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This double blind study investigated the effect of oral creatine supplementation (CrS) on 4 x 20 s of maximal sprinting on an air-braked cycle ergometer. Each sprint was separated by 20 s of recovery. A group of 16 triathletes [mean age 26.6 (SD 5.1) years. mean body mass 77.0 (SD 5.8) kg, mean body fat 12.9 (SD 4.6)%, maximal oxygen uptake 4.86 (SD 0.7) l.min-1] performed an initial 4 x 20 s trial after a muscle biopsy sample had been taken at rest. The subjects were then matched on their total intramuscular creatine content (TCr) before being randomly assigned to groups to take by mouth either a creatine supplement (CRE) or a placebo (CON) before a second 4 x 20 s trial. A muscle biopsy sample was also taken immediately before this second trial. The CrS of 100 g comprised 4 x 5 g for 5 days. The initial mean TCr were 112.5 (SD 8.7) and 112.5 (SD 10.7) mmol.kg-1 dry mass for CRE and CON, respectively. After creatine loading and placebo ingestion respectively, CRE [128.7 (SD 11.8) mmol.kg-1 dry mass] had a greater (P = 0.01) TCr than CON [112.0 (SD 10.0) mmol.kg-1 dry mass]. While the increase in free creatine for CRE was statistically significant (P = 0.034), this was not so for the changes in phosphocreatine content [trial 1: 75.7 (SD 6.9), trial 2: 84.7 (SD 11.0) mmol.kg-1 dry mass, P = 0.091]. There were no significant differences between CRE and CON for citrate synthase activity (P = 0.163). There was a tendency towards improved performance in terms of 1 s peak power (in watts P = 0.07; in watts per kilogram P = 0.05), 5 s peak power (in watts P = 0.08) and fatigue index (P = 0.08) after CrS for sprint 1 of the second trial. However, there was no improvement for mean power (in watts P = 0.15; in watts per kilogram P = 0.1) in sprint 1 or for any performance values in subsequent sprints. Our results suggest that, while CrS elevates the intramuscular stores of free creatine, this does not have an ergogenic effect on 4 x 20 s all-out cycle sprints with intervening 20-s rest periods.

Six endurance-trained men [peak oxygen uptake (V(O(2))) = 4.58 +/- 0.50 (SE) l/min] completed 60 min of exercise at a workload requiring 68 +/- 2% peak V(O(2)) in an environmental chamber maintained at 35 degrees C (<50% relative humidity) on two occasions, separated by at least 1 wk. Subjects ingested either a 6% glucose solution containing 1 microCi [3-(3)H]glucose/g glucose (CHO trial) or a sweet placebo (Con trial) during the trials. Rates of hepatic glucose production [HGP = glucose rate of appearance (R(a)) in Con trial] and glucose disappearance (R(d)), were measured using a primed, continuous infusion of [6,6-(2)H]glucose, corrected for gut-derived glucose (gut R(a)) in the CHO trial. No differences in heart rate, V(O(2)), respiratory exchange ratio, or rectal temperature were observed between trials. Plasma glucose concentrations were similar at rest but increased (P < 0.05) to a greater extent in the CHO trial compared with the Con trial. This was due to the absorption of ingested glucose in the CHO trial, because gut R(a) after 30 and 50 min (16 +/- 5 micromol. kg(-1). min(-1)) was higher (P < 0.05) compared with rest, whereas HGP during exercise was not different between trials. Glucose R(d) was higher (P < 0.05) in the CHO trial after 30 and 50 min (48.0 +/- 6.3 vs 34.6 +/- 3.8 micromol. kg(-1). min(-1), CHO vs. Con, respectively). These results indicate that ingestion of carbohydrate, at a rate of approximately 1.0 g/min, increases glucose R(d) but does not blunt the rise in HGP during exercise in the heat.

Much of the research that has examined the interaction between metabolism and exercise has been conducted in comfortable ambient conditions. It is clear, however, that environmental temperature, particularly extreme heat, is a major practical issue one must consider when examining muscle energy metabolism. When exercise is conducted in very high ambient temperatures, the gradient for heat dissipation is significantly reduced which results in changes to thermoregulatory mechanisms designed to promote body heat loss. This can ultimately impact upon hormonal and metabolic responses to exercise which act to alter substrate utilisation. In general, the literature examining metabolic responses to exercise and heat stress has demonstrated a shift towards increased carbohydrate use and decreased fat use. Although glucose production appears to be augmented during exercise in the heat, glucose disposal and utilisation appears to be unaltered. In contrast, glycogen use has been consistently demonstrated to be augmented during exercise in the heat. This increase in glycogenolysis is observed via both aerobic and anaerobic pathways. Although several hypotheses have been proposed as mechanisms for the substrate shift towards greater carbohydrate metabolism during exercise and heat stress, recent work suggests that an augmented sympatho-adrenal response and intramuscular temperature may be responsible for such a phenomenon.

We examined the effect of caffeine co-ingested with either carbohydrate or fat on metabolism and performance in eight endurance-trained subjects who performed a random order of four experimental trials consisting of 120 min of steady-state ergometer cycling at 70 % of maximal O(2) uptake (SS) followed by a time trial in which subjects completed a set amount of work (7 kJ kg-1) as quickly as possible. One hour before SS subjects ingested either 2.6 g kg-1 carbohydrate (CHO); 2.6 g kg-1 CHO + 6 mg kg-1 caffeine (CHO + CAF); 1.2 g kg-1 fat with 2000 U I.V. heparin (FAT); or 1.2 g kg-1 fat with 2000 U I.V. heparin + 6 mg kg-1 caffeine (FAT + CAF). The rate of carbohydrate oxidation was higher (micromol kg-1 min-1: CHO, 243 +/- 39 and CHO + CAF, 239 +/- 30 vs. FAT, 196 +/- 48 and FAT + CAF, 191 +/- 55; P < 0.05, values are means +/- S.D.) and the rate of fat oxidation lower (micromol kg-1 min-1: CHO, 19 +/- 8 and CHO + CAF, 22 +/- 7 vs. FAT, 35 +/- 19 and FAT + CAF, 37 +/- 17; P < 0.05) with carbohydrate than fat ingestion. Yet despite lower carbohydrate use with fat feeding, the time taken to complete the time trial was less after carbohydrate than after fat ingestion (min: CHO, 30.37 +/- 7.42 and CHO + CAF, 29.12 +/- 5.62 vs. FAT, 33.02 +/- 8.50 and FAT + CAF, 32.78 +/- 7.70; P < 0.05). We conclude that (1) caffeine co-ingested with either carbohydrate or fat meals has no additive effect on substrate utilization or exercise performance and (2) carbohydrate ingestion before exercise improves subsequent time trial performance compared with fat ingestion. Experimental Physiology (2001) 86.1, 137-144.

We investigated the effect of carbohydrate (CHO) ingestion before and during exercise and in combination on glucose kinetics, metabolism and performance in seven trained men, who cycled for 120 min (SS) at approximately 63% of peak power output, followed by a 7 kJ/kg body wt time trial (TT). On four separate occasions, subjects received either a placebo beverage before and during SS (PP); placebo 30 min before and 2 g/kg body wt of CHO in a 6.4% CHO solution throughout SS (PC); 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and placebo throughout SS (CP); or 2 g/kg body wt of CHO in a 25.7% CHO beverage 30 min before and 2 g/kg of CHO in a 6.4% CHO solution throughout SS (CC). Ingestion of CC and CP markedly (>8 mM) increased plasma glucose concentration ([glucose]) compared with PP and PC (5 mM). However, plasma [glucose] fell rapidly at the onset of SS so that after 80 min it was similar (6 mM) between all treatments. After this time, plasma [glucose] declined in both PP and CP (P < 0.05) but was well maintained in both CC and PC. Ingestion of CC and CP increased rates of glucose appearance (R(a)) and disappearance (R(d)) compared with PP and PC at the onset of, and early during, SS (P < 0.05). However, late in SS, both glucose R(a) and R(d) were higher in CC and PC compared with other trials (P < 0.05). Although calculated rates of glucose oxidation were different when comparing the four trials (P < 0.05), total CHO oxidation and total fat oxidation were similar. Despite this, TT was improved in CC and PC compared with PP (P < 0.05). We conclude that 1) preexercise ingestion of CHO improves performance only when CHO ingestion is maintained throughout exercise, and 2) ingestion of CHO during 120 min of cycling improves subsequent TT performance.

For 5 days, eight well-trained cyclists consumed a random order of a high-carbohydrate (CHO) diet (9.6 g. kg(-1). day(-1) CHO, 0.7 g. kg(-1). day(-1) fat; HCHO) or an isoenergetic high-fat diet (2.4 g. kg(-1). day(-1) CHO, 4 g. kg(-1). day(-1) fat; Fat-adapt) while undertaking supervised training. On day 6, subjects ingested high CHO and rested before performance testing on day 7 [2 h cycling at 70% maximal O(2) consumption (SS) + 7 kJ/kg time trial (TT)]. With Fat-adapt, 5 days of high-fat diet reduced respiratory exchange ratio (RER) during cycling at 70% maximal O(2) consumption; this was partially restored by 1 day of high CHO [0.90 +/- 0.01 vs. 0.82 +/- 0.01 (P < 0.05) vs. 0.87 +/- 0.01 (P < 0.05), for day 1, day 6, and day 7, respectively]. Corresponding RER values on HCHO trial were [0. 91 +/- 0.01 vs. 0.88 +/- 0.01 (P < 0.05) vs. 0.93 +/- 0.01 (P < 0.05)]. During SS, estimated fat oxidation increased [94 +/- 6 vs. 61 +/- 5 g (P < 0.05)], whereas CHO oxidation decreased [271 +/- 16 vs. 342 +/- 14 g (P < 0.05)] for Fat-adapt compared with HCHO. Tracer-derived estimates of plasma glucose uptake revealed no differences between treatments, suggesting muscle glycogen sparing accounted for reduced CHO oxidation. Direct assessment of muscle glycogen utilization showed a similar order of sparing (260 +/- 26 vs. 360 +/- 43 mmol/kg dry wt; P = 0.06). TT performance was 30.73 +/- 1.12 vs. 34.17 +/- 2.48 min for Fat-adapt and HCHO (P = 0.21). These data show significant metabolic adaptations with a brief period of high-fat intake, which persist even after restoration of CHO availability. However, there was no evidence of a clear benefit of fat adaptation to cycling performance.

The present study was undertaken to examine the effect of exercise and carbohydrate (CHO) ingestion on intracellular monocyte cytokine production. Subjects performed 2 h of cycling at 70 % peak pulmonary O2 uptake (VO2,peak) while ingesting either an 8 % CHO beverage or a sweet placebo. Whole blood was incubated with (stimulated) or without (spontaneous) lipopolysaccharide (LPS) and surface stained for monocyte surface antigens. The cells were permeabilised, stained for intracellular cytokines and analysed using flow cytometry. Exercise had no effect on the number of monocytes spontaneously producing cytokines, but the number of stimulated IL-1alpha-, TNF-alpha- and IL-6-positive monocytes were elevated (P < 0.01) immediately post-exercise and 2 h post-exercise. These stimulated cells produced less (P < 0.05) TNF-alpha immediately post-exercise, and less (P < 0.05) TNF-alpha and IL-1alpha 2 h post-exercise. There was a small, but significant increase (P < 0.05) in the plasma IL-6 concentration immediately post-exercise. Exercise resulted in an elevation (P < 0.01) in the plasma adrenaline concentration in the placebo trial, and ingestion of CHO attenuated this increase. CHO ingestion had no effect on monocyte cytokine production, plasma IL-6 or circulating leukocyte numbers. These data suggest that circulating monocytes are not the origin of increased levels of plasma IL-6 during exercise: prolonged cycling exercise increased the number of monocytes producing cytokines upon stimulation, but these cells produced less cytokines post-exercise. In addition, attenuation of plasma adrenaline levels had no effect on plasma IL-6 or monocyte cytokine production.

Eight trained men cycled at 70% peak oxygen uptake for 120 min followed by a 30-min performance cycle after ingesting either a high-glycemic index (HGI), low-glycemic index (LGI), or placebo (Con) meal 30 min before exercise. Ingestion of HGI resulted in an elevated (P<0.01) blood glucose concentration compared with LGI and Con. At the onset of exercise, blood glucose fell (P<0.05) such that it was lower (P<0.05) in HGI compared with LGI and Con at 15 and 30 min during exercise. Plasma insulin concentration was higher (P<0.01) throughout the rest period after ingestion of HGI compared with LGI and Con. Plasma free fatty acid concentrations were lower (P<0.05) throughout exercise in HGI compared with LGI and Con. The rates of [6,6-(2)H]glucose appearance and disappearance were higher (P<0.05) at rest after ingestion and throughout exercise in HGI compared with LGI and Con. Carbohydrate oxidation was higher (P<0.05) throughout exercise, whereas glycogen use tended (P = 0.07) to be higher in HGI compared with LGI and Con. No differences were observed in work output during the performance cycle when comparing the three trials. These results demonstrate that preexercise carbohydrate feeding with a HGI, but not a LGI, meal augments carbohydrate utilization during exercise but does not effect exercise performance.

It has been suggested that exercise performance in the heat is limited by the degree of hyperthermia, which, in some circumstances, compromises cardiovascular function and/or the central nervous system. However, this review presents evidence that a temperature-induced dysfunction to skeletal muscle contraction may contribute to a reduction in performance during exercise in the heat.

To examine the effect of exercise on heat shock protein (HSP) 72 mRNA expression in skeletal muscle, five healthy humans (20 +/- 1 yr; 64 +/- 3 kg; peak O(2) uptake of 2.55 +/- 0.2 l/min) cycled until exhaustion at a workload corresponding to 63% peak O(2) uptake. Muscle was sampled from the vastus lateralis, and muscle temperature was measured at rest (R), 10 min of exercise (Min10), approximately 40 min before fatigue (F-40 = 144 +/- 7 min), and fatigue (F = 186 +/- 15 min). Muscle samples were analyzed for HSP72 mRNA expression, as well as glycogen and lactate concentration. Muscle temperature increased (P < 0.05) during the first 10 min of exercise but then remained constant for the duration of the exercise. Similarly, lactate concentration increased (P < 0.05) when Min10 was compared with R but decreased (P < 0.05) thereafter, such that concentrations at F-40 and F were not different from those at R. In contrast, muscle glycogen concentration fell progressively throughout exercise (486 +/- 74 vs. 25 +/- 7 mmol/kg dry weight for R and F, respectively; P < 0.05). HSP72 mRNA was detected at R but did not increase by Min10. However, HSP72 mRNA increased (P < 0.05) 2.2 +/- 0.5- and 2.6 +/- 0.9-fold, respectively, when F-40 and F were compared with R. These data demonstrate that HSP72 mRNA increases progressively during acute cycling, suggesting that processes that take place throughout concentric exercise are capable of initiating a stress response.

This study examined the effect of heat stress on physiological responses and exercise performance in elite road cyclists. Eleven members of the Australian National Road Cycling Squad completed two 30 min cycling time-trials in an environmental chamber set at either 32 degrees C, (HT) or 23 degrees C (NT) with a relative humidity of 60% in each circumstance. The trials were separated by two days, with six subjects performing HT first. Power output was 6.5% lower (P<0.05) during HT compared with NT. Mean skin temperature and sweat rate were higher (P<0.05) in HT compared with NT. In contrast, rectal temperature was remarkably similar throughout each trial. During the first 10 min of exercise in HT when power output was not different between trials, blood lactate was higher (P<0.05), and blood pH lower (P<0.05). In contrast, during the last 10 min of exercise when power output was reduced (P<0.05), blood lactate was lower (P<0.05), and pH higher (P<0.05), in HT. These data indicate that heat stress is associated with a reduced power output during self-paced exercise in highly trained men. This decrease in performance appears to be associated with factors associated with body temperature rather than metabolic capacity.

The present study was undertaken to examine the effect of carbohydrate ingestion on plasma and muscle ammonia (NH(3) denotes ammonia and ammonium) accumulation during prolonged exercise. Eleven trained men exercised for 2 h at 65% peak pulmonary oxygen consumption while ingesting either 250 ml of an 8% carbohydrate-electrolyte solution every 15 min (CHO) or an equal volume of a sweet placebo. Blood glucose and plasma insulin levels during exercise were higher in CHO, but plasma hypoxanthine was lower after 120 min (1.7 +/- 0.3 vs. 2.6 +/- 0.1 micromol/l; P < 0. 05). Plasma NH(3) levels were similar at rest and after 30 min of exercise in both trials but were lower after 60, 90, and 120 min of exercise in CHO (62 +/- 9 vs. 76 +/- 9 micromol/l; P < 0.05). Muscle NH(3) levels were similar at rest and after 30 min of exercise but were lower after 120 min of exercise in CHO (1.51 +/- 0.21 vs. 2.07 +/- 0.23 mmol/kg dry muscle; P < 0.05; n = 5). These data are best explained by carbohydrate ingestion reducing muscle NH(3) production from amino acid degradation, although a small reduction in net AMP catabolism within the contracting muscle may also make a minor contribution to the lower tissue NH(3) levels.

The relationship between changes in the muscle total adenine nucleotide pool (TAN = ATP + ADP + AMP) and IMP during and after 30 s of sprint cycling was examined. Skeletal muscle samples were obtained from the vastus lateralis muscle of seven untrained men (23. 9 +/- 2.3 yr, 74.4 +/- 3.6 kg, and 55.0 +/- 2.9 ml. kg(-1). min(-1) peak oxygen consumption) before and immediately after exercise and after 5 and 10 min of passive recovery. The exercise-induced increase in muscle IMP was linearly related to the decrease in muscle TAN (r = -0.97, P < 0.01), and the slope of this relationship (-0.83) was not different from 1.0 (P > 0.05), indicating a 1:1 stoichiometric relationship. This interpretation must be treated cautiously, because all subjects displayed a greater decrease in TAN compared with the increase in IMP content, and the TAN + IMP + inosine + hypoxanthine content was lower (P < 0.05) immediately after exercise compared with during rest. During the first 5 min of recovery, the increase in TAN was not correlated with the decrease in IMP (r = -0.18, P > 0.05). In all subjects, the magnitude of TAN increase was higher than the magnitude of IMP decrease over this recovery period. In contrast, the increase in TAN was correlated with the decrease in IMP throughout the second 5 min of recovery (r = -0.80, P < 0.05), and it was a 1:1 stoichiometric relationship (slope = -1.12). These data indicate that a small proportion of the TAN pool was temporarily lost from the muscle purine stores during sprinting but was rapidly recovered after exercise.

Purpose: We investigated the effects of acute plasma volume expansion on exercise performance in the heat., Methods: Six moderately trained men cycled for 40 min at 64 +/- 2% peak pulmonary oxygen uptake (VO2peak) followed by an individual performance time trial, where subjects completed a set amount of work (267 +/- 15 kJ) in as little time as possible. Exercise trials were performed at 35 degrees C with a relative humidity of 40%. Subjects performed two exercise trials: one after 13.1 +/- 1% acute plasma volume expansion (PVE), which was achieved by the intravenous infusion of 8 mL x kg(-1) body weight of Hemaccel (35 g x L(-1) polygeline, 145 mmol x L(-1) Na+, and 145 mmol x L(-1) Cl-) and the other without prior treatment (CON)., Results: Core temperature, skin blood flow, and heart rate progressively increased (P < 0.05) during exercise, but no differences were observed between trials. Plasma glucose and lactate were similar at rest and during exercise, as was VO2 during exercise. Exercise performance was not influenced by plasma volume expansion (CON 17.5 +/- 0.4 min and PVE 17.1 +/- 0.2 min)., Conclusion: These data suggest that, in moderately trained men, plasma volume expansion alone does not enhance thermoregulatory function and exercise performance during moderate intensity exercise in the heat.

This study examined the effectiveness of ingesting a carbohydrate or carbohydrate + medium-chain triglycerides (MCT) on metabolism and cycling performance. Eight endurance-trained men [peak O(2) uptake = 4.71 +/- 0.09 (SE) l/min] completed 35 kJ/kg as quickly as possible [time trial (TT)] while consuming 250 ml/15 min of either a 6% (wt/vol) carbohydrate solution (C), a 6% carbohydrate + 4.2% MCT solution (C+M), or a sweet placebo (P). Time to complete the set amount of work was reduced in both C and C+M compared with P by 7 and 5%, respectively (C: 166 +/- 7 min; C+M: 169 +/- 7 min; P: 178 +/- 11 min; P < 0.01). Plasma glucose concentration was maintained at or above resting values throughout both C and C+M trials but decreased (P < 0.05) below resting values in P at the completion of the TT. The estimated rate of carbohydrate oxidation was not different during the first 90 min of exercise but thereafter was reduced (P < 0.05) in P and was maintained in both C and C+M. These data demonstrate that carbohydrate ingestion during exercise improves 100-km TT performance compared with a sweet placebo, but the addition of MCT does not provide any further performance enhancement.

A depletion of phosphocreatine (PCr), fall in the total adenine nucleotide pool (TAN = ATP + ADP + AMP), and increase in TAN degradation products inosine 5'-monophosphate (IMP) and hypoxanthine are observed at fatigue during prolonged exercise at 70% maximal O(2) uptake in untrained subjects [J. Baldwin, R. J. Snow, M. F. Carey, and M. A. Febbraio. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R295-R300, 1999]. The present study aimed to examine whether these metabolic changes are also prevalent when exercise is performed below the blood lactate threshold (LT). Six healthy, untrained humans exercised on a cycle ergometer to voluntary exhaustion at an intensity equivalent to 93 +/- 3% of LT ( approximately 65% peak O(2) uptake). Muscle biopsy samples were obtained at rest, at 10 min of exercise, approximately 40 min before fatigue (F-40 =143 +/- 13 min), and at fatigue (F = 186 +/- 31 min). Glycogen concentration progressively declined (P < 0.01) to very low levels at fatigue (28 +/- 6 mmol glucosyl U/kg dry wt). Despite this, PCr content was not different when F-40 was compared with F and was only reduced by 40% when F was compared with rest (52. 8 +/- 3.7 vs. 87.8 +/- 2.0 mmol/kg dry wt; P < 0.01). In addition, TAN concentration was not reduced, IMP did not increase significantly throughout exercise, and hypoxanthine was not detected in any muscle samples. A significant correlation (r = 0.95; P < 0. 05) was observed between exercise time and glycogen use, indicating that glycogen availability is a limiting factor during prolonged exercise below LT. However, because TAN was not reduced, PCr was not depleted, and no correlation was observed between glycogen content and IMP when glycogen stores were compromised, fatigue may be related to processes other than those involved in muscle high-energy phosphagen metabolism.

To examine the effect of acute plasma volume expansion (PVE) on substrate selection during exercise, seven untrained men cycled for 40 min at 72 +/- 2% peak oxygen uptake (VO(2 peak)) on two occasions. On one occasion, subjects had their plasma volume expanded by 12 +/- 2% via an intravenous infusion of the plasma substitute Haemaccel, whereas on the other occasion no such infusion took place. Muscle samples were obtained before and immediately after exercise. In addition, heart rate and pulmonary gas and venous blood samples were obtained throughout exercise. No differences in oxygen uptake or heart rate during exercise were observed between trials, whereas respiratory exchange ratio, blood glucose, and lactate were unaffected by PVE. Muscle glycogen and lactate concentrations were not different either before or after exercise. In addition, there was no difference in total carbohydrate oxidation between trials (control: 108 +/- 2 g; PVE group: 105 +/- 2 g). Plasma catecholamine levels were not affected by PVE. These data indicate that substrate metabolism during submaximal exercise in untrained men is unaltered by acute hypervolemia.

To study the effect of temperature on muscle metabolism during submaximal exercise, six endurance-trained men had one thigh warmed and the other cooled for 40 min prior to exercise using water-perfused cuffs. One cuff was perfused with water at 50-55 degrees C (HL) with the other being perfused with water at 0 degree C (CL). With the cuffs still in position, subjects performed cycling exercise for 20 min at a work load corresponding to 70% VO2,peak (where VO2,peak is peak pulmonary oxygen uptake) in comfortable ambient conditions (20-22 degrees C). Muscle biopsies were obtained prior to and following exercise and forearm venous blood was collected prior to and throughout the exercise period. Muscle temperature (Tmus) was not different prior to treatment, but treatment resulted in a large difference in pre-exercise Tmus (difference = 6.9 +/- 0.9 degrees C; P < 0.01). Although this difference was reduced following exercise; it was nonetheless significant (difference = 0.4 +/- 0.1 degree C; P < 0.05). Intramuscular [ATP] was not affected by either exercise or muscle temperature. [Phosphocreatine] decreased (P < 0.01) and [creatine] increased (P < 0.01) with exercise but were not different when comparing HL with CL. Muscle lactate concentration was not different prior to treatment nor following exercise when comparing HL with CL. Muscle glycogen concentration was not different when comparing the trials before treatment, but the post-exercise value was lower (P < 0.05) in HL compared with CL. Thus, net muscle glycogen use was greater during exercise with heating (208 +/- 23 vs. 118 +/- 22 mmol kg-1 for HL and CL, respectively; P < 0.05). These data demonstrate that muscle glycogen use is augmented by increases in intramuscular temperature despite no differences in high energy phosphagen metabolism being observed when comparing treatments. This suggests that the increase in carbohydrate utilization occurred as a direct effect of an elevated muscle temperature and was not secondary to allosteric activation of enzymes mediated by a reduced ATP content.

To examine the effect of training status on muscle metabolism during exercise, seven endurance-trained [peak oxygen uptake (VO(2 peak)) = 65.8 +/- 2.4 ml. kg(-1). min(-1)] and six untrained (VO(2 peak) = 46. 2 +/- 1.9 ml. kg(-1). min(-1)) men cycled to fatigue at a work rate calculated to require 70% VO(2 peak). Time to exhaustion was 36% longer (P < 0.01) in trained (TR) compared with untrained (UT) men (148 +/- 11 vs. 95 +/- 8 min). Although intramuscular glycogen content was reduced (P < 0.05) in both TR and UT at fatigue, IMP, a marker of a mismatch between ATP supply and demand, was only elevated (P < 0.01) in UT muscle at fatigue and was approximately fourfold higher at this point in UT compared with TR. These data demonstrate that fatiguing submaximal exercise was associated with a similar low level of intramuscular glycogen in both TR and UT men, but a mismatch between ATP supply and demand only occurred in UT individuals.

To examine the effect of ambient temperature on metabolism during fatiguing submaximal exercise, eight men cycled to exhaustion at a workload requiring 70% peak pulmonary oxygen uptake on three separate occasions, at least 1 wk apart. These trials were conducted in ambient temperatures of 3 degrees C (CT), 20 degrees C (NT), and 40 degrees C (HT). Although no differences in muscle or rectal temperature were observed before exercise, both muscle and rectal temperature were higher (P < 0.05) at fatigue in HT compared with CT and NT. Exercise time was longer in CT compared with NT, which, in turn, was longer compared with HT (85 +/- 8 vs. 60 +/- 11 vs. 30 +/- 3 min, respectively; P < 0.05). Plasma epinephrine concentration was not different at rest or at the point of fatigue when the three trials were compared, but concentrations of this hormone were higher (P < 0.05) when HT was compared with NT, which in turn was higher (P < 0.05) compared with CT after 20 min of exercise. Muscle glycogen concentration was not different at rest when the three trials were compared but was higher at fatigue in HT compared with NT and CT, which were not different (299 +/- 33 vs. 153 +/- 27 and 116 +/- 28 mmol/kg dry wt, respectively; P < 0.01). Intramuscular lactate concentration was not different at rest when the three trials were compared but was higher (P < 0.05) at fatigue in HT compared with CT. No differences in the concentration of the total intramuscular adenine nucleotide pool (ATP + ADP + AMP), phosphocreatine, or creatine were observed before or after exercise when the trials were compared. Although intramuscular IMP concentrations were not statistically different before or after exercise when the three trials were compared, there was an exercise-induced increase (P < 0.01) in IMP. These results demonstrate that fatigue during prolonged exercise in hot conditions is not related to carbohydrate availability. Furthermore, the increased endurance in CT compared with NT is probably due to a reduced glycogenolytic rate.

Purpose: This study aimed to examine the effect of glycemic index of pre-exercise carbohydrate (CHO) ingestion on exercise metabolism and performance., Methods: Eight endurance trained men ingested a high glycemic index (HGI), low glycemic index (LGI), or a placebo (CON) meal 45 min before exercise and then cycled for 50 min at 67% VO2max. Subjects subsequently performed a 15-min self-paced performance ride in which total work (kJ) was recorded., Results: Plasma glucose concentrations were higher (P < 0.01) after ingestion in HGI compared with LGI and CON (7.53 +/- 0.64 vs 5.55 +/- 0.21 and 4.65 +/- 0.14 mmol.L-1 for HGI, LGI, and CON, respectively, 30 min postprandial; mean +/- SE) but declined at the onset of exercise and were lower (P < 0.01) compared with LGI and CON (4.03 +/- 0.31 vs 4.64 +/- 0.24 and 5.09 +/- 0.16 mmol.L-1 for HGI, LGI, and CON respectively; mean +/- SE) at 10 min of exercise. Plasma glucose remained depressed (P < 0.01) until 30 min into exercise in HGI compared with other trials. Plasma insulin concentrations were higher (P < 0.01) following ingestion during rest and exercise in HGI compared with LGI and CON. Plasma FFA concentrations were lower (P < 0.05) following ingestion in HGI and LGI compared with CON and higher (P < 0.05) in LGI compared with HGI at the start and end of exercise. RER and CHO oxidation was higher (P < 0.01) in HGI compared with LGI and CON during submaximal exercise. There were no differences in work output during the performance cycle., Conclusions: These data indicate that pre-exercise CHO feedings with varying glycemic indexes do not affect exercise performance following short term submaximal exercise despite alterations in metabolism.

Six men were studied during four 30-s "all-out" exercise bouts on an air-braked cycle ergometer. The first three exercise bouts were separated by 4 min of passive recovery; after the third bout, subjects rested for 4 min, exercised for 30 min at 30-35% peak O2 consumption, and rested for a further 60 min before completing the fourth exercise bout. Peak power and total work were reduced (P < 0. 05) during bout 3 [765 +/- 60 (SE) W; 15.8 +/- 1.0 kJ] compared with bout 1 (1,168 +/- 55 W, 23.8 +/- 1.2 kJ), but no difference in exercise performance was observed between bouts 1 and 4 (1,094 +/- 64 W, 23.2 +/- 1.4 kJ). Before bout 3, muscle ATP, creatine phosphate (CP), glycogen, pH, and sarcoplasmic reticulum (SR) Ca2+ uptake were reduced, while muscle lactate and inosine 5'-monophosphate were increased. Muscle ATP and glycogen before bout 4 remained lower than values before bout 1 (P < 0.05), but there were no differences in muscle inosine 5'-monophosphate, lactate, pH, and SR Ca2+ uptake. Muscle CP levels before bout 4 had increased above resting levels. Consistent with the decline in muscle ATP were increases in hypoxanthine and inosine before bouts 3 and 4. The decline in exercise performance does not appear to be related to a reduction in muscle glycogen. Instead, it may be caused by reduced CP availability, increased H+ concentration, impairment in SR function, or some other fatigue-inducing agent.

To test the hypothesis that an elevation in circulating epinephrine increases intramuscular glycogen utilization, six endurance-trained men performed two 40-min cycling trials at 71 +/- 2% of peak oxygen uptake in 20-22 degrees C conditions. On the first occasion, subjects were infused with saline throughout exercise (Con). One week later, after determination of plasma epinephrine levels in Con, subjects performed the second trial (Epi) with an epinephrine infusion, which resulted in a twofold higher (P < 0.01) plasma epinephrine concentration in Epi compared with Con. Although oxygen uptake was not different when the two trials were compared, respiratory exchange ratio was higher throughout exercise in Epi compared with Con (0.93 +/- 0.01 vs. 0.89 +/- 0.01; P < 0.05). Muscle glycogen concentration was not different when the trials were compared preexercise, but the postexercise value was lower (P < 0.01) in Epi compared with Con. Thus net muscle glycogen utilization was greater during exercise with epinephrine infusion (224 +/- 37 vs. 303 +/- 30 mmol/kg for Con and Epi, respectively; P < 0.01). In addition, both muscle and plasma lactate and plasma glucose concentrations were higher (P < 0.05) in Epi compared with Con. These data indicate that intramuscular glycogen utilization, glycolysis, and carbohydrate oxidation are augmented by elevated epinephrine during submaximal exercise in trained men.

This study examined the effect of delaying the ingestion of carbohydrate on muscle glycogen storage following prolonged exhaustive exercise. Six endurance trained men cycled on two separate occasions at a workload corresponding to 70% VO2max for 2 h followed by four "all-out" 30-s sprints. Following exercise, subjects were fed five high glycemic index (HGI) meals over a 24-h period, with the first three being fed either at 0-4 h (IT) or 2-6 h (DT) at 2-h intervals. Muscle biopsies were taken immediately after exercise and at 8 and 24 h post-exercise and analyzed for glycogen and glucose-6-phosphate. Blood samples were obtained prior to and at 30, 60, and 90 min after each meal and analyzed for glucose and insulin. No differences were observed in the incremental glucose and insulin areas after each meal when IT and DT were compared. In addition, no differences were observed in muscle glycogen or glucose-6-phosphate any time in the two trials. These data indicate that delayed feeding of a HGI meal by 2 h has no effect on the rate of muscle glycogen resynthesis at 8 and 24 h post-exercise, providing that sufficient carbohydrate is ingested during the recovery period.

Two series of experiments were conducted to examine the effect of ingesting beverages with differing carbohydrate (CHO) concentrations and osmolalities on metabolism and performance during prolonged exercise in different environmental conditions. In series 1, 12 subjects performed three cycling exercise trials to fatigue at 70% VO2peak in either 33 degrees C (N = 6) (HT1) or 5 degrees C (N = 6) (CT). Subjects ingested either a 14% CHO solution (osmolality = 390 mosmol.1(-1) (HCHO); a 7% CHO solution (330 mosmol.1(-1) (NCHO) or a placebo (90 mosmol.1(-1) (CON1). In series 2, six subjects performed the same three trials at 33 degrees C (HT2), while ingesting either NCHO, a 4.2% CHO solution (240 mosmol.1(-1) (LCHO) or a placebo) (240 mosmol.1(-1) (CON2). Plasma glucose was higher (P < 0.05) in HCHO than NCHO, which in turn was higher (P < 0.05) than CON1 in both CT and HT1. Plasma glucose was lower (P < 0.05) in CON2 compared with NCHO and LCHO in HT2. The fall in plasma volume was greater (P < 0.05) in HCHO than other trials in both CT and HT1 but was not different when comparing the three trials in HT2. Exercise time was not different when comparing the trials in either HT1 or HT2 but was longer (P < 0.05) in NCHO compared with HCHO, which, in turn, was longer (P < 0.05) than CON1 in CT. These data demonstrate that, during prolonged exercise in the heat, fatigue is related to factors other than CHO availability. In addition, during exercise in 5 degrees C a 7% CHO solution is more beneficial for exercise performance than a 14% CHO solution.

This study examined the effects of elevated muscle temperature on muscle metabolism during exercise. Seven active but untrained men completed two cycle ergometer trials for 2 min at a workload estimated to require 115% maximal oxygen uptake (VO2) either without pretreatment (CT) or after having their thigh wrapped in a heating blanket for 60 min before exercise (HT). HT increased (P < 0.01) muscle temperature (Tm) and resulted in a difference in Tm between the two trials before (delta = 1.9 +/- 0.1 degrees C, P < 0.01) and after exercise (delta = 0.6 +/- 0.2 degree C, P < 0.05). HT did not affect rectal temperature or plasma catecholamines. In addition, these parameters were not different between CT and HT either before or after exercise. No differences in resting intramuscular concentrations of the adenine nucleotides (ATP, ADP, AMP) or their degradation products (inosine 5'-monophosphate, ammonia), lactate, glycogen, creatine phosphate, or creatine were observed between HT and CT. During exercise, the magnitude of ATP degradation and inosine 5'-monophosphate and ammonia accumulation was higher (P < 0.05) in HT compared with CT. Although preexercise concentrations of glycogen and lactate were not different between the two trials, postexercise lactate concentration was higher (P < 0.05) and glycogen lower (P < 0.05) in HT compared with CT. In addition, net muscle glycogen use was higher (P < 0.05) in HT. It is concluded that an elevated Tm per se increases muscle glycogenolysis, glycolysis, and high-energy phosphate degradation during exercise. These alterations may be the result of an increased rate of ATP turnover associated with the exercise and/or changes in the anaerobic/aerobic contribution to ATP resynthesis.

This study examined the effect of preexercise carbohydrate (CHO) ingestion on muscle CHO metabolism and performance during prolonged exercise. Six endurance-trained men performed three exercise trials on a cycle ergometer after ingesting either a high glycemic index (HGI), low glycemic index (LGI), or placebo (Con) meal 45 min before exercise. During each trial, subjects cycled at a workload corresponding to 70% peak oxygen uptake for 120 min, followed by a 15-min performance cycle where total work (kJ) was measured. Ingestion of HGI resulted in an elevated (P < 0.01) blood glucose concentration 15 min after ingestion, compared with LGI and Con, but there were no differences in the glycemic responses to the meals thereafter, despite plasma insulin concentration being higher (P < 0.01) throughout the rest period after ingestion of HGI compared with LGI and Con. Plasma free fatty acid concentrations were lower (P < 0.05) throughout exercise in HGI compared with LGI and Con. In addition, concentrations of this metabolite were lower (P < 0.05) during the first hour of exercise in LGI compared with Con. Despite these results, no differences were observed in either the rate of muscle glycogen utilization during submaximal exercise or work output during the performance cycle when the three trials were compared. These results demonstrate that preexercise CHO ingestion has no effect on muscle glycogen utilization or exercise performance, irrespective of the glycemic or insulinemic responses to the ingested meals.

To examine the effect of blunting the rise in body temperature on exercise metabolism, seven endurance-trained men cycled for 40 min at 65% of maximal oxygen consumption (VO2,max) in an environmental chamber at either 20 degrees C and 20% relative humidity (RH) (T20) or 3 degrees C and approximately 50% RH (T3). The trials were conducted in random order at least 1 week apart. Mean oxygen consumption (VO2) during exercise was not different when comparing the two trials. In contrast, the mean respiratory exchange ratio (RER) was lower (P < 0.05) at T20 compared with T3. Heart rate, rectal temperature and plasma catecholamines were higher (P < 0.05) during exercise at T20 compared with T3, as was post-exercise muscle temperature (P < 0.01). Muscle and blood lactate and blood glucose concentrations were not significantly different when comparing T20 with T3. Net muscle glycogen utilization was greater (P < 0.05) at T20 compared with T3. These results suggest that glycogenolysis in contracting skeletal muscle is reduced during exercise when the rise in body core temperature is attenuated. These changes in carbohydrate metabolism appear to be influenced by alterations in muscle temperature and/or sympatho-adrenal activity.

This study examined the effect of (a) creatine supplementation on exercise metabolism and performance and (b) changes in intramuscular total creatine stores following a 5 day supplementation period and a 28 day wash-out period. Six men performed four exercise trials, each consisting of four 1 min cycling bouts, punctuated by 1 min of rest followed by a fifth bout to fatigue, all at a workload estimated to require 115 or 125% VO2,max. After three familiarization trials, one trial was conducted following a creatine monohydrate supplementation protocol (CREAT); the other after 28 d without creatine supplementation, in which the last 5 d involved placebo ingestion (CON). Intramuscular TCr was elevated (P < 0.05) in CREAT compared with the final familiarization trial (FAM 3) and CON. Concentrations of this metabolite in these latter trials were not different. In addition, a main effect (P < 0.05) for treatment was observed for PCr when the data from CREAT were compared with CON. In contrast, no differences were observed in the total adenine nucleotide pool (ATP+ADP+AMP), inosine 5'-monophosphate, ammonia, lactate or glycogen when comparing CREAT with CON. Despite the differences in TCr and PCr concentrations when comparing CREAT with other trials, no difference was observed in exercise duration in the fifth work bout. These data demonstrate that creatine supplementation results in an increase in TCr but this has no effect on performance during exercise of this nature, where the creatine kinase system is not the principal energy supplier. In addition 28 d without supplementation is a sufficient time to return intramuscular TCr stores to basal levels.

To examine the effect of heat stress on muscle energy metabolism during submaximal exercise, 12 endurance-trained men cycled on two occasions for approximately 40 min at 70% maximal O2 uptake in an environmental chamber at either 20 degrees C and 20% relative humidity (T20) or 40 degrees C and 20% relative humidity (T40). Trials were conducted > or = 1 wk apart in random order. No difference in mean O2 uptake was observed when exercise in T40 was compared with that in T20. In contrast, exercise in T40 resulted in a higher mean heart rate (P < 0.01) and respiratory exchange ratio (P < 0.05) compared with that in T20. Postexercise rectal and muscle temperatures were also higher (P < 0.01) in T40 than in T20. Lower (P < 0.01) postexercise creatine phosphate and higher creatine (P < 0.01) and ammonia (P < 0.05) were observed in muscle after exercise in T40 compared with T20. In addition, an increased (P < 0.01) muscle glycogenolysis and higher (P < 0.01) postexercise muscle lactate accumulation were observed during exercise in T40 compared with T20. In contrast, no differences were observed in postexercise concentrations of total adenine nucleotide pool (ATP+ADP+AMP), ATP/ADP ratio, or inosine 5'-monophosphate (IMP) when T40 was compared with T20. These results indicate that the rate of ATP utilization may be increased during exercise in the heat but that this increased energy demand is predominantly met by an increase in anaerobic glycolysis and creatine phosphate hydrolysis, preventing a reduction in total adenine nucleotide pool.(ABSTRACT TRUNCATED AT 250 WORDS)

To examine the effect of sprint training on human skeletal muscle purine nucleotide metabolism, eight active untrained subjects completed a maximal 30-s sprint bout on a cycle ergometer before and after 7 wk of sprint training. Resting muscle ATP and total adenine nucleotide content were reduced (P < 0.05) by 19 and 18%, respectively, after training. Training resulted in a 52% attenuation (P < 0.05) in the magnitude of ATP depletion after exercise and a similar reduction (P < 0.05) in the accumulation of inosine 5'-monophosphate and ammonia. During recovery, muscle inosine 5'-monophosphate (P < 0.05) and inosine (P < 0.01) content were reduced after training, as was the accumulation of inosine (P < 0.05). Plasma ammonia was higher (P < 0.05) after training early in recovery; in contrast, plasma hypoxanthine concentrations were reduced (P < 0.05) during the latter stages of recovery. The attenuated resting ATP and total adenine nucleotide contents after training probably result from the acute effects of prior training sessions. The reduction in the magnitude of ATP depletion during a 30-s sprint bout after training must reflect an improved balance between ATP hydrolysis and resynthesis. It is unclear which mechanism(s) is responsible for the reduction in the magnitude of ATP degradation after training.

Exercise metabolism was examined in 13 endurance athletes who exercised on three occasions for 40 min at 70% of maximal O2 uptake in an environmental chamber at either 20 degrees C and 20% relative humidity (RTT) or 40 degrees C and 20% relative humidity before (PRE ACC) or after (POST ACC) 7 days of acclimation. Exercise in the heat resulted in a lower (P < 0.05) mean O2 uptake (0.13 l/min) and higher (P < 0.01) heart rate and respiratory exchange ratio. Acclimation resulted in a lower (P < 0.01) mean heart rate and respiratory exchange ratio. Postexercise rectal temperature, muscle temperature, muscle and blood lactate, and blood glucose were higher (P < 0.01) in the PRE ACC than in the RTT trial, but all were reduced (P < 0.01) in the POST ACC compared with the PRE ACC trial. Muscle glycogenolysis and percentage of type I muscle fibers showing glycogen depletion were greater (P < 0.05) in the PRE ACC than in the RTT trial. Muscle glycogenolysis was unaffected by acclimation during exercise in the heat, although the percentage of depleted type I fibers was higher (P < 0.05) in the unacclimated state. Plasma epinephrine was higher (P < 0.01) during exercise in the heat in the unacclimated individual relative to RTT but was lower (P < 0.01) in the POST ACC than in the PRE ACC trial. The greater reliance on carbohydrate as a fuel source during exercise in the heat appears to be partially reduced after acclimation. These alterations are consistent with the observed changes in plasma epinephrine concentrations.

Seven men were studied during 40 min of exercise at 70% VO2 peak, in an environmental chamber maintained at either 20 or 40 degrees C, to examine the effect of heat stress on ammonia metabolism during exercise. Heart rate and rectal and muscle temperatures were higher during exercise in the heat, while no differences were observed in pulmonary oxygen uptake or respiratory exchange ratio. Plasma ammonia levels and muscle ammonia accumulation were higher during exercise at 40 degrees C compared with 20 degrees C. Such metabolic alterations may be associated with reduced performance during exercise in the heat.