Central and peripheral muscle fatigue following repeated-sprint running in moderate and severe hypoxia

New Findings: What is the central question of this study? Increasing severity of arterial hypoxaemia induces a shift towards greater central, relative to peripheral, mechanisms of fatigue during exhaustive exercise. Does a similar pattern exist for ‘all-out’ repeated-sprint running? What is the main finding and its importance? Severe normobaric hypoxia [fraction of inspired oxygen ((Formula presented.)) = 0.13] did not induce a greater contribution from central fatigue, but indices of muscle fatigue were elevated compared with normoxia ((Formula presented.) = 0.21) and moderate hypoxia ((Formula presented.) = 0.17). This suggests a different fatigue response to repeated-sprint running versus other exercise modalities and, consequently, that task specificity might modulate the effect of hypoxia on the central versus peripheral contribution to fatigue. Abstract: We examined the effects of increasing hypoxia severity on repeated-sprint running performance and neuromuscular fatigue. Thirteen active males completed eight sprints of 5 s (recovery = 25 s) on a motorized sprint treadmill in normoxia (sea level, SL; (Formula presented.) = 0.21), in moderate hypoxia (MH; (Formula presented.) = 0.17) and in severe hypoxia (SH; (Formula presented.) = 0.13). After 6 min of passive recovery, in all conditions a second set of four sprints of 5 s was conducted in normoxia. Neuromuscular function of the knee extensors was assessed at baseline (Pre-) and 1 min after set 1 (Post-set 1) and set 2 (Post-set 2). In set 1, the mean distance covered in SL (22.9 ± 1.2 m) was not different to MH (22.7 ± 1.3 m; P = 0.71) but was greater than in SH (22.3 ± 1.3 m; P = 0.04). No significant differences between conditions for mean distance occurred in set 2. There was a decrease in maximal voluntary contraction torque (Δ = −31.4 ± 18.0 N m, P < 0.001) and voluntary activation (%VA; Δ = −7.1 ± 5.1%, P = 0.001) from Pre- to Post-set 1, but there was no effect of hypoxia. No further change from Post-set 1 to Post-set 2 occurred for either maximal voluntary contraction or %VA. The decrease in potentiated twitch torque in SL (Δ = −13.3 ± 5.2 N m) was not different to MH (Δ = −13.3 ± 6.3 N m) but was lower than in SH (Δ = −16.1 ± 4 N m) from Pre- to Post-set 1 (interaction, P < 0.003). Increasing severity of normobaric hypoxia, up to an equivalent elevation of 3600 m, can increase indices of peripheral fatigue but does not impact central fatigue after ‘all-out’ repeated-sprint running.