Isaak-Alexandros Koutsoklenis

Limits to Human Performance

Master programme of Sport and Exercise Science – Human Performance
Halmstad University

Assignment 1 – Muscle Fatigue

3. Explain and discuss the difference between central and peripheral fatigue
models, both at the whole body and cellular level.

“Muscle fatigue” is a complicated phenomenon that has been investigated and

analyzed through time in the sports science area. It is considered as one of the most
important factors concerning human performance and its limitations. ACSM (2011, p.
178) defines “muscle fatigue” as “a condition in which there is a loss in the capacity
for developing force and/or velocity of a muscle, resulting from muscle activity under
load which is reversible by rest”. Losses in force, velocity and power are the main
factors of performance effected by fatigue and can appear both at the whole body and
at cellular level. “Muscle fatigue” can also be divided into two categories, “peripheral
fatigue” which is about deleterious changes in the muscle itself and “central fatigue”
which concerns changes in the central nervous system (CNS) (ACSM, 2011).

Central fatigue
“Central fatigue” can be shown not only in elite high level trained athletes but
also in common people at their workplace. Taylor and Gandevia (2007) define
“central fatigue” as “a progressive exercise-induced failure of voluntary activation of
the muscle.” On cellular level, the assumptions for the determiners of “central
fatigue” lie on a) afferent inputs from group 1 to 4 muscle afferents, b)
suprasegmental centers involved in planning of willed movements, c) motor cortical
and other corticospinal outputs, d) other supraspinal and propriospinal outputs and e)
α- and γ- motor neurons or their axons (ASCM, 2011). Additionally, “central fatigue
is associated and is more obvious in sustained maximal contractions than in
submaximal contractions. To be more specific, during a maximal voluntary effort,
there is an increase in the increment of the force evoked by nerve stimulation which is
an indicator of fatigue (Taylor and Gandevia, 2007).

Peripheral fatigue
Peripheral fatigue is related more with the decrease in force production after exercise
that happens in the neuromuscular junction, instead of the central fatigue which is
shown mostly at voluntary activations of the muscle, where the force gradually fails
after exercise (Taylor and Gandevia, 2007).
These are the models of “peripheral fatigue”:

Cross bridge cycle

Fitts (2008) states that that force velocity and power, which are the mains factors that
get affected from fatigue, are influenced by the molecular factors which control the
quantity and force of the strongly bound cross bridges, and the rate of cross-bridge
cycling. During high-intensity contractions the high accumulation of Pi and H+ reduces
the force per strongly bound, high-force bridge. In addition, it is very important for
the fatigue procedure that myofibrillar sensitivity is decreased by both Pi and H+ (Fitts,
2008).

Impaired calcium release

One of the main causes of peripheral muscle fatigue in the isolated skeletal muscle
fibers is the impaired calcium release from the sarcoplasmic reticulum (SR) (Allen et
al, 2007). The major mechanisms that contribute to this are the decrease in the
amplitude of action potential, probably because by the extracellular K+ accumulation,
that may reduce the voltage sensor activation (Allen et al, 2007). All in all, the same
study of Allen et al, (2007) highlights the reduction of force as a consequence of the
reduction of SR Ca2+ release.

Muscle K+, Na+, Cl- Disturbances

The study of McKenna et al, (2007) focuses on another critical contributor of fatigue
which is the pronounced perturbations in extracellular (interstitial) and intracellular
K+ and Na+ concentrations, induced by Intense fatiguing contractions induce cellular
K+ efflux and Na+ and Cl- influx. Furthermore, during intense contraction
some Na+ and K+ pumps are disabled and along with more ionic disturbances,
probably precipitate muscle fatigue (Allen et al, 2008).

Respiratory muscle fatigue

According to the study of Romer and Polkey, (2008), whole body endurance exercise
with high intensity can induce fatigue to the diaphragm and abdominal muscles. This
fatigue is caused by the increased levels of respiratory muscle work in combination
with an increased competition for blood flow with limb locomotor muscles.
Respiratory muscle fatigue has a great effect in exercise tolerance and the main is the
increased sympathetic vasoconstrictor outflow to working skeletal muscle through a
respiratory muscle metaboreflex, by means of that reducing limb blood flow and
increasing the acuteness of exercise-induced locomotor muscle fatigue (Romer and
Polkey, 2008).

4. Select your “favorite” muscle fatigue mechanism, find another article

investigating the same fatigue mechanism; argue for your fatigue model against
the other models.

First of all the respiratory muscle fatigue is a model of fatigue that is

considered as both central and peripheral, in contrast to the other fatigue models such
as the cross- bridge cycling, the failure of sarcoplasm reticulum, the Ca handling and
the suprispinal and spinal mechanisms. Also, the major consequence of respiratory
muscle fatigue is an increased sympathetic vasoconstrictor outflow to working
skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb
flow and increasing the severity of exercise-induced locomotor muscle fatigue.
Another factor in which the respiratory fatigue differs from the others is the
intensity and time of appearance (Romer et al, 2008). Specifically, it appears on
submaximal intensity of ~ 80% and prolonged exercise of ~10 minutes. These factors
indicate that the respiratory model is a unique one, among the other models of fatigue.
 SUMMARY

Article:
BABCOCK MA, PEGELOW DF, HARMS CA, & DEMPSEY JA. (2002). Effects of
respiratory muscle unloading on exercise-induced diaphragm fatigue. Journal of
Applied Physiology.93, 201-6.

Past research, showed that the amount of diaphragmatic force output required
to cause fatigue was reduced significantly during exercise. This study examines the
role of diaphragmatic force output per se on diaphragmatic fatigue caused by whole
body exercise, by using proportional assist mechanical ventilation (PAV) to unload
the respiratory muscles during heavy endurance cycling exercise.
Ιnitially, the subjects were consisting of seven male with normal lung function
and no signs of arterial hypoxemia during the maximal oxygen uptake. In the
beginning, was used an inspiratory muscle unloading through a feedback-controlled
PAV that reduces the work of inspiratory muscles through exercise. Afterwards, the
Pair-stimuli technique took place to show the level of supramaximal bilateral phrenic
nerve stimulation (BPNS). Then, the High-frequency response was measured. Then,
there was a collection of exercise data which provides a conservative estimate of the
total amount of work done by respiratory muscles during exercise. The next step was
the exercise test protocols, where the subjects exercised on an electromagnetically
braked cycle ergometer testing the Vo2max and the arterial blood O2 saturation. At
the end, the statistical analyses were done by the statistical program Sigma Stat.
The results in respiratory muscle force output and oxygen uptake showed that
in control conditions the force output of the diaphragm was 88-100% and fell to 80%
by the end of exercise and with PAV, remained relatively constant at 67-72% of the
exercise duration. Also, Wb was decreased both in inspiration and expiration. Oxygen
uptake rose throughout the exercise period during the control-exercise trial, but was
reduced significantly with PAV. The ventilatory responses to exercise indicate a rise
in control exercise and a decrease with PAV. The Twitch Pdi was not significantly
changed from preexercise control after PAV exercise.
These findings point a dual cause o exercise induced diaphragmatic fatigue. In the
first place, whole body exercise fatigue factor is likely due to less blood flow
availability to the diaphragm during exercise in the face of demands by the locomotor
muscles. The other general cause is the work of the diagram incurred during high-
intensity whole blood exercise is critical to causing diaphragmatic fatigue.
In conclusion, the present research postulates that the magnitude of force output
required b the diaphragm during high-intensity whole body exercise is a significant
determinant of exercise-induced diaphragmatic fatigue. In addition, it is shown that
mechanically reducing respiratory muscle work during high-intensity resulted in 1)
increased vascular conductance and blood flow to working limb locomotor muscles
and 2) significant increases in endurance-exercise performance.
References
ALLEN, D. G., LAMB, G. D., & WESTERBLAD, H. (2007). Impaired calcium
release during fatigue. Journal of Applied Physiology. 104, 296-305.

FARRELL, P. A., JOYNER, M. J., & CAIOZZO, V. J. (2011). ACSM's advanced

exercise physiology. Philadelphia, Wolters Kluwer Health/Lippincott Williams &
Wilkins.

FITTS R.H. (2008). The cross-bridge cycle and skeletal muscle fatigue. Journal of
Applied Physiology. 104, 551-558.

MCKENNA, M. J., BANGSBO, J., & RENAUD, J.-M. (2008). Muscle K+, Na+, and
Cl disturbances and Na+-K+ pump inactivation: implications for fatigue. Journal of
Applied Physiology. 104, 288-295.

ROMER, L. M., & POLKEY, M. I. (2008). Exercise-induced respiratory muscle

fatigue: implications for performance. Journal of Applied Physiology. 104, 879-888.

TAYLOR, J. L., & GANDEVIA, S. C. (2007). A comparison of central aspects of

fatigue in submaximal and maximal voluntary contractions. Journal of Applied
Physiology. 104, 542-550.