Abstract
Astaxanthin is a carotenoid pigment and has been shown to be an effective inhibitor of oxidative damage. We tested the hypothesis that astaxanthin intake would attenuate immobilization‐induced muscle atrophy in rats. Male Wistar rats (14‐week old) were fed for 24 days with either astaxanthin or placebo diet. After 14 days of each experimental diet intake, the hindlimb muscles of one leg were immobilized in plantar flexion position using a plaster cast. Following 10 days of immobilization, both the atrophic and the contralateral plantaris muscles were removed and analyzed to determine the level of muscle atrophy along with measurement of the protein levels of CuZn‐superoxide dismutase (CuZn‐SOD) and selected proteases. Compared with placebo diet animals, the degree of muscle atrophy in response to immobilization was significantly reduced in astaxanthin diet animals. Further, astaxanthin supplementation significantly prevented the immobilization‐induced increase in the expression of CuZn‐SOD, cathepsin L, calpain, and ubiquitin in the atrophied muscle. These results support the postulate that dietary astaxanthin intake attenuates the rate of disuse muscle atrophy by inhibiting oxidative stress and proteolysis via three major proteolytic pathways.
Highlights
Skeletal muscles produce abundant reactive oxygen species (ROS) during both aerobic contractions and inactivity, such as bed rest and limb immobilization (Powers et al 2005, 2007, 2011; Powers and Jackson 2008)
Oxidative stress has been shown to participate in the activation of proteolysis via three major proteolytic pathways, lysosomal proteases, Ca2+-activated proteases, and the ubiquitin–proteasome system, all of which are activated during disuse muscle atrophy (Powers et al 2005, 2007)
The immobilization-induced decrease of heat-shock protein 72 (HSP72) levels was not observed in both astaxanthin-treated groups. The mechanisms of this effect are still unclear, these findings suggest that maintenance of HSP72 levels induced by dietary intake of astaxanthin could maintain the beneficial functions of HSP72 described above during immobilization, which resulted in reducing plantaris muscle atrophy
Summary
Skeletal muscles produce abundant reactive oxygen species (ROS) during both aerobic contractions and inactivity, such as bed rest and limb immobilization (Powers et al 2005, 2007, 2011; Powers and Jackson 2008). Kondo et al provided the first evidence regarding the relationship between oxidative stress and disuse muscle atrophy (Kondo et al 1991), and their group indicated that generation of various types of ROS is promoted in atrophied muscle induced by immobilization (Kondo et al 1992, 1993a,b, 1994). It is considered that disuse-induced oxidative stress in skeletal muscle contributes to muscular atrophy via the activation of these proteolytic pathways. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society
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