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POINT-COUNTERPOINT
O2 is at its highest value, not supramaximal exercise when O2 often declines. In our Counterpoint, we attempted to provide a balanced assessment of the literature, acknowledging variability in the SV response, but highlighting the ability of the trained myocardium to increase SV during incremental to maximal exercise. There is clear evidence that in endurance athletes (O2max > 65 ml·kg–1·min–1) the SV at O2max is higher than that attained at submaximal and supramaximal workloads (2, 5, 9, 10). It is instructive to address the inherent assumptions and/or inferences that serve as the foundation for Dr. González-Alonso's Point (3). For example, the relationship between heart rate and workload during incremental exercise cannot strictly be considered linear (6). Furthermore, a high heart rate does not by default cause a reduction in SV. The left ventricular diastolic pressure-volume relationship is only affected at heart rates above 170 beats/min. Ventricular interaction, reduced myocardial compliance, and/or pericardial constraint likely explain the invariant filling and SV at much lower heart rates in sedentary individuals (1, 4). Also, it remains that many untrained and moderately trained individuals are able to maintain and even increase SV during maximal exercise (5).
Clearly, it is difficult to attain valid and reliable measures of cardiac output during maximal exercise (8). When familiarization procedures and supramaximal confirmatory intensities (plateau or decreasing O2 values) are used, previous research from independent laboratories supports the ability to achieve maximal SV at O2max (2, 10). Moreover, techniques that are not as affected by movement artifact and that are reliable during strenuous exercise reveal the ability to increase SV in the face of increasing workload (particularly in endurance athletes; Refs. 2, 5). It should be noted that studies reporting a decline in SV during exercise often evaluated individuals who were not highly trained and who exercised at peak power outputs well below predicted.
We believe that owing to the potential for cardiac fatigue (7) and marked changes in vascular volumes, the discussion of cardiac function during prolonged strenuous exercise provides little insight into the SV response to short-term incremental upright exercise.
There is considerable interindividual variability in the response to most cardiovascular parameters during exercise, and much is lost in the translation of this knowledge when mean data is reported from small sample sizes. Individual results from various studies reveal that most trained and many untrained individuals maintain or increase their SV during maximal exercise.
REFERENCES
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