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

Abstract

Key pointsr Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown.r We show that changes in myofibrillar protein synthesis (MyoPS) after an initial resistance exercise (RE) bout in the first week of RT (T1) were greater than those seen post-RE at the third (T2) and tenth week (T3) of RT, with values being similar at T2 and T3.r Muscle damage (Z-band streaming) was the highest during post-RE recovery at T1, lower at T2 and minimal at T3.r When muscle damage was the highest, so was the integrated MyoPS (at T1), but neither were related to hypertrophy; however, integrated MyoPS at T2 and T3 were correlated with hypertrophy.r We conclude that muscle hypertrophy is the result of accumulated intermittent increases in MyoPS mainly after a progressive 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 and assessed muscle damage at the beginning (T1), at 3 weeks (T2) and at 10 weeks of RT (T3). Ten young men (27 (1) years, mean (SEM)) 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 (post-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. Initial MyoPS response post-RE in an RT programme is not directed to support muscle hypertrophy, coinciding with the greatest muscle damage. However, integrated MyoPS is quickly 'refined' by 3 weeks 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 attenuation of muscle damage.

Post-absorptive muscle protein turnover affects resistance training hypertrophy

“…Throughout the exercise training, protein turnover in the post-absorptive state could be a time frame that characterizes high responders to RET through maintenance of protein mass and/or a limiting of muscle loss in the fasted state. Although our study design is unable to define the precise role and time course of the post-absorptive state during RET on muscle hypertrophy, it is clear that this period is important for muscle hypertrophy as several elegant reports have demonstrated (Brook et al 2015; Damas et al 2016). Until recently, the hours following exercise have received the most focus regarding the accrual of new proteins supporting muscle hypertrophy (Mitchell et al 2014).…”

“…In particular, after a period of RET, individuals experience a shorter duration of the acute elevation of MPS following a bout of RE (Damas et al 2015), and a higher rate of basal post-absorptive MPS compared to pre-training levels (Damas et al 2015). Therefore, the adaptation of muscle protein turnover throughout chronic RET may be an important contributor to muscle hypertrophy as more recent studies are starting to reveal (Brook et al 2015; Damas et al 2016). However, the role of muscle protein turnover, specifically in the basal post-absorptive state, during resistance exercise-induced muscle hypertrophy is unknown.…”

Molecular Regulation of Exercise-Induced Muscle Fiber Hypertrophy

“…Forexample, Mitchell et al reported no correlation between the myofibrillar protein synthesis (MyoPS) response 1–6 h after an initial resistance exercise bout and the magnitude of long-term, RT-induced muscle hypertrophy (Mitchell et al 2014). In an interesting subsequent study, Damas et al (2016) confirmed no relationship between the 24–48 h MyoPS response and eventual myofiber hypertrophy when studying MyoPS during the first week of training; however, strong correlations were noted when MyoPS was quantified in response to exercise during weeks 3 and 10 of a 10-week RT program. The investigators’ assessments of muscle damage suggest that the week-1 MyoPS response was driven largely by damage/repair, whereas the later responses after a few weeks of training were more reflective of anabolism supporting myofiber hypertrophy (Damas et al 2016).…”

“…In an interesting subsequent study, Damas et al (2016) confirmed no relationship between the 24–48 h MyoPS response and eventual myofiber hypertrophy when studying MyoPS during the first week of training; however, strong correlations were noted when MyoPS was quantified in response to exercise during weeks 3 and 10 of a 10-week RT program. The investigators’ assessments of muscle damage suggest that the week-1 MyoPS response was driven largely by damage/repair, whereas the later responses after a few weeks of training were more reflective of anabolism supporting myofiber hypertrophy (Damas et al 2016). Thus, much like the magnitude of myofiber hypertrophy (Bamman et al 2007), the acute muscle protein synthesis response to RT is variable between individuals and the relationship between the two appears to strengthen as training progresses.…”

Sex differences in the effect of fish-oil supplementation on the adaptive response to resistance exercise training in older people: a randomized controlled trial

“…To determine whether the acute resistance exercise induction of p70s6k activity differed between placebo and long-chain n–3 PUFA groups, p70s6k activity was measured before and 2 h after a training session in the last week of the intervention. The last week of training was chosen because the incorporation of long-chain n–3 PUFAs would be maximized at this point and to remove any of the contribution from the acute muscle-damage responses when beginning exercise training (24). …”