Endurance training in humans leads to fiber type-specific increases in levels of peroxisome proliferator-activated receptor-[gamma] coactivator-1 and peroxisome proliferator-activated receptor-[alpha] in skeletal muscle


Autoria(s): Russell, Aaron; Feilchenfeldt, Jonas; Schreiber, Sylvia; Praz, Manu; Crettenand, Antoinette; Gobelet, Charles; Meier, Christoph; Bell, David; Kralli, Anastasia; Giacobino, Jean-Paul; Deriaz, Olivier
Data(s)

01/12/2003

Resumo

The peroxisome proliferator-activated receptor (PPAR)-γ coactivator-1 (PGC-1) can induce mitochondria biogenesis and has been implicated in the development of oxidative type I muscle fibers. The PPAR isoforms α, β/δ, and γ control the transcription of genes involved in fatty acid and glucose metabolism. As endurance training increases skeletal muscle mitochondria and type I fiber content and fatty acid oxidative capacity, our aim was to determine whether these increases could be mediated by possible effects on PGC-1 or PPAR-α, -β/δ, and -γ. Seven healthy men performed 6 weeks of endurance training and the expression levels of PGC-1 and PPAR-α, -β/δ, and -γ mRNA as well as the fiber type distribution of the PGC-1 and PPAR-α proteins were measured in biopsies from their vastus lateralis muscle. PGC-1 and PPAR-α mRNA expression increased by 2.7- and 2.2-fold (<i>P</i> < 0.01), respectively, after endurance training. PGC-1 expression was 2.2- and 6-fold greater in the type IIa than in the type I and IIx fibers, respectively. It increased by 2.8-fold in the type IIa fibers and by 1.5-fold in both the type I and IIx fibers after endurance training (<i>P</i> < 0.015). PPAR-α was 1.9-fold greater in type I than in the II fibers and increased by 3.0-fold and 1.5-fold in these respective fibers after endurance training (<i>P</i> < 0.001). The increases in PGC-1 and PPAR-α levels reported in this study may play an important role in the changes in muscle mitochondria content, oxidative phenotype, and sensitivity to insulin known to be induced by endurance training.<br />

Identificador

http://hdl.handle.net/10536/DRO/DU:30004098

Idioma(s)

eng

Publicador

American Diabetes Association

Relação

http://dro.deakin.edu.au/eserv/DU:30004098/n20062095.pdf

http://ovidsp.tx.ovid.com/spb/ovidweb.cgi?

Direitos

2003, American Diabetes Association

Tipo

Journal Article