Dietary astaxanthin supplementation attenuates disuse-induced muscle atrophy and myonuclear apoptosis in the rat soleus muscle.
Extended periods of skeletal muscle disuse results in muscle atrophy and weakness. Currently, no therapeutic treatment is available for the prevention of this problem. Nonetheless, growing evidence suggests that prevention of disuse-induced oxidative stress in inactive muscle fibers can delay inactivity-induced muscle wasting. Therefore, this study tested the hypothesis that dietary supplementation with the antioxidant astaxanthin would protect against disuse muscle atrophy, in part, by prevention of myonuclear apoptosis. Wistar rats (8 weeks old) were divided into control (CT, n = 9), hindlimb unloading (HU, n = 9), and hindlimb unloading with astaxanthin (HU + AX, n = 9) groups. Following 2 weeks of dietary supplementation, rats in the HU and HU + AX groups were exposed to unloading for 7 days. Seven-day unloading resulted in reduced soleus muscle weight and myofiber cross-sectional area (CSA) by ~30 and ~47 %, respectively. Nonetheless, relative muscle weights and CSA of the soleus muscle in the HU + AX group were significantly greater than those of the HU group. Moreover, astaxanthin prevented disuse-induced increase in the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive nuclei. We conclude that astaxanthin supplementation prior to and during hindlimb unloading attenuates soleus muscle atrophy, in part, by suppressing myonuclear apoptosis.
Graduate School of Health and Sports Science, Juntendo University, 1-1 Hirakagakuendai, Inzai, Chiba, 270-1695, Japan. t-yoshih@juntendo.ac.jp.
Toshinori
T
Yoshihara
Sports Research and Development Core, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, Japan.
Yuki
Y
Yamamoto
Graduate School of Frontier Biosciences, Osaka University, 1-17 Machikaneyama-cho, Toyonaka, Osaka, Japan.
Tsubasa
T
Shibaguchi
Toyo Koso Kagaku Co. Ltd., 4-4-27 Horie, Urayasu, Chiba, Japan.
Nobuyuki
N
Miyaji
Faculty of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, Japan.
Ryo
R
Kakigi
Graduate School of Health and Sports Science, Juntendo University, 1-1 Hirakagakuendai, Inzai, Chiba, 270-1695, Japan.
Hisashi
H
Naito
Graduate School of Health Sciences, Toyohashi SOZO University, 20-1 Matsushita, Toyohashi, Aichi, Japan.
Katsumasa
K
Goto
Department of Chemistry, School of Medicine, Juntendo University, 1-1 Hrakagakuendai, Inzai, Chiba, Japan.
Daijiro
D
Ohmori
Hirosaki Gakuin University, 13-1 Minori-cho, Hirosaki, Aomori, Japan.
Toshitada
T
Yoshioka
Faculty of Education, Yamaguchi University, 1677-1 Yoshida, Yamaguchi, Japan.
Takao
T
Sugiura
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects*; D019417:Hindlimb Suspension / Q000502:physiology; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000473:pathology; D009133:Muscular Atrophy / Q000188:drug therapy* / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D024341:Xanthophylls / Q000494:pharmacology / Q000627:therapeutic use
D000975:Antioxidants; D024341:Xanthophylls; C005948:astaxanthine
Antioxidant; Apoptosis; Disuse muscle atrophy; Protein degradation