Abstract

PURPOSE: The asymptote of the hyperbolic power-endurance relationship (Critical Power, CP) has been suggested to represent a sustainable power output using renewable aerobic energy. Work rates above CP would result in blood [lactate] rising until peak VO2 is attained and exhaustion would occur when the curvature of the power-endurance relationship, defined as a fixed Anaerobic Work Capacity (AWC), is totally depleted. Since CP is dependent on aerobic energy supply, we tested the hypothesis that it should be reduced systematically under hypoxia while AWC would remain unaltered. METHODS: Seventeen subjects (8 males; age: 37 ± 3; mass: 71 ± 2 kg) performed a ramp test to determine peak VO2, and three to four constant-load tests to exhaustion in order to model the linear P-t-1 relationship (using a 2-parameter model where CP is the intercept, and AWC the slope). All tests were performed in a random order under moderate hypoxia (FiO2=0.15; pre-exercise SaO2 of 93.5 ± 0.8%) and normoxia (pre-exercise SaO2 of 98.3 ± 0.3%) on a SRM cycle ergometer with VO2 measurement using a breath-by-breath analyzer (Ergocard; Medi-Soft). Paired t-tests were performed to identify differences. Relationships were explored using the Spearman correlation coefficient. The significance was set at P<0.05. RESULTS: Peak VO2 (3.55 ± 0.17 L.min-1vs 3.11 ± 0.15 L.min-1; P<0.01) and CP (225 ± 10W vs 193 ± 8 W; 2.86 ± 0.13 L.min-1 vs 2.45 ± 0.12 L.min-1; P<0.01) were both significantly reduced by hypoxia. The decrease in CP (-14 ± 2%; range from 1 to -26%) and peak VO2 (-12 ± 1% decrease; range from -1 to -21%) were significantly correlated (r=0.82; P<0.05). AWC was not significantly different under hypoxia (11.8 ± 1.2 kJ vs 12.2 ± 0.9 kJ; P>0.05) with the changes in AWC (+12 ± 8%; range from +60 to -36%) being highly correlated with the changes in CP (r=-0.80; P<0.05). CONCLUSION: The present study demonstrates the aerobic nature of the intercept of the P-t-1 relationship. A reduction in the systemic O2 transport systematically affects CP, with 67% of its change being explained by peak VO2 changes. The extreme changes in AWC in individuals whose CP were most affected by hypoxia, challenges the current interpretation of this parameter.

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