We compared the effects of caffeinated vs non-caffeinated carbohydrate electrolyte (CE) drinks on urine volume (UV), free water clearance (CH2O), fractional excretion of water (FEH2O), and osmolar excretion during 4 h of rest or 1 h rest followed by 3 h of cycling at 60% VO2max in six subjects. We also tested maximal performance at 85% VO2max following the 3-h exercise trials. Throughout the two resting trials and the two rest + exercise trials, subjects ingested CE (total volume = 35 ml/kg) without (PLAC) or with (CAFF) caffeine (25 mg/dl). Blood samples were collected, and body weight and UV were recorded every hour. Urine and blood were analyzed for osmolality and creatinine, and plasma catecholamine concentrations were determined. At rest, mean (+/-SE) UV between 60 min and 240 min was greater for CAFF (1843 +/- 166 ml) vs PLAC (1411 +/- 181 ml) (p < 0.01); during exercise the difference in UV between CAFF (398 +/- 32 ml) and PLAC (490 +/- 57 ml) was not significant. Cycling performance was unaffected by caffeine. Plasma catecholamine concentrations were not different between PLAC and CAFF but were greater during exercise than rest (p < 0.01) and may have counteracted the diuretic effect of caffeine observed at rest. Thus, CAFF consumed in CE during moderate endurance exercise apparently does not compromise bodily hydration status.

We investigated the role of glycogen synthase in supranormal resynthesis (supercompensation) of skeletal muscle glycogen after exhaustive exercise. Six healthy men exercised 60 min by cycling with one leg at 75% VO2max, recovered 3 days on a low-carbohydrate diet, exercised again, and recovered 4 days on high-carbohydrate diet. Glycogen and glycogen synthase activities at several glucose-6-phosphate (G6P) concentrations were measured in biopsy samples of m. vastus lateralis. Dietary alterations alone did not affect glycogen, whereas exercise depleted glycogen stores. After the second exercise bout, glycogen returned to normal within 24 h and reached supercompensated levels by 48 h of recovery. Glycogen synthase activation state strikingly increased after exercise in exercised muscle and remained somewhat elevated for the first 48 h of recovery in both muscles. We suggest that 1) forms of glycogen synthase intermediate to I (G6P-independent) and D (G6P-dependent) forms are present in vivo, and 2) glycogen supercompensation can in part be explained by the formation of intermediate forms of glycogen synthase that exhibit relatively low activity ratios, but an increased sensitivity to activation by G6P.

The belief that high-carbohydrate diets enhance training capacity (mean power output) has been extrapolated from studies that have varied dietary carbohydrate over a few days and measured muscle glycogen but did not assess power output during training. We hypothesized that a high-carbohydrate (HI) diet (10 g.kg body mass-1.day-1) would promote greater muscle glycogen content and greater mean power output during training than a moderate-carbohydrate (MOD) diet (5 g.kg body mass-1.day-1) over 4 wk of intense twice-daily rowing training. Dietary protein intake was 2 g.kg body mass-1.day-1, and fat intake was adjusted to maintain body mass. Twelve male and 10 female collegiate rowers were randomly assigned to the treatment groups. Training was 40 min at 70% peak O2 consumption (VO2) (A.M.) and either three 2,500-m time trials to assess power output or interval training at 70-90% peak VO2 (P.M.). Mean daily training was 65 min at 70% peak VO2 and 38 min at greater than or equal to 90% peak VO2. Mean muscle glycogen content increased 65% in the HI group (P less than 0.05) but remained constant at 119 mmol/kg in the MOD group over the 4 wk. Mean power output in time trials increased 10.7 and 1.6% after 4 wk in the HI and MOD groups, respectively (P less than 0.05). We conclude that a diet with 10 g carbohydrate.kg body mass-1.day-1 promotes greater muscle glycogen content and greater power output during training than a diet containing 5 g carbohydrate.kg body mass-1.day-1 over 4 wk of intense twice-daily rowing training.(ABSTRACT TRUNCATED AT 250 WORDS)

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A simple low-cost procedure was developed to compare the temporal profiles of deuterium oxide (D2O) accumulation in body fluids after ingestion of D2O-labeled solutions. D2O concentration was measured in plasma and saliva samples taken at various intervals after ingestion of 20 ml of D2O mixed with five solutions differing in carbohydrate and electrolyte concentrations. An infrared spectrometer was used to measure D2O in purified samples obtained after a 48-h incubation period during which the water (D2O and H2O) in the sample was equilibrated with an equal volume of distilled water in a sealed diffusion dish. The procedure yields 100% recoveries of 60-500 ppm D2O with an average precision of 5%. When compared with values for distilled water, D2O accumulation in serial samples of plasma and saliva was slower for ingested solutions containing 40 and 15% glucose and faster for hypotonic saline and a 6% carbohydrate-electrolyte solution. These differences appear to reflect known differences in gastric emptying and intestinal absorption of these beverages. Therefore this technique may provide a useful index of the rate of water uptake from ingested beverages into the body fluids.

The effect of the temperature of ingested water on the rise in core temperature (Tco) during exercise is not clear. Seven trained subjects were recruited to complete 2 hr of recumbent cycling at 51% VO2peak in a temperate environment (Ta = 26 degrees C, relative humidity = 40%) on four occasions, while ingesting either no fluid (trial NF26), cold water (0.5 degree C; trial CD26), cool water (19 degrees C; trial CL26), or warm water (38 degrees C; trial WA26) during the second hour of exercise. A fifth trial was conducted during which convective and radiative heat loss were reduced by raising Ta to 31 degrees C. During this trial, subjects ingested cold water (0.5 degree C; trial CD31). When compared to WA26, over the second hour of exercise, CD26 attenuated the time-averaged changes in (Tco) and forearm blood flow and decreased whole-body sweat rate and forearm sweat rate (p < .05). Similarly, relative to WA26, the CL26 trial attenuated the time-averaged changes in Tco and reduced whole-body sweat rate (p < .05) during the second hour of exercise, but CL26 had no significant effect on forearm sweat rate or blood flow. Finally, regardless of beverage temperature, water ingestion (vs. NF26) reduced the time-averaged changes in Tco and in heat storage during the second hour of exercise (p < .05).

We hypothesized that central fatigue may have a role in limiting the endurance capacity of horses. Therefore, we tested the effect of infusing tryptophan and/or glucose on endurance time and plasma concentrations of free tryptophan and other substrates thought to affect tryptophan uptake into the brain of seven mares (3-4 yr of age, 353-435 kg) that ran on a treadmill at 50% of maximal O2 consumption to fatigue. With use of a counterbalanced crossover design, the horses were infused with tryptophan (100 mg/kg in saline solution) or a similar volume of saline solution (placebo) before exercise. During exercise, horses received infusions of glucose (2 g/min, 50% wt/vol) or a similar volume of saline. Thus the treatments were 1) tryptophan and glucose (T & G), 2) tryptophan and placebo (T & P), 3) placebo and glucose (P & G), and 4) placebo and placebo (P & P). Mean heart rate, hematocrit, and concentration of plasma total solids before and during exercise were similar for all trials. Mean time to exhaustion was reduced (P < 0.05) for T & P and T & G compared with P & P [86.1 +/- 6.9 and 87.1 +/- 6.8 vs. 102.3 +/- 10.3 (SE) min], whereas endurance for P & G (122.4 +/- 11.9 min) was greater than for all other trials (P < 0.05). Compared with nontryptophan trials, during the tryptophan trials plasma prolactin increased (P < 0.05) nearly threefold before exercise and almost twofold early in exercise. Muscle glycogen concentrations were reduced (P < 0.05) below preexercise values in the P & G and P & P trials only. However, glucose infusions (P & G) did not affect (P > 0.05) concentrations of plasma free fatty acids or ratios of branched-chain amino acids to free tryptophan. In conclusion, tryptophan infusion reduced endurance time, which was consistent with the central fatigue hypothesis. The failure of glucose infusion to alleviate the effects of tryptophan and the absence of significant muscle glycogen reduction in the tryptophan trials suggest that the early onset of fatigue in the tryptophan trials is not due to a lack of readily available substrate.

The effects of moderate- or high-carbohydrate diets on muscle glycogen and performance in runners and cyclists over 7 consecutive days of training were determined. Muscle biopsies were performed on 4 separate days before exercise for 1 h at 75% peak oxygen consumption (VO2) followed by five, 1-min sprints. After the training session on day 7, subjects ran or cycled to exhaustion at 80% peak VO2. Muscle glycogen for cyclists and runners was maintained with the high-carbohydrate diet but was reduced 30-36% (P < 0.05) with the moderate-carbohydrate diet. All subjects completed all training sessions, and there were no differences in times to exhaustion on day 7. For cyclists and runners, consuming a moderate-carbohydrate diet over 7 d of intense training reduces muscle glycogen but has no apparent deleterious effect on training capability or high-intensity exercise performance. A high-carbohydrate diet maintains muscle glycogen, but this has no apparent benefit on training capability or high-intensity exercise performance.