Factors “Limiting” Exercise Performance in Hypoxia

Dear Editor-in-Chief: Some of the findings reported by Woorons et al. (8) cannot be explained by the Archibald V. (A. V.) Hill cardiovascular/anaerobic/catastrophic model that these authors prefer, but are more readily understood according to the central governor model. This model predicts that the increasing levels of arterial hypoxemia that develop at progressively higher altitudes will limit the extent of skeletal muscle recruitment specifically to protect the brain from hypoxia (4–6). That lower limb EMG activity is reduced during maximal exercise at moderate altitude is established (3). Woorons et al. (8) report that, at an altitude of 4500 m, “maximum” heart rate, ventilation, power output, and oxygen consumption were all lower than at sea level (Table 2 in (8)). Although peak blood lactate concentrations were insignificantly lower at that altitude, pH at exercise termination was significantly increased. These findings are compatible with the conclusion that exercise did not terminate at altitude because of a “catastrophic” failure of oxygen flow to the exercising muscles. Rather, homeostasis of muscle metabolism was better protected in hypoxia as shown by (i) higher arterial pH and (ii) submaximal levels of heart rate and ventilation at exhaustion in hypoxia. Applying the accepted criteria (2) for a maximal, oxygen-limited test according to the A. V. Hill model (4,5) leads to the conclusion that “maximal” exercise at altitude is submaximal and therefore not “oxygen limited.” Criteria for a maximum effort were originally developed to identify subjects who terminated exercise because of a “lack of motivation.” The submaximal nature of “maximum” exercise at altitude must indicate that subjects terminate exercise because of a “lack of motivation” and not because of skeletal muscle anerobiosis. The criteria for a “maximal” exercise test must be the same at both sea level and at altitude. If novel criteria for “maximal” effort at altitude must be developed, then we do not understand the phenomena we are trying to describe (4,5). Finally, the authors state that it is necessary “to determine whether 𝑄̇max (maximal cardiac output) actually decreases with altitude and the consequences of this decrement in the drop of V̇O2max” (p. 153). It is well established that 𝑄̇max is reduced during maximal exercise at increasing altitude or increasing levels of hypoxia (1,4,5,7). Furthermore, the cardiac output is reduced in proportion to the reduction in external work rate (4). This is compatible with the central governor model that proposes that the extent of muscle recruitment sets the work rate, which then determines the cardiac output and the oxygen consumption (4,5), and not the reverse. My contention is that the extent of skeletal muscle recruitment at maximum effort becomes increasingly submaximal with the progressive hypoxia that develops at higher altitudes. This maintains the arterial pO2 above some critical value at which hypoxic brain damage occurs. The conclusive evidence for this explanation is the proven decrease in the extent of skeletal muscle recruitment at exhaustion during “maximal” exercise at altitude (3) and the instantaneous increase in work capacity when the pO2 of the inspired air is normalized (1,3). Timothy D. Noakes, MBChB, MD, DSc, FACSM Sports Science Institute of South Africa Newlands, South Africa