4.6 Article

Aerobic Exercise Alters Skeletal Muscle Molecular Responses to Resistance Exercise

期刊

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
卷 44, 期 9, 页码 1680-1688

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0b013e318256fbe8

关键词

ENDURANCE; HUMAN SKELETAL MUSCLE; mTOR; MUSCLE POWER; PGC-1 alpha; P70S6K

资金

  1. Swedish National Centre for Research in Sports
  2. Swedish National Space Board
  3. Swedish Medical Association
  4. Karolinska Institutet Foundation
  5. Marianne and Marcus Wallenberg Foundation

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LUNDBERG, T. R., R. FERNANDEZ-GONZALO, T. GUSTAFSSON, and P. A. TESCH. Aerobic Exercise Alters Skeletal Muscle Molecular Responses to Resistance Exercise. Med. Sci. Sports Exerc., Vol. 44, No. 9, pp. 1680-1688, 2012. Purpose: This study assessed the influence of an acute aerobic exercise bout on molecular responses to subsequent resistance exercise (RE). Methods: Nine physically active men performed a 45-min one-legged cycle ergometry exercise and 4 x 7 maximal concentric eccentric knee extensions for each leg 6 h later. Thus, one limb was subjected to aerobic and resistance exercise (AE+RE), and the contralateral limb to resistance exercise (RE) only. Knee extensor peak power was determined. Biopsies were obtained from the m vastus lateralis before (PRE) and 15 mm (POST1) and 3 h after RE. Analysis determined glycogen content, mRNA levels (vascular endothelial growth factor, peroxisome proliferator activated receptor-gamma coactivator-1, muscle RING-finger protein-1, atrogin-1, myostatin), and phosphorylated proteins (mammalian target of rapamycin, p70S6 kinase, ribosomal protein S6, eukaryotic elongation factor 2). Results: Peak power was similar in AE + RE and RE. After RE, the time course of glycogen utilization and protein signaling was similar across legs. However, phosphorylation of mammalian target of rapamycin and p70S6 kinase was elevated in AE + RE versus RE (main effect, P < 0.05). Vascular endothelial growth factor and peroxisome proliferator activated receptor-gamma coactivator-1 were higher in AE + RE than in RE at PRE and POST1 (P < 0.05). Myostatin was lower in AE + RE versus RE at PRE and POST1 (P < 0.05) and downregulated after resistance exercise only. Atrogin-1 was higher in AE + RE than in RE at PRE and POST1 (P < 0.05) and decreased after RE in AE + RE. Muscle RING-finger protein-1 was similar across legs. No difference for any marker was evident 3 h after RE. Conclusions: These results suggest that acute aerobic exercise alters molecular events regulating muscle protein turnover during the early recovery period from subsequent RE.

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