Stroke volume does/does not decline during exercise at maximal effort in healthy individuals
2007; American Physiological Society; Volume: 104; Issue: 1 Linguagem: Inglês
10.1152/japplphysiol.01073.2007
ISSN8750-7587
Autores Tópico(s)Heart Rate Variability and Autonomic Control
ResumoPOINT-COUNTERPOINT COMMENTSStroke volume does/does not decline during exercise at maximal effort in healthy individualsAlejandro Lucia, and Carl FosterAlejandro Lucia, and Carl FosterPublished Online:01 Jan 2008https://doi.org/10.1152/japplphysiol.01073.2007This is the final version - click for previous versionMoreSectionsPDF (47 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat The following letters are in response to Point:Counterpoint: Stroke volume does/does not decline during exercise at maximal effort in healthy individuals.To the Editor: Disagreement between studies showing a decrease (3) or no decrease in the stroke volume (SV) of healthy humans approaching volitional exhaustion during large muscle mass exercise (6) can be explained by differences in methods for SV assessment, body position, training status, exercise mode and protocol, the subject's motivation to cope with symptoms of fatigue, and individual differences in the behavior of heart rate (HR) and SV as peak exercise is approached (4). In most motivated, well trained athletes, maximal SV and cardiac output (Q) tend to level off during maximal efforts engaging large muscle mass. This is related to an unfavorable change in the balance between myocardial contractility, left ventricular filling (preload), and resistance to left ventricular emptying (afterload; Ref. 1). During graded exercise, the HR-workload relationship shows a negative acceleration in individuals where SV decreases, potentially attempting to defend diastolic filling time (4). Conversely, in ∼20% of healthy, well trained individuals where SV increases, the HR-workload relationship remains linear up to maximal exertion (4). The reasons for this individuality of response are unclear, but may depend on the ability to promote high vascular conductance (e.g., low afterload) during incremental exercise (1); the contractility of the myocardium, which may depend on cardiac dimensions (5); and the ability of venous return and myocardial compliance to maintain/allow adequate cardiac filling in the face of a shrinking diastolic filling time (2). However, any two individuals may solve the equation of defending SV and, indeed, Q in different ways that are yet to be elucidated.REFERENCES1 Foster C, Gall RA, Murphy P, Port SC, Schmidt DH. Left ventricular function during exercise testing and training. Med Sci Sports Exerc 29: 297–305, 1997.ISI | Google Scholar2 Glehdill N, Cox D, Jamnik R. Endurance athlete's stroke volume does not plateau: major advantage in diastolic function. Med Sci Sports Exerc 26: 1116–1121, 1994.Crossref | PubMed | ISI | Google Scholar3 González-Alonso J. Point :Stroke volume does decline during exercise at maximal effort in healthy humans. J Appl Physiol; doi:10.1152/japplphysiol. 00595.2007.Google Scholar4 Lepretre PM, Foster C, Koralsztein JP, Billat VL. Heart rate deflection point as a strategy to defend stroke volume during incremental exercise. J Appl Physiol 98: 1660–1665, 2005.Link | ISI | Google Scholar5 Lucia A, Carvajal A, Boraita A, Serratosa L, Hoyos J, Chicharro JL. Heart dimensions may influence the occurrence of the heart rate deflection point in highly trained cyclists. Br J Sports Med 33: 387–392, 1999.Crossref | ISI | Google Scholar6 Warburton ER, Gledhill N. Counterpoint: Stroke volume does not decline during exercise at maximal effort in healthy humans. J Appl Physiol: doi:10.1152/japplphysiol.00595.2007a.Google ScholarjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyPierre-Marie LeprêtreLaboratoire de Biomécanique et de Physiologie Insitut National du Sport et de l'Education PhysiqueJanuary2008Egil Henriksen, M. Sundstedt, and P. HedbergDepartment of Clin Physiol Central Hospital Väsreaas SwedenJanuary2008Chantal A. Vella, and Robert A. RobergsUniversity of Texas at El PasoJanuary2008Edward F. Coyle, and Joel D. TrinityThe University of Texas at Austin Human Performance LaboratoryJanuary2008Veronique Louise BillatUniversity Evry INSERM U902 Faculty of Sport Sciences Laboratory LEPHE EA3872 Genopole Evry-University of Evry-Val d'Essonne Evry, FranceJanuary2008To the Editor: Endurance performance is classicaly associated with the heart capacity to pump unusually large blood volume to muscles. It is so logical to speculate that maximal exercise terminates after a significant decrease in stroke volume value (SV). In this way, Professor Gonzalez-Alonso argues a “regulatory limit of the heart” supported by previous observations of a significant decline in SV at peak exercise compared with a 50% V̇o2max in healthy individuals (1). In 22 endurance-trained subjects who presented similar maximal SV and V̇o2, Lepretre et al. (3) also reported an increase in SV to 78.3 ± 9.3% V̇o2max followed by a significant decline until exhaustion. However, six of their subjects did not show a SV plateau before fatigue (3). Other human research has already shown varied SV responses to exercise (6). These SV behaviors could be explained by different cardiac adaptations induced by miscellaneous physical activity (2), genetic characteristics, or both. Individual SV responses to upright exercise, moreover, indicate that the SV pattern during maximal incremental or constant protocol is greatly dependent on intensity and duration. In fact, McCole et al. (5) reported that a 6-min ramp test resulted in a significantly greater SV and, therefore, cardiac output, than a 12-min progressive exercise despite no difference in maximal V̇o2 value. Indeed, V̇o2max is reached with a lower SV in heavy compared with maximal exhaustive constant exercises (4). This raises the question about the nature of the exercise to be prescribed to induce SV adaptations according to the individual fitness level. To the Editor: Despite the large quantity of data on LV performance during exercise, basic data on left ventricular (LV) performance are conflicting. Many of these inconsistencies can certainly be explained by methodological differences, measurement variability, supine versus upright exercise, athletes versus sedentary subjects, and different exercise protocols (1, 4).We used contrast echocardiography to assess changes in left ventricular volumes during incremental upright submaximal bicycle exercise in male endurance athletes (2). Maximal oxygen uptake and oxygen pulse were measured by using cardiopulmonary exercise testing. We found an almost linear increase in stroke volume (SV; from 105 to 152 ml from rest to a heart rate of 160 beats/min) mainly explained by an almost linear increase in LV end-diastolic volume and an initial small decrease in end-systolic volume during upright exercise. No significant differences were observed between stroke volume calculated from LV volumes with contrast echocardiography and SV calculated from oxygen pulse at heart rates of 130 and 160 beats/min. To explain the VAO2 during maximal exercise, the SV had to increase an additional 10% from submaximal to maximal exercise. Additional data suggesting an incremental increase in SV during upright exercise was that the mean transmitral pressure gradient, peak transmitral velocity, and LV filling rate showed a almost linear increase with exercise findings not easily explained by the decrease in LV filling time alone (3). In a hitherto unpublished paper, we showed that the increase in LV end-diastolic volume is explained by a significant augment in the inner transverse LV diameters creating a more spherical LV end-diastolic cavity during exercise.To the Editor: Endurance training, resistance training, body composition, or different disease states can lead to diverse adaptations in cardiac structure and/or function. It is currently unknown if these adaptations contribute to the ability, or the inability, to maintain SV during near-maximal or maximal exercise.Contrary to Warburton and Gledhill's (6) statement that the SV response to exercise is “highly reliant on fitness level,” not all endurance-trained individuals maintain SV (3, 4) and not all sedentary individuals show a drop in SV at maximal exercise (2). These responses have been demonstrated in cross-sectional and longitudinal studies (3–5).Gonzalez-Alonso (1) correctly points out that most of the published research in this area has not measured SV at maximal exercise and, thus, SV may have been overestimated. However, we (5) measured cardiac output and SV (CO2 rebreathing) 20–30 s prior to volitional fatigue and demonstrated three different SV responses at maximal exercise: drop, plateau, and continued increase. Scientists must refrain from concluding absolute interpretations, resulting in oversimplified explanations and understanding. This is especially true in exercise physiology, where multiple control systems combine with a multitude of individual differences in numerous exercise scenarios to create varied physiological responses.To the Editor: The parties involved in the debate (4, 6) appear to be discussing two different experimental conditions: incremental vs. constant-power cycling. On the basis of the title of the original Point:Counterpoint, we will offer our opinion on the SV response during or throughout 4–8 min of constant-power exercise that elicits V̇o2 max. Only a few investigations have reported SV and cardiac function during several minutes at constant maximal aerobic intensity (2, 5). These investigations have shown that SV reached maximal values 2–3 minutes into the exercise bout and then decreased prior to fatigue. Cardiac output (CO) and oxygen delivery also declined prior to exhaustion, suggesting a central limitation (e.g., myocardial) to maximal aerobic power. Unfortunately these data demonstrating reduced SV after several minutes of exercise at 95–100% V̇o2max were compiled primarily by one laboratory using invasive techniques (2, 5). Therefore, other laboratories should consider investigating these fundamental cardiovascular responses to maximal exercise. Data pertaining to prolonged exercise at 65–75% V̇o2 max with ensuing hyperthermia (1, 3) should not be ignored as the pattern of cardiovascular instability (reduced SV, CO, and MAP) is remarkably similar and just accelerated during high intensity exercise compared with prolonged moderate-intensity exercise. A common denominator linking high-intensity, short-term exercise and prolonged moderate-intensity exercise eliciting dehydration may be the development of hyperthermia (esophageal temperature of 39.3°C), which has been shown to reduce SV by 8% independent of dehydration and elevated skin temperature (4).To the Editor: This (4, 8) is the same debate as that on the occurrence of a V̇o2 drop after the achievement of a V̇o2 peak or V̇o2max plateau. For incremental model (7), the stroke volume should be expressed per unit of time since the independent factor is the power output for comparing stroke volume independently of the heart rate values. For constant load exercise, we must distinguish exercise below and above the maximal lactate steady state and not consider the intensity in percentage of since catecholamine concentration influences the vascular regulation (3, 5, 6). Indeed, exercise at 80% of can be below the maximal lactate steady state in well trained endurance athletes and above for sprinters (2). The kinetics of oxygen uptake must also be taken into consideration and the stroke volume must be expressed per unit of oxygen uptake when is not stable (1). In a marathon, stroke volume increased until the 24th kilometer and then was maintained despite a decrease in speed (personal data). Consequently, the stroke volume per unit of meter ran increased while the number of heart beats per unit of meter run was maintained constant. This result could be due to a cardiovascular endurance training adaptation for avoiding the increase in heart beat (and then the myocardium oxygen consumption) as reported for incremental exercise (7). Free-pace exercise models must also be studied since sudden deaths occur and the stroke volume kinetics could be one candidate for this sudden death due to dehydration or heart pathology.REFERENCES1. González-Alonso J. Point: Stroke volume does decline during exercise at maximal effort in healthy individuals. J Appl Physiol; doi:10.1152/ japplphysiol.00595.2007. Google Scholar2. D'Andrea A, Limongelli G, Caso P, Sarubbi B, Della Pietra A, Brancaccio P, Cice G, Scherillo M, Limongelli F, Calabrò R. Association between left ventricular structure and cardiac performance during effort in two morphological forms of athlete's heart. Int J Cardiol 86: 177–1784, 2002. Crossref | PubMed | ISI | Google Scholar3. Lepretre PM, Foster C, Koralsztein JP, Billat VL. Heart rate deflection point as a strategy to defend stroke volume during incremental exercise. J Appl Physiol 98: 1660–1665, 2005. Link | ISI | Google Scholar4. Lepretre PM, Koralsztein JP, Billat VL. Effect of exercise intensity on relationship between VO2max and cardiac output. Med Sci Sports Exerc 36: 1357–1363, 2004. Crossref | PubMed | ISI | Google Scholar5. McCole SD, Davis AM, Fueger PT. Is there a disassociation of maximal oxygen consumption and maximal cardiac output? Med Sci Sports Exerc 33: 1265–1269, 2001. Crossref | ISI | Google Scholar6. Warburton D, Gledhill N. Counterpoint: Stroke volume does not decline during exercise at maximal effort in healthy individuals. J Appl Physiol; doi:10.1152/japplphysiol.00595.2007a. Google ScholarREFERENCES1. González-Alonso J. Point: Stroke volume does decline during exercise at maximal effort in healthy individuals. J App Physiol; doi:10.1152/ japplphysiol.00595.2007. Google Scholar2. Sundstedt M, Hedberg P, Jonason T, Ringqvist I, Brodin LA, Henriksen E. Left ventricular volumes during exercise in endurance athletes assessed by contrast echocardiography. Acta Physiol Scand 182: 45–51, 2004. Crossref | PubMed | Google Scholar3. Sundstedt M, Hedberg P, Jonason T, Ringqvist I, Henriksen E. Echocardiographic Doppler assessments of left ventricular filling and ejection during upright exercise in endurance athletes. Clin Physiol Funct Imaging 27: 36–41, 2007. Crossref | ISI | Google Scholar4. Warburton D, Gledhill N. Counterpoint: Stroke volume does not decline during exercise at maximal effort in healthy individuals. J App Physiol; doi:10.1152/japplphysiol.00595.2007a. Google ScholarREFERENCES1. González-Alonso J. Point: Stroke volume does decline during exercise at maximal effort in healthy individuals. J Appl Physiol; doi:10.1152/ japplphysiol.00595.2007. Google Scholar2. Martino M, Gledhill N, Jamnik V. 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Endurance athletes' stroke volume does not plateau: major advantage is diastolic function. Med Sci Sports Exerc 26: 1116–1121, 1994. Crossref | PubMed | ISI | Google Scholar4. Gonzalez-Alonso J. Point: Stroke volume does decline during exercise at maximal effort in healthy individuals. J Appl Physiol; doi:10.1152/ japplphysiol.00595.2007. Google Scholar5. Gonzalez-Alonso J, Calbet JA. Reductions in systemic and skeletal muscle blood flow and oxygen delivery limit maximal aerobic in humans. Circulation 107: 824–830, 2003. Crossref | PubMed | ISI | Google Scholar6. Gonzalez-Alonso J, Dalsgaard MK, Osada T, Volianitis S, Dawson EA, Yoshiga CC, Secher NH. Brain and central haemodynamics and oxygenation during maximal exercise in humans. J Physiol 557: 331–342, 2004. Crossref | PubMed | ISI | Google Scholar7. Lepretre PM, Foster C, Koralsztein JP, Billat V. Heart rate deflection point as a strategy to defend stroke volume during incremental exercise. J Appl Physiol 98: 1660–1665, 2005. Link | ISI | Google Scholar8. Warburton DER, Gledhill N. Counterpoint: Stroke volume does decline during exercise at maximal effort in healthy individuals. J Appl Physiol; doi:10.1152/japplphysiol.00595.2007a. Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationCited ByHeavy cycling exercise at fixed heart rate prevent the decline of stroke volume and delay time to exhaustion in trained adolescentsScience & Sports, Vol. 32, No. 1Long-term stability of the oxygen pulse curve during maximal exerciseClinics, Vol. 66, No. 2Cardiac Dimensions over 5 Years in Highly Trained Long-Distance Runners and Sprinters13 March 2015 | The Physician and Sportsmedicine, Vol. 38, No. 4Running-Specific Prostheses Permit Energy Cost Similar to NonamputeesMedicine & Science in Sports & Exercise, Vol. 41, No. 5Last Word on Point:Counterpoint: Stroke volume does/does not decline during exercise at maximal effort in healthy individualsJosé González-Alonso1 January 2008 | Journal of Applied Physiology, Vol. 104, No. 1 More from this issue > Volume 104Issue 1January 2008Pages 281-283 Copyright & PermissionsCopyright © 2008 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.01073.2007PubMed17975122History Published online 1 January 2008 Published in print 1 January 2008 Metrics Downloaded 1,864 times
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