Abstract
Skeletal muscle disuse rapidly decreases muscle mass. Resistance training (RT) is believed as the most effective way to gain muscle mass via an increase in mTORC1 activity and muscle protein synthesis (MPS). However, it remains unclear whether muscle atrophy by disuse alters the mTORC1 activation and MPS response to an acute resistance exercise (RE) and chronic RT–mediated skeletal muscle hypertrophy. This study investigated the influence of disuse muscle atrophy on the response of mTORC1 activation and MPS to an acute RE. We also evaluated whether disuse muscle atrophy affects the response of RT-induced muscle mass gain. Thirty male Sprague-Dawley rats were randomly divided into control (CON) or hindlimb suspension (HS) groups. A 14-day HS via the tail was used as the model for gastrocnemius muscle disuse in the HS group. Unilateral lower limb muscle contraction using by percutaneous electrical stimulation was used to mimic the stimuli of RE. Ten bouts of RE were performed in 3-week as chronic RT. Our results showed that MPS and mTORC1 activity was unchanged after HS at basal state. However, the ribosomal RNA (rRNA) level was reduced in HS rats compared to that in CON rats at basal state. MPS and rRNA increased in both HS and CON rats in response to acute RE to the same extent. However, the level of mTORC1 activation in response to an acute RE was significantly higher in HS than that in the CON group at 12 h after exercise, even though no difference was observed at 3 h after exercise. The 10-bout RT significantly increased gastrocnemius muscle mass in both CON and HS rats. The response of muscle hypertrophy did not differ between the groups. Therefore, MPS in response to acute RE and muscle hypertrophy in response to chronic RT were unaltered after disuse muscle atrophy.
Highlights
Skeletal muscle is known to have a broad range of plasticity, such as hypertrophy in response to mechanical loading [i.e., functional overload, resistance training (RT)] (Goodman et al, 2011a; Ogasawara et al, 2016a), and atrophy in response to disuse
We investigated whether skeletal muscle disuse atrophy would alter the Muscle protein synthesis (MPS) response to an acute resistance exercise (RE) and chronic RT-induced muscle mass gain
The response of muscle hypertrophy to RT was not changed after disuse muscle atrophy as compared with RT from basal conditions
Summary
Skeletal muscle is known to have a broad range of plasticity, such as hypertrophy in response to mechanical loading [i.e., functional overload, resistance training (RT)] (Goodman et al, 2011a; Ogasawara et al, 2016a), and atrophy in response to disuse (i.e., space flight, bed rest, and inactivity; Allen et al, 1996; Glover et al, 2008; Drummond et al, 2012). Muscle Atrophy and Resistance Training metabolism that is regulated by protein synthesis and breakdown is one of the key determinant factors of muscle mass (Russell, 2010). Muscle protein synthesis (MPS) is believed to be regulated by translational efficiency and translational capacity. Previous studies revealed that mTORC is a key regulator of muscle contraction-induced MPS and skeletal muscle hypertrophy (Goodman et al, 2011a; West et al, 2016; Ogasawara et al, 2016b; Ogasawara and Suginohara, 2018; You et al, 2018). Recent evidence suggests that the capacity of ribosome biogenesis is relevant to the response of load-induced skeletal muscle hypertrophy (von Walden et al, 2012; Kirby et al, 2015; Figueiredo and McCarthy, 2019)
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