This study examined the possible effects of caffeine ingestion on muscle metabolism and endurance during brief intense exercise. We tested 14 subjects after they ingested placebo or caffeine (6 mg/kg) with an exercise protocol in which they cycled for 2 min, rested 6 min, cycled 2 min, rested 6 min, and then cycled to voluntary exhaustion. In each exercise the intensity required the subject's maximal O2 consumption. Eight subjects had muscle and venous blood samples taken before and after each exercise period. The caffeine ingestion resulted in a significant increase in endurance (4.12 +/- 0.36 and 4.93 +/- 0.60 min for placebo and caffeine, respectively) and resulted in a significant increase in plasma epinephrine concentration throughout the protocol but not in norepinephrine concentration. During the first two exercise bouts, the power and work output were not different; blood lactate concentrations were not affected significantly by caffeine ingestion, but during the exercise bouts muscle lactate concentration was significantly increased by caffeine. The net decrease in muscle glycogen was not different between treatments at any point in the protocol, and even at the time of fatigue there was at least 50% of the original glycogen concentration remaining. the data demonstrated that caffeine ingestion can be an effective ergogenic aid for exercise that is as brief as 4-6 min. However, the mechanism is not associated with muscle glycogen sparing. It is possible that caffeine is exerting actions directly on the active muscle and/or the neural processes that are involved in the activity.
Monosodium glutamate (MSG) ingestion is known to increase plasma glutamate concentration, and MSG infusion stimulates insulin secretion. We investigated the impact of MSG ingestion on both the plasma and intramuscular amino acid pools. Nine postprandial adults ingested MSG (150 mg/kg) and rested for 105 min. Venous blood was sampled preingestion and then every 15 min; vastus lateralis muscle biopsies were taken preingestion and at 45, 75, and 105 min postingestion. Venous plasma glutamate and aspartate concentrations increased (P = 0.05) approximately 700-800 and 300-400%, respectively, after 30-45 min. Although several other plasma amino acids increased modestly, the rise in glutamate accounted for approximately 80% of the increase in total plasma amino acids. In addition, plasma insulin increased threefold after 15 min; this occurred before a significant increase in plasma glutamate, indicating a feed-forward stimulation from the gastrointestinal tract. The intramuscular amino acid pool was remarkably constant, with only glutamate increasing (P = 0.05) by 3.56 mmol/kg dry wt. By 105 min, the plasma and muscle amino acids had returned to resting concentrations. This increase in muscle glutamate concentration could account for approximately 40% of the MSG ingested; we propose that resting skeletal muscle is a major sink for the glutamate and metabolizes it to aspartate.
This two-part investigation compared the ergogenic and metabolic effects of theophylline and caffeine. Initially (part A), the ergogenic potential of theophylline on endurance exercise was investigated. Eight men cycled at 80% maximum O(2) consumption to exhaustion 90 min after ingesting either placebo (dextrose), caffeine (6 mg/kg; Caff), or theophylline (4.5 mg/kg Theolair; Theo). There was a significant increase in time to exhaustion in both the Caff (41.2+/-4.8 min) and Theo (37.4+/-5.0 min) trials compared with placebo (32.6+/-3.4 min) (P<0.05). In part B, the effects of Theo on muscle metabolism were investigated and compared with Caff. Seven men cycled for 45 min at 70% maximum O(2) consumption (identical treatment protocol as in part A). Neither methylxanthines (MX) affected muscle glycogen utilization (P>0.05). Only Caff increased plasma epinephrine (P<0.05), but both MX increased blood glycerol levels (P<0.05). Muscle cAMP was increased (P<0.05) by both MX at 15 min and remained elevated at 45 min with Theo. This demonstrates that both MX are ergogenic and that this can be independent of muscle glycogen.
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