The purpose of the study was to investigate whether a combination of sago and soy protein ingested during moderate-intensity cycling exercise can improve subsequent high-intensity endurance capacity compared with a carbohydrate in the form of sago and with a placebo. The participants were 8 male recreational cyclists with age, weight, and VO2max of 21.5 +/- 1.1 yr, 63.3 +/- 2.4 kg, and 39.9 +/- 1.1 ml . kg(-1) . min(-1), respectively. The design of the study was a randomized, double-blind placebo-controlled crossover comprising 60 min of exercise on a cycle ergometer at 60% VO2max followed by a time-to-exhaustion ride at 90% VO2max. The sago feeding provided 60 g of carbohydrate, and the sago-soy combination provided 52.5 g of carbohydrate and 15 g of protein, both at 20-min intervals during exercise. Times to exhaustion for the placebo, sago, and sago-soy supplementations were 4.09 +/- 1.28, 5.49 +/- 1.20, and 7.53 +/- 2.02 min, respectively. Sago-soy supplementation increased endurance by 84% (44-140%; p < .001) and by 37% (15-63%; p < .05) relative to placebo and sago, respectively. The plasma insulin response was elevated above that with placebo during sago and sago-soy supplementations. The authors conclude that a combination of sago and soy protein can delay fatigue during high-intensity cycling.
Inophyllin A (INO-A), a pyranoxanthone isolated from the roots of Calophyllum inophyllum represents a new xanthone with potential chemotherapeutic activity. In this study, the molecular mechanism of INO-A-induced cell death was investigated in Jurkat T lymphoblastic leukemia cells. Assessment of phosphatidylserine exposure confirmed apoptosis as the primary mode of cell death in INO-A-treated Jurkat cells. INO-A treatment for only 30 min resulted in a significant increase of tail moment which suggests that DNA damage is an early apoptotic signal. Further flow cytometric assessment of the superoxide anion level confirmed that INO-A induced DNA damage was mediated with a concomitant generation of reactive oxygen species (ROS). Investigation on the thiols revealed an early decrease of free thiols in 30 min after 50 μM INO-A treatment. Using tetramethylrhodamine ethyl ester, a potentiometric dye, the loss of mitochondrial membrane potential (MPP) was observed in INO-A-treated cells as early as 30 min. The INO-A-induced apoptosis progressed with the simultaneous activation of caspases-2 and -9 which then led to the processing of caspase-3. Taken together, these data demonstrate that INO-A induced early oxidative stress, DNA damage and loss of MMP which subsequently led to the activation of an intrinsic pathway of apoptosis in Jurkat cells.