Resistance training-induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage

Abstract

Skeletal muscle hypertrophy is one of the main outcomes of resistance training (RT) but how hypertrophy is modulated and the mechanisms regulating it are still unknown. To investigate how muscle hypertrophy is modulated through RT, we measured day-to-day integrated myofibrillar protein synthesis (MyoPS) using deuterium-oxide ingestion and assessed muscle damage at the beginning (T1), at 3wk (T2), and 10wk of RT (T3). Ten young men (27(1) y) had muscle biopsies (vastus lateralis) taken to measure integrated MyoPS and muscle damage (Z-band streaming and indirect parameters) before and 24 h and 48 h post-resistance exercise (RE) at T1, T2 and T3. Fibre cross-sectional area (fCSA) was evaluated using biopsies at T1, T2 and T3. Increases in fCSA were observed only at T3 (P = 0.017). Changes in MyoPS post-RE at T1, T2 and T3 were greater at T1 (P < 0.03) than at T2 and T3 (similar values between T2 and T3). Muscle damage was the highest during post-RE recovery at T1, attenuated at T2 and further attenuated at T3. The change in MyoPS post-RE at both T2 and T3, but not at T1, was strongly correlated (r∼0.9, P < 0.04) with muscle hypertrophy (T3−T1). Initial MyoPS response post-RE in a RT program is not directed to support muscle hypertrophy, coinciding with the highest magnitude of muscle damage. However, integrated MyoPS is quickly 'refined', by 3wk of RT, and is related to muscle hypertrophy. We conclude that muscle hypertrophy is the result of accumulated intermittent changes in MyoPS post-RE in RT, which coincides with progressive muscle damage attenuation.

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