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Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process.
Int J Biochem Cell Biol. 2010 Sep; 42(9):1371-5.IJ

Abstract

Muscle cells (fibres) are post-mitotic and thus undergo changes in phenotype by modifying their existing structure. Hypertrophy is a hallmark change that occurs in response to increased loading and can be achieved in humans through repeated bouts of resistance exercise (i.e., training). In resistance exercise, contractions are initiated by neural drive leading to immediate perturbations such as calcium influx, cross-bridge cycling and tension/stress on the cytoskeleton, sarcolemma and extracellular matrix, as well as more delayed cellular events such as the production/release of potential local growth factors (e.g., IGF-1). Resistance exercise can also elevate the systemic concentration of certain hormones (growth hormone, testosterone, IGF-1) that are hypothesized to drive hypertrophy. However, while these hormones are clearly anabolic during childhood and puberty, or when given at supraphysiological exogenous doses, the transient post-exercise elevations in hormone concentration are of little consequence to the either the acute protein synthetic response or to a hypertrophic phenotype after resistance training. Thus, the acute post-exercise increases in systemic hormones are in no way a proxy marker for anabolism since they do not underpin the capacity of the muscle to hypertrophy in any measurable way. In contrast, the acute activation of intrinsically located signalling proteins such as p70(S6K) and the acute elevation of muscle protein synthesis are more reflective of the potential to increase in muscle mass with resistance training. Ultimately, local mechanisms are activated by the stress imposed by muscle loading and prime the muscle for protein accretion. Membrane-derived molecules and tension-sensing pathways are two intrinsic mechanisms implicated in upregulating the synthesis and incorporation of muscle proteins into the myofibre in response to mechanical stress derived from loaded contractions.

Authors+Show Affiliations

Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Canada.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20541030

Citation

West, Daniel W D., et al. "Human Exercise-mediated Skeletal Muscle Hypertrophy Is an Intrinsic Process." The International Journal of Biochemistry & Cell Biology, vol. 42, no. 9, 2010, pp. 1371-5.
West DW, Burd NA, Staples AW, et al. Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process. Int J Biochem Cell Biol. 2010;42(9):1371-5.
West, D. W., Burd, N. A., Staples, A. W., & Phillips, S. M. (2010). Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process. The International Journal of Biochemistry & Cell Biology, 42(9), 1371-5. https://doi.org/10.1016/j.biocel.2010.05.012
West DW, et al. Human Exercise-mediated Skeletal Muscle Hypertrophy Is an Intrinsic Process. Int J Biochem Cell Biol. 2010;42(9):1371-5. PubMed PMID: 20541030.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process. AU - West,Daniel W D, AU - Burd,Nicholas A, AU - Staples,Aaron W, AU - Phillips,Stuart M, Y1 - 2010/06/09/ PY - 2009/12/22/received PY - 2010/04/13/revised PY - 2010/05/30/accepted PY - 2010/6/15/entrez PY - 2010/6/15/pubmed PY - 2010/11/3/medline SP - 1371 EP - 5 JF - The international journal of biochemistry & cell biology JO - Int. J. Biochem. Cell Biol. VL - 42 IS - 9 N2 - Muscle cells (fibres) are post-mitotic and thus undergo changes in phenotype by modifying their existing structure. Hypertrophy is a hallmark change that occurs in response to increased loading and can be achieved in humans through repeated bouts of resistance exercise (i.e., training). In resistance exercise, contractions are initiated by neural drive leading to immediate perturbations such as calcium influx, cross-bridge cycling and tension/stress on the cytoskeleton, sarcolemma and extracellular matrix, as well as more delayed cellular events such as the production/release of potential local growth factors (e.g., IGF-1). Resistance exercise can also elevate the systemic concentration of certain hormones (growth hormone, testosterone, IGF-1) that are hypothesized to drive hypertrophy. However, while these hormones are clearly anabolic during childhood and puberty, or when given at supraphysiological exogenous doses, the transient post-exercise elevations in hormone concentration are of little consequence to the either the acute protein synthetic response or to a hypertrophic phenotype after resistance training. Thus, the acute post-exercise increases in systemic hormones are in no way a proxy marker for anabolism since they do not underpin the capacity of the muscle to hypertrophy in any measurable way. In contrast, the acute activation of intrinsically located signalling proteins such as p70(S6K) and the acute elevation of muscle protein synthesis are more reflective of the potential to increase in muscle mass with resistance training. Ultimately, local mechanisms are activated by the stress imposed by muscle loading and prime the muscle for protein accretion. Membrane-derived molecules and tension-sensing pathways are two intrinsic mechanisms implicated in upregulating the synthesis and incorporation of muscle proteins into the myofibre in response to mechanical stress derived from loaded contractions. SN - 1878-5875 UR - https://www.unboundmedicine.com/medline/citation/20541030/Human_exercise_mediated_skeletal_muscle_hypertrophy_is_an_intrinsic_process_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1357-2725(10)00192-5 DB - PRIME DP - Unbound Medicine ER -