{"id":10839,"date":"2023-10-23T06:00:44","date_gmt":"2023-10-23T05:00:44","guid":{"rendered":"https:\/\/blogs.bmj.com\/bjsm\/?p=10839"},"modified":"2023-10-27T14:07:58","modified_gmt":"2023-10-27T13:07:58","slug":"the-error-of-easy-running-in-terms-of-stroke-volume-response-to-exercise-or-why-peter-coe-was-right","status":"publish","type":"post","link":"https:\/\/blogs.bmj.com\/bjsm\/2023\/10\/23\/the-error-of-easy-running-in-terms-of-stroke-volume-response-to-exercise-or-why-peter-coe-was-right\/","title":{"rendered":"The error of easy running in terms of stroke volume response to exercise, or why Peter Coe was right"},"content":{"rendered":"

Author: Sergey Roussakow, MD, PhD (0000-0002-2548-895X)<\/span><\/p>\n

This blog reconsiders the traditional point of view about the training effect and physiological mechanisms of easy running and low heart rate training.<\/span><\/p><\/blockquote>\n

The Miracle of Long Slow Distance<\/span><\/h2>\n

If you ask a novice runner what the benefits of long slow distance running (LSD) (also known as low-heart rate running or easy running) are, you may hear them say “heart training.” If you then ask how this happens, they may explain to you that the heart stroke volume representing the \u201cheartbeat strength\u201d peaks at a low heart rate of only about 100 bpm and then practically does not increase, so \u201cfairly easy running is a good developer of the heart muscle, and although it doesn\u2019t feel as if you are working very hard, your heart is\u201d [1]. Thus, there is no point in further increasing the load, because one can benefit from this training effect without extra effort, and you can literally \u201crace faster by training slower\u201d [2]. That’s why you always hear from LSD and 80\/20 adherents something like \u201cIt\u2019s (more like) a ninety-minute social hour\u201d when we \u201cjust run side by side at a relaxed pace and carry on a conversation\u201d [2]. It sounds great and attracts many newcomers every year, but is it true?<\/span><\/p>\n

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 \u201ceffortless training\u201d, and the laws of thermodynamics cannot be deceived.<\/span><\/p>\n

Where did this come from?<\/span><\/h2>\n

Where did the idea of low heart rate training come from? It seems that it was first voiced by Woldemar Gerschler in the late 1930s. This famous inventor of interval training, at least in the early stages of development of this concept, attributed the training effect mainly to intervals, that is, the recovery periods between high-intensity sessions when the heart contracts at \u201cmaximum stroke volume.\u201d And it really worked… in combination with submaximal load. Arthur Lydiard certainly played the main role in popularizing the idea of LSD, or rather, he is considered its father, although in fact the Lydiard system was more of a type of fartlek with increased LSD mileage. However, in the 70s, it was the idea of \u201ceffortless training\u201d that was popularized as the essence of the Lydiard system and gave birth to the \u201crunning boom\u201d of the 70s in the United States. It was a brilliant marketing ploy. Selling the idea of training hard to the masses is difficult, but the idea of “effortless running” certainly caught on. As Jim Fixx, one of the fathers of the American “running revolution”, wrote in his bestseller The Complete Book of Running<\/em>, \u201cIf you feel that you’re running, no matter how slow you’re going, no one can say you’re not\u201d [3]. The idea of \u201ceasy running at maximum stroke volume\u201d had taken root in sports physiology [1].<\/span><\/p>\n

What really happens?<\/span><\/h2>\n

Everything old is new again. In fact, the stroke volume response to exercise was described exhaustively by Robert Rushmer [4, 5] back in the late 50s (Fig. 1).\u00a0<\/span><\/p>\n

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Fig. 1. Dynamics of the components of cardiac output at rest and during exercise (dashed line \u2013 in an upright position, solid line \u2013 in recumbent position, red line \u2013 trend transition point) [5].<\/span><\/i><\/p>\n

In the recumbent position, when venous return is almost not limited by gravity, the heart chambers fill quickly and stretch to their maximum, so the stroke volume peaks thanks to the Frank-Starling law, a type of the so-called myotatic reflex that works at the level of muscle fiber. The Frank-Starling mechanism consists of two components: (1) active contraction is activated by the compression of muscle mechanoreceptors when a muscle is stretched, and (2) passive response is determined by the fact that the muscle fiber, when stretched, accumulates elastic energy, and the more it is stretched, the stronger it contracts. This phenomenon is known as residual eccentric force. In general, it\u2019s like with a balloon: the more you inflate, the stronger the air flow. It is important to understand that this does not \u201ctrain\u201d the balloon, which is simply working within its natural range.<\/span><\/p>\n

In an upright position (standing or sitting), gravity limits venous return. The volume of blood in the venous part of the systemic circulation is about 80% of the circulating blood volume, while the arterial part accounts for only 12-15%, and the capillaries for the resting 5-8%, but in an upright position, the venous blood is additionally redistributed to the veins of the lower extremities and abdominal cavity, which decreases the filling of the heart chambers and, according to Starling\u2019s law, decreases the force of contraction, stroke volume and cardiac output. <\/span>The magnitude of the decrease in stroke volume varies greatly from study to study, but on average it can be estimated at 10-30%. Already with minor physical activity of <60% V\u0307O<\/span>2<\/span>max, that is, with a heart rate of 100-110 bpm, stroke volume is restored to the maximum value observed in the recumbent position [5, 6]. The main mechanism in this case is an increase in sympathetic tone, which leads to contraction of the veins and an increase in venous return. It is often overlooked that the venous bed has 3-4 times more abundant sympathetic innervation than the arterial bed, so an increase in venous tone is no less, if not a more significant component of the sympathetic effect.<\/span><\/p>\n

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 \u201ctrain lying down\u201d, 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.<\/span><\/p>\n

Where is the error?<\/span><\/h2>\n

In fact, the error is on the surface: it is the identification of stroke volume with myocardial contractility. In fact, although these concepts are related, they are not equivalent. This raises a related error of misunderstanding the relationship between stroke volume and exercise. Cardiac output increases in response to an increase in metabolic demand during exercise due to the increase in heart rate and stroke volume, but if the linear pattern of heart rate-exercise dependence is well known, the pattern of the dependence of stroke volume on exercise has not been established. Three main patterns have been described [7, 8]:\u00a0<\/span><\/p>\n

    \n
  1. Ascending, when stroke volume increases as the load increases up to V\u0307O<\/span>2<\/span>max.<\/span><\/li>\n
  2. Horizontal, when the stroke volume does not change in the recumbent position or reaches a \u201cplateau\u201d at a certain value of V\u0307O<\/span>2<\/span> (40-50% V\u0307O<\/span>2<\/span>max) in the upright position.<\/span><\/li>\n
  3. Descending, when stroke volume decreases in the recumbent position or after recovery in the upright position.<\/span><\/li>\n<\/ol>\n

    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 \u2013 exercise physiology.\u00a0<\/span><\/p>\n

    Some physiology<\/span><\/h2>\n

    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.<\/span><\/p>\n

    \"\"<\/p>\n

    Fig. 2. Lewis-Wiggers cardiac cycle (left) and left atrium cy\u0441le (right) [10].<\/span><\/i><\/p>\n

    When load increases above 60% V\u0307O<\/span>2<\/span>max, 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 \u201cy\u201d 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 \u201ca\u201d) occurs as a short booster contraction, which \u201cpumps\u201d 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%. <\/span><\/p>\n

    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 \u2013 already at 120 bpm.<\/span><\/p>\n

    This has important hemodynamic consequences, as shortened diastole reduces filling time and hence EDV. This is actively counteracted by increased left atrial contraction (Fig. 3). EDV, therefore, is determined by the balance of heart rate and the force of atrial contraction and always decreases with increasing heart rate, slightly in athletes and significantly in untrained and especially weakened people. This decrease is compensated by an increase in myocardium contractility, i.e. ejection fraction, so stroke volume is determined by the balance of EDV and ejection fraction, or, ultimately, heart rate and myocardial contractility.<\/span><\/p>\n

    \"\"<\/p>\n

    Fig.3. Response of stroke volume and cardiac output to exercise.<\/span><\/i>
    \n<\/span><\/i>Note: SNS, sympathetic nervous system; SV, stroke volume; CO, cardiac output; LV, left ventricle; LA, left atrium; ESV, end-systolic volume; EDV, end-diastolic volume; EF, ejection fraction; HR, heart rate.<\/span><\/i><\/p>\n

    Hypothesis: The pattern of stroke volume response to exercise depends on cardiorespiratory fitness<\/span><\/h2>\n

    Based on the above, all three patterns of stroke volume versus exercise should occur depending on myocardial contractility or cardiorespiratory fitness.<\/span><\/p>\n

      \n
    1. With high myocardial contractility (athletes), stroke volume increases, since a progressive increase in myocardial contractility and ejection fraction outpaces the decrease in EDV (which is minimized by the increased filling of the left ventricle due to increased contractions of the left atrium) and compensates for the shortening of diastole.<\/span><\/li>\n
    2. In normal myocardium contractility, stroke volume remains constant, as the increase in ejection fraction compensates for the decrease in EDV. It is logical to assume that this pattern would be the most common, which is why stroke volume remains unchanged in most studies.<\/span><\/li>\n
    3. With myocardial weakness, a stroke volume decreases, since the decrease in EDV outpaces the increase in the ejection fraction, which, moreover, may not increase at all.\u00a0<\/span><\/li>\n<\/ol>\n

      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 \u2013 i.e. age, gender, fitness, diseases, etc. \u2013 so we can hypothesize that there should be a correlation between the parameters of fitness (primarily V\u0307O<\/span>2<\/span>max) and myocardial contractility (ejection fraction or stroke volume <\/span>per se<\/span><\/i>) and the pattern of exercise-dependence of stroke volume. It seems that the available data is sufficient to verify this.<\/span><\/p>\n

      Hypothesis testing<\/span><\/h2>\n

      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 V\u0307O<\/span>2<\/span>max (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 V\u0307O<\/span>2<\/span>max 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.<\/span><\/p>\n

      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 V\u0307O<\/span>2<\/span>max (r=0.42, p=0.013, t=2.6, n=35) and the stroke volume <\/span>per se<\/span><\/i> (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.<\/span><\/p>\n

      Additionally, there was a significant strong correlation between physical fitness (V\u0307O<\/span>2<\/span>max) and stroke volume (r=0.80) with statistical power of 100% (p=1.5\u00d710<\/span>-7<\/span>, t=6.9, n=30), which is not surprising. What is surprising is the strength of the correlation, given that stroke volume is a surrogate measure of myocardial contractility, and taking into account the above limitations of the model. It is likely that the correlation of V\u0307O<\/span>2<\/span>max with ejection fraction, which is a more direct measure of myocardial contractility, would be much stronger, as well as the correlation between ejection fraction and the stroke volume pattern.<\/span><\/p>\n

      What did we find?<\/span><\/h3>\n

      So, here we found out two fundamental points: <\/span><\/p>\n

      (1) The effect of slow running is not associated with training myocardial contractility, and;<\/span><\/p>\n

      (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.<\/span><\/p>\n

      What does it mean?<\/span><\/h3>\n

      This suggests that the force of myocardial contraction in most cases increases with increasing load, manifested by an increase in ejection fraction and not always in an increase in stroke volume, which is an indirect measure of myocardial contractility distorted by the effect of heart rate on EDV. This exposes two major pitfalls of the concept of \u201cmaximum stroke volume training\u201d at easy running:<\/span><\/p>\n