How much oxygen consumption increase with exercise intensity before it plateaus?

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While exercising, the human body tries to optimize the use of oxygen captured in the lungs.

During intense exercise, the oxygen consumption of the human body can increase up to 8 times, compared to the consumption at rest, before it plateaus. This higher demand for oxygen is usually covered through increased heart rate, which increases the cardiac output, and thus, the amount of blood (and oxygen) reaching the muscles.

However, cardiac output cannot increase as much as oxygen demand does. When this limit is surpassed, the human body has another mechanism to ensure oxygen supply to the muscles. Once cardiac output cannot increase more, the only solution is to remove more oxygen from hemoglobin, in this way, the same volume of blood will provide more oxygen. This happens because when muscles increase their metabolic rate, they produce high amounts of carbon dioxide and H+, which lower the pH. Lower pH reduces the affinity of hemoglobin for oxygen, making it easier for oxygen to be transferred from hemoglobin to the muscle tissue.

A review of the stroke volume response to upright exercise in healthy subjects

1. C A Vella,
2. R A Robergs

1. University of New Mexico, Albuquerque, New Mexico, USA

1. Correspondence to: Dr Vella University of New Mexico, MSC 04 2610, 1, Albuquerque 87131, USA; cvellasalud.unm.edu

Abstract

Traditionally, it has been accepted that, during incremental exercise, stroke volume plateaus at 40% of Vo2max. However, recent research has documented that stroke volume progressively increases to Vo2max in both trained and untrained subjects. The stroke volume response to incremental exercise to Vo2max may be influenced by training status, age, and sex. For endurance trained subjects, the proposed mechanisms for the progressive increase in stroke volume to Vo2max are enhanced diastolic filling, enhanced contractility, larger blood volume, and decreased cardiac afterload. For untrained subjects, it has been proposed that continued increases in stroke volume may result from a naturally occurring high blood volume. However, additional research is needed to evaluate the importance of blood volume, or other mechanisms, that influence the stroke volume response to exercise in untrained subjects.

• cardiac output
• contractility
• diastolic filling
• maximum oxygen uptake

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• cardiac output
• contractility
• diastolic filling
• maximum oxygen uptake

HISTORICAL PERSPECTIVE

It is commonly accepted that, during incremental, upright exercise to maximum, stroke volume increases from rest to exercise and plateaus at 40–50% of Vo2max.1 The theory of a stroke volume plateau developed from early research based on a few subjects during two or three exercise intensities,1–3 with the latter characteristic limiting the number of data points used to describe the stroke volume response to exercise.2,3 The concept of a plateau in stroke volume was attributed mainly to a decrease in the diastolic filling time that occurs during exercise of increasing intensity.4

Interestingly, a progressive increase in stroke volume was reported in the literature as early as 1960. In a study by Chapman and others5 the stroke volume responses during discontinuous treadmill exercise were evaluated in 26 normal, male subjects aged 19–63 years. The fitness level of the subjects was not noted, but the mean (SD) Vo2max was 3.38 (0.46) litres/min. Stroke volume increased progressively with increasing levels of exercise in most subjects, but the relation between stroke volume and Vo2 was not linear. Similarly, Ekblom and Hermansen6 reported that stroke volume progressively increased during treadmill exercise at workloads of 40–80% of Vo2max and at Vo2max in nine of 13 well trained athletes (subject sex was not stated). Unfortunately, these findings were largely ignored and it became accepted that stroke volume plateaus during exercise of increasing intensity.

More recent investigations have reported that stroke volume progressively increases in certain people.7–12 The mechanisms for the continual increase in stroke volume are not completely understood. Gledhill et al7 proposed that enhanced diastolic filling and subsequent enhanced contractility are responsible for the increased stroke volume in trained subjects. However, an increase in stroke volume with an increase in exercise intensity has also been reported in untrained subjects.8,9 Table 1 presents a summary of the past research that has quantified stroke volume during exercise.

Table 1

Summary of the literature on stroke volume response to exercise

Current research indicates that there is a range of responses in stroke volume to reflect the range of a subject’s training status. In addition, training may not be the only factor affecting the stroke volume response to exercise. Four main types of stroke volume responses to exercise have been reported in the literature: plateau,1,4,10,13–16 plateau with a drop,14,15,17–19 plateau with a secondary increase,5,11,20 and progressive increase6–10,12,14,21 (fig 1). The implications of a progressive increase in stroke volume to Vo2max have yet to be completely understood.

This review will examine recent discussions and evidence describing the stroke volume response to increasing exercise intensity. In addition, the role of fitness level, age, and sex on the stroke volume response to incremental exercise will be clarified.

FITNESS LEVEL

Gledhill and coworkers7 were the first to recognise the difference in the stroke volume response between trained and untrained young men. The study compared the stroke volume response in competitive, male endurance cyclists (22.5 (2.1) years; mean (SD)) and normally active males (22.2 (4.9) years) at matched heart rates ranging from 90 to190 beats/min during cycle ergometry. The stroke volume of the competitive endurance cyclists increased progressively throughout exercise, whereas that of the normally active males plateaued at an average heart rate of 120 beats/min or 40% of Vo2max. In addition, the stroke volumes of the trained subjects were significantly larger than those of the untrained subjects at all heart rates (p<0.001).

There is accumulating evidence that, in some endurance trained men and women, stroke volume continues to increase to Vo2max. Zhou et al12 compared the stroke volume response in untrained men (28.1 (7.5) years), male distance runners (25.5 (4.3) years), and elite male runners (29.8 (2.5) years) during incremental exercise to exhaustion on the treadmill. The stroke volume of the untrained and distance runners plateaued at about 40% of Vo2max, whereas in elite distance runners, it continued to increase throughout exercise to maximum. Although the distance runners’ Vo2max averaged 72.1 ml/kg/min, 12 ml/kg/min lower than that of the elite runners, they still exhibited a plateau in stroke volume, indicating that endurance training may not be the only factor influencing the stroke volume response to exercise.

Crawford et al23 studied the stroke volume response in male and female competitive marathon runners and non-competitive runners. The stroke volume of the non-competitive runners plateaued at 70% of maximal heart rate, whereas that of the competitive marathon runners progressively increased to maximal heart rate. Although the stroke volume of the latter group progressively increased to maximal heart rate, the authors noted that the increase in stroke volume from 70% to 100% of maximal heart rate was not significant.

Vanfraechem22 studied healthy, male soccer players (21 (0.2) years) during cycle exercise at 25, 50, and 75% of Vo2max and reported significant increases in stroke volume at each workload. Although stroke volume was not measured at an intensity greater than 75% of Vo2max, this study suggested that it may not plateau in young, healthy male soccer players.

Warburton and coworkers21 studied the stroke volume response in male endurance trained cyclists during incremental exercise to Vo2max (22 (1) years) under two conditions: a 500 ml plasma volume expansion and control. In both the plasma volume expansion and control trials, stroke volume increased progressively throughout incremental cycle exercise to Vo2max. In addition, stroke volume and cardiac output were elevated after plasma volume expansion, suggesting that blood volume has a significant influence on the stroke volume response to exercise. Warburton et al26 reported similar findings in highly trained male cyclists (18–30 years) during supine and upright cycle exercise to Vo2max. In both supine and upright exercise, stroke volume increased progressively to Vo2max.

In contrast, Spina et al19 reported a plateau in stroke volume after 12 weeks of endurance training in healthy sedentary men and women (25 (1) years). Before endurance training, stroke volume fell significantly in all subjects when exercise intensity was increased from 50% to 100% of Vo2max. The authors concluded that endurance training attenuated the decrease in stroke volume at maximal exercise.

Rivera et al10 also reported a plateau in stroke volume in endurance trained younger and older men. All of the young athletes (27–39 years) and five of 11 master athletes (59–81 years) attained a plateau in stroke volume at 30% of Vo2max. The stroke volume of six of the master athletes continued to increase to 85% of Vo2max, but the increase in stroke volume from 30% to 85% of Vo2max was not significant.

Similarly, unpublished data from our laboratory suggested that not all endurance trained subjects exhibit a progressive increase in stroke volume during incremental exercise to Vo2max. We tested 21 endurance trained men and women (29.4 (6.1) years) during cycle exercise to Vo2max. Eighteen subjects reached a plateau in stroke volume at 37% of Vo2max, with one subject unable to maintain maximal stroke volume as exercise intensity increased to Vo2max. Only three subjects showed a progressive increase in stroke volume to Vo2max.

Although most of the available data on the stroke volume response to exercise are from male subjects, there is also evidence to support a progressive increase in stroke volume in female subjects. Ferguson et al20 compared the stroke volume response in moderately active and endurance trained women (18–30 years) during incremental cycle exercise to exhaustion. Stroke volume increased progressively to Vo2max in both groups. The stroke volume was significantly greater in endurance trained women at all workloads. In moderately trained women, stroke volume increased from rest to exercise, plateaued, and then showed a secondary increase to maximum. Wiebe and colleagues11 reported similar results in women 20–63 years of age. This type of rise in stroke volume is consistent with data from others.5,9,11

Three studies to date provide evidence that stroke volume does not plateau in untrained subjects.5,8,9 Martino and colleagues9 studied healthy, young men (19–22 years) with no history of training, but unusually high Vo2max. Untrained subjects with a high Vo2max (65.3 (0.6) ml/kg/min; HI group) were matched with similar subjects who had a normal Vo2max (46.2 (0.9) ml/kg/min; LO group). Subjects were chosen from a group of 1900 healthy, young men who underwent prior Vo2max testing. Despite no history of training, the Vo2max and mean blood volume of the HI group were comparable with that of an endurance trained athlete. In both groups, stroke volume increased progressively from rest to 50% of Vo2max, plateaued from 50% to 75% of Vo2max, then increased from 75% to 100% of Vo2max. Martino and colleagues concluded that the high Vo2max observed in the untrained subjects was due to a naturally occurring high blood volume that contributes to a high maximal stroke volume and cardiac output. Krip and colleagues8 reported similar results in endurance trained male cyclists and untrained male control subjects (18–30 years) during cycle exercise to exhaustion. The stroke volume of all of the subjects increased progressively throughout exercise to Vo2max, although the trained subjects had higher blood volumes, faster diastolic filling rates, and faster systolic emptying rates than the untrained controls.

Current research supports a continual increase in stroke volume during exercise of increasing intensity in some trained and untrained subjects. The physiological characteristics that promote this progressive increase are not yet fully understood. Data support endurance training as a mechanism of improving the stroke volume response to exercise. However, the data of Martino et al9 show that blood volume, independent of training, may be a major determinant of the stroke volume response to exercise.

AGE

Studies on the effects of age on the stroke volume response to exercise have produced conflicting results. Whereas most studies have reported a plateau or a fall in stroke volume,14,15,17,18 two have reported a progressive increase in stroke volume in older men and women.10,11 The age related effects on the stroke volume response to exercise may be due to increases in end systolic volume, decreases in end diastolic volume, or a combination of both.

The results of Wiebe et al11 and Rivera et al10 provide evidence of a progressive increase in stroke volume in older subjects. Wiebe and others11 examined the stroke volume response during incremental cycle exercise to Vo2max in endurance trained women (20–63 years). The subjects were matched for lean body mass, then divided into four age groups: 20–29, 40–45, 49–54, and 58–63 years. In all groups, stroke volume increased progressively throughout incremental exercise to Vo2max. Maximal stroke volume was lower in endurance trained women aged 40–63 years than in those aged 20–29 years. The authors hypothesised that the age related differences in maximal stroke volume may be due to decreases in end diastolic volume or end systolic volume. These data suggest that older subjects have the ability to progressively increase stroke volume during exercise of increasing intensity.

Rivera and colleagues10 reported similar results when comparing the stroke volume response of master athletes (59–81 years) and young athletes (27–39 years) during incremental treadmill exercise to 85% of Vo2max. The stroke volume of all of the young runners and five of 11 master runners plateaued during exercise, whereas the stroke volume of the other six master runners progressively increased to 85% of Vo2max. The authors noted that, in all groups, the average stroke volume did not significantly increase after 30% of Vo2max; however, visual inspection of individual data revealed that stroke volume progressively increased in six of 11 master runners.

In contrast, several authors have reported a plateau or fall in stroke volume during exercise in older subjects.13,14,17,18 Proctor and others14 compared younger (20–31 years) and older (51–72 years) endurance trained men and women during cycle exercise at 40%, 70%, and 90% of Vo2max. The stroke volume in the young men continued to increase progressively throughout exercise to 90% of Vo2max, whereas the stroke volume of older men and younger women exhibited a plateau which was maintained throughout exercise. The older women showed an impaired ability to maintain stroke volume when intensity was increased from 70% to 90% of Vo2max. Several of the oldest men also showed a modest decline in stroke volume at exercise intensities above 70% of Vo2max. The authors noted that the stroke volume response in both the older men and women was related to age (r = −0.50), with the oldest subjects having the largest decrease in stroke volume.

McCole et al18 reported similar results in postmenopausal competitive master athletes, physically active women, and sedentary women (63 (5) years) during treadmill exercise to Vo2max. In all groups, stroke volume reached maximal values at 40–60% of Vo2max and decreased significantly as exercise intensity increased from 60% to 100% of Vo2max. The decrease in stroke volume was similar across all physical activity groups.

Ogawa et al17 studied healthy younger (18–31 years) and older (51–72 years) sedentary and endurance trained men and women. The subjects were divided into eight groups based on age (younger versus older), training status (sedentary versus trained), and sex. In all groups, the highest stroke volume was attained at 50% of Vo2max, and a fall in stroke volume occurred between 50% and 100% of Vo2max.

Hagberg et al24compared master athletes (56 (5) years), young runners matched in training and performance to the master athletes (25 (3) years), competitive young runners (26 (3) years), and healthy older sedentary subjects (58 (5) years) during treadmill exercise at 50%, 60%, and 70% of Vo2max. In all groups, stroke volume plateaued at 50% of Vo2max and was maintained up to 70% of Vo2max. Although the stroke volume of the older subjects did not decline, stroke volume measurements were only obtained up to 70% of Vo2max. Several studies have reported a fall in stroke volume at intensities above 70% of Vo2max in older subjects,14,17,18 therefore it is difficult to ascertain if the plateau in stroke volume in older subjects would have been maintained up to Vo2max.

McLaren and colleagues13 reported a stroke volume plateau in trained older male cyclists (65 (2.1) years), trained older male runners (65 (3.5) years), and healthy but untrained older male controls (66 (1.2) years). The stroke volume of the older trained runners plateaued at about 40% of Vo2max, whereas the stroke volume of the older trained cyclists and controls plateaued at an average of 30% of Vo2max.

In a training study by Spina et al,15 the stroke volume of older men and women decreased as exercise intensity increased from 50% to 100% of Vo2max before and after 9–12 months of endurance training, suggesting that the adaptability in the stroke volume response to exercise may be influenced by age.

Current evidence indicates that older subjects (men and women) have an impaired ability to maintain stroke volume at near maximal exercise. Although there is evidence of a progressive increase in stroke volume in older subjects, additional longitudinal research is needed to evaluate the effects of age on the stroke volume response to exercise.

SEX DIFFERENCES

The studies on sex differences in the stroke volume response to exercise have produced conflicting results. Sullivan and others16 investigated the effects of sex on stroke volume control during cycle exercise to Vo2max in healthy men (20–70 years) and women (20–63 years). In both men and women, stroke volume reached its maximum at 50% of Vo2max and remained unchanged through maximal exercise. There were no differences in stroke volume index (ml/m2) at rest or during exercise between groups. In addition, the increase in stroke volume index from rest to exercise was similar in men and women. These authors concluded that, in healthy subjects, matched for body size and fitness level, sex is not an important determinant of the stroke volume response to exercise.

In contrast, although Ogawa et al17 reported similar stroke volume responses in healthy younger (18–31 years) and older (52–27 years) sedentary and endurance trained men and women, the stroke volume of the women was lower at all workloads compared with the men, even after normalisation to body weight. After normalisation of stroke volume to fat free mass, the sex difference was eliminated in sedentary subjects, but only reduced in the endurance trained subjects. The authors concluded that the sex difference in the stroke volume of the endurance trained subjects was due to a greater percentage of body fat in women.

Proctor and others14 examined the influence of age and sex on cardiovascular responses to exercise. The stroke volume response of younger (20–31 years) and older (51–72 years) endurance trained men and women were compared during cycle exercise at 40%, 70%, and 90% of Vo2max. The stroke volume in the young men had not yet reached a plateau at 90% of Vo2max, whereas the stroke volume of older men and younger women reached a plateau at 40% of Vo2max which was maintained throughout exercise. The older women showed an impaired ability to maintain stroke volume at exercise intensities above 90% of Vo2max, which was also evident, to a lesser degree, in the oldest men. Spina and coworkers15 studied sex differences in the cardiovascular responses before and after training in older men and women (64 (3) years). Before and after training, stroke volume decreased as exercise intensity was increased from 50% to 100% of Vo2max in both sexes. However, the decrease in stroke volume was greater in women than in men.

Current evidence suggests that the stroke volume response to exercise may differ between men and women. However, sex differences cannot be elucidated at this time because of conflicting results and a lack of relevant studies.

MECHANISMS OF ENHANCED STROKE VOLUME

With increasing exercise intensity, diastolic filling time, as well as systolic ejection time, decreases.7 This decrease is thought to lead to a plateau in stroke volume with increasing exercise intensity. However, current research is suggesting that, in young endurance trained subjects, diastolic filling, as well as ventricular emptying, is enhanced, leading to a progressive increase in stroke volume during exercise to Vo2max.7,8,20 Interestingly, research has shown that endurance trained subjects have significantly longer ventricular ejection times,7,8,27 greater myocardial contractility,16,22 greater left ventricular diameter and mass,28–31 and significantly shorter diastolic filling times7,8,27 than untrained subjects.

Gledhill et al7 reported that, in endurance trained men, ventricular ejection times were longer, and diastolic filling times were shorter, than in untrained men (figs 2 and 3). If athletes are able to increase end diastolic volume in less time than untrained subjects, this suggests that the rates of ventricular filling are dramatically increased in trained subjects. What allows for this increased rate of filling? Gledhill and coworkers7 suggested that the higher blood volumes in the trained subjects maintained an adequate ventricular filling pressure during exercise, thereby enhancing diastolic filling. The longer ejection times and enhanced diastolic emptying reported by Gledhill et al7 were attributed to lower systolic and diastolic blood pressures in trained subjects, which reduced cardiac afterload and facilitated ventricular emptying. Further support for enhanced diastolic filling in athletes was reported by Vinereanu et al.31 Using tissue Doppler echocardiography, they reported augmented left ventricular diastolic filling velocities in endurance trained subjects compared with strength trained and control subjects.

Wolfe and others27 reported similar findings in trained male athletes. The athletes tested had shorter pre-ejection periods, longer ejection times, and faster mean systolic ejection rates at the same exercise heart rates than subjects who were moderately trained and untrained. The authors hypothesised that an enhanced end diastolic volume and ejection fraction were involved in the increased stroke volume in athletes.

What is already known on this topic

Research data on the stroke volume response to incremental exercise are conflicting. Early research supports a plateau in stroke volume in healthy untrained and trained subjects. Recent research has documented that stroke volume progressively increases to Vo2max in both trained and untrained subjects, but this finding has not been consistently reported.

Ferguson and colleagues20 suggested that, in endurance trained women, the increase in stroke volume at higher exercise intensities was due to an enhanced ventricular preload, not myocardial contractility. In contrast, Jensen-Urstad and colleagues32 reported that training induced increases in myocardial contractility, and possibly a decreased afterload, were the main contributing factors to the increase in stroke volume during incremental exercise in elite male runners. Similarly, Vanfraechem22 reported that left ventricular ejection times decreased at each workload in male soccer players. The author hypothesised that the continued increase in stroke volume, despite the decrease in ventricular ejection time, may be due to an increase in ejection fraction during exercise of increasing intensity.

In addition, left ventricular eccentric hypertrophy may be related to enhanced diastolic filling and stroke volume. Data indicate that endurance trained athletes develop an increase in both left ventricular diameter and wall thickness (eccentric hypertrophy), as the heart adapts to both volume and pressure loads.28–31 Longitudinal data from Levy et al30 indicate that endurance training significantly increases left ventricular mass and is associated with improvements in early diastolic filling rates at rest and during exercise. Similarly, Hoogsteen et al29 reported greater left ventricular end diastolic diameter and early filling rates in endurance trained subjects compared with previously established normal values. However, data are conflicting in this area.28,30

The above findings indicate that endurance trained subjects may have enhanced diastolic filling, greater left ventricular diameter and mass, greater ventricular compliance, greater myocardial contractility, and may depend more on the Frank Starling mechanism (preload) as exercise intensity increases, compared with untrained subjects. Although research suggests that untrained subjects with a naturally occurring high blood volume may have enhanced diastolic filling,8,9 there is currently no evidence to suggest that untrained people have enhanced ventricular compliance, greater left ventricular diameter and mass, or myocardial contractility, as seen in trained subjects.

What this study adds

This is the first review of stroke volume responses to exercise in healthy subjects. This study adds to the understanding of the various stroke volume responses to increasing exercise intensity, the effects of endurance training, sex, and age on the stroke volume response to exercise, and the mechanisms responsible for a progressive increase in stroke volume during exercise.

CONCLUSIONS

Current findings indicate that the stroke volume response to exercise may depend on many factors, including age, fitness level, sex, and genetics. Those with a high blood volume may be more likely to exhibit a progressive increase in stroke volume during exercise of increasing intensity. The progressive increase in stroke volume with endurance training has some training implications and clinical relevance. In terms of myocardial oxygen demand, increasing stroke volume is much more efficient than increasing heart rate during exercise. In athletes, increasing stroke volume for a given heart rate may increase work output and performance. The physiological mechanisms for an enhanced stroke volume during exercise may include enhanced diastolic filling due to increases in blood volume, left ventricular diameter, and ventricular compliance, enhanced systolic emptying due to increases in myocardial contractility and decreases in ventricular afterload, or both.

Future investigations should evaluate the type and amount of endurance training needed to facilitate a progressive increase in stroke volume during incremental exercise and determine if the adaptability in the stroke volume response to exercise is influenced by age, sex, type of training, and training status.

REFERENCES

1. ↵

   Astrand PO, Cuddy TE, Saltin B, et al. Cardiac output during submaximal and maximal work. J Appl Physiol 1964;19:268–74.

2. ↵

   Bevegard S, Holmgren A, Jonsson B. Circulatory studies in well trained athletes at rest and during heavy exercise, with special reference to stroke volume and the influence of body position. Acta Physiol Scand1963;57:26–50.

3. ↵

   Grimby G, Nilsson NJ, Saltin B. Cardiac output during submaximal and maximal exercise in active middle-aged athletes. J Appl Physiol1966;21:1150–6.

4. ↵

   Higginbotham MB, Morris KG, Williams RS. et al Regulation of stroke volume during submaximal and maximal upright exercise in normal man. Circ Research1986;58:281–91.

5. ↵

   Chapman CB, Fisher JN, Sproule BJ. Behavior of stroke volume at rest and during exercise in human beings. J Clin Investigation1960;30:1208–13.

6. ↵

   Ekblom B, Hermansen L. Cardiac output in athletes. J Appl Physiol1968;25:619–25.

7. ↵

   Gledhill N, Cox D, Jamnik R. Endurance athletes’ stroke volume does not plateau; major advantage is diastolic function. Med Sci Sports Exerc 1994;26:1116–21.

8. ↵

   Krip B, Gledhill N, Jamnik V, et al. Effect of alterations in blood volume on cardiac function during maximal exercise. Med Sci Sports Exerc 1997;29:1469–76.

9. ↵

   Martino M, Gledhill N, Jamnik V. High VO2 max with no history of training is primarily due to high blood volume. Med Sci Sports Exerc 2002;34:966–71.

10. ↵

    Rivera AM, Pels III, Sady AE, et al. Physiological factors associated with the lower maximal oxygen consumption of master runners. J Appl Physiol 1989;66:949–54.

11. ↵

    Wiebe CG, Gledhill N, Jamnik VK, et al. Exercise cardiac function in young through elderly endurance trained women. Med Sci Sports Exerc 1999;31:684–91.

12. ↵

    Zhou B, Conlee RK, Jensen R, et al. Stroke volume does not plateau during graded exercise in elite male distance runners. Med Sci Sports Exerc 2001;33:1849–54.

13. ↵

    McLaren PF, Nurhayati Y, Boutcher SH. Stroke volume response to cycle ergometry in trained and untrained older men. Eur J Appl Physiol1997;57:537–42.

14. ↵

    Proctor DN, Beck KC, Shen PH, et al. Influence of age and gender on cardiac output VO2 relationships during submaximal cycle ergometry. J Appl Physiol 1998;84:599–605.

15. ↵

    Spina RJ, Ogawa T, Kohrt WM, et al. Differences in cardiovascular adaptations to endurance exercise training between older men and women. J Appl Physiol 1993;75:849–55.

16. ↵

    Sullivan MJ, Cobb FR, Higginbotham MB. Stroke volume increases by similar mechanisms during upright exercise in normal men and women. Am J Cardiol1991;67:1405–12.

17. ↵

    Ogawa T, Spina RJ, Martin III WH, et al. Effects of aging, sex, and physical training on cardiovascular responses to exercise. Circulation 1992;86:494–503.

18. ↵

    McCole SD, Brown MD, Moore GE, et al. Cardiovascular hemodynamics with increasing exercise intensities in postmenopausal women. J Appl Physiol 1999;87:2334–40.

19. ↵

    Spina RJ, Ogawa T, Martin III WH, et al. Exercise training prevents decline in stroke volume during exercise in young healthy subjects. J Appl Physiol 1992;72:2458–62.

20. ↵

    Ferguson S, Gledhill N, Jamnik VK, et al. Cardiac performance in endurance trained and moderately active young women. Med Sci Sports Exer 2001;33:1114–17.

21. ↵

    Warburton DER, Gledhill N, Jamnik VK, et al. Induced hypervolemia, cardiac function, VO2 max, and performance of elite cyclists. Med Sci Sports Exerc 1999;31:800–8.

22. ↵

    Vanfraechem JHP. Stroke volume and systolic time interval adjustments during bicycle ergometer. J Appl Physiol1979;46:588–92.

23. ↵

    Crawford MH, Petru MA, Rabinowitz C. Effect of isotonic exercise training on left ventricular volume during upright exercise. Circulation1985;72:1237–43.

24. ↵

    Haberg JM, Allen WK, Seals DR, et al. A hemodynamic comparison of young and older endurance trained athletes during exercise. J Appl Physiol 1985;58:2041–6.

25. ↵

    Leyk D, Ebfeld D, Hoffmann U, et al. Postural effect on cardiac output, oxygen uptake and lactate during cycle exercise of varying intensity. Eur J Appl Physiol 1994;68:30–5.

26. ↵

    Warburton DER, Haykowsky MJ, Quinney HA, et al. Myocardial response to incremental exercise in endurance-trained athletes: influence of heart rate, contractility and the Frank-Starling effect. Exp Physiol 2002;87:613–22.

27. ↵

    Wolfe LA, Cunningham DA, Davis GM, et al. Relationship between maximal oxygen uptake and left ventricular function in exercise. J Appl Physiol 1978;44:44–9.

28. ↵

    Finkelhor RS, Hanak LJ, Bahler RC. Left ventricular filling in endurance-trained subjects. J Am Coll Cardiol1986;8:289–93.

29. ↵

    Hoogsteen J, Hoogeveen A, Schaffers H, et al. Left atrial and ventricular dimensions in highly trained cyclists. Int J Cardiovasc Imaging 2003;19:211–17.

30. ↵

    Levy WC, Cerqueira MD, Abrass IB, et al. Endurance exercise training augments diastolic filling at rest and during exercise in healthy young and older men. Circulation 1993;88:116–26.

31. ↵

    Vinereanu D, Florescu N, Sculthorpe N, et al. Left ventricular long-axis diastolic function is augmented in the hearts of endurance-trained compared with strength-trained athletes. Clin Sci 2002;103:249–57.

32. ↵

    Jensen-Urstad M, Bouvier F, Nejat M, et al. Left ventricular function in endurance runners during exercise. Acta Physiol Scand 1998;164:167–72.

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  British Journal of Sports Medicine 2005; 39 688-688 Published Online First: 23 Aug 2005. doi: 10.1136/bjsm.2004.013037corr1

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