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Biomedical subjects

M A Febbraio

Publications and source records attributed to M A Febbraio.

At least 37 records · Page 2Linked to original sources

Effect of creatine supplementation on metabolism and performance in humans during intermittent sprint cycling.

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.

Adult↗

The influence of whole-body vs. torso pre-cooling on physiological strain and performance of high-intensity exercise in the heat.

Little research has been reported examining the effects of pre-cooling on high-intensity exercise performance, particularly when combined with strategies to keep the working muscle warm. This study used nine active males to determine the effects of pre-cooling the torso and thighs (LC), pre-cooling the torso (ice-vest in 3 degrees C air) while keeping the thighs warm (LW), or no cooling (CON: 31 degrees C air), on physiological strain and high-intensity (45-s) exercise performance (33 degrees C, 60% rh). Furthermore, we sought to determine whether performance after pre-cooling was influenced by a short exercise warm-up. The 45-s test was performed at different (P<0.05) mean core temperature [(rectal+oesophageal)/2] [CON: 37.3+/-0.3 (S.D.), LW: 37.1+/-0.3, LC: 36.8+/-0.4 degrees C] and mean skin temperature (CON: 34.6+/-0.6, LW: 29.0+/-1.0, LC: 27.2+/-1.2 degrees C) between all conditions. Forearm blood flow prior to exercise was also lower in LC (3.1+/-2.0 ml 100 ml tissue(-1) x min(-1)) than CON (8.2+/-2.5, P=0.01) but not LW (4.3+/-2.6, P=0.46). After an exercise warm-up, muscle temperature (Tm) was not significantly different between conditions (CON: 37.3+/-1.5, LW: 37.3+/-1.2, LC: 36.6+/-0.7 degrees C, P=0.16) but when warm-up was excluded, T(m) was lower in LC (34.5+/-1.9 degrees C, P=0.02) than in CON (37.3+/-1.0) and LW (37.1+/-0.9). Even when a warm-up was performed, torso+thigh pre-cooling decreased both peak (-3.4+/-3.8%, P=0.04) and mean power output (-4.1+/-3.8%, P=0.01) relative to the control, but this effect was markedly larger when warm-up was excluded (peak power -7.7+/-2.5%, P=0.01; mean power -7.6+/-1.2%, P=0.01). Torso-only pre-cooling did not reduce peak or mean power, either with or without warm-up. These data indicate that pre-cooling does not improve 45-s high-intensity exercise performance, and can impair performance if the working muscles are cooled. A short exercise warm-up largely removes any detrimental effects of a cold muscle on performance by increasing Tm.

Adult↗

Effect of pre-cooling, with and without thigh cooling, on strain and endurance exercise performance in the heat.

Body cooling before exercise (i.e. pre-cooling) reduces physiological strain in humans during endurance exercise in temperate and warm environments, usually improving performance. This study examined the effectiveness of pre-cooling humans by ice-vest and cold (3 degrees C) air, with (LC) and without (LW) leg cooling, in reducing heat strain and improving endurance performance in the heat (35 degrees C, 60% RH). Nine habitually-active males completed three trials, involving pre-cooling (LC and LW) or no pre-cooling (CON: 34 degrees C air) before 35-min cycle exercise: 20 min at approximately 65% VO2peak then a 15-min work-performance trial. At exercise onset, mean core (Tc, from oesophagus and rectum) and skin temperatures, forearm blood flow (FBF), heart rate (HR), and ratings of exertion, body temperature and thermal discomfort were lower in LW and LC than CON (P<0.05). They remained lower at 20 min [e.g. Tc: CON 38.4+/-0.2 (+/-S.E.), LW 37.9+/-0.1, and LC 37.8+/-0.1 degrees C; HR: 177+/-3, 163+/-3 and 167+/-3 b.p.m.), except that FBF was equivalent (P=0.10) between CON (15.5+/-1.6) and LW (13.6+/-1.0 ml.100 ml tissue(-1) x min(-1)). Subsequent power output was higher in LW (2.95+/-0.24) and LC (2.91+/-0.25) than in CON (2.52+/-0.28 W kg(-1), P=0.00, N=8), yet final Tc remained lower. Pre-cooling by ice-vest and cold air effectively reduced physiological and psychophysical strain and improved endurance performance in the heat, irrespective of whether thighs were warmed or cooled.

Adult↗

Effects of ovarian hormones on exercise metabolism.

Growing evidence suggests that the ovarian hormones have major effects on lipid and carbohydrate metabolism, and may also play a major role in up-stream molecular signaling mechanisms for regulating substrate metabolism. It appears that the absence of estrogen can impair glucose uptake during exercise. In contrast, progesterone not only impairs contraction-mediated glucose uptake when solely administered, but impairs glucose uptake when physiological concentrations of both estrogen and progesterone are administered. Likewise, progesterone administered to rodents for 14 days decreases glucose transporter (GLUT) 4 protein content in skeletal muscle and adipose tissue. Furthermore removing the ovaries decreases the activity of key oxidative enzymes while estrogen treatment restores the activity of these enzymes. It appears, therefore, that estrogen increases the metabolic capacity for both carbohydrate and lipid metabolism, perhaps increasing the overall metabolic flexibility of skeletal muscle. Conversely, progesterone negates both these effects, and could therefore result in a state of relative metabolic inflexibility, similar to that observed in the metabolic syndrome.

Animals↗

Effect of caffeine co-ingested with carbohydrate or fat on metabolism and performance in endurance-trained men.

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.

Adult↗

Effect of glycerol-induced hyperhydration on thermoregulation and metabolism during exercise in heat.

This study examined the effect of glycerol ingestion on fluid homeostasis, thermoregulation, and metabolism during rest and exercise. Six endurance-trained men ingested either 1 g glycerol in 20 ml H2O x kg(-1) body weight (bw) (GLY) or 20 ml H2O x kg(-1) bw (CON) in a randomized double-blind fashion, 120 min prior to undertaking 90 min of steady state cycle exercise (SS) at 98% of lactate threshold in dry heat (35 degrees C, 30% RH), with ingestion of CHO-electrolyte beverage (6% CHO) at 15-min intervals. A 15-min cycle, where performance was quantified in kJ, followed (PC). Pre-exercise urine volume was lower in GLY than CON (1119 +/- 97 vs. 1503 +/- 146 ml x 120 min(-1); p < .05). Heart rate was lower (p < .05) throughout SS in GLY, while forearm blood flow was higher (17.1 +/- 1.5 vs. 13.7 +/- 3.0 ml x 100 g tissue x min(-1); p < .05) and rectal temperature lower (38.7 +/- 0.1 vs. 39.1 +/- 0.1 degrees C; p < .05) in GLY late in SS. Despite these changes, skin and muscle temperatures and circulating catecholamines were not different between trials. Accordingly, no differences were observed in muscle glycogenolysis, lactate accumulation, adenine nucleotide, and phosphocreatine degradation or inosine 5'-monophosphate accumulation when comparing GLY with CON. Of note, the work performed during PC was 5% greater in GLY (252 +/- 10 vs. 240 +/- 9 kJ; p < .05). These results demonstrate that glycerol, when ingested with a bolus of water 2 hours prior to exercise, results in fluid retention, which is capable of reducing cardiovascular strain and enhancing thermoregulation. Furthermore, this practice increases exercise performance in the heat by mechanisms other than alterations in muscle metabolism.

Adult↗

Circulating monocytes are not the source of elevations in plasma IL-6 and TNF-alpha levels after prolonged running.

The present study was undertaken to examine the effect of prolonged running on monocyte intracellular cytokine production and plasma cytokine concentration. Blood samples were collected 1 h before, immediately after, 2 h after, and 24 h after a competitive marathon run. There was no change in the number of cells spontaneously producing tumor necrosis factor (TNF)-alpha; however, there was a decrease in the number of cells producing interleukin (IL)-1alpha and IL-6 (P < 0.01) postexercise. In contrast, there was an increase in the number of monocytes that responded to lipopolysaccharide stimulation by producing IL-1alpha, TNF-alpha, and IL-6 (P < 0.01) immediately and 2 h postexercise; however, these cells contained less cytokine (P < 0.05). Plasma IL-6, TNF-alpha, epinephrine, norepinephrine, and cortisol concentrations were markedly increased (P < 0.01) postexercise. These data demonstrate that circulating monocytes are not the source of elevated levels of plasma IL-6 and TNF-alpha after prolonged running. In addition, it is likely that stress hormones result in a decrease in the amount of cytokine produced by LPS-stimulated cells postexercise.

Epinephrine↗

Effect of adrenergic blockade on lymphocyte cytokine production at rest and during exercise.

To examine the effect of exercise and adrenergic blockade on lymphocyte cytokine production, six men ingested either a placebo (control) or an alpha- (prazosin hydrochloride) and beta-adrenoceptor antagonist (timolol malate) capsule (blockade, or BLK) 2 h before performing 19 +/- 1 min of supine bicycle exercise at 78 +/- 3% peak pulmonary uptake. Blood was collected before and after exercise, stimulated with phorbol 12-myristate 13-acetate and ionomycin, and surface stained for T (CD3(+)) and natural killer [NK (CD3(-)CD56(+))] lymphocyte surface antigens. Cells were permeabilized, stained for the intracellular cytokines interleukin (IL)-2 and interferon (IFN)-gamma, and analyzed using flow cytometry. BLK had no effect on the resting concentration of stimulated cytokine-positive T and NK lymphocytes or the amount of cytokine they were producing. Exercise resulted in an increase (P < 0.05) in the concentration of stimulated T and NK lymphocytes producing cytokines in the circulation, but these cells produced less (P < 0.05) cytokine post- compared with preexercise. BLK attenuated (P < 0.05) the elevation in the concentration of lymphocytes producing cytokines during exercise; however, BLK did not affect the amount of IL-2 and IFN-gamma produced. These results suggest that adrenergic stimulation contributes to the exercise-induced increase in the concentration of lymphocytes in the circulation; however, it does not appear to be responsible for the exercise-induced suppression in cytokine production.

Adrenergic alpha-Antagonists↗

Effect of ovarian hormones on mitochondrial enzyme activity in the fat oxidation pathway of skeletal muscle.

To examine the roles of 17beta-estradiol (E(2)) and progesterone (Prog) in lipid metabolism, skeletal muscle enzyme activities were studied in female Sprague-Dawley rats. Groups included sham-operated rats (C) and ovariectomized rats treated with placebo (O), E(2) (E), Prog (P), both hormones at physiological doses (P + E), or both hormones with a high dose of E(2) (P + HiE). Hormone (or vehicle only) delivery was via time-release pellets inserted at the time of surgery, 15 days before metabolic testing. Results demonstrated that carnitine palmitoyltransferase maximal activity was 19, 21, and 19% lower (P < 0.01) in O, P, and P + E rats, respectively, compared with C rats. Conversely, activity in E and P + HiE rats was 14 and 19% higher (P < 0.01) than in C. beta-Hydroxyacyl-CoA dehydrogenase (beta-HAD) maximal activity was 20% lower (P < 0.01) in O than in C rats; similarly, P and P + E rats were 18 and 19% lower, respectively (P < 0.01); however, treatment with E(2) returned beta-HAD activity to C levels. These results suggest that E(2) plays a role in lipid metabolism by increasing the maximal activity of key enzymes in the fat oxidative pathway of skeletal muscle.

3-Hydroxyacyl CoA Dehydrogenases↗

Glucose kinetics and exercise performance during phases of the menstrual cycle: effect of glucose ingestion.

To study the effect of menstrual cycle phase and carbohydrate ingestion on glucose kinetics and exercise performance, eight healthy, moderately trained, eumenorrheic women cycled at 70% of peak O(2) consumption for 2 h and then performed a 4 kJ/kg body wt time trial. A control (C) and a glucose ingestion (G) trial were completed during the follicular (F) and luteal (L) phases of the menstrual cycle. Plasma substrate concentrations were similar before the commencement of exercise. Glucose rates of appearance and disappearance were higher (P < 0.05) during the 2nd h of exercise in FC than in LC. The percent contribution of carbohydrate to total energy expenditure was greater in FC than in LC, and subjects performed better (13%, P < 0.05) in FC. Performance improved (19% and 26% in FG and LG compared with FC and LC, respectively, P < 0.05) with the ingestion of glucose throughout exercise. These data demonstrate that substrate metabolism and exercise performance are influenced by the menstrual cycle phase, but ingestion of glucose minimizes these effects.

Adult↗

Effect of carbohydrate ingestion on glucose kinetics during exercise in the heat.

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.

Adult↗

No effect of mild heat stress on the regulation of carbohydrate metabolism at the onset of exercise.

To investigate the influence of heat stress on the regulation of skeletal muscle carbohydrate metabolism, six active, but not specifically trained, men performed 5 min of cycling at a power output eliciting 70% maximal O2 uptake in either 20 degrees C (Con) or 40 degrees C (Heat) after 20 min of passive exposure to either environmental condition. Although muscle temperature (T(mu)) was similar at rest when comparing trials, 20 min of passive exposure and 5 min of exercise increased (P < 0.05) T(mu) in Heat compared with Con (37.5 +/- 0.1 vs. 36.9 +/- 0.1 degrees C at 5 min for Heat and Con, respectively). Rectal temperature and plasma epinephrine were not different at rest, preexercise, or 5 min of exercise between trials. Although intramuscular glycogen phosphorylase and pyruvate dehydrogenase activity increased (P < 0.05) at the onset of exercise, there were no differences in the activities of these regulatory enzymes when comparing Heat with Con. Accordingly, glycogen use in the first 5 min of exercise was not different when comparing Heat with Con. Similarly, no differences in intramuscular concentrations of glucose 6-phosphate, lactate, pyruvate, acetyl-CoA, creatine, phosphocreatine, or ATP were observed at any time point when comparing Heat with Con. These results demonstrate that, whereas mild heat stress results in a small difference in contracting T(mu), it does not alter the activities of the key regulatory enzymes for carbohydrate metabolism or glycogen use at the onset of exercise, when plasma epinephrine levels are unaltered.

Adult↗

Exercise increases serum Hsp72 in humans.

Recent evidence suggests that heat shock proteins (Hsps) may have an important systemic role as a signal to activate the immune system. Since acute exercise is known to induce Hsp72 (the inducible form of the 70-kDa family of Hsp) in a variety of tissues including contracting skeletal muscle, we hypothesized that such exercise would result in the release of Hsp72 from stressed cells into the blood. Six humans (5 males, 1 female) ran on a treadmill for 60 minutes at a workload corresponding to 70% of their peak oxygen consumption. Blood was sampled from a forearm vein at rest (R), 30 minutes during exercise, immediately postexercise (60 minutes), and 2, 8, and 24 hours after exercise. These samples were analyzed for serum Hsp72 protein. In addition, plasma creatine kinase (CK) was measured at these time points as a crude marker of muscle damage. With the exception of the sample collected at 30 minutes, muscle biopsies (n = 5 males) were also obtained from the vastus lateralis at the time of blood sampling and analyzed for Hsp72 gene and protein expression. Serum Hsp72 protein increased from rest, both during and after exercise (0.13 0.10 vs 0.87+/-0.24 and 1.02+/-0.41 ng/mL at rest, 30 and 60 minutes, respectively, P < 0.05, mean SE). In addition, plasma CK was elevated (P < 0.05) 8 hours postexercise. Skeletal muscle Hsp72 mRNA expression increased 6.5-fold (P < 0.05) from rest 2 hours postexercise, and although there was a tendency for Hsp72 protein expression to be elevated 2 and 8 hours following exercise compared with rest, results were not statistically significant. The increase in serum Hsp72 preceded any increase in Hsp72 gene or protein expression in contracting muscle, suggesting that Hsp72 was released from other tissues or organs. This study is the first to demonstrate that acute exercise can increase Hsp72 in the peripheral circulation, suggesting that during stress these proteins may indeed have a systemic role.

Adult↗

Alterations in energy metabolism during exercise and heat stress.

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.

Adaptation, Physiological↗

Effect of prolonged, submaximal exercise and carbohydrate ingestion on monocyte intracellular cytokine production in humans.

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.

Adult↗

Effects of heat stress on physiological responses and exercise performance in elite cyclists.

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.

Adult↗

Effect of altering substrate availability on metabolism and performance during intense exercise.

The purpose of this study was to determine the effect of altering substrate availability on metabolism and performance during intense cycling. Seven highly trained men ingested a random order of three isoenergetic meals 90 min before cycling at 80% maximal oxygen uptake (VO2max) for 20 min (about 310 W), followed by a 600 kJ time trial lasting about 30 min. Meals consisted of either 1.2 g saturated fat/kg body mass (BM) with 3500 U heparin intravenously (HIFAT) to elevate circulating plasma free fatty acid (FA) concentration, 2.5 g carbohydrate/kg BM (CHO) to elevate plasma glucose and insulin concentrations or 2.5 g carbohydrate +20 mg nicotinic acid/kg BM (NA) to suppress lipolysis and reduce free FA concentration. HIFAT elevated free FA concentration (HIFAT 1.3 (sem 0.2), CHO 0.2 (sem 0.1), NA 0.1 (sem 0.1) mm; P < 0.001) lowered the RER (HIFAT 0.94 (sem 0.01), CHO 0.97 (sem 0.01), NA 0.98 (sem 0.01); P < 0.01) and increased the rate of fat oxidation (HIFAT 24 (sem 3), CHO 12 (sem 2), NA 8 (sem 3) micromol/kg per min; P < 0.01) during the 20 min ride. Marked differences in fat availability and fuel utilisation, however, had little effect on performance in the subsequent time trial (HIFAT 320 (sem 16), CHO 324 (sem 15), NA 315 (sem 13) W). We conclude: (1) increased fat availability during intense cycling increases the rate of fat oxidation; but (2) the reduction in the rate of carbohydrate oxidation in the presence of high circulating plasma free FA is unlikely to enhance intense exercise performance lasting about 1 h; (3) substrate selection during intense (about 80% VO2max) exercise is dominated by carbohydrate oxidation.

Adult↗

Effect of acute plasma volume expansion on thermoregulation and exercise performance in the heat.

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.

Acclimatization↗