SKELETAL MUSCLE ADAPTATIONS TO REPEATED SPRINT TRAINING IN SYSTEMIC HYPOXIA VERSUS WITH BLOOD FLOW RESTRICTION

Author(s): ZANOU, N., LANFRANCHI, C., WILLIS, S., SIRAGO, G., REUGE, J., LARAMÉE, L., CONDE ALONSO, S., KAYSER, B., PLACE, N., MILLET, G., Institution: UNIVERSITY OF LAUSANNE, Country: SWITZERLAND, Abstract-ID: 2082

INTRODUCTION:
Repeated sprint training (RST) enhances high-intensity performance, and adding hypoxia may further improve repeated sprint ability (RSA). This study compared RST performed under systemic hypoxia (RSH; FIO₂ = 13.6%) with RST under local hypoxia induced by blood flow restriction (RSO; 45% arterial occlusion pressure), examining performance and skeletal muscle metabolic adaptations.
METHODS:
Seventeen healthy young men completed nine RST sessions in either RSH or RSO conditions. Pre- and post-training assessments included RSA, Wingate test, and a 10 km time trial (10 km TT), along with neuromuscular evaluation. Muscle biopsies (vastus lateralis) were analyzed using proteomics and Western blotting to identify molecular adaptations, and plasma metabolomics was performed.
RESULTS:
Both groups showed comparable improvements in RSA, Wingate, and 10 km TT performance, with no significant changes in neuromuscular function. At the muscular level, RSH and RSO induced a shift toward a more glycolytic phenotype, marked by increased glucose transporter type 4, key glycolytic enzymes, and S100A13, alongside reduced oxidative phosphorylation protein content.
Mitochondrial dynamics were altered in both groups, with increased dynamin-related protein 1 and optic atrophy protein 1 expression. However, only RSO increased peroxisome proliferator-activated receptor gamma coactivator 1, suggesting modality-specific stimulation of mitochondrial biogenesis. Markers of muscle protein synthesis (fast and slow myosin heavy chain isoforms) and antioxidant enzymes were unchanged.
Muscle proteomic analysis revealed distinct molecular responses. RSH uniquely increased proteins related to ribosomal machinery and cytoplasmic translation, whereas RSO specifically upregulated proteins associated with inflammation and immune responses.
Plasma metabolomics showed both shared and distinct changes. Suberate, a byproduct of incomplete beta-oxidation, was commonly regulated. Only RSH increased kynurenate while decreasing kynurenine, raising the kynurenate/kynurenine ratio, which suggests activation of the muscle-brain axis that counteracts brain disorders during exercise. In contrast, RSO markedly increased histamine, reduced cAMP, and elevated hypoxanthine, xanthine, and inosine, indicating activation of the purine nucleotide pathway.

CONCLUSION:
In summary, although RSH and RSO similarly improved performance, they induced both shared and modality-specific muscle and systemic adaptations.