Abstract
Cellular adaptations that occur during skeletal muscle hypertrophy in response to high-volume resistance training are not well-characterized. Therefore, we sought to explore how actin, myosin, sarcoplasmic protein, mitochondrial, and glycogen concentrations were altered in individuals that exhibited mean skeletal muscle fiber cross-sectional area (fCSA) hypertrophy following 6 weeks of high-volume resistance training. Thirty previously resistance-trained, college-aged males (mean ± standard deviation: 21±2 years, 5±3 training years) had vastus lateralis (VL) muscle biopsies obtained prior to training (PRE), at week 3 (W3), and at week 6 (W6). Muscle tissue from 15 subjects exhibiting PRE to W6 VL mean fCSA increases ranging from 320–1600 μm2 was further interrogated using various biochemical and histological assays as well as proteomic analysis. Seven of these individuals donated a VL biopsy after refraining from training 8 days following the last training session (W7) to determine how deloading affected biomarkers. The 15 fCSA hypertrophic responders experienced a +23% increase in mean fCSA from PRE to W6 (p<0.001) and, while muscle glycogen concentrations remained unaltered, citrate synthase activity levels decreased by 24% (p<0.001) suggesting mitochondrial volume decreased. Interestingly, repeated measures ANOVAs indicated that p-values approached statistical significance for both myosin and actin (p = 0.052 and p = 0.055, respectively), and forced post hoc tests indicated concentrations for both proteins decreased ~30% from PRE to W6 (p<0.05 for each target). Phalloidin-actin staining similarly revealed actin concentrations per fiber decreased from PRE to W6. Proteomic analysis of the sarcoplasmic fraction from PRE to W6 indicated 40 proteins were up-regulated (p<0.05), KEGG analysis indicated that the glycolysis/gluconeogenesis pathway was upregulated (FDR sig. <0.001), and DAVID indicated that the following functionally-annotated pathways were upregulated (FDR value <0.05): a) glycolysis (8 proteins), b) acetylation (23 proteins), c) gluconeogenesis (5 proteins) and d) cytoplasm (20 proteins). At W7, sarcoplasmic protein concentrations remained higher than PRE (+66%, p<0.05), and both actin and myosin concentrations remained lower than PRE (~-50%, p<0.05). These data suggest that short-term high-volume resistance training may: a) reduce muscle fiber actin and myosin protein concentrations in spite of increasing fCSA, and b) promote sarcoplasmic expansion coincident with a coordinated up-regulation of sarcoplasmic proteins involved in glycolysis and other metabolic processes related to ATP generation. Interestingly, these effects seem to persist up to 8 days following training.
Highlights
Weeks to months of resistance training increases skeletal muscle mean fiber cross-sectional area [1,2,3,4,5,6,7,8,9,10]
Citrate synthase activity decreased from PRE to week 3 (W3) (p
In retrospect, it would have been interesting to observe if strength changes plateaued or even decreased at these time points relative to PRE, and if these changes were associated with decrements in actin and myosin protein concentrations. It remains to be determined what other myofibrillar proteins may be expressed to differing degrees in response to various training interventions beyond myosin and actin, which are considered to occupy the majority of the myofibril, and what specific training stimuli instigate the expression of specific myofibrillar proteins. These data challenge current dogma suggesting fiber cross-sectional area (fCSA) increases during high-volume resistance training are primarily driven through increases contractile protein content
Summary
Weeks to months of resistance training increases skeletal muscle mean fiber cross-sectional area (fCSA) [1,2,3,4,5,6,7,8,9,10]. The ingestible deuterium oxide tracer has enabled scientists to measure integrated MPS and MyoPS for prolonged periods [14, 15], and results have suggested that rates are elevated weeks into training Such findings have led to a general consensus that resistance training-induced skeletal muscle hypertrophy occurs via: a) increased myofibrillar protein accretion at the cellular level, and b) an increase in muscle fiber size and diameter due to said protein accretion. Our laboratory recently reported that untrained college-aged males with high pre-training myofibrillar protein concentrations, as assessed through biochemical methods, experienced the largest decrease in myofibrillar protein concentrations following 12 weeks of resistance training [19] These findings collectively suggest that the hypertrophic response to resistance training may include fiber growth through sarcoplasmic expansion (e.g., intracellular fluid, sarcoplasmic proteins, and glycogen) prior to the accretion of contractile proteins. We noted a severe lack of research into this area and persuaded further exploration
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