Effect of hydroxytyrosol supplementation on mitochondrial biogenesis, aerobic capactiy, and endurance exercise performance in healthy men
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The purpose of this study was to investigate the effects of hydroxytyrosol (HT) supplementation on markers of mitochondrial biogenesis, aerobic capacity, and endurance exercise performance in recreationally active men. Sixty-one (n = 61) subjects (21.46 ± 0.22 yrs, 179.46 ± 0.79 cm, 78.91 ± 1.19 kg) consumed either a high dose (HI) HT supplement (150 mg HT), a low dose (LO) HT supplement (50 mg HT), or a placebo (PLA) every day for 6 weeks. Muscle biopsies from the vastus lateralis were obtained at baseline and after 6 weeks of supplement consumption and analyzed for markers of mitochondrial biogenesis: succinate dehydrogenase (SDH), citrate synthase (CS), and peroxisome proliferator-activated receptor ɣ coactivator (PGC)-1α. Subjects completed exercise testing on a bicycle ergometer at baseline and after 3 and 6 weeks of supplement consumption to measure changes in maximal aerobic power (VO2MAX), lactate threshold, respiratory exchange ratio (RER), substrate utilization, and endurance exercise performance on a 20 km time trial course. The primary findings were that HT supplementation increased muscle oxidative enzyme activity suggesting increased oxidative capacity. HT also increased time trial performance at midpoint and endpoint and this corresponded with an improvement in lactate threshold and a lower RER for the LO HT treatment. Time trial performance was also improved at endpoint for PLA, however, unlike LO an HI HT, this was accompanied by a significant increase in rating of perceived exercise (RPE) and not associated with improvements in muscle oxidative capacity. Our results indicate that HT ranging from 50 to 150 mg/day for 6 weeks can improve muscle oxidative capacity and aerobic performance, and suggests that HT may be used chronically to improve mitochondrial function. HT may be used as an effective means to increase mitochondria to improve exercise performance, and limit diseases associated with mitochondrial dysfunction such as cardiovascular disease, type II diabetes, and some cancers.