Investigations examining the ergogenic and metabolic influence of caffeine during short-term high-intensity exercise are few in number and have produced inconsistent results. This study examined the effects of caffeine on repeated bouts of high-intensity exercise in recreationally active men. Subjects (n = 9) completed four 30-s Wingate (WG) sprints with 4 min of rest between each exercise bout on two separate occasions. One hour before exercise, either placebo (P1; dextrose) or caffeine (Caf; 6 mg/kg) capsules were ingested. Caf ingestion did not have any effect on power output (peak or average) in the first two WG tests and had a negative effect in the latter two exercise bouts. Plasma epinephrine concentration was significantly increased 60 min after Caf ingestion compared with P1; however, this treatment effect disappeared once exercise began. Caf ingestion had no significant effect on blood lactate, O2 consumption, or aerobic contribution at any time during the protocol. After the second Wingate test, plasma NH3 concentration increased significantly from the previous WG test and was significantly higher in the Caf trial compared with P1. These data demonstrate no ergogenic effect of caffeine on power output during repeated bouts of short-term, intense exercise. Furthermore, there was no indication of increased anaerobic metabolism after Caf ingestion with the exception of an increase in NH3 concentration.

The relationship of leptin to thyroid and sex hormones, insulin, energy intake, exercise energy expenditure, and reproductive function was assessed in 39 female athletes. They comprised elite athletes who were either amenorrheic (EAA; n = 5) or cyclic (ECA; n = 8) and recreationally active women who were either cyclic (RCA; n = 13) or taking oral contraceptives (ROC; n = 13). Leptin was significantly lower in EAA (1.7 +/- 0.2 ng/ml) than in ECA (2.9 +/- 0.3 ng/ml), RCA (5.8 +/- 0.9 ng/ml), and ROC (7.4 +/- 1.3 ng/ml). Hypoleptinemia in EAA was paralleled by reductions (P < 0.05) in caloric intake, insulin, estradiol, and thyroid hormones. Leptin increased by 40-46% (P < 0.05) in the luteal phase of the menstrual cycle in RCA and ECA. Plasma leptin was similar in the placebo and active pill phases in ROC despite a significant increase in ethinylestradiol. Leptin correlated (P < 0.05) with triiodothyronine and insulin but not with estrogen, energy intake, or exercise energy expenditure. These data suggest that in female athletes 1) leptin may be a metabolic signal that provides a link between adipose tissue, energy availability, and the reproductive axis and 2) sex hormones do not directly regulate leptin secretion.

The influence of gender, exercise, and thermal stress on caffeine pharmacokinetics is unclear. We hypothesized that these factors would not have an effect on the metabolism of caffeine. Eight women participated in four 8-h trials and six men participated in two 8-h trials after the ingestion of 6 mg/kg caffeine. The women performed two resting trials (1 in the follicular phase and 1 in the luteal phase of the menstrual cycle) and two exercise trials (90 min of cycling exercise at 65% of maximal O(2) uptake, 1 h after caffeine ingestion) in the follicular phase (1 without and 1 with an additional thermal stress). The men performed one exercise and one resting trial. Menstrual cycle, gender, and exercise, with or without an additional thermal stress, had no effect on the pharmacokinetic measurements or urine caffeine. There was a trend for higher plasma caffeine and lower plasma paraxanthine concentrations in the women. These results confirm that gender, exercise, and thermal stress have no effect on caffeine pharmacokinetics in men and women.

We examined the hypothesis that increasing the rate of branched-chain amino acid (BCAA) oxidation, during conditions of low glycogen availability, reduces the level of muscle tricarboxylic acid cycle intermediates (TCAI) by placing a carbon "drain" on the cycle at the level of 2-oxoglutarate. Six men cycled at approximately 70% of maximal oxygen uptake for 15 min under two conditions: 1) low preexercise muscle glycogen (placebo) and 2) low glycogen combined with BCAA ingestion. We have previously shown that BCAA ingestion increased the activity of branched-chain oxoacid dehydrogenase, the rate-limiting enzyme for BCAA oxidation in muscle, compared with low glycogen alone [M. L. Jackman, M. J. Gibala, E. Hultman, and T. E. Graham. Am. J. Physiol. 272 (Endocrinol. Metab. 35): E233-E238, 1997]. Muscle glycogen concentration was 185 +/- 22 and 206 +/- 22 mmol/kg dry wt at rest for the placebo and BCAA-supplemented trials, respectively, and decreased to 109 +/- 18 and 96 +/- 10 mmol/kg dry wt after exercise. The net increase in the total concentration of six measured TCAI ( approximately 95% of TCAI pool) during exercise was not different between trials (3.97 +/- 0. 34 vs. 3.88 +/- 0.34 mmol/kg dry wt for the placebo and BCAA trials, respectively). Muscle 2-oxoglutarate concentration decreased from approximately 0.05 at rest to approximately 0.03 mmol/kg dry wt after exercise in both trials. The magnitude of TCAI pool expansion in both trials was similar to that seen previously in subjects who performed an identical exercise bout after a normal mixed diet [M. J. Gibala, M. A. Tarnopolsky, and T. E. Graham. Am. J. Physiol. 272 (Endocrinol. Metab. 35): E239-E244, 1997]. These data suggest that increasing the rate of BCAA oxidation has no measurable effect on muscle TCAI during exercise with low glycogen in humans. Moreover, it appears that low resting glycogen per se does not impair the increase in TCAI during moderate exercise.

Saliva was collected from six healthy young men at hourly intervals at sea level and after 1-2, 8-9 and 15-16 days at 4450 m on Mount Kenya for measurement of aldosterone (SA) and glucocorticoid (SGC, cortisol + cortisone) concentrations. Blood samples were collected simultaneously with some of the saliva samples and analysis of these showed that plasma and saliva concentrations of aldosterone and glucocorticoids were highly correlated (r = 0.91 and 0.75 respectively; p less than 0.01 for both hormones). Mean SA for the group was reduced to approximately 50% of the sea-level value (p less than 0.05) by the time the first saliva samples were collected at altitude, and remained at this depressed level throughout the 2-week period on Mount Kenya, although there was considerable inter-subject variation. SGC concentration also tended to be lower on Mount Kenya than at sea level. Though SA was lower throughout the day at altitude compared to sea level, the principal difference in the temporal pattern of SA was the reduction or complete absence of the marked rise in SA that normally occurs in the first few hours after rising. SA and SGC responses to exercise, which consisted of stepping on and off and 0.4-m high stool 60 times/min for 25 min, were assessed at sea level and after various periods at 4450 m.(ABSTRACT TRUNCATED AT 250 WORDS)