The purpose of this study was to investigate the effects of a proprietary blend of soybean peptides, taurine, Pueraria isoflavone, and ginseng saponin complex (STPG capsule) on exercise performance in humans. Fourteen male volunteers were randomly assigned to two crossover treatments in which they consumed either four STPG capsules (STPG treatment) or placebo (P treatment) for 15 days before a 75% maximal oxygen uptake (VO(2max)) exhaustive cycling test. Blood samples and respiratory gas were collected prior to the exercise (Pre-Ex), at 10 (Ex-10), 15 (Ex-15), 20 (Ex-20), and 25 (Ex-25) minutes during exercise, and immediately after exercise (exhaustion) to assess the blood metabolites, cardiorespiratory responses, and energy substrate utilization. The result showed that exercise time to exhaustion of the 75% (VO(2max)) exhaustive cycling test of the STPG-treated subjects was significantly greater than with the P treatment (30.99 ± 2.01 vs. 28.05 ± 1.48 minutes). The plasma lactate concentrations at Ex-20 and Ex-25 in the STPG treatment were significantly lower with STPG treatment than with P treatment (10.5 ± 0.7 vs. 11.5 ± 0.8 and 10.7 ± 0.9 vs.12.3 ± 1.0 mmol/L, respectively). Nonesterified fatty acid levels at Ex-15, Ex-20, Ex-25, and exhaustion in the STPG group (0.27 ± 0.03, 0.32 ± 0.04, 0.32 ± 0.06, and 0.37 ± 0.05 mmol/L, respectively) were significantly higher than those in the P treatment (0.21 ± 0.03, 0.23 ± 0.03, 0.24 ± 0.03, and 0.25 ± 0.03 mmol/L, respectively). It was concluded that supplementation of four capsules (2 g) of STPG complex, consisting of soybean peptides, taurine, Pueraria isoflavone, and ginseng saponin, for 15 days was effective in promoting utilization of free fatty acids and improving exhaustive cycling test performance in humans.
BackgroundAngelica Sinensis (AS), a folk medicine, has long been used in ergogenic aids for athletes, but there is little scientific evidence supporting its effects. We investigated whether AS induces hypertrophy in myotubes through the phosphatidylinositol 3-kinase (PI3K)/Akt (also termed PKB)/mammalian target of the rapamycin (mTOR) pathway.MethodsAn in vitro experiment investigating the induction of hypertrophy in myotubes was conducted. To investigate whether AS promoted the hypertrophy of myotubes, an established in vitro model of myotube hypertrophy with and without AS was used and examined using microscopic images. The role of the PI3K/Akt/mTOR signaling pathway in AS-induced myotube hypertrophy was evaluated. Two inhibitors, wortmannin (an inhibitor of PI3K) and rapamycin (an inhibitor of mTOR), were used.ResultThe results revealed that the myotube diameters in the AS-treated group were significantly larger than those in the untreated control group (P < 0.05). Wortmannin and rapamycin inhibited AS-induced hypertrophy. Furthermore, AS increased Akt and mTOR phosphorylation through the PI3K pathway and induced myotube hypertrophy.ConclusionThe results confirmed that AS induces hypertrophy in myotubes through the PI3K/Akt/mTOR pathway.
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