The Acute Response of Pericytes to Muscle-Damaging Eccentric Contraction and Protein Supplementation in Human Skeletal Muscle

Michael De Lisio, Jean Farup, Richard A Sukiennik, Nicole Clevenger, Julian Nallabelli, Brett Nelson, Kelly Ryan, Stine Klejs Rahbek, Frank de Paoli, Kristian Vissing, Marni D Boppart

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Abstract

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 hours following ECC. Reflective of the damaging protocol, integrin subunits, including α7, β1A and β1D increased (3.8-fold, 3.6-fold and 3.9-fold, p<0.01) 24 hours 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 SRF, and the number of pericytes expressing SRF did not differ as a function of time post-ECC or supplement. These data demonstrate that acute muscle-damaging ECC increases α7β1 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 towards pericyte contribution to repair and adaptation post-exercise.

OriginalsprogEngelsk
TidsskriftJournal of Applied Physiology
Vol/bind119
Nummer8
Sider (fra-til)900-907
Antal sider8
ISSN8750-7587
DOI
StatusUdgivet - 15 okt. 2015

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