Abstract

[Purpose]We investigated the effects of endurance training on the expression of long-chain fatty acid transport proteins in the skeletal muscle and whole-body fat oxidation during endurance exercise.[Methods]Seven-week-old male ICR mice (n = 12) were divided into 2 groups, namely, Sed (sedentary; non-trained) and Tr (endurance-trained) groups. The Tr group was adapted to treadmill training at a fixed intensity (15 m/min, 8° slope) for 3 days. Next, the exercise intensity was increased while maintaining the 8° slope. In the last week of training, the exercise intensity was set at 25 m/min for 50 min (about 70–75% maximal oxygen uptake for 4 weeks). After the protocol ended, the mice were sacrificed, and tissues were collected for western blot analysis.[Results]Four weeks of endurance training resulted in a significant increase in the protein levels of FAT/CD36 and CPTІ. The FAT/ CD36 protein level in the Tr group was about 1.3-fold greater than that in the Sed group (p < 0.01). Furthermore, the increased CPTІ indicated higher activity (19% upregulation) in the Tr group compared to the Sed group (p < 0.05). The FAT/CD36 protein level and the estimated whole-body fat oxidation rate during 1-h exercise were found to be significantly correlated (r = 0.765, p < 0.01).[Conclusion]We suggest that the increase in FAT/CD36 protein in skeletal muscle by endurance training might be positively associated with whole-body fat oxidation, which might enhance endurance exercise capacity.

Highlights

  • Muscle adaptations to aerobic endurance training include increased capillary density and mitochondrial number and size[1]

  • [Conclusion] We suggest that the increase in FAT/CD36 protein in skeletal muscle by endurance training might be positively associated with whole-body fat oxidation, which might enhance endurance exercise capacity

  • Four weeks of endurance training resulted in a significant increase in the protein expression of FAT/CD36 and CPTІ

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Summary

Introduction

Muscle adaptations to aerobic endurance training include increased capillary density and mitochondrial number and size[1]. Aerobic endurance training increases the activity of the enzymes of the tricarboxylic acid cycle and of other oxidative enzymes (hormone-sensitive lipase, catecholamines, β-oxidation enzymes, etc.), with a concomitant increase in the capacity to oxidize both fat and carbohydrate. A consequence of and a likely contributing factor to the improvement of exercise capacity after endurance training is the metabolic shift to a greater use of fat and a concomitant sparing of glycogen[3]. Some evidence suggests that increases in plasma FFA concentration can suppress the rate of muscle glycogen utilization. This action might theoretically be beneficial, because muscle glycogen depletion is one of the prime causes of fatigue[4]

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