Abstract
It is now well established that resistance exercise stimulates muscle protein synthesis and promotes gains in muscle mass and strength. However, considerable variability exists following standardized resistance training programs in the magnitude of muscle cross-sectional area and strength responses from one individual to another. Several studies have recently posited that alterations in satellite cell population, myogenic gene expression and microRNAs may contribute to individual variability in anabolic adaptation. One emerging factor that may also explain the variability in responses to resistance exercise is circadian rhythms and underlying molecular clock signals. The molecular clock is found in most cells within the body, including skeletal muscle, and principally functions to optimize the timing of specific cellular events around a 24 h cycle. Accumulating evidence investigating the skeletal muscle molecular clock indicates that exercise-induced contraction and its timing may regulate gene expression and protein synthesis responses which, over time, can influence and modulate key physiological responses such as muscle hypertrophy and increased strength. Therefore, the circadian clock may play a key role in the heterogeneous anabolic responses with resistance exercise. The central aim of this Hypothesis and Theory is to discuss and propose the potential interplay between the circadian molecular clock and established molecular mechanisms mediating muscle anabolic responses with resistance training. This article begins with a current review of the mechanisms associated with the heterogeneity in muscle anabolism with resistance training before introducing the molecular pathways regulating circadian function in skeletal muscle. Recent work showing members of the core molecular clock system can regulate myogenic and translational signaling pathways is also discussed, forming the basis for a possible role of the circadian clock in the variable anabolic responses with resistance exercise.
Highlights
Skeletal muscle encompasses ∼40% of total bodily mass and is a highly malleable tissue with the capacity to alter its structure and metabolism in response to internal and external stress signals such as muscle contraction and nutrition (Hawley et al, 2014; Camera et al, 2016)
Accumulating evidence investigating molecular clock mechanisms and peripheral circadian rhythmicity in skeletal muscle tissues suggests that exercise-induced contraction and its timing may regulate gene expression and protein synthesis related to muscle anabolism and metabolism (Zambon et al, 2003; Schroder and Esser, 2013)
These findings suggest the potential for transient, but chronic, elevations in Myogenic Differentiation (MyoD) and myogenin gene expression with each exercise session are necessary signals that lead to greater muscle hypertrophy induced by resistance training (Bamman et al, 2007)
Summary
Skeletal muscle encompasses ∼40% of total bodily mass and is a highly malleable tissue with the capacity to alter its structure and metabolism in response to internal and external stress signals such as muscle contraction and nutrition (Hawley et al, 2014; Camera et al, 2016). As Booth and Laye correctly communicate, the generalized term “non-responder” can be misleading as “it implies that no exercise-induced adaptations occur” (Booth and Laye, 2010) This point was clearly supported in a retrospective analysis study by the van Loon group that demonstrated participants were able to positively respond to at least one training outcome (i.e., lean body mass, muscle fiber size, strength, or physical work function) following 24 weeks resistance training in older (>65 years) men and women (Churchward-Venne et al, 2015). These findings do not explain the basis for why variability still existed within each of these specific adaptation responses. This aspect of exercise and muscle physiology is largely unconsidered within the research field despite the potential for the circadian clock to modulate adaptation responses with resistance training
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