Combined isometric, concentric, and eccentric resistance exercise prevents unloading-induced muscle atrophy in rats.
Previously, we reported that an isometric resistance training program that was effective in stimulating muscle hypertrophy in ambulatory rats could not completely prevent muscle atrophy during unloading (Haddad F, Adams GR, Bodell PW, Baldwin KM. J Appl Physiol 100: 433-441, 2006). These results indicated that preventing muscle atrophy does not appear to be simply a function of providing an anabolic stimulus. The present study was undertaken to determine if resistance training, with increased volume (3-s contractions) and incorporating both static and dynamic components, would be effective in preventing unloading-induced muscle atrophy. Rats were exposed to 5 days of muscle unloading via tail suspension. During that time one leg received electrically stimulated resistance exercise (RE) that included an isometric, concentric, and eccentric phase. The results of this study indicate that this combined-mode RE provided an anabolic stimulus sufficient to maintain the mass and myofibril content of the trained but not the contralateral medial gastrocnemius (MG) muscle. Relative to the contralateral MG, the RE stimulus increased the amount of total RNA (indicative of translational capacity) as well as the mRNA for several anabolic/myogenic markers such as insulin-like growth factor-I, myogenin, myoferlin, and procollagen III-alpha-1 and decreased that of myostatin, a negative regulator of muscle size. The combined-mode RE protocol also increased the activity of anabolic signaling intermediates such as p70S6 kinase. These results indicate that a combination of static- and dynamic-mode RE of sufficient volume provides an effective stimulus to stimulate anabolic/myogenic mechanisms to counter the initial stages of unloading-induced muscle atrophy.
Adams
G R
GR
Dept. of Physiology and Biophysics, Univ. of California, Irvine, CA 92697-4560, USA.
Haddad
F
F
Bodell
P W
PW
Tran
P D
PD
Baldwin
K M
KM
D000818:Animals; D001835:Body Weight; D024061:Collagen Type III / Q000378:metabolism; D056741:Cyclin D; D016213:Cyclins / Q000378:metabolism; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005260:Female; D019417:Hindlimb Suspension; D018974:Insulin-Like Growth Factor Binding Protein 4 / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007537:Isometric Contraction; D009119:Muscle Contraction; D024510:Muscle Development; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000201:enzymology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009133:Muscular Atrophy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D018008:Myogenin / Q000378:metabolism; D009929:Organ Size; D010766:Phosphorylation; D005082:Physical Exertion; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012107:Research Design; D038762:Ribosomal Protein S6 Kinases, 70-kDa / Q000378:metabolism; D044843:SKP Cullin F-Box Protein Ligases / Q000378:metabolism; D015398:Signal Transduction; D013997:Time Factors
D024061:Collagen Type III; D056741:Cyclin D; D016213:Cyclins; D018974:Insulin-Like Growth Factor Binding Protein 4; D009124:Muscle Proteins; C503803:Myog protein, rat; D018008:Myogenin; D012333:RNA, Messenger; D007334:Insulin-Like Growth Factor I; D044843:SKP Cullin F-Box Protein Ligases; D038762:Ribosomal Protein S6 Kinases, 70-kDa