Respiratory muscle training and maximum aerobic power in hypoxia

Abstract

In a recent paper, Keramidas et al. (2010) investigated the effects of respiratory muscle training (RMT) on endurance exercise performance in normoxia (N) and hypoxia (H; FIO2 = 0.12). Participants were randomly assigned either to RMT or control training group. Both groups performed regular (1 h/day, 5 days/week at 50% of peak power output) aerobic training on a cycle ergometer, while RMT group performed an additional specific training programme of respiratory muscles (isocapnic hyperpnoea) prior to the cycle ergometry. After 4 weeks of training, both groups enhanced maximum oxygen uptake _ VO2max in N, but only the RMT group improved _ VO2max (only specific, not absolute) significantly in H. The enhanced _ VO2max in H in the RMT group was accompanied by increased maximum ventilation _ VE , but at an identical peak power output, most likely resulting in an increased metabolic demand of the respiratory muscles. However, in this study, peak power output was calculated as the last workload completed of a ramp test (30 W/min). If this is the case, peak power output would be a supramaximal power, which both aerobic and anaerobic energy sources would contribute to, and thus cannot be defined as the maximum aerobic mechanical power, which corresponds to the lowest power requiring a _ VO2 equal to _ VO2max. Always, whether in N or in H, an increase in _ VO2max is accompanied by an increase in maximum mechanical power. In a similar paper, Esposito et al. (2010) assessed the effects of 8 weeks RMT (isocapnic hyperpnoea, 5 training sessions per week, 10–20 min each including warm up; the volume and the frequency of respiratory cycles were increased progressively, based on participants’ response to training work loads) on _ VO2max in N and H (FIO2 = 0.11). After 8 weeks of RMT, no changes in cardiorespiratory and metabolic variables were detected at maximal exercise in N. On the contrary, in H _ VE and alveolar ventilation _ VA at maximal exercise were significantly higher than in pre-training condition. Accordingly, alveolar O2 partial pressure (PAO2 ) after RMT significantly increased by *10%. Nevertheless, arterial PO2 and _ VO2max did not change with respect to pre-training condition. Thus, the authors provided evidence that RMT did not have any effect on _ VO2max, under either normoxic or hypoxic condition. They concluded that in H, the significant increase in _ VE and _ VA at maximum exercise after RMT lead to higher alveolar but not arterial PO2 values, revealing an increased A–a gradient. Thus, a possible role of increased ventilation–perfusion mismatch was suggested. According to multifactorial models of _ VO2max limitation (di Prampero 1985; di Prampero and Ferretti 1990), the O2 transfer from ambient air to mitochondria is set by a cascade of resistances in series, each resistance being overcome by a specific O2 partial pressure gradient. Four major resistances have been identified in the studies cited above (1) ventilatory (RV) between ambient and alveoli; (2) lung (RL) between alveoli and arterial blood; (3) circulatory (RQ) between arterial blood and muscle capillaries; (4) peripheral (Rp) between muscle capillaries and Communicated by Susan Ward.