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The Error of Easy Running in Terms of S... Log - Social Media - S Leading SEM Voice
The Error of Easy Running in Terms of S... Log - Social Media - S Leading SEM Voice
Actually, I respect attempts to cheat the laws of nature. This is creativity, and I
would be delighted if someone finally created a perpetual motion machine.
But until this happens, I remain a rationalist and consider it my duty to explain
that there’s no such thing as a free lunch and “effortless training”, and the laws
of thermodynamics cannot be deceived.
The low-heart rate increase in stroke volume is thus restorative and reflex, i.e.
not associated with increased myocardial contractility. In other words, based
on this, the idea of maximum stroke volume-based low-heart rate training is
untenable: you can just as well “train lying down”, since the recumbent stroke
volume is the same as at the low-heart rate training, and the effort is much
less. In fact, we “bed train” for 8 hours every day while we sleep, but for some
reason this does not lead to increased heart muscle strength.
Vieira et al. (2016) in their systematic review [7] failed to draw a conclusion
which pattern was true due to conflicting evidence, as were Vella et al. (2005)
in a previous review [8], so the problem is still unresolved. To solve it here, we
need to dive deeper to the heart of the matter – exercise physiology.
Some physiology
The mechanisms underlying the dependence of stroke volume on exercise
have been well known [9]. To begin with, stroke volume is the difference
between the end-diastolic volume (EDV) of the left ventricle, i.e. its volume
before the ventricle contraction (systole), and the end-systolic volume (ESV),
i.e. volume at the end of systole with maximum contraction of the left
ventricle. The ratio of stroke volume to EDV is called the ejection fraction and,
in fact, it is the ejection fraction, and not the stroke volume, that determines
myocardial contractility.
Fig. 2. Lewis-Wiggers cardiac cycle (left) and left atrium cyсle (right) [10].
When load increases above 60% V̇O2max, i.e. after restoration of the postural
decrease in stroke volume, cardiac output increases due to a further increase
in heart rate and enforced heart contractions, i.e. increase in ejection fraction,
and the key issue in the dynamics of stroke volume becomes the dynamics of
EDV, determined by the filling of the left ventricle in diastole. This filling occurs
in three phases (Fig. 2): (1) the first phase of active-passive filling occurs under
the action of elastic traction of the stretched atrium following the Starling law
and quickly empties the atrium and reduces its pressure to a minimum (the
“y” wave); (2) the blood then flows passively from the pulmonary veins, and the
atrium acts simply as a conduit; (3) and finally, during the last 100 ms of
ventricular diastole, active atrial systole (wave “a”) occurs as a short booster
contraction, which “pumps” the remaining 15% to 20% of EDV into the left
ventricle. It is important to understand that this remaining EDV is much more
significant in terms of stroke volume, which increases by 20-30%.
As the heart rate increases, the cardiac cycle shortens, and it is important that
diastole shortens faster than systole, so that at a heart rate of ~150 bpm their
ratio decreases to 1:1 from about 1.6:1 at rest (i.e., when the systole is
shortened by half (from 300 ms to 150 ms), the diastole is shortened more
than 3 times (from 500 ms to 150 ms)). Moreover, in almost 40% of cases the
diastole/systole ratio is reversed at high heart rates, i.e. diastole becomes
shorter than systole [11]. The pattern of the ratio change depends on the
cardiorespiratory fitness: in healthy men the ratio remains >1 up to the
maximum heart rate; in weakened men (patients) it is reversed at about 160
bpm, and in women – already at 120 bpm.
Thus, the error of all studies and reviews is that they try to establish a single
correct pattern, when, in fact, all three patterns occur. If so, then the stroke
volume pattern should depend on the parameters affecting myocardial
contractility – i.e. age, gender, fitness, diseases, etc. – so we can hypothesize
that there should be a correlation between the parameters of fitness (primarily
V̇O2max) and myocardial contractility (ejection fraction or stroke volume per
se) and the pattern of exercise-dependence of stroke volume. It seems that
the available data is sufficient to verify this.
Hypothesis testing
An impressive sample of 50 groups and 577 subjects was taken from the Vella
et al. review [8], where the data are well prepared, so that almost nothing to
add or change (see full table at the end of the blog in the Additional Materials).
Minor changes included converting absolute V̇O2max (l/min) to relative
(ml/kg/min) using a 70 kg body weight reference (there may be an error here,
but within the entire data set it is negligible, as confirmed by sensitivity
analysis) and exclusion of groups with uncertain V̇O2max and/or stroke
volume (i.e., if presented as a range). Patterns A, B and C were digitized by
assigning values of 1, 0 and -1, respectively.
Patterns A, B and C were found in 30%, 48%, and 22% of groups, respectively ,
consistent with expectations. Correlation analysis showed a moderately strong
and statistically significant correlation of the stroke volume pattern with
V̇O2max (r=0.42, p=0.013, t=2.6, n=35) and the stroke volume per se (r=0.42,
p=0.014, t=2.6, n=33). Sensitivity analysis does not affect the conclusion
(r=0.39-0.42, p=0.013-0.021). Considering that the analysis model is extremely
unfavorable for detecting correlation because it is based on mean values that
smooth out correlation, uses the crudest trinary outcome measure (instead of
a more precise continuous measure such as slope, etc.), and includes a
number of confounders, the strength of the correlation far exceeds
expectations. So much so that this result can be considered sufficient proof of
the hypothesis.
(1) The effect of slow running is not associated with training myocardial
contractility, and;
(2) The pattern of stroke volume versus exercise depends on physical fitness
and / or myocardial contractility, so that in trained subjects the pattern is
rather ascending (A), in the weakened it is more likely to descend (C), and on
average the probability of a horizontal pattern is highest (B). While the first
finding is actually an open secret, forgotten or neglected knowledge, the
second is new knowledge, albeit derived from existing data.
Simply put, the concept assumes a training effect where there is none, and
misses it where it exists, that is, it is turned upside down.
This does not mean that low heart rate running is useless. Its good tolerance
allows for higher volumes of running, which results in increased basic
endurance, from the muscle recapillarization, strengthening of muscles,
bones, joints and ligaments to dilated myocardial hypertrophy and brain and
fatigue resistance, but increased myocardial contractility is not in the list. This
means that you still have to run fast to race faster, so, in my opinion, the
marketing slogan “run slow to race faster” is misleading. Rather, it seems to
me that Peter Coe was right when he said: “Long slow distance makes you a
long slow runner.”
References
[1] Daniels J. Daniels’ running formula. Human Kinetics; 2013.
[2] Fitzgerald M. 80/20 Running: Run Stronger and Race Faster By Training
Slower. Penguin, 2014, 272 p.
[3] Fixx J. The Complete Book of Running. Random House, 1977, 314 p.
[6] Grimby G, Nilsson NJ, Saltin B. Cardiac output during submaximal and
maximal exercise in active middle-aged athletes. J Appl Physiol.
1966;21:1150–6.
[7] Vieira SS, Lemes B, de Carvalho PTC, de Lima RN, Bocalini DS, Junior JAS,
Arsa G, Casarin CA, Andrade EL, Serra AJ. Does Stroke Volume Increase During
an Incremental Exercise? A Systematic Review. Open Cardiovasc Med J.
2016;10:57-63.
[8] Vella CA, Robergs RA. A review of the stroke volume response to upright
exercise in healthy subjects. British J Sports Med. 2005;39:190-195.
[9] Higginbotham MB, Morris KG, Williams RS, McHale PA, Coleman RE, Cobb
FR. Regulation of stroke volume during submaximal and maximal upright
exercise in normal man. Circ Res. 1986;58(2):281-91.
[10] Walklate J, Ferrantini C, Johnson CA, Tesi C, Poggesi C, Geeves MA. Alpha
and beta myosin isoforms and human atrial and ventricular contraction. Cell
Mol Life Sci. 2021;78(23):7309-7337.
Author information
Sergey Roussakow, MD, PhD (0000-0002-2548-895X)
roussakow@gmail.com
Additional Materials
Tab. 1. Stroke volume response to exercise (Vella et al., 2005 [8]).
N 577 35 30 33 50
Note: N, sample size; SV, Stroke volume; * reference numbers are according to
Vella et al. [8]; r – Pearson correlation coefficient; t, t-statistic; p, p-value.
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