Effect of dietary antioxidant-rich foods combined with aerobic training on energy metabolism in healthy young men.

Although supplementation with several antioxidants has been suggested to improve aerobic metabolism during exercise, whether dietary foods containing such antioxidants can exert the metabolic modulation is unclear. This study aimed to investigate the effect of intake of the specific antioxidant-rich foods coupled with exercise training on energy metabolism. Twenty young healthy, untrained men were assigned to antioxidant and control groups: participants in the antioxidant group were encouraged to consume foods containing catechin, astaxanthin, quercetin, glutathione, and anthocyanin. All participants performed cycle training at 60% maximum oxygen consumption for 30 min, 3 days per week for 4 weeks. Maximum work load was significantly increased by training in both groups, while oxygen consumption during exercise was significantly increased in the antioxidant group only. There were positive correlations between maximum work load and fat/carbohydrate oxidations in the antioxidant group. Carbohydrate oxidation during rest was significantly higher in the post-training than that in the pre-training only in the antioxidant group. More decreased levels of serum insulin and HOMA-IR after training were observed in the antioxidant group than in the control group. This study suggests that specific antioxidant-rich foods could modulate training-induced aerobic metabolism of carbohydrate and fat during rest and exercise.

The astaxanthin-induced improvement in lipid metabolism during exercise is mediated by a PGC-1α increase in skeletal muscle.

Astaxanthin, a xanthophyll carotenoid, accelerates lipid utilization during aerobic exercise, although the underlying mechanism is unclear. The present study investigated the effect of astaxanthin intake on lipid metabolism associated with peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in mice. Mice were divided into 4 groups: sedentary, sedentary and astaxanthin-treated, exercised, and exercised and astaxanthin-treated. After 2 weeks of treatment, the exercise groups performed treadmill running at 25 m/min for 30 min. Immediately after running, intermuscular pH was measured in hind limb muscles, and blood was collected for measurements. Proteins were extracted from the muscle samples and PGC-1α and its downstream proteins were measured by western blotting. Levels of plasma fatty acids were significantly decreased after exercise in the astaxanthin-fed mice compared with those fed a normal diet. Intermuscular pH was significantly decreased by exercise, and this decrease was inhibited by intake of astaxanthin. Levels of PGC-1α and its downstream proteins were significantly elevated in astaxanthin-fed mice compared with mice fed a normal diet. Astaxanthin intake resulted in a PGC-1α elevation in skeletal muscle, which can lead to acceleration of lipid utilization through activation of mitochondrial aerobic metabolism.