This investigation determined whether carbohydrate ingestion during prolonged moderate-intensity exercise enhanced endurance performance when the exercise was preceded by carbohydrate supercompensation. Seven male trained cyclists performed two trials at an initial power output corresponding to 71 ± 1 % of their peak oxygen consumption. During the trials, subjects ingested either a 6% glucose/sucrose (C) solution or an equal volume of artificially flavored and sweetened placebo (P) every 20 min throughout exercise. Both C and P were preceded by a 6-day carbohydrate supercompensation procedure in which subjects undertook a depletion-taper exercise sequence in conjunction with a moderate- and high-carbohydrate diet regimen. Statistical analysis of time to exhaustion, plasma glucose concentration, carbohydrate oxidation rate, fat oxidation rate, and plasma glycerol concentration indicated that in spite of a carbohydrate supercompensation procedure administered prior to exercise, carbohydrate ingestion during exercise can exert an additional ergogenic effect by preventing a decline in blood glucose levels and maintaining carbohydrate oxidation during the later stages of moderate-intensity exercise.
Jie Kang, Robert J. Robertson, Bart G. Denys, Sergio G. DaSilva, Paul Visich, Richard R. Suminski, Alan C. Utter, Fredric L. Goss and Kenneth F. Metz
Joshua Lowndes, Robert F. Zoeller, George A. Kyriazis, Mary P. Miles, Richard L. Seip, Niall M. Moyna, Paul S. Visich, Linda S. Pescatello, Paul M. Gordon, Paul D. Thompson and Theodore J. Angelopoulos
The purpose of this study was to examine whether leptin levels affect the response of leptin to exercise training (ET) and whether this is also affected by C-reactive protein (CRP) or the three common Apolipoprotein E genotypes (APOE). Ninety-seven (male = 45, female = 52) sedentary individuals underwent 6 months of supervised ET. Blood was sampled before the initiation of ET, and again 24 and 72 hr after completion of the final training session. ET resulted in a small reduction in body mass (80.47 ± 18.03 vs 79.42 ± 17.34 kg, p < .01). Leptin was reduced 24 hr after the final exercise session (p < .01), but returned to normal after 72 hr (p > .05)—Pre: 13.51 ± 12.27, 24hr: 12.14 ± 12.34, 72hr: 12.98 ± 11.40 ng/ml. The most hyperleptinemic individuals had a greater initial response, which was sustained through to 72 hr after the final session in the pooled study population (p < .01), and in both males (p < .05) and females (p < .05) separately. CRP was related to leptin independently of body weight and positively related to the reductions in leptin. APOE genotype was not related to leptin levels and did not affect the response to ET. Leptin levels may only be reduced by ET in those with hyperleptinemia. In addition, both the initial extent of hyperleptinemia and the subsequent reduction in leptin may be related to low grade chronic systemic inflammation.