期刊
JOURNAL OF APPLIED PHYSIOLOGY
卷 103, 期 5, 页码 1488-1495出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.01194.2006
关键词
resistance training; muscle growth; cell cycle; muscle fiber
资金
- NCRR NIH HHS [M01 RR 00032] Funding Source: Medline
- NIA NIH HHS [R01 AG017896] Funding Source: Medline
Myostatin is a potent inhibitor of myogenesis; thus differential expression might be expected across individuals varying in responsiveness to myogenic stimuli. We hypothesized that myostatin would be differentially regulated across humans with markedly different hypertrophic responses to resistance training (RT; 16 wk). Targets were assessed in muscle biopsies at baseline (T1) and 24 h after the first (T2) and last (T3) loading bouts in previously untrained subjects statistically clustered based on mean myofiber hypertrophy as extreme (Xtr; n = 17, 2,475 mu m(2)), modest (n = 32, 1,111 mu m2), and nonresponders (n = 17, - 16 mu m2). We assessed protein levels of latent full- length myostatin protein complex and its propeptide; mRNA levels of myostatin, cyclin D1, p21(cip1), p27(kip1), and activin receptor IIB; and serum myostatin protein concentration. Total RNA concentration increased by T3 in nonresponders (37%) and modest responders (40%), while it increased acutely (T2) only in Xtr (26%), remaining elevated at T3 (40%). Myostatin mRNA decreased at T2 (-44%) and remained suppressed at T3 (- 52%), but not differentially across clusters. Cyclin D1 mRNA increased robustly by T2 (38%) and T3 (74%). The increase at T2 was driven by Xtr (62%, P < 0.005), and Xtr had the largest elevation at T3 (82%, P < 0.001). No effects were found for other target transcripts. Myostatin protein complex increased 44% by T3 (P < 0.001), but not differentially by cluster. Myostatin protein complex propeptide and circulating myostatin were not influenced by RT or cluster. Overall, we found no compelling evidence that myostatin is differentially regulated in humans demonstrating robust RT- mediated myofiber hypertrophy vs. those more resistant to growth.
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