It has been demonstrated that exercise induces heat shock proteins (HSPs) . However, no study has investigated changes in HSPs following endurance training at different speeds. Therefore, this study was designed to investigate the effect of treadmill training at different running speeds on induction HSPs. One group of male Wistar rats was assigned as a sedentary control, three groups were assigned for exercise training (10 m/min, 20 m/min and 30 m/min) and another three groups for one acute bout of exercise (10 m/min, 20 m/min and 30 m/min) . Each training group ran at each speed for 30 min/day, 5 days a week for 8 weeks. The acute exercise group performed the exercise only once. Forty-eight hours after the last exercise session was completed, the rats were sacrificed and the plantaris (PLA) and soleus (SOL) muscles were dissected. In the acute exercise group, the content of HSP72 in both the PLA and SQL increased (p<0.05) at all speeds, and the content of HSP60 increased significantly (p<0.05) at all speeds for the PLA, but not for the SOL. On the other hand, in the endurance group, the content of HSP72 and HSP60 in both muscles increased in 30 m/min groups. These results indicate that an increase in HSP72 and HSP60 by endurance training is induced by high intensity training in both muscles. This was not found to be the case with the acute exercise groups.

In the present study, we investigated the effect of heat stress on disuse atrophy from changes in the muscle protein levels of desmin and calpain. Wistar strain female rats (6-8 months old) were randomly assigned to two experimental groups: control (C) and heat stress (H). One hindlimb of all animals was immobilized in plantar flexion with plaster. Before immobilization, animals in H group were placed in a heat chamber (42°C for 60 min). Following 6 days of immobilization, the soleus muscles were removed and analyzed. Although immobilization resulted in significant muscle atrophy in all experimental animals, the soleus weight-to-body weight ratio in immobilized limbs of H group was significantly higher compared to that of C group. Expression of desmin and HSP72 in the atrophied soleus muscle from C group was significantly lower compared with the contralateral muscle; but this was not the case in H group. Further, in C group, the ratio of autolyzed calpains I increased significantly in the atrophied muscle compared to the contralateral muscle. These results show that the effect of heat stress on disuse skeletal muscle atrophy is attributed to the decreasing degradation of desmin by suppressing the activation of calpain.

Oxidative stress is thought to be a significant contributing factor of age-related sarcopenia. We tested the hypothesis that long-term dietary antioxidant (astaxanthin) intake attenuates sarcopenia. Wistar strain male rats, aged 45 weeks old, were given either control (Cont) or astaxanthin feed (0.004%, Ax) for 1 year. The soleus muscle weight and muscle weight-to-body weight ratios in Ax group were significantly higher than in Cont group, but tibialis anterior muscle mass was similar between the two dietary groups. The level of ubiquitinated proteins was significantly lower in the soleus muscles of Ax group, but not in tibialis anterior muscles when compared with Cont group. Tibialis anterior levels of cathepsin L, especially, and caspase-3 tended to be lower in Ax group than in Cont group. Cathepsin L levels were significantly lower. Whereas no differences between Cont and Ax were observed in soleus levels. There were no significant differences in Ax supplementation on calpain 1 and 2, UBC3B, Cu/Zn SOD and nitrotyrosine levels in either soleus or tibialis anterior muscles. Our data suggest that long-term dietary astaxanthin intake attenuates age-related muscle atrophy, due in part, to reduction in ubiquitination of myofibrillar protein in slow soleus muscles, but not in fast tibialis anterior muscles.

The purpose of this study was to examine the effects of combination of a heat stress and astaxanthin supplementation, known as a potent anti-oxidative nutrient, on muscle protein degradation and disuse muscle atrophy. Fifty-two male Wistar rats (261.7±1.17 g) were divided into five groups: control (Cont, n=10), suspension (Sus, n=11), heat stress and suspension (Heat, n=10), astaxanthin and suspension (Ax, n=10), and heat stress, astaxanthin and suspension (H+A, n=11). There were no significant differences in Cu,Zn-SOD, cathepsin L and caspase-3 levels among the Heat, Ax and H+A groups in the soleus and plantaris muscles. Although levels of calpain 2 and ubiquitinated protein in the myofibrillar fraction in the soleus muscle were not significantly different among the Heat, Ax and H+A groups, levels in the H+A group were significantly (p<0.05) lower than Sus. Concerning atrophied plantaris muscles, the H+A group significantly (p<0.05) suppressed the expression of calpain 1 in the myofibrillar fraction, but there were no marked changes of proteolytic indexes. These data indicate that the combination of the heat stress and astaxanthin supplementation could be effective in inhibiting muscle protein degradation in disuse atrophy of the soleus.

We examined the effect of a combination of astaxanthin (AX) supplementation, repeated heat stress, and intermittent reloading (IR) on satellite cells in unloaded rat soleus muscles. Forty-nine male Wistar rats (8-week-old) were divided into control, hind-limb unweighting (HU), IR during HU, IR with AX supplementation, IR with repeated heat stress (41.0-41.5 °C for 30 min), and IR with AX supplementation and repeated heat stress groups. After the experimental period, the antigravitational soleus muscle was analyzed using an immunohistochemical technique. Our results revealed that the combination of dietary AX supplementation and heat stress resulted in protection against disuse muscle atrophy in the soleus muscle. This protective effect may be partially due to a higher satellite cell number in the atrophied soleus muscle in the IR/AX/heat stress group compared with the numbers found in the other groups. We concluded that the combination treatment with dietary AX supplementation and repeated heat stress attenuates soleus muscle atrophy, in part by increasing the number of satellite cells.
Animals ; Body Weight ; Dietary Supplements ; Fibrinolytic Agents/pharmacology* ; Heat-Shock Response ; Hindlimb ; Hot Temperature ; Immunohistochemistry ; Male ; Muscle, Skeletal ; Muscular Atrophy/drug therapy* ; Oxidative Stress ; Rats ; Rats, Wistar ; Satellite Cells, Skeletal Muscle/cytology* ; Xanthophylls/pharmacology*