4.4 Article

N-acetyl-4-aminophenol and musculoskeletal adaptations to resistance exercise training

期刊

EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY
卷 113, 期 5, 页码 1127-1136

出版社

SPRINGER
DOI: 10.1007/s00421-012-2529-z

关键词

Resistance exercise; Acetaminophen; Muscle hypertrophy; Osteogenesis; Mechanotransduction; Lean tissue mass

资金

  1. National Institutes of Health [R21 AG027809, R01 AG018857, P30 DK048520]
  2. Colorado Clinical Translational Science Institute [UL1 TR000154]

向作者/读者索取更多资源

N-acetyl-4-aminophenol (ACET) may impair musculoskeletal adaptations to progressive resistance exercise training (PRT) by inhibiting exercise-induced muscle protein synthesis and bone formation. To test the hypothesis that ACET would diminish training-induced increases in fat-free mass (FFM) and osteogenesis, untrained men (n = 26) aged a parts per thousand yen50 years participated in 16 weeks of high-intensity PRT and bone-loading exercises and were randomly assigned to take ACET (1,000 mg/day) or placebo (PLAC) 2 h before each exercise session. Total body FFM was measured by DXA at baseline and week 16. Serum bone-specific alkaline phosphatase (BAP) and C-terminal crosslinks of type-I collagen (CTX) were measured at baseline and week 16. Vastus lateralis muscle biopsies were performed at baseline and weeks 3 and 16 for prostanoid, anabolic, and catabolic gene expression by RT-PCR. In exercise-compliant men (ACET, n = 10; PLAC, n = 7), the increase in FFM was not different between groups (p = 0.91). The changes in serum BAP and CTX were not different between groups (p > 0.7). There were no significant changes in any of the target genes at week 3. After 16 weeks of PRT, the mRNA expressions of the anabolic marker p70S6K (p = 0.003) and catabolic marker muscle-atrophy F-box (MAFbx) (p = 0.03) were significantly reduced as compared to baseline in ACET. The mRNA expression of the prostanoids were unchanged (all p a parts per thousand yen 0.40) in both groups. The administration of ACET (1,000 mg) prior to each exercise session did not impair PRT-induced increases in FFM or significantly alter bone formation markers in middle aged and older men.

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