This study aimed to determine the effects of hypoxia and/or blood flow restriction (BFR) on an arm-cycling repeated sprint ability test (aRSA) and its impact on elbow flexor neuromuscular function.
Fourteen volunteers performed an aRSA (10 s sprint/20 s recovery) to exhaustion in four randomized conditions: normoxia (NOR), normoxia plus BFR (N _BFR ), hypoxia (FiO ₂ = 0.13, HYP) and hypoxia plus BFR (H _BFR ). Maximal voluntary contraction (MVC), resting twitch force (Db10), and electromyographic responses from the elbow flexors [biceps brachii (BB)] to electrical and transcranial magnetic stimulation were obtained to assess neuromuscular function. Main effects of hypoxia, BFR, and interaction were analyzed on delta values from pre- to post-exercise.
BFR and hypoxia decreased the number of sprints during aRSA with no significant cumulative effect (NOR 16 ± 8; N _BFR 12 ± 4; HYP 10 ± 3 and H _BFR 8 ± 3; P < 0.01). MVC decrease from pre- to post-exercise was comparable whatever the condition. M-wave amplitude (- 9.4 ± 1.9% vs. + 0.8 ± 2.0%, P < 0.01) and Db10 force (- 41.8 ± 4.7% vs. - 27.9 ± 4.5%, P < 0.01) were more altered after aRSA with BFR compared to without BFR. The exercise-induced increase in corticospinal excitability was significantly lower in hypoxic vs. normoxic conditions (e.g., BB motor evoked potential at 75% of MVC: - 2.4 ± 4.2% vs. + 16.0 ± 5.9%, respectively, P = 0.03).
BFR and hypoxia led to comparable aRSA performance impairments but with distinct fatigue etiology. BFR impaired the muscle excitation-contraction coupling whereas hypoxia predominantly affected corticospinal excitability indicating incapacity of the corticospinal pathway to adapt to fatigue as in normoxia.