Influence of shortened recovery between resistance exercise sessions on muscle‐hypertrophic effect in rat skeletal muscle

Abstract

Resistance exercise training induces muscle hypertrophy, and recovery between sessions is one of the major determinants of this effect. However, the effect of the recovery period between sessions on muscle hypertrophy following resistance exercise training remains unclear. To elucidate the effect of recovery period on hypertrophy, in the present study, we investigated changes in protein degradation systems and hypertrophic responses in rat skeletal muscle to resistance training with variable recovery periods. In the conventional recovery group (exercised every 72 h) and a shorter recovery group (exercised every 24 h), 18 bouts of resistance exercise consisting of 50 repetitions of a 3‐sec maximal isometric contraction caused muscle hypertrophy and slight activation of muscle protein degradation systems. By contrast, in an excessively shorter recovery group (exercised every 8 h), 18 bouts of resistance exercise did not cause hypertrophy and markedly activated protein degradation systems, accompanied by inflammatory responses. These observations indicate that excessive shortening of recovery between sessions does not cause skeletal muscle hypertrophy, likely due to the activation of proteolysis induced by inflammatory responses to resistance exercise training.

Effect of mechanistic/mammalian target of rapamycin complex 1 on mitochondrial dynamics during skeletal muscle hypertrophy

“…We did not observe any significant difference in the protein expression of PGC‐1α between the groups, although the expression levels of OXPHOS proteins were significantly decreased by functional overload regardless of rapamycin administration. Chronic muscle contraction has been demonstrated to enhance expression levels of PGC‐1α and OXPHOS proteins (Kitaoka et al, 2015; Ogasawara et al, 2016; Takegaki, Ogasawara, et al, 2019). While these previous studies employed a model of muscle hypertrophy induced by 4 weeks of muscle contraction, our study employed a model of rapid muscle hypertrophy in 14 days, and we believe that adequate adaptation of mitochondrial biogenesis and mitochondrial content would not occur in this short‐term muscle hypertrophy model.…”

The distribution of eukaryotic initiation factor 4E after bouts of resistance exercise is altered by shortening of recovery periods

“…Additionally, repetitive resistance exercise with excessively short recovery is known to highly activate mTORC1 [2][3][4]. On the other hand, as mentioned above, this type of exercise training does not induce the acute activation of muscle protein synthesis and chronic muscle hypertrophy even though mTORC1 is highly activated [2][3][4]. These facts indicate the possibility that an excessively shortened recovery influences the downstream targets of the mTORC1 pathway.…”

“…A recent study reported that mTORC1 plays a minor role in the acute activation of muscle protein synthesis but is essential for muscle hypertrophy induced by chronic mechanical overload [8]. Additionally, repetitive resistance exercise with excessively short recovery is known to highly activate mTORC1 [2][3][4]. On the other hand, as mentioned above, this type of exercise training does not induce the acute activation of muscle protein synthesis and chronic muscle hypertrophy even though mTORC1 is highly activated [2][3][4].…”

“…The recovery period is one of the determinants of the training effect, and a period of 2 or 3 days is regarded as adequate for inducing muscle hypertrophy [1]. Resistance exercise training with an excessively short recovery period can lead to inadequate responses, such as suppression of protein synthesis and activation of muscle protein degradation systems [2][3][4]. However, little information is available on the mechanisms underlying the suppression of acute and chronic responses of muscle anabolism after bouts of resistance exercise training with insufficient recovery.…”

“…Repetitive resistance exercise with insufficient recovery is also known to activate inflammation [2][3][4]. Therefore, this type of exercise training possibly impairs eIF4F complex formation, even though mTORC1 is highly activated, which may contribute to the attenuation of chronic muscle hypertrophy and/or acute activation of muscle protein synthesis.…”