Impact of resistance exercise during bed rest on skeletal muscle sarcopenia and myosin isoform distribution

Author:

Bamman Marcas M.1,Clarke Mark S. F.2,Feeback Daniel L.2,Talmadge Robert J.3,Stevens Bruce R.4,Lieberman Steven A.5,Greenisen Michael C.2

Affiliation:

1. Department of Human Studies, University of Alabama at Birmingham, Birmingham, Alabama 35294;

2. Life Sciences Research Laboratories, National Aeronautics and Space Administration Johnson Space Center, Houston, Texas 77058;

3. Department of Physiological Sciences, University of California, Los Angeles, California 90095;

4. Department of Physiology, University of Florida, Gainesville, Florida 32611; and

5. Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas 77550

Abstract

Bamman, Marcas M., Mark S. F. Clarke, Daniel L. Feeback, Robert J. Talmadge, Bruce R. Stevens, Steven A. Lieberman, and Michael C. Greenisen. Impact of resistance exercise during bed rest on skeletal muscle sarcopenia and myosin isoform distribution. J. Appl. Physiol. 84(1): 157–163, 1998.—Because resistance exercise (REx) and bed-rest unloading (BRU) are associated with opposing adaptations, our purpose was to test the efficacy of REx against the effects of 14 days of BRU on the knee-extensor muscle group. Sixteen healthy men were randomly assigned to no exercise (NoEx; n = 8) or REx ( n = 8). REx performed five sets of leg press exercise with 80–85% of one repetition maximum (1 RM) every other day during BRU. Muscle samples were removed from the vastus lateralis muscle by percutaneous needle biopsy. Myofiber distribution was determined immunohistochemically with three monoclonal antibodies against myosin heavy chain (MHC) isoforms (I, IIa, IIx). MHC distribution was further assessed by quantitative gel electrophoresis. Dynamic 1-RM leg press and unilateral maximum voluntary isometric contraction (MVC) were determined. Maximal neural activation (root mean squared electromyogram) and rate of torque development (RTD) were measured during MVC. Reductions ( P < 0.05) in type I (15%) and type II (17%) myofiber cross-sectional areas were found in NoEx but not in REx. Electrophoresis revealed no changes in MHC isoform distribution. The percentage of type IIx myofibers decreased ( P < 0.05) in REx from 9 to 2% and did not change in NoEx. 1 RM was reduced ( P < 0.05) by 9% in NoEx but was unchanged in REx. MVC fell by 15 and 13% in NoEx and REx, respectively. The agonist-to-antagonist root mean squared electromyogram ratio decreased ( P < 0.05) 19% in REx. RTD slowed ( P < 0.05) by 54% in NoEx only. Results indicate that REx prevented BRU-induced myofiber atrophy and also maintained training-specific strength. Unlike spaceflight, BRU did not induce shifts in myosin phenotype. The reported benefits of REx may prove useful in prescribing exercise for astronauts in microgravity.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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