Resistance Exercise Training Attenuates Wasting of the EDL Muscle in Mice Bearing the Colon-26 Adenocarcinoma
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Biological Research for Nursing
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Progressive wasting of skeletal muscle is a significant side effect of malignancy. Perturbations in protein metabolism contribute to this state of wasting. Resistance exercise increases protein synthesis and mass of healthy muscles and counteracts muscle wasting associated with several catabolic conditions. It is not known whether resistance exercise training can counteract cancer-induced muscle wasting. This study examined the effect of resistance exercise training on muscle mass and protein content in 9 mice bearing the colon-26 adenocarcinoma. The dorsiflexor (extensor digitorum longus [EDL] and tibialis anterior) and plantar flexor (soleus, plantaris, and gastrocnemius) muscles of 1 leg of the tumor-bearing and the control mice were stimulated to contract eccentrically and concentrically, respectively, using an electrical stimulation protocol consisting of 10 sets of 6 repetitions per session. The muscles were stimulated on alternate days for a total of 8 sessions. The weight and protein content of the stimulated EDL muscle in the tumorbearing mice were significantly higher (62% and 25%, respectively) than those of the nonstimulated EDL. Training did not have significant effects on the weight or protein content of the other muscles of the tumorbearing mice, nor did it have significant effects on the muscles of the controls. These findings demonstrated that resistance training attenuated cancer-induced muscle wasting and protein depletion in the EDL muscle. The lack of an effect of the same training protocol on the ED Lmuscle in the control mice suggests that the amount and intensity of exercise training that is adequate to attenuate muscle wasting may not be adequate to induce hypertrophy of healthy muscles.
McCarthy, Donna O., "Resistance Exercise Training Attenuates Wasting of the EDL Muscle in Mice Bearing the Colon-26 Adenocarcinoma" (2001). College of Nursing Faculty Research and Publications. 205.