Medicine & Science in Sports & Exercise:
Presidential Closing Remarks 12:05 PM - 12:15 PM: Immediately Following President's Lectures ROOM: Ballroom 2/3 and Ballroom 1: C-18 Free Communication/Slide - Muscle Hypertrophy/Atrophy THURSDAY, JUNE 1, 2006 8:00 AM - 10:00 AM ROOM: 401
1Institute of Sport Science and Clinical Biomechanics, University of Southern Denmark, Denmark, Odense M, Denmark.
2Department of Endocrinology, Odense University Hospital, Denmark, Odense, Denmark.
3Dept. of Molecular Muscle Biology, CMRC, Rigshospitalet, Denmark, Copenhagen, Denmark
Endogenous testosterone (ET) interacts with skeletal muscle and is a component of an integrated endocrine system that seems to mediate the adaptive changes in muscles as a result of strength training (ST). In addition, the myogenic regulating factors (MRFs) including myoD and myogenin seem to play an essential role in the ST induced muscle hypertrophy. The interaction between ST, levels of ET, myoD and myogenin, muscle hypertrophy and increased strength has not been examined.
PURPOSE: Suppression of ET will inhibit the adaptation to ST with a concomitant decrease in the mRNA expression of myoD and myogenin, leading to a less pronounced increase in lean mass and muscle strength.
METHODS: Twenty-two moderately trained young men with no experience of ST volunteered to participate in this randomized, placebo-controlled, intervention study. The subjects were divided in two groups (zoladex (Z) n = 1 2 and placebo (P) n = 1 0). ET levels were suppressed using injections of GnRH-analogue (Zoladex, AstraZeneca). Zoladex (3.6 mg) or placebo (saline) was administered sub cutaneous ly every 4 wk for a period of 12 wk. The ST period started 3 wk after the first injection and the subjects were assigned to a full body ST program emphasizing the legs for 8 wk. Subjects trained 6–10 reps with corresponding 6–10 RM loads x 3 – 4 sets per exercise, 3/wk. Before and after the ST period strength test (Kin-Com 500H, USA) and whole body DEXA scan (Hologic 4500) were performed. Biopsies were taken in the right vastus lateralis at 4 time points to measure the mRNA expression of myoD and myogenin. Before (biopsy nr. 1.) and after (nr. 2.) the ST period and in relation to the last ST session (pre (nr. 2.), 4 h post (nr. 3.) and 24 h post (nr. 4.)). MyoD and myogenin mRNA expression were normalized to GAPDH.
RESULTS: Absolute isometric strength increased significantly after 8 wk of ST in P from 240.2 ± 41.3 (SD) Nm to 264.1 ± 35.3 Nm (p<0.05) while Z showed no changes 224.8 ± 44.4 to 230.0 ± 39.8 Nm (p = 0.05 between groups). Lean mass for the legs increased 0.38 ± 0.1 kg in Z and 0.57 ± 0.3 kg in P (p<0.05 within and p = 0.05 between groups). MyoD expression showed no changes between different time points, whereas myogenin expression was nearly 4 fold higher when comparing biopsy nr. 3. with biopsy nr. 2. (p<0.05). In addition, biopsy nr. 3. and 4. was significantly higher than biopsy nr. 1. and 2. (p<0.05). There were no differences between the myogenin expression in the two groups.
CONCLUSIONS: This study showed that ST with suppression of ET production does not inhibit local cellular mRNA expression of myogenin but leads to a less pronounced increase in lean mass and no increase in muscle strength.