Endurance training in humans leads to fiber type-specific increases in levels of peroxisome proliferator-activated receptor-γ coactivator-1 and peroxisome proliferator …

AP Russell, J Feilchenfeldt, S Schreiber, M Praz… - Diabetes, 2003 - Am Diabetes Assoc
AP Russell, J Feilchenfeldt, S Schreiber, M Praz, A Crettenand, C Gobelet, CA Meier…
Diabetes, 2003Am Diabetes Assoc
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 …
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 (P < 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 (P < 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 (P < 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.
Am Diabetes Assoc