Severity of arterial hypoxaemia affects the relative contributions of peripheral muscle fatigue to exercise performance in healthy humans

Abstract

We examined the effects of hypoxia severity on peripheral versus central determinants of exercise performance. Eight cyclists performed constant-load exercise to exhaustion at various fractions of inspired O-2 fraction (F-IO2 0.21/0.15/0.10). At task failure (pedal frequency < 70% target) arterial hypoxaemia was surreptitiously reversed via acute O-2 supplementation (F-IO2 = 0.30) and subjects were encouraged to continue exercising. Peripheral fatigue was assessed via changes in potentiated quadriceps twitch force (Delta Q(tw,pot)) as measured pre- versus post-exercise in response to supramaximal femoralnerve stimulation. At task failure in normoxia (haemoglobin saturation (S-pO2) similar to 94%, 656 +/- 82 s) and moderate hypoxia (S-pO2 similar to 82%, 278 +/- 16 s), hyperoxygenation had no significant effect on prolonging endurance time. However, following task failure in severe hypoxia (S-pO2, similar to 67%; 125 +/- 6 s), hyperoxygenation elicited a significant prolongation of time to exhaustion (171 6 1 %). The magnitude of A Q(tw,pot) at exhaustion was not different among the three trials (-35% to -36%, P = 0.8). Furthermore, quadriceps integrated EMG, blood lactate, heart rate, and effort perceptions all rose significantly throughout exercise, and to a similar extent at exhaustion following hyperoxygenation at all levels of arterial oxygenation. Since hyperoxygenation prolonged exercise time only in severe hypoxia, we repeated this trial and assessed peripheral fatigue following task failure prior to hyperoxygenation (125 +/- 6 s). Although Q(tw,pot) was reduced from pre-exercise baseline (-23%; P < 0.01), peripheral fatigue was substantially less (P < 0.01) than that observed at task failure in normoxia and moderate hypoxia. We conclude that across the range of normoxia to severe hypoxia, the major determinants of central motor output and exercise performance switches from a predominantly peripheral origin of fatigue to a hypoxia-sensitive central component of fatigue, probably involving brain hypoxic effects on effort perception.