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We aimed to test whether high-intensity high-volume training (HIHVT) swimming would induce more robust signaling than sprint interval training (SIT) swimming within the  m .  triceps brachii  due to lower metabolic and oxidation. Nine well-trained swimmers performed the two training procedures on separate randomized days. Muscle biopsies from  m .  triceps brachii  and blood samples were collected at three different time points: a) before the intervention (pre), b) immediately after the swimming procedures (post) and c) after 3 h of rest (3 h). Hydroperoxides, creatine kinase (CK), and lactate dehydrogenase (LDH) were quantified from blood samples, and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) and the AMPK pTHR172 /AMPK ratio were quantified by Western blot analysis. PGC-1α, sirtuin 3 (SIRT3), superoxide-dismutase 2 (SOD2), and vascular endothelial growth factor (VEGF) mRNA levels were also quantified. SIT induced a higher release of LDH ( p  < 0.01 at all time points) and CK ( p  < 0.01 at post) than HIHVT, but neither SIT nor HIHVT altered systemic hydroperoxides. Additionally, neither SIRT3 nor SOD2 mRNA levels increased, while PGC-1α transcription increased at 3 h after SIT ( p  < 0.01) and after HIHVT ( p  < 0.001). However, PGC-1α protein was higher after HIHVT than after SIT ( p  < 0.05). Moreover, the AMPK pTHR172 /AMPK ratio increased at post after SIT ( p  < 0.05), whereas this effect was delayed after HIHVT as it increased after 3 h ( p  < 0.05). In addition, VEGF transcription was higher in response to HIHVT (p < 0.05). In conclusion, SIT induces higher muscular stress than HIHVT without increasing systemic oxidation. In addition, HIHVT may induce more robust oxidative adaptations through PGC-1α and AMPK.

plos one

High-intensity high-volume swimming induces more robust signaling through PGC-1α and AMPK activation than sprint interval swimming in m. triceps brachii