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POINT-COUNTERPOINT
Centre for Sports Medicine and Human Performance
Brunel University, Uxbridge
Middlesex, United Kingdom
e-mail: j.gonzalez-alonso{at}brunel.ac.uk
POINT: STROKE VOLUME DOES DECLINE DURING EXERCISE AT MAXIMAL EFFORT IN HEALTHY INDIVIDUALS
A widely held theory explaining the physiological factors limiting maximal aerobic power (
O2max) in humans postulates that the perfusion capacity of skeletal muscle greatly exceeds the capacity of the heart to pump blood into the systemic circulation (1, 2, 20, 22, 27). This theory implies that any human being would be able to recruit more motor units and produce more work during maximal exercise if cardiac output (Q) did not reach such a hypothetical upper limit. In this debate, I will argue that the decline in stroke volume (SV) underpinning the plateau or drop in Q during incremental and constant maximal exercise supports the idea of a regulatory limit of the heart. The approach is necessarily integrative to be able to support the contention that SV does decline during exercise at maximal effort in healthy individuals. It is emphasized that the question under debate is whether the SV value preceding fatigue (i.e., 10–30 s before exhaustion) is lower than the values observed at submaximal intensities during incremental exercise to exhaustion or during the initial stages of maximal constant-load exercise. It is important to note, however, that due to methodological difficulties, only a handful of studies in the literature report measures of SV and Q in the few seconds before exhaustion. The common observation that heart rate and systemic a-vO2 difference increase progressively during exercise to maximum makes the behavior of Q the central issue of the debate.
A number of observations made with a variety of experimental techniques provide evidence that SV declines during maximal incremental exercise in humans, a response that accompanies the attenuation in the rate of rise, the plateau, or the decline in Q (9, 10, 12, 14, 16, 18, 21, 25, 26, 28, 29). In the early 1980s, Keul et al. (16) provided the first echocardiographic data supporting that SV falls during upright cycling to exhaustion. Using right heart catheterization, radionuclide angiography, and expired gas analysis, Higginbotham et al. (14) later showed a slight decline in SV at peak exercise following the "classic" plateau response from 40–50% O2max (3), which was attributed to the effects of tachycardia on left ventricular filling. In the same year and using a dye-dilution method for determining Q, Yamaguchi et al. (30) reported a decline in SV during incremental supine cycling in 31 subjects showing an attenuation or levelling off in Q. Adding inconsistency to their results, however, they reported a plateau in SV in 9 subjects displaying a linear increase in Q and a conflicting levelling off in the calculated systemic a-vO2 difference above 50% O2max (30). In the 1990s, a number of independent research groups showed an 8–11% decline in SV at peak exercise using angiographic, acetylene rebreathing, and echocardiographic techniques (9, 25, 26). Recent experiments employing the Fick principle to estimate Q expand on these early observations by showing a significant fall in SV during incremental exercise accompanying nonlinear locomotor muscle blood flow and Q dynamics leading to a plateau in exercising limb muscle O2 (19, 28, 29). Of note is the strikingly similar pattern of response in Stringer et al. (28, 29) and in our recent study during incremental exercise to exhaustion (19). Both studies found a significant decline in SV at peak exercise compared with 50% O2max, which accompanied the attenuation and subsequent plateau in Q above 90% O2max (19, 28, 29). Because the methods available to assess heart rate, a-vO2 difference, and O2 are more sensitive than the methods used to measure SV or Q, a concerted examination of components of the Fick equation (O2 = Q x a-vO2 difference, where Q = SV x heart rate) is warranted to ascertain the validity of the measured or estimated SV. In our study, heart rate and O2 increased in a linear fashion (r2 = 0.99; P< 0.001) in agreement with studies in the literature. Interestingly, Stringer et al. (28, 29) showed that systemic a-vO2 differences display a linear rather than a hyperbolic profile, thus indicating that Q as a function of O2 must be curvilinear and that SV must decline during incremental exercise to exhaustion. Indeed, direct measures of blood oxygen content demonstrate that systemic and leg oxygen extraction increases continuously until exhaustion, reaching values ranging from 80 to 95%, with the extraction across the exercising legs being higher than across the systemic circulation (6, 10, 12, 23, 24). The continuously increasing a-vO2 difference and the linear increase in heart rate during incremental exhausting exercise suggest that the fall in SV may be more accentuated in individuals showing a plateau in O2max because Q must decline in that setting (4, 17).
Another approach to determine whether SV declines during exercise at maximal effort is to examine the hemodynamic responses to short duration (3–10 min) constant-load exercise. An advantage of this protocol is that it assesses the capacity of the body to sustain O2max and the capacity of the cardiovascular system to sustain maximal systemic and locomotor muscle blood flow and O2 delivery. In three studies involving 29 subjects, we consistently observed significant reductions in SV and Q prior to exhaustion in both the presence and absence of heat stress (10, 12, 19). These responses were associated with high core temperature, catecholamines, and plasma ATP, near-maximal heart rate, altered or stable central venous, and mean arterial pressures and reduced locomotor muscle blood flow. This suggests that the fall in SV might have resulted from the interaction of several factors transiently depressing preload and/or left ventricular function. The similar cardiovascular instability during exhausting incremental and constant-load exercise points toward an upper limit in cardiovascular regulation, which might implicate both central and peripheral factors (4–6, 10, 12, 19). Interestingly, the rate-pressure product of heart rate and mean arterial pressure increases until exhaustion, indicating that myocardial oxygen demand is rising when SV declines during constant and incremental maximal exercise. Under these conditions, an increase in myocardial O2 can only occur by an increase in O2 delivery provided by augmented coronary blood flow because the O2 extraction reserve is minimal. The blunted Q raises the possibility that impaired coronary circulation sets a limit to cardiac function (19), an inference already advanced by Hill and Lupton (15) 84 years ago.
The cardiovascular instability described here is not unique to maximal exercise. A similar drop in SV occurs during prolonged submaximal exercise as part of the classical phenomenon termed "cardiovascular drift" (7, 8) or the cardiovascular strain evoked by severe dehydration and hyperthermia, which also features reductions in Q and exercising muscle blood flow (11, 13). In conclusion, comprehensive studies measuring Q and other components of the Fick principle during both incremental and constant load cycling support the position that SV does decline during exercise at maximal effort. These observations are consistent with the idea of a central limitation to O2max.
GRANTS
The studies were supported by the Copenhagen Muscle Research Centre, Team Denmark, and the Gatorade Sports Science Institute.
ACKNOWLEDGMENTS
The author thanks all the coinvestigators who made possible the research projects discussed in this article.
REFERENCES
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  S. P. Mortensen, R. Damsgaard, E. A. Dawson, N. H. Secher, and J. Gonzalez-Alonso Restrictions in systemic and locomotor skeletal muscle perfusion, oxygen supply and VO2 during high-intensity whole-body exercise in humans J. Physiol., May 15, 2008; 586(10): 2621 - 2635. [Abstract] [Full Text] [PDF]
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 L. Nybo Hyperthermia and fatigue J Appl Physiol, March 1, 2008; 104(3): 871 - 878. [Abstract] [Full Text] [PDF]
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