Effects of astaxanthin supplementation and electrical stimulation on muscle atrophy and decreased oxidative capacity in soleus muscle during hindlimb unloading in rats

Abstract

The effects of a combination of the antioxidant astaxanthin (AX) and electrical stimulation (ES) on muscle mass and mitochondrial oxidative capacity were investigated in the soleus muscle of hindlimb unloaded rats. Five groups of male Sprague-Dawley rats were used; control, 1-week hindlimb unloading (HU), HU + AX, HU + ES, and HU + AX + ES. Respective rats in the AX groups received 50-mg/kg AX twice daily during HU. Calf muscles of rats in the ES groups were electrically stimulated for 240 s/day during HU. One-week HU decreased muscle mass along with decreased FoxO3a phosphorylation and increased ubiquitinated proteins expressions, decreased oxidative enzymatic activity accompanied with decline in PGC-1α protein expression, and increased reactive oxygen species production. However, the combination treatment could synergistically attenuate/suppress all HU-related changes, suggesting protective effects on muscle atrophy and decreased muscle oxidative capacity due to chronic neuromuscular inactivity.

Improved Tetanic Force and Mitochondrial Calcium Homeostasis by Astaxanthin Treatment in Mouse Skeletal Muscle

“…It should be noted that the observed effect sizes-increase in tetanic force and reduction in mitochondrial calcium accumulation following repetitive stimulation-were modest. This however is consistent with former measurements using either other antioxidants or AX to improve muscle function or to modify body metabolism by AX [54][55][56].…”

Effects of astaxanthin on the protection of muscle health (Review)

“…Using an exercised mouse model, Liu et al (63) suggested that astaxanthin accelerated lipid utilization in skeletal muscle and reduced intermuscular pH during aerobic exercise through elevation of PGC-1α. Studies conducted by Kanazashi et al (31,32) identified a similar pattern to astaxanthin alone, astaxanthin with intermittent loading and astaxanthin with electrical stimulation retained mitochondrial biogenesis by raising PGC-1α and eNOS expression in the soleus muscle of hindlimb unloaded mice. The total 5'-adenosine monophosphate-activated protein kinase (AMPK) content in skeletal muscle was also significantly augmented in the exercised animals fed with astaxanthin from H. pluvialis than the control group.…”

“…The data from this study showed that increases in 4-hydroxy-2-nonenal (4-HNE)-modified protein, 8-hydroxy-2'-deoxyguanosine (8-OHdG), plasma CK activity and myeloperoxidase (MPO) activity in the gastrocnemius and heart caused by exercise were attenuated by astaxanthin (52). Astaxanthin treatment was effective in lowering the concentrations of malondialdehyde (MDA) or TBARS, ROS and carbonylated protein in various animal models (28)(29)(30)(31)(32)38,39,41,53).…”

“…The combined therapy was more efficient than astaxanthin alone in reversing the adverse changes due to hindlimb unloading. The combination of astaxanthin and electrical stimulation increased absolute soleus muscle mass and fibre cross-sectional area (FCSA) (32). Another group of researchers reported that dietary astaxanthin supplementation prior to and during hindlimb unloading suppressed soleus muscle atrophy.…”

“…High doses of astaxanthin (15 or 30 mg/kg) were shown to be effective in suppressing the levels of GPx, CAT and CK and raising SOD activity in plasma and muscle of mice after moderate-intensity swimming training (53). Another group of researchers pinpointed the reduction in SOD-1 expression in animals with muscle atrophy induced by hindlimb unloading treated with astaxanthin alone (30) or in combination with other interventions such as intermittent loading (31) or electrical stimulation (32). In line with these studies, a lowered SOD-1 level was also detected in two other studies using animals subjected to hindlimb immobilization-induced muscle atrophy (38,39).…”