suggested (27). Nevertheless, it is
likely that the mechanisms all ultimately
work through a common pathway, which is
to alter either [A] the susceptibility of mus-
cle fibers to the presence of calcium ions,
or [B] the amount of calcium ions that can
enter the muscle fiber during or after exer-
cise. These factors are what determine the
losses in strength after a workout, either
through excitation-contraction coupling
failure or myofibrillar damage (and the
subsequent central nervous system fatigue
due to the inflammatory response).
Conclusions
In untrained subjects, strength training
which involves muscles reaching a long
maximum muscle length on each rep (as
the hamstrings do during a seated leg
curl) tends to cause greater hypertrophy
than strength training which involves
muscles reaching a short maximum
muscle length (as the hamstring do in
a prone leg curl). Yet, the two types of
exercise cause similar protection against
sustained post-workout fatigue.
Analysis
This is why changes in fascicle length can
affect the RBE (28). A change in fasci-
cle length alters the amount of calcium
ions that can enter muscle fibers through
stretch-activated ion channels. Similar-
ly, this is why making muscle fibers more
oxidative alters the RBE (29). More oxida-
tive fibers have more mitochondria, which
act to remove calcium ions from the cyto-
plasm. Interestingly, by identifying that the
magnitude of the RBE is similar after train-
ing at long and short maximum muscle
lengths, this study suggests that changes
in fascicle length (and therefore alterations
in the amount of calcium ions introduced
into muscle fibers) are less important than
changes in muscle fiber type (and there-
fore alterations in the amount of calcium
ions removed from muscle fibers), since it
would be reasonably expected that training
at a long maximum muscle length would
cause greater increases in fascicle length.
Practical implications
Strength training exercises that involve
reaching different maximum muscle
lengths (either because of a difference in
a position of the neighboring joint or due
to a difference in the range of motion)
are likely to produce differences in re-
gional hypertrophy (both within muscles
and within muscle groups). Bodybuilders
may therefore benefit from using a va-
reity of exercises and exercise ranges of
motion.

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 Why do muscles have a memory of
previous training?

M uscles tend to grow more quickly as a result of a

retraining period (following a period of training
and then detraining) compared to as a result of an
initial training period (from an untrained state). This
phenomenon is commonly called “muscle memory”
and has been attributed variously to the retention of
myonuclei gained after the initial training period and
to an epigenetic memory. However, while several
studies have found that myonuclei are retained after
an initial training period, other studies have shown
that myonuclei are actually lost during detraining.

Key findings
In a rodent model, detraining caused fast twitch muscles (and fibers) to reduce in size,
to display a shift towards a less oxidative type, and to reduce the number of myonuclei,
suggesting that a retention of myonuclei might not contribute to any “muscle memory”
effect in these muscles. In contrast, there was no loss of muscle size or myonuclei or any
reversal of fiber type shifts after detraining in the slow twitch muscle.

Practical implications
Although many studies have observed the muscle memory effect, it is still unknown how
gains in muscular strength and size are faster during retraining compared to during an
initial training bout. This study suggests that detraining may produce a smaller impact on
muscles that contain a greater proportion of slow twitch muscle fibers, although the exact
reasons for this are unclear.

Muscle memory: myonuclear accretion, maintenance, morphology, and miRNA

levels with training and detraining in adult mice. Murach, K. A., Mobley, C. B.,
Zdunek, C. J., Frick, K. K., Jones, S. R., McCarthy, J. J. & Dungan, C. M. (2020).
Journal of Cachexia, Sarcopenia and Muscle. (PubMed)
Background
OBJECTIVE To explore the changes in myonuclear number after two months of
training and six months of detraining, in the slow twitch (soleus) and
fast twitch (gastrocnemius) muscles of rodents.

INTERVENTION
POPULATION
Female mice were assigned to various training (and detraining)
and control groups to enable assessment of the effects of both HSA-GFP female adult
training and detraining. Training involved 2 months of progres- mice, produced by cross-
sive weighted wheel running, which has previously been shown to ing C57BL/6J mice with
produce hypertrophy and myonuclear addition in adult mice. The HSA-rtTA mice
detraining period involved 6 months without access to a wheel for
running.

MEASUREMENTS
Muscle size: By muscle mass
and by muscle fiber cross-sec-
tional area (CSA) of muscle
fibers of each type by immuno-
histochemistry.
RESULTS
Soleus muscle mass, type IIA (but not type I) fiber CSA
increased after training, and these changes were retained
after detraining. Gastrocnemius muscle mass, type I fiber
CSA, and type IIX/B fiber CSA did not change after either
training or detraining. Gastrocnemius type IIA fiber CSA
increased after training, but this change was reversed after
detraining.

Muscle fiber type: By immu-
nohistochemistry.
Soleus fiber type shifted to type I and away from type IIA
after training, and this shift was retained after detraining.
Conversely, gastrocnemius fiber type shifted to type I and
type IIA and away from type IIX/B after training, and this
shift was reversed after detraining.

Myonuclear number: By Soleus myonuclear number (and the number of central-

measuring the number of myo-
nuclei per muscle fiber, using
immunohistochemistry
ized nuclei, which are indicative of muscle fiber damage)
increased after training in both type I and type IIA fibers.
These changes were retained after detraining. Conversely,
gastrocnemius myonuclear number increased only in type
IIA fibers, and this increase was reversed after detraining.

SUMMARY
In a rodent model, detraining caused fast twitch muscles (and fibers)
to reduce in size, to display a shift towards a less oxidative type, and to reduce the num-
ber of myonuclei, suggesting that a retention of myonuclei might not contribute to any
“muscle memory” effect in these muscles. In contrast, there was no loss of muscle size or
myonuclei or any reversal of fiber type shifts after detraining in the slow twitch muscle.

T his study used a rodent model to iden-
tify that detraining caused fast twitch
muscles (and fibers) to reduce in size, to
display a shift towards a less oxidative
type, and to reduce the number of myonu-
clei inside each muscle fiber. This suggests
that a retention of myonuclei during de-
training does not contribute to any “muscle
memory” effect in fast twitch muscles or
fast twitch muscle fibers (which as those
muscle fibers that are most easily altered
by strength training). In contrast, detrain-
ing did not cause a loss of muscle size or
myonuclear number in slow twitch muscles
(and fibers). This suggests that a retention
of myonuclei during detraining might con-
tribute to a “muscle memory” effect in slow
twitch muscles or slow twitch muscle fibers
(which can be controlled by high-threshold
motor units and therefore modified after
strength training).
The “muscle memory” effect is the ob-
servation that increases in strength and
muscle size occur at a faster rate during
retraining (after detraining) compared to
during an initial training period (1–6). This
has traditionally been explained by way of
the retention of myonuclei during detrain-
ing. More recent research has identified
that epigenetic changes during training
could contribute. Alternatively, improve-
ments in voluntary activation during train-
ing (and retained during detraining) could
affect adaptations during retraining.
Analysis
1. Retention of myonuclei
Myonuclei are key for myofibrillar pro-
tein synthesis (MYOPS). Therefore, when
there are more myonuclei, it is possible
to achieve faster MYOPS rates during the
post-workout period. Consequently, when
a muscle fiber contains a higher density of
myonuclei, each workout has the poten-
tial to stimulate it to grow more than if the
same muscle fiber contains a lower density
of myonuclei. The myonuclear domain hy-
pothesis suggests that muscle fibers gen-
erally contain a constant density of myo-
nuclei, and that new myonuclei are added
in conjunction with increasing muscle fiber
size, while existing myonuclei are lost with
decreasing muscle fiber size. Even so, this
relationship between muscle fiber size and
the number of myonuclei is not perfect,
and muscle fibers have been observed to
increase somewhat in size without adding
new myonuclei, as well as decreasing in
size without losing myonuclei. Indeed, it
has been suggested that the muscle mem-
ory effect could arise when myonuclei are
not lost during detraining, and can there-
fore provide a faster MYOPS rate after each
workout during a retraining period than
was achieved in the original training peri-
od. Yet, while many studies have found ev-
idence for myonuclei being retained during
detraining (7–9), other studies have found
that myonuclei are lost during detraining
(10,11), or otherwise do not explain the
muscle memory effect (6,12).

2. Epigenetic changes
More recent research has identified that
epigenetic changes during training could
contribute to the muscle memory effect
(13–15), and this might occur either with
or without an effect on the number of myo-
nuclei inside each muscle fiber. Even so,
only a small number of studies have been
performed in this area to date.
3. Maintained voluntary activation
One possibility that is rarely discussed in
the literature is that changes in volun-
tary activation could contribute to muscle
growth during retraining. Voluntary acti-
vation is a measurement of the ability to
access high-threshold motor units. The
high-threshold motor units of a muscle
control large numbers of highly-respon-
sive muscle fibers, which adapt quickly and
easily to strength training. Untrained lifters
have access to far fewer of these motor
units than well-trained lifters. Indeed, an
increase in voluntary activation is one of
the key adaptations to strength training
that contributes to increased maximum
strength. Crucially, increases in voluntary
activation that are obtained through train-
ing are not easily lost during detraining
(16–19). Therefore, lifters who experience
detraining (and muscle loss) will rarely lose
access to any of the high-threshold motor
units that they gained access to as a result
of an initial training block.
Analysis
Consequently, when we compare the train-
ing effects of the same lifter undergoing
the same training program on two separate
occasions (once when training for the first
time and once when training for the second
time, after undergoing a period of detrain-
ing), the number of high-threshold motor
units that can be used will be different in
each iteration of the training program. In
the retraining period, the same lifter will
have access to more high-threshold motor
units, and will therefore be able to train a
larger number of highly-responsive muscle
fibers, which will stimulate greater overall
hypertrophy.
Nevertheless, this study was important,
because it suggested that the myonuclear
response to training differed between slow
twitch and fast twitch muscle fibers. The
slow twitch muscles (and fibers) gained
myonuclei both to support hypertrophy
and also to increase myonuclear density,
which the increased number of centralized
nuclei suggest may have been in order
to mediate damage repair. Moreover, the
increased muscle size, myonuclear number,
and increased number of centralized nuclei
were not lost after detraining. In contrast,
the fast twitch muscles (and fibers) gained
myonuclei only to increase muscle fiber
size, and these were lost in tandem with
losses in muscle size during detraining.

Conclusions
In a rodent model, detraining caused fast
twitch muscles (and fibers) to reduce
in size, to display a shift towards a less
oxidative type, and to reduce the number
of myonuclei, suggesting that a reten-
tion of myonuclei might not contribute
to any “muscle memory” effect in these
muscles. In contrast, there was no loss of
muscle size or myonuclei or any reversal
of fiber type shifts after detraining in the
slow twitch muscle.
Analysis
Practical implications
Although many studies have observed the
muscle memory effect, it is still unknown
how gains in muscular strength and size
are faster during retraining compared to
during an initial training bout. This study
suggests that detraining may produce a
smaller impact on muscles that contain a
greater proportion of slow twitch muscle
fibers, although the exact reasons for this
are unclear.

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