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1 Department of Physiology and Biophysics, university of California Irvine, Irvine, CA, USA
* To whom correspondence should be addressed. E-mail: fhaddad{at}uci.edu.
This study tested the hypothesis that an isometric resistance training (RT) paradigm targeting the medial gastrocnemius (MG) of adult rodents is effective in preventing muscle atrophy during the early stages of hindlimb unloading by maintaining normal activation of the IRS-1/ PI3K/Akt signaling pathway. This pathway has been shown to simultaneously create an anabolic response while inhibiting processes upregulating catabolic processes involving expression of key enzymes in the ubiquitination of proteins for degradation. The findings show that during the five days of unloading 1) absolute MG muscle weight reduction occurred by ~ 20%, but muscle weight corrected to body weight was not different from normal weight bearing controls (P< .05); 2) normalized myofibril fraction concentration and content were decreased; and 3) a robust isometric training program, known to induce a hypertrophy response, failed to maintain the myofibril protein content. This response occurred in spite of fully blunting the increases in the mRNA for of atrogin-1, MURF-1, and myostatin, e.g., sensitive gene markers of an activated catabolic state. Analyses of the IRS-1/ PI3K/Akt markers indicated that abundance of insulin receptor subrate-1 (IRS-1) and phosphorylation state of Akt and p70S6 kinase were decreased relative to normal control rats, and the RT failed to maintain these signaling markers at normal regulatory level. Our findings suggest that in order to fully prevent muscle atrophy responses affecting the myofibril system during unloading, the volume of mechanical stress must be augmented sufficiently to maintain optimal activity of the IRS-1/ PI3K/Akt pathway to provide an effective anabolic stimulus on the muscle.
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