4.5 Article

The acute response of pericytes to muscle-damaging eccentric contraction and protein supplementation in human skeletal muscle

期刊

JOURNAL OF APPLIED PHYSIOLOGY
卷 119, 期 8, 页码 900-907

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.01112.2014

关键词

mesenchymal stem cell; whey; muscle damage; muscle regeneration

资金

  1. Abbott Nutrition
  2. Center for Nutrition, Learning, and Memory at the University of Illinois [392 Abbott CNLM ZA68]
  3. ARLA Foods

向作者/读者索取更多资源

Skeletal muscle pericytes increase in quantity following eccentric exercise (ECC) and contribute to myofiber repair and adaptation in mice. The purpose of the present investigation was to examine pericyte quantity in response to muscle-damaging ECC and protein supplementation in human skeletal muscle. Male subjects were divided into protein supplement (WHY; n = 12) or isocaloric placebo (CHO; n = 12) groups and completed ECC using an isokinetic dynamometer. Supplements were consumed 3 times/day throughout the experimental time course. Biopsies were collected prior to (PRE) and 3, 24, 48, and 168 h following ECC. Reflective of the damaging protocol, integrin subunits, including alpha 7, beta 1A, and beta 1D, increased (3.8-fold, 3.6-fold and 3.9-fold, respectively, P < 0.01) 24 h post-ECC with no difference between supplements. Pericyte quantity did not change post-ECC. WHY resulted in a small, but significant, decrease in ALP(+) pericytes when expressed as a percentage of myonuclei (CHO 6.8 +/- 0.3% vs. WHY 5.8 +/- 0.3%, P < 0.05) or per myofiber (CHO 0.119 +/- 0.01 vs. WHY 0.098 +/- 0.01, P < 0.05). The quantity of myonuclei expressing serum response factor and the number of pericytes expressing serum response factor, did not differ as a function of time post-ECC or supplement. These data demonstrate that acute muscle-damaging ECC increases alpha 7 beta 1 integrin content in human muscle, yet pericyte quantity is largely unaltered. Future studies should focus on the capacity for ECC to influence pericyte function, specifically paracrine factor release as a mechanism toward pericyte contribution to repair and adaptation postexercise.

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