Abstract
The purpose of this study was to evaluate the effect of chronic quercetin treatment on mitochondrial biogenesis, endurance exercise performance and activation levels of AMP-activated protein kinase (AMPK) in rat skeletal muscle. Rats were assigned to a control or quercetin group and were fed for 7 days. Rats treated with quercetin showed no changes in the protein levels of citrate synthase or cytochrome C oxidase IV or those of sirtuin 1, peroxisome proliferator-activated receptor gamma coactivator-1α or phosphorylated AMPK. After endurance swimming exercise, quercetin-treated rats demonstrated no differences in blood and muscle lactate levels or glycogen utilization speed compared to control rats. These results indicate that quercetin treatment does not stimulate mitochondrial biogenesis in skeletal muscle and does not influence metabolism in a way that might enhance endurance exercise capacity. On the other hand, the AMPK phosphorylation level immediately after exercise was significantly lower in quercetin-treated muscles, suggesting that quercetin treatment might provide a disadvantage to muscle adaptation when administered with exercise training. The molecular results of this study indicate that quercetin treatment may not be advantageous for improving endurance exercise performance, at least after high-dose and short-term therapy.
Highlights
Quercetin is one of the most common flavonoids found in many foods, including onions, red wines, blueberries and leeks [1]
In addition to focusing on the effects of quercetin treatment on the basal level of AMPK in skeletal muscle, we investigated the impact of quercetin on exercise-induced AMPK activation
Our results clearly demonstrated that quercetin treatment did not stimulate mitochondrial biogenesis in skeletal muscle regardless of muscle fiber type
Summary
Quercetin is one of the most common flavonoids found in many foods, including onions, red wines, blueberries and leeks [1]. Several human and rodent studies [6,7,8,9] demonstrated that quercetin treatment increased VO2 max and time to fatigue and improved performance in the 30-km time trial and maximal 12-min test. It is well known that mitochondrial biogenesis in skeletal muscle plays a substantial role in determining endurance exercise performance. Exercise training improves performance and increases mitochondrial content. From this perspective, a landmark study conducted by Davis et al [7] has received the most attention in the field of quercetin-related research. The authors demonstrated that relatively short-term (7 days) quercetin supplementation increased mitochondrial biogenesis in mouse skeletal muscle in the absence of exercise training and resulted in a remarkable improvement in endurance exercise capacity. A subsequent study in humans did not replicate this exercise-like
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