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One exercise (EX) bout increases PPAR‐gamma coactivator (PGC)‐1 alpha expression in skeletal muscle from healthy and insulin resistant humans
Author(s) -
De Filippis Elena A.,
Alvarez Guy,
Berria Rachele,
Meyer Christian,
Mandarino Lawrence
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1279-c
Insulin resistance in muscle is characterized by mitochondrial (Mito) dysfunction and decreased PGC‐1α expression. EX improves Mito function but the mechanism is unclear. This study was undertaken to determine the pattern of EX induced changes in expression of transcription factors regulating Mito function and if EX effects are normal in insulin resistance. Obese (Ob) and lean control (LC) volunteers (n = 8, BMI 32 ± 0.6 vs. 25 ±1; P<0.05) performed one 45 min bout of cycle EX at 70–90% of max heart rate. Muscle biopsies were taken before and after EX (30 and 300 min). Glucose clamps assessed insulin action; RT‐quantitative PCR measured mRNA for PGC‐1α, nuclear respiratory factor (NRF)‐1, Mito transcription factor A (Tfam/mtTFA), cytochrome c oxidase (COX) VIc and voltage dependent anion channel (VDAC). Ob had reduced insulin stimulated glucose disposal (5.4 ± 1 vs. 8 ± 0.5 mg/(kg.min), P<0.05). In LC, EX increased PGC‐1α mRNA (1.7 ± 0.2 and 9.5 ± 3.1 fold basal values, 30 and 300 min, P<0.05), and COX subunit VIc (2.0 ± 0.5 and 2.5 ± 0.6 fold over basal, P<0.05); mtTFA and VDAC mRNA did not change. In Ob, PGC‐1α mRNA increased (P<0.05) only at 5 hrs post EX (0.7 ± 0.1 and 4.1 ± 1.2 fold over basal, 30 and 300 min) and COX VIc and other mRNAs did not change. Therefore, one bout of EX increases expression of PGC‐1α and other PGC‐1α regulated genes by 30 min. However, in obesity there is delayed onset of changes in PGC‐1α and delay or block in downstream gene expression.