Physiological Differences Between Low Versus High Skeletal Muscle Hypertrophic Responders to Resistance Exercise Training: Current Perspectives and Future Research Directions.

Michael D Roberts,Petey W Mumford,Christopher G Vann,Matthew A Romero,John J Mccarthy,Cody T Haun,Paul A Roberson,Christopher B Mobley

doi:10.3389/fphys.2018.00834

Michael D Roberts, Petey W Mumford + Show 6 more

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https://doi.org/10.3389/fphys.2018.00834

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Abstract

Numerous reports suggest there are low and high skeletal muscle hypertrophic responders following weeks to months of structured resistance exercise training (referred to as low and high responders herein). Specifically, divergent alterations in muscle fiber cross sectional area (fCSA), vastus lateralis thickness, and whole body lean tissue mass have been shown to occur in high versus low responders. Differential responses in ribosome biogenesis and subsequent protein synthetic rates during training seemingly explain some of this individual variation in humans, and mechanistic in vitro and rodent studies provide further evidence that ribosome biogenesis is critical for muscle hypertrophy. High responders may experience a greater increase in satellite cell proliferation during training versus low responders. This phenomenon could serve to maintain an adequate myonuclear domain size or assist in extracellular remodeling to support myofiber growth. High responders may also express a muscle microRNA profile during training that enhances insulin-like growth factor-1 (IGF-1) mRNA expression, although more studies are needed to better validate this mechanism. Higher intramuscular androgen receptor protein content has been reported in high versus low responders following training, and this mechanism may enhance the hypertrophic effects of testosterone during training. While high responders likely possess “good genetics,” such evidence has been confined to single gene candidates which typically share marginal variance with hypertrophic outcomes following training (e.g., different myostatin and IGF-1 alleles). Limited evidence also suggests pre-training muscle fiber type composition and self-reported dietary habits (e.g., calorie and protein intake) do not differ between high versus low responders. Only a handful of studies have examined muscle biomarkers that are differentially expressed between low versus high responders. Thus, other molecular and physiological variables which could potentially affect the skeletal muscle hypertrophic response to resistance exercise training are also discussed including rDNA copy number, extracellular matrix and connective tissue properties, the inflammatory response to training, and mitochondrial as well as vascular characteristics.

Highlights

Physiological factors that affect trait responsiveness to exercise training have gained widespread research interest
Contrary to the findings of Petrella et al (2008), as well as the hypothesis that increases in satellite cells are obligatory for resistance exercise training-induced muscle hypertrophy, we reported that training-induced increases in satellite cell number and increases in types I and II fiber myonuclear number were similar between high versus low responders following 12 weeks of resistance exercise training (Mobley et al, 2018a)
There are human reports from several laboratories suggesting the degree of ribosome biogenesis during training associates with the degree of hypertrophy, and the importance of ribosome biogenesis in facilitating muscle hypertrophy is strengthened by numerous in vitro and rodent studies

Summary

Introduction

Physiological factors that affect trait responsiveness to exercise training (e.g., changes in aerobic capacity, strength, or muscle growth) have gained widespread research interest. Van Etten et al (1994) examined the skeletal muscle hypertrophic response in individuals that were classified as “slender” of “solid” following 12 weeks of resistance exercise training. Subjects were classified on the basis of their fat-free mass index (FFMI) determined by skinfolds, in which slender subjects had comparatively lower values relative to solid subjects. These authors reported solid subjects presented significant increases in fat-free mass following training (+1.6 kg), while slender subjects experienced virtually no gain in fat-free mass. While this paper did not examine potential biomarkers which could have facilitated these divergent responses, the authors did conclude that future research should “study the mechanism responsible for differences in weight-training-induced changes in fat free mass.”

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