Skeletal Muscle and Systemic Adaptations to Repeated Sprint Training with Blood Flow Restriction or in Normobaric...

Repeated sprint training in hypoxia (RSH) or with blood flow restriction (RS-BFR) are known to enhance the repeated-sprint ability. However, studies directly comparing their underlying molecular mechanisms are scarce.

Here we used a comprehensive approach combining pre- and post-intervention testing including sprint performance tests, neuromuscular assessments, skeletal muscle biopsies for protein levels quantification, and blood samples for systemic metabolites analyses to characterize the specific adaptations induced by RSH and RS-BFR. Recreationally active men performed 9 sessions of RSH (FiO₂ ~0.136; n=9) or RS-BFR (45% arterial occlusion; n=8).

Both RSH and RS-BFR similarly improved exercise performance without significant changes in knee extensor maximal voluntary contraction force. Both training modalities reduced the levels of oxidative phosphorylation proteins while increasing markers of mitochondrial dynamics and mitochondrial translation proteins. Glycolytic remodelling was evident in both groups, with increased levels of the glucose transporter 4 and phosphofructokinase proteins, accompanied by marked upregulation of the S100A13-Akt signalling. Unbiased muscle proteomics and plasma metabolomics also revealed common and more specific signatures. Both RSH and RS-BFR increased plasma levels of intermediates metabolites of lipid metabolism. RSH specifically upregulated cytoplasmic translation pathways in muscle and increased the kynurenate/kynurenine ratio in plasma, whereas RS-BFR was characterized by an upregulation of immune and inflammatory pathways both in muscle and plasma.

In summary, 3-week of RS-BFR elicits performance adaptations comparable to RSH, supported by largely shared muscular and systemic metabolic adaptations. The specific characteristics of the adaptations induced by each method, however, are particularly interesting and could influence the outcome of regular training.