Respiratory muscle training and maximum aerobic power in hypoxia

Excerpt

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 \( \left( {\dot{V}{\text{O}}_{{ 2 {\text{max}}}} } \right) \) in N, but only the RMT group improved \( \dot{V}{\text{O}}_{{ 2 {\text{max}}}} \) (only specific, not absolute) significantly in H. The enhanced \( \dot{V}{\text{O}}_{{ 2 {\text{max}}}} \) in H in the RMT group was accompanied by increased maximum ventilation \( \left( {\dot{V}{\text{E}}} \right) \), 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 \( \dot{V}{\text{O}}_{ 2} \) equal to \( \dot{V}{\text{O}}_{{ 2 {\text{max}}}} \). Always, whether in N or in H, an increase in \( \dot{V}{\text{O}}_{{ 2 {\text{max}}}} \) is accompanied by an increase in maximum mechanical power. …