Autophagic responses to vigorous endurance exercise in men vary by training status but are similar in PBMCs and skeletal muscle: A pilot study
Vigorous exercise triggers signaling cascades that activate autophagy markers like the degradation of sequestosome 1 (p62) and accumulation of Light Chain 3 II (LC3II). Limited human data exist on autophagic responses across different local and systemic tissues and how training status affects these relationships. This study investigates the vigorous exercise‐induced changes in p62 and LC3II expression in peripheral blood mononuclear cells (PBMCs) and skeletal muscle between endurance‐trained and untrained men. Twelve men (endurance‐trained n = 7, untrained n = 5) completed 60 min of cycling at their second ventilatory threshold. Skeletal muscle biopsy samples and PBMCs were collected pre‐ and 3‐h post‐exercise and analyzed for p62 and LC3II protein expression. We found significant interaction effects of time and training status for p62 (p < 0.001) and LC3II (p = 0.002). In untrained men, p62 decreased in PBMCs (FC = 0.50 ± 0.14; p < 0.001) and skeletal muscle (FC = 0.57 ± 0.21; p < 0.001), while LC3II increased in both tissues (FC = 1.74 ± 0.79; p = 0.019 for PBMCs; FC = 1.69 ± 0.47; p = 0.033 for skeletal muscle). No changes were observed in endurance‐trained men (all p > 0.05). These results suggest that a bout of vigorous endurance exercise increased autophagy‐related markers in both skeletal muscle and PBMCs in the untrained men only, suggesting a diminished autophagic response in the trained men.