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 (FI,O2) = 0.13] did not induce a greater contribution from central fatigue, but indices of muscle fatigue were elevated compared with normoxia (FI,O2 = 0.21) and moderate hypoxia (FI,O2 = 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. 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; FI,O2 = 0.21), in moderate hypoxia (MH; FI,O2 = 0.17) and in severe hypoxia (SH; FI,O2 = 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. [ABSTRACT FROM AUTHOR]