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Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signalling and microRNA expression in human skeletal muscle.

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AJP Regulatory Integrative and Comparative Physiology

Published online on

Abstract

We compared the effects of concurrent exercise, incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT), on mTORC1 signalling and microRNA expression in skeletal muscle, relative to resistance exercise (RE) alone. Eight males (mean ± SD: age, 27 ± 4 y; "V" O2peak, 45.7 ± 9 ml•kg-1•min-1) performed three experimental trials in a randomised order: i) RE (8 x 5 leg press repetitions at 80% 1RM) performed alone, and RE preceded by either ii) HIT cycling (10 x 2 min at 120% lactate threshold [LT]; HIT+RE) or iii) work-matched MICT cycling (30 min at 80% LT; MICT+RE). Vastus lateralis muscle biopsies were obtained immediately before RE, either without (REST) or with (POST) preceding endurance exercise, +1 h (RE+1 h) and +3 h (RE+3 h) after RE. Prior HIT and MICT similarly reduced muscle glycogen content and increased ACCSer79 and p70S6KThr389 phosphorylation before subsequent RE (i.e., at POST). Compared with MICT, HIT induced greater mTORSer2448 and rps6Ser235/236 phosphorylation at POST. RE-induced increases in p70S6K and rps6 phosphorylation were not influenced by prior HIT or MICT; however, mTOR phosphorylation was reduced at RE+1 h for MICT+RE vs. both HIT+RE and RE. Expression of miR-133a, miR-378 and miR-486 was reduced at RE+1 h for HIT+RE vs. both MICT+RE and RE. Post-exercise mTORC1 signalling following RE is therefore not compromised by prior HIT or MICT, and concurrent exercise incorporating HIT, but not MICT, reduces post-exercise expression of miRNAs implicated in skeletal muscle adaptation to RE.