Stroke Volume: What It Is, What Changes It — and What It Means for Athletes
Table of Contents
Key Takeaways: Stroke Volume
- Stroke volume is the amount of blood the left ventricle ejects with each heartbeat. Multiplied by heart rate, it gives cardiac output — the volume of blood the heart delivers per minute.
- Maximal heart rate is strongly associated with age; stroke volume can improve with endurance training. Maximal heart rate is predicted largely by age, and the age relationship did not differ by sex or habitual physical activity [7], and training-induced gains in VO₂max are largely facilitated by an expanded red blood cell volume and an accompanying improvement in how much blood the heart ejects per beat [10].
- Cardiac output tracks VO₂max. In a meta-analysis of healthy young adults, endurance training increased both VO₂max and maximal cardiac output, while oxygen extraction at maximal exercise did not change significantly [8].
- The classic “plateau” is not universal. In one study, untrained students and university runners showed the classic levelling-off at about 40% of VO₂max, while elite runners kept increasing all the way to maximal exercise, who reached 187 mL per beat versus 128 mL in the untrained group [4].
- Blood volume is a major lever. After six weeks of endurance training in previously untrained adults, removing the training-induced gain in blood volume returned maximal cardiac output to pre-training levels [9].
- Dehydration shrinks the output per beat. At 2.8% hypohydration, each heartbeat during cycling ejected 18 mL less blood and heart rate was 18 beats per minute higher than when the same subjects were euhydrated [13].
- It can be built — and lost. Aerobic interval training increased stroke volume by approximately 10% in moderately trained men [11], whereas short-term detraining in highly trained athletes lowers blood volume and output per beat, reducing maximal cardiac output [16].
- It shows up in everyday clinical signs. In my clinical experience, a fairly low heart rate in an athlete and a rising heart rate in a dehydrated patient are two familiar examples.
- Your own numbers may reflect training. In my case, resting heart rate rose slightly when I stopped competing and fell again when I returned to interval training — though a wearable’s resting heart rate is only an indirect marker.
- Cardiac output is not the only limit in hard intervals. In my own experience as an interval athlete, lactate clearance rather than cardiac output has usually been the limiting factor.
Introduction: Stroke Volume
Heart rate is a familiar training metric. Stroke volume is less visible in everyday training, even though it is the other half of the equation that decides how much blood — and therefore oxygen — the heart can deliver to working muscles.
Put simply, it is the amount of blood the heart pumps out with each beat. It sounds like a textbook term, but it sits behind many things athletes notice in training: why VO₂max improves, why heart rate drifts upward during a long session in the heat, why fitness fades surprisingly quickly during a break, and why an endurance athlete’s heart can look large on an ultrasound.
For a long time, the standard teaching was that stroke volume rises at the start of exercise and then levels off at around 40% of VO₂max. A 2005 review in the British Journal of Sports Medicine pointed out that later studies had documented it continuing to increase up to VO₂max in both trained and untrained people, and that the response may be influenced by training status, age and sex [1].
In this article, I explain what stroke volume is, what determines it, how it behaves during exercise, and what the research shows about how athletes can increase it — and what makes it fall.
Stroke volume is not something most people think about, and in a general practitioner’s office it rarely comes up on a daily basis. Still, there are many clinical situations in which it has to be taken into account. In my clinical experience, it often surfaces quietly: an athlete is sitting in the consulting room, and on auscultation the heart rate is fairly low. This is usually explained by a large stroke volume. I recognise this from my own case, as I have had a low resting heart rate for as long as I can remember, having exercised throughout my life — and I still do.
What Is Stroke Volume?
Stroke volume (SV) — the heart’s output per beat — is the volume of blood ejected by the left ventricle in a single contraction, usually expressed in millilitres per beat (mL/beat). It is the difference between how much blood the ventricle holds when it has finished filling (end-diastolic volume) and how much is left once it has contracted (end-systolic volume).
Three relationships explain most of what follows:
- SV = end-diastolic volume − end-systolic volume
- Ejection fraction = SV ÷ end-diastolic volume
- Cardiac output = heart rate × SV
Ejection fraction is the number most people see on an echocardiography report, but it is a percentage, not a volume. Because SV equals ejection fraction multiplied by end-diastolic volume, a larger ventricle can eject more blood per beat at exactly the same ejection fraction. And because cardiac output is the product of heart rate and SV, a heart that ejects more per beat can deliver the same output with fewer beats. What a low resting pulse does and does not tell you is a separate topic, covered in the article on resting heart rate changes in overtrained athletes.
Outside sport, stroke volume matters most when something goes wrong. In patients with sepsis, I sometimes see a clearly raised heart rate. In my trauma training we were taught a blunt rule of thumb: when the heart rate is higher than the systolic blood pressure, the demand for cardiac output is high and the risk of shock is often evident. This applies especially to trauma patients and patients with sepsis. A more dramatic example is resuscitation. In my clinical experience, the stroke volume produced by chest compressions is clearly not that of a normal heart, and maintaining blood pressure with compressions alone is often difficult. I have had to resuscitate patients on several occasions myself, and supporting the circulation this way is challenging.
Is There a “Normal” Stroke Volume?
There is no single normal value. In 434 healthy young adults (mean age 26) studied with cardiac MRI, left and right ventricular stroke volumes were larger in men than in women [2]. Results also depend heavily on how they are measured: in a meta-analysis of male athletes, left ventricular end-diastolic volume — the volume from which each stroke is ejected — averaged 178 mL in studies using cardiac MRI and 135 mL in studies using echocardiography [3]. Because these figures come from different study populations, the gap cannot be attributed to the imaging technique alone.
Exercise studies give a sense of scale. At maximal exercise, untrained male university students in one study averaged 128 mL per beat [4], while moderately trained women in another reached 82.7 mL per beat at VO₂max [5]. These figures come from different measurement methods and populations, so they are illustrations rather than reference ranges.
What Determines Stroke Volume?
Physiologically, stroke volume is governed by three classic factors:
- Preload — how much the ventricle fills before it contracts. Venous return, total blood volume and the time available for filling all influence it, and in a dehydration study reduced filling lowered stroke volume [6].
- Contractility — how forcefully the heart muscle contracts.
- Afterload — the resistance the ventricle has to pump against.
In endurance-trained people, the mechanisms proposed to explain a continued rise at high intensities are better diastolic filling, greater contractility, a larger blood volume and a lower cardiac afterload. In untrained people who show the same continued rise, a naturally high blood volume has been suggested as the explanation [1].
The importance of filling becomes clear when it fails. In a study of eight participants (three women and five men) cycling for two hours in the heat, the dehydrated trial — 4.0% body mass loss — reduced SV, end-diastolic volume, cardiac filling time, blood volume and cardiac output compared with the euhydrated trial. Markers of the heart muscle’s own contraction and relaxation were not reduced; if anything, they tended to be higher. The authors concluded that the decline reflected compromised filling of the left ventricle and reduced venous return, not impaired left ventricular function [6].
A related clinical sign is visible in the neck. In patients with congestion, the jugular veins may be visibly distended, because the heart is not able to move the blood forward as it should. This does not always mean congestion — in a lying position, for example, prominent neck veins can also be normal — but I see this from time to time in the clinic, and I find it a good rule of thumb. In patients with heart failure, I often pay attention to it.
The most extreme example I have seen is cardiac tamponade. I have encountered it once: cardiac output and stroke volume fell dramatically, and an emergency pericardial puncture was needed. Cardiac tamponade is a very dangerous situation for the patient, and resuscitation often does not help either.
Several of these mechanisms concern how well the heart is filled rather than the strength of the heart muscle itself — a theme that returns throughout the rest of this article.
What Happens During Exercise?
When exercise starts, SV rises; what happens after that has long been debated [1].
In a study comparing five elite male distance runners, ten university distance runners and ten untrained university students on a graded treadmill test, no statistically significant differences in SV responses were detected between the three groups in the transition from rest to light exercise. From light to maximal exercise, however, the rate of change stayed flat in the untrained students and the university runners — consistent with the classic plateau at about 40% of VO₂max — whereas in the elite runners it rose sharply throughout the test, with a further increase once heart rate exceeded 160 beats per minute. Average maximal SV was 187 ± 14 mL per beat in the elite runners, 145 ± 8 mL in the university runners and 128 ± 14 mL in the untrained students [4].
A study in women found a continued rise in both groups. Thirteen elite female endurance athletes (VO₂max 67.1 mL/kg/min) and eleven moderately trained women (VO₂max 49.5 mL/kg/min) were measured at rest and while running at 40%, 60%, 80% and 100% of VO₂max. Both groups increased SV significantly from 40% of VO₂max to VO₂max — from 105.3 to 129.1 mL per beat in the elite athletes and from 68.7 to 82.7 mL per beat in the moderately trained women. No statistically significant difference in the size of the increase was detected between the groups, although the elite athletes had larger values at every intensity [5].
The honest summary is that the plateau is not a universal law. Whether a plateau appears seems to depend on who is being tested — training status, age and sex have all been proposed as influences [1] — and the studies use different measurement techniques. Imaging method can have a significant impact on how cardiac volumes are interpreted [3], so absolute numbers from different studies should not be compared directly.
Stroke Volume and VO₂max
According to the Fick principle, VO₂max equals maximal cardiac output multiplied by the arteriovenous oxygen content difference at maximal exercise — the amount of oxygen the working muscles extract from each unit of blood. Maximal cardiac output, in turn, is maximal heart rate multiplied by stroke volume.
Maximal heart rate is largely set by age rather than by activity level. In a meta-analysis combined with a laboratory study, maximal heart rate was predicted largely by age alone, following the equation 208 − 0.7 × age, and the relationship did not differ between men and women or with habitual physical activity [7]. The practical implications are discussed in the article on max heart rate and age.
Because maximal heart rate is strongly associated with age and differs little across habitual activity groups, stroke volume and oxygen extraction are the main components to consider when looking at training-related changes in VO₂max — and the evidence points mainly at cardiac output. A systematic review and meta-analysis of endurance training studies in healthy young adults (mean age under 40, training lasting at least three weeks, programmes ranging from 5 to 12.9 weeks) found that training increased VO₂max (standardised mean difference 0.75) and maximal cardiac output (0.64), but not the arteriovenous oxygen difference at maximal exercise (0.21, P = 0.23). The change in maximal cardiac output was positively associated with the change in VO₂max (B = 0.91, P = 0.007), whereas the change in oxygen extraction was not (B = 0.20, P = 0.40) [8].
These were relatively short training programmes, so the meta-analysis says less about what limits further progress in athletes who have already trained for many years.
What Stroke Volume Means for Athletes
Endurance Athletes Have Larger Hearts
A systematic review and meta-analysis of elite young male athletes found that every left ventricular structural measure was larger in athletes than in controls. Left ventricular end-diastolic volume was larger in endurance athletes than in resistance athletes — 171 mL versus 131 mL — and right ventricular end-diastolic volume, right ventricular mass and left atrial diameter were larger in endurance athletes than in controls [3].
A larger end-diastolic volume provides more blood in the ventricle before contraction and can contribute to a greater stroke volume, depending on how much blood remains after systole. This is consistent with the large maximal values measured in elite endurance runners, although these studies did not establish a causal link [4].
In my clinical experience, an enlarged heart is occasionally seen on the chest X-ray of an athlete. This is worth distinguishing from the enlargement seen in some patients with hypertension, where left ventricular hypertrophy is pathological. In athletes, the growth of the heart often looks more even, and on a chest X-ray it may appear somewhat rounder, rather than as one-sided as in people with hypertension.
Blood Volume: A Major Driver
One of the clearest experiments took blood back out. Nine healthy but untrained volunteers (VO₂max 47 ± 5 mL/kg/min) trained for 60 minutes, four times a week at 65% of VO₂max, for six weeks. Plasma volume rose by 147 mL (5%), red blood cell volume by 235 mL (10%) and total blood volume by 382 mL (7%). Resting echocardiography showed no structural changes in the heart. Maximal cardiac output increased from 18.9 to 20.4 L/min (9%), and VO₂max rose by 10%. When the researchers then removed blood to bring blood volume back to pre-training levels, maximal cardiac output returned to pre-training values (18.1 L/min) and VO₂max fell by 8%. The authors concluded that the increase in blood volume was the main mechanism behind the rise in maximal cardiac output after six weeks of training in previously untrained people [9].
A review of VO₂max biology reached a consistent conclusion: training-induced increases in VO₂max are largely facilitated by an expanded red blood cell volume and an associated improvement in SV — although it also adapts independently of changes in red blood cell volume [10].
When plasma volume rises proportionally more than red blood cell mass, hemoglobin concentration can look lower on a routine blood test through dilution, as explained in the article on blood volume expansion in athletes.
Interval Training
In a randomised study, 40 healthy, moderately trained men were assigned to one of four programmes matched for total oxygen consumption and performed three days a week for eight weeks: long slow distance running at 70% of maximal heart rate; lactate-threshold running at 85%; 15/15 intervals (15 seconds at 90–95% of maximal heart rate alternating with 15 seconds of active rest at 70%); or 4 × 4-minute intervals at 90–95% of maximal heart rate with 3 minutes of active rest at 70%. The interval groups improved VO₂max significantly more than the long slow distance and lactate-threshold groups, and SV increased significantly in the two interval groups, by approximately 10%. The authors noted a close correspondence between the changes in VO₂max and the changes in the heart’s output per beat [11].
This is a single eight-week study in moderately trained men, so it should not be read as proof that easier training does nothing for the heart. How hard and easy sessions are best combined across a training week is a separate question, discussed in the article on polarized training.
Interval training is often discussed in terms of VO₂max and stroke volume, but those numbers are only part of how hard efforts feel. In my own experience as an interval athlete, the limiting factor has usually not been cardiac output but lactate. After a hard sparring session or a competition I am of course out of breath, but it is not so much a feeling of oxygen hunger; the problem is more the clearance of lactate. I can tell because my heart rate is where I would expect it to be, while the breathlessness is relatively mild. I notice this especially in interval-type sport.
Female Athletes
In healthy young adults, stroke volume is larger in men than in women [2]. In female athletes, it also continues to rise at high intensities, and elite female endurance athletes had larger values than moderately trained women at every exercise intensity tested [5].
The training response, however, may differ between the sexes. A systematic review and meta-analysis of 26 endurance training studies in 468 healthy, untrained people (287 men and 181 women, aged 22 to 72) found that left ventricular end-diastolic volume increased more in men than in women (+15.6 vs +5.2 mL), and left ventricular SV increased significantly only in men (+9.2 mL). Left ventricular mass, by contrast, increased similarly in both sexes (+10.2 vs +7.0 g). In women — but not in men — older age was associated with smaller left ventricular adaptations [12].
Two caveats matter. The programmes were mainly moderate-intensity, lower-body endurance exercise lasting 12 to 52 weeks in untrained people, so the findings do not show that women cannot improve it. Elite female athletes had larger SV than moderately trained women at every intensity [5], although a cross-sectional comparison cannot show how much of that difference comes from training. They do suggest that, at least with moderate training, the cardiac response in women may be smaller and more age-dependent than in men.
Dehydration, Heat and Cardiovascular Drift
During prolonged exercise, heart rate can creep up even when pace or power stays the same. This is called cardiovascular drift: a rising heart rate accompanied by a falling stroke volume [13].
Hydration has a graded effect on it. In one study, nine subjects first dehydrated by exercising in the heat (32 °C) until body weight fell by 2.5%, then rested for two hours either without fluid or while drinking water equal to the fluid lost. They then cycled at 65% of peak oxygen consumption in a 21 °C environment while hypohydrated by 0.9% (water trial) or 2.8% (no-fluid trial). Compared with euhydrated cycling, heart rate was 10 ± 2 and 18 ± 2 beats per minute higher, and SV 9 ± 3 and 18 ± 2 mL per beat lower, respectively. Blood volume during exercise stayed at euhydrated levels, so under these conditions the drift was graded in proportion to hypohydration rather than explained by a smaller blood volume [13].
In hotter conditions with greater fluid loss, the heat study described earlier found that dehydration reduced the output per beat by compromising filling of the heart and venous return [6].
For athletes, the practical implication is that a heart rate drifting upward late in a long session may partly reflect hydration status, as shown under controlled experimental conditions [13]. Fluid replacement strategies are covered in the article on rehydration after exercise. Other contributors to a session that feels harder than it should are covered in the article on fatigue in athletes.
In my clinical practice, I often see a rising heart rate in a dehydrated patient, as if the body were compensating for the dehydrated state. To me it is one useful clinical pearl for recognising dehydration, and I occasionally look for it myself, although there are of course other clinical signs as well. In my experience, patients with diarrhoea or vomiting can become dehydrated quite acutely.
Heat Acclimation
Repeated exercise in the heat also triggers cardiovascular adaptations. A review of the cardiovascular side of heat acclimation lists an increase in total body water, plasma volume expansion, better maintenance and/or elevation of SV, a lower heart rate, improved ventricular filling and myocardial efficiency, and enhanced skin blood flow and sweating. The size of these adaptations varies with exercise intensity, exposure duration, the frequency and total number of exposures, and whether the heat is dry or humid [14].
A small randomised study illustrates the cardiac side. Thirteen male endurance-trained cyclists completed either five consecutive days of exercise with controlled hyperthermia at 32 °C and 70% relative humidity, or five days of exercise in temperate conditions (21 °C, 36% relative humidity). Resting echocardiography afterwards showed significantly greater increases in left ventricular end-diastolic volume, SV, left atrial volume and inferior vena cava diameter in the heat group, which the authors interpreted as consistent with increased preload and improved ventricular compliance [15].
These are resting measurements in a small group of male cyclists, so they show that heat acclimation can change cardiac filling — not how much it improves performance.
Detraining: The Gains Fade Quickly
These gains also fade quickly during a break. A review of short-term detraining (less than four weeks of insufficient training stimulus) described a rapid decline in VO₂max and blood volume in highly trained athletes. Exercise heart rate rises, but not enough to compensate for the smaller output per beat, so maximal cardiac output falls. In recently trained people, these changes are more moderate [16].
This is consistent with the phlebotomy experiment described above, in which removing the training-induced gain in blood volume was enough to erase the gain in maximal cardiac output [9].
Detraining shows up in everyday numbers as well. I stopped competing in 2019, after winning a world championship, and at that time my resting heart rate was quite low. When I trained less after my competitive career, my resting heart rate rose slightly, and I have seen the same when looking back at the data from my wearable devices. Now that I have started to train more again and do intervals, my resting heart rate has come down again. A wearable’s resting heart rate is of course only an indirect marker, and I have not measured my stroke volume, so I cannot say what changed in the heart itself. Still, the pattern is consistent with the idea that adaptations fade when training stops and return when it resumes.
Can You Measure It?
The studies in this article measured SV or cardiac volumes with cardiac MRI and echocardiography [2][3], inert gas rebreathing during cycling [9], and single-breath acetylene uptake during treadmill running [5].
Two points matter when interpreting a result. First, the method matters: in male athletes, left ventricular end-diastolic volume averaged 178 mL in MRI-based studies versus 135 mL in echocardiography-based studies [3], although these were different study populations rather than paired measurements. Second, body size matters: in the same meta-analysis, body surface area was positively associated with left ventricular mass, right ventricular mass and left atrial diameter [3]. Comparing an athlete’s values with a general reference range — or with someone measured using a different technique — can therefore mislead; for repeat measurements, using a consistent method may help limit method-related differences, and results from different techniques should be interpreted cautiously rather than assumed to be interchangeable.
Consumer devices that claim to estimate SV were not evaluated in the research reviewed for this article.
In cardiological examinations, stroke volume is often described indirectly through the ejection fraction. From a clinical perspective, the ejection fraction is generally regarded as a measure of the severity of heart failure, and it influences clinical decision-making in many cases when cardiologists assess its level. When we measure a patient’s actual oxygen uptake, a fitness test with VO₂max is the one we usually use in our practice. Lactate is also used in many situations, but in my understanding it measures something a little different.
Conclusion: Stroke Volume
Stroke volume — the volume of blood the heart ejects with each beat — is closely tied to VO₂max. Maximal heart rate is largely set by age [7], training-induced gains in VO₂max are largely facilitated by an expanded red blood cell volume and an improved output per beat [10], and gains in maximal cardiac output track gains in VO₂max [8].
The research also shows how much SV depends on how well the heart is filled. A training-induced expansion of blood volume was the main driver of a higher maximal cardiac output after six weeks of training in previously untrained people [9], while dehydration [13] and short-term detraining [16] push it down. Endurance athletes’ larger hearts [3], interval training [11] and heat acclimation [15] all relate to the same capacity.
Outside sport, stroke volume becomes visible mostly when something goes wrong — a rising heart rate in dehydration, distended neck veins in congestion, or a dramatic fall in output in conditions such as cardiac tamponade. In my clinical experience, an athlete’s slow resting heart rate is the quieter version of the same physiology. In my own case, resting heart rate rose slightly when I stopped competing and came down again when I returned to interval training, and in hard interval work lactate clearance rather than cardiac output has usually been my limiting factor.
For athletes, the practical message is straightforward: stroke volume is trainable, it is sensitive to hydration and time off, and it should not be judged from a single number measured with an unknown method.
Bibliography
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[7] https://pubmed.ncbi.nlm.nih.gov/11153730/
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[13] https://doi.org/10.1055/s-2007-1021023
[14] https://doi.org/10.1016/j.autneu.2016.02.002
