Key result
Severe hypoxia reduced the mean distance covered during repeated sprints compared to normoxia (22.3 vs 22.9 m; P=0.04) and increased peripheral fatigue without impacting central fatigue.
Why the study?
Increasing arterial hypoxaemia induces greater central versus peripheral fatigue during exhaustive exercise, but whether this occurs during repeated-sprint running was unknown.
Does increasing severity of normobaric hypoxia affect repeated-sprint running performance and neuromuscular fatigue in active males?
Does increasing severity of normobaric hypoxia affect repeated-sprint running performance and neuromuscular fatigue in active males?
Absolute Event Rate: 22.3% vs 22.9%
p-value: p=0.04
Severe normobaric hypoxia increases peripheral muscle fatigue but does not impact central fatigue after 'all-out' repeated-sprint running, suggesting task specificity modulates the effect of hypoxia on fatigue mechanisms.
Severe hypoxia does not increase central fatigue in repeated sprints; leaves open sprint-specific fatigue mechanisms in 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 ( ) = 0.13] did not induce a greater contribution from central fatigue, but indices of muscle fatigue were elevated compared with normoxia ( = 0.21) and moderate hypoxia ( = 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; = 0.21), in moderate hypoxia (MH; = 0.17) and in severe hypoxia (SH; = 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.
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Townsend et al. (2020) studied Healthy (active males) (n=13). Severe hypoxia vs. Normoxia (FiO2 = 0.21) was evaluated on Mean distance covered in set 1 (p=0.04). Severe hypoxia reduced the mean distance covered during repeated sprints compared to normoxia (22.3 vs 22.9 m; P=0.04) and increased peripheral fatigue without impacting central fatigue.
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