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Vol. 84, Issue 1, 157-163, January 1998
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
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.
muscle atrophy; spaceflight; immunohistochemistry; strength; neural activation; unloading
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