Carbohydrate supplementation improves moderate and high-intensity exercise in the heat

The aim of the present study was to clarify the effect of carbohydrate (CHO) supplementation on moderate and high-intensity endurance exercise in the heat. Eight endurance-trained men [maximal oxygen uptake ( VO(2max)) 59.5+/-1.6 ml kg(-1) bw(-1), mean+/-SE] cycled to exhaustion twice at 60% VO(2max) and twice at 73% VO(2max) at an ambient temperature of 35 degrees C. Subjects ingested either a 6.4% maltodextrin solution (CHO) or an artificially flavoured and coloured placebo (PLA). Time to fatigue was significantly greater with CHO in both the 60% and 73% VO(2max) trials (14.5% and 13.5% improvement, respectively). Heart rate and oxygen uptake ( VO(2)) did not differ at any point between PLA and CHO. Hypoglycaemia was not seen in any condition but plasma glucose concentrations tended to be higher at both intensities when CHO was fed. CHO oxidation rates were similar at 60% VO(2max) between CHO and PLA. There were no differences between PLA and CHO in the rate of rise of rectal temperatures ( T(rec)) at either intensity but there was a trend for subjects to fatigue at a high temperature when taking CHO. Ratings of perceived exertion (RPE) tended to be lower throughout both CHO trials; this was significant at 80 min and at fatigue at 60% VO(2max). It is concluded that supplementation with CHO improves exercise performance in the heat at both moderate and high endurance intensities. In the absence of a clear metabolic explanation, a central effect involving an increased tolerance of rising deep body temperature merits further investigation.     

No effect of carbohydrate feeding on 16 km cycling time trial performance

The aim of this study is to investigate the effects of CHO ingestion during high intensity exercise performance lasting approximately 25 min. Twelve endurance trained male cyclists (age 19-41 years; body mass 73.2 +/- 4.2 kg; VO(2)max 66.4 +/- 6.2 ml kg(-1) min(-1)) completed a simulated 16 km time trial (457 +/- 37 kJ) time trial in the lab on three occasions. Once they received a 6% carbohydrate electrolyte solution (CHO) and twice they received the same electrolyte containing placebo drink (PLA). Carbohydrate or placebo drinks were ingested 5 min before the start (4 ml kg(-1)) and at 25, 50, and 75% of completion of the time trial (1.4 ml kg(-1)). The CHO drink was a 6% sucrose-glucose-electrolyte solution. No differences were observed in the time to complete the time trials with either treatment. Time in min:s were 25:30 +/- 1:34 and 25:27 +/- 1:46 for the two placebo trials and 25:38 +/- 1:59 in the CHO trial. Power output during the time trials was also remarkably similar: 300 +/- 37 W, 301 +/- 39 W and 299 +/- 40 W, respectively. Pacing strategies and heart rate were identical in all three trials. From the two placebo trials, a coefficient of variation for this performance task was calculated to be 1.1%. Data from this study provides evidence that carbohydrate ingestion during short high intensity exercise (approximately 30 min, 85-90% VO(2)max) does not improve performance. Furthermore, this study found a very low coefficient of variation (1.1%) for a simulated 16 km time trial.     

Muscle carnitine metabolism during incremental dynamic exercise in humans

The changes in muscle content of carnitine and acetylcarnitine have been studied during incremental dynamic exercise. Six subjects exercised for 10 min on an ergometer at 40 and 75% of their maximal oxygen uptake (VO2 max) and to fatigue at 100% of VO2 max (about 4 min). Muscle samples were taken from the quadriceps femoris muscle at rest and after exercise. Muscle content of free carnitine was (means +/- SE) 15.9 +/- 1.7 mmol kg-1 d.wt (dry weight) at rest and remained unchanged after exercise at low intensity but decreased to 5.9 +/- 0.6 and 4.6 +/- 0.5 mmol kg-1 d.wt after exercise at 75 and 100% of VO2 max respectively. Acetylcarnine content at rest was 6.9 +/- 1.9 mmol kg-1 d.wt and increased during exercise in correspondence with the decrease in free carnitine. Muscle content of pyruvate and lactate was unchanged after exercise at 40% of VO2 max but increased at the higher intensities. The parallel increases in acetylcarnitine, pyruvate and lactate indicate that formation of acetylcarnitine is augmented when the availability of glycolytic three-carbon metabolites is high and is consistent with the idea that acetylcarnitine provides a sink for pyruvate and acetyl CoA. This could be of importance for the maintenance of an adequate level of CoA and thus function of the tricarboxylic acid cycle.     

The effect of treadmill incline on maximal oxygen uptake,gas exchange and the metabolic response to exercise in the horse

In healthy man, conditions that change muscle O2 delivery affect the achievable maximum rate of O2 uptake as well as the metabolic (e.g. lactate threshold, LT) and gas exchange (e.g. gas exchange threshold, Tge) responses to incremental exercise. Inclined (I) compared to level (L) running increases locomotory muscle EMG at a given speed in the horse, indicative of elevated metabolic demand. To our knowledge, the effect of treadmill incline on VO2,max, LT and Tge has not been addressed in the exercising quadruped. We used blood sampling and breath-by-breath expired gas analysis to test the hypothesis that I (10% gradient) would increase VO2,max and the rate of O2 uptake (VO2) at LT and Tge in six Thoroughbred horses during incremental running to volitional fatigue. VO2,max was significantly higher for I (I, 77.8 +/- 4.1; L, 65.5 +/- 5.3 1 min(-1); P < 0.05), but peak plasma lactate concentration was not (I, 28.0 +/- 3.7; L, 25.9 +/- 3.0 mM). Arterial Pco2 increased to 62.1 +/- 3.3 and 57.9 +/- 2.7 Torr (I vs. L; P < 0.05), yet despite this relative hypoventilation, a distinct Tge was present. This Tge occurred at a significantly different absolute (I, 49.6 +/- 3.2; L, 42.4 +/- 3.21 min(-1); P < 0.05), but nearly identical relative VO2 (I, 63.6 +/- 1.2; L, 63.9 +/- 1.6% VO2max) in I and L. Similarly, LT occurred at a significantly greater absolute VO2 (I, 37.3 +/- 2.8; L, 26.9 +/- 2.1 1 min(-1)), but a relative VO2 that was not different (I, 47.9 +/- 2.1; L, 43.9 +/- 4.5% VO2,max). In addition, Tge occurred at a significantly higher (P < or = 0.05) absolute and relative VO2 than LT for both I and L tests. In conclusion, VO2,max is higher during inclined than level running and both LT and Tge in the horse occur at a similar percentage of VO2,max irrespective of the absolute level of VO2,max. In contrast to humans, LT is a poor analogue of Tge in the horse.     

Effects of bicarbonate ingestion on the respiratory compensation threshold and maximal exercise performance

Six males performed cycle ergometer exercise on two occasions in random order. Each exercise was preceded by a 2-h period in which matched capsules were administered orally, containing either starch (C) or NaHCO3 (E) in a dose of a 0.2 g.kg-1 body wt; pre-exercise blood pH and [HCO3-] were 7.34 +/- 0.01 and 23.7 +/- 0.5 mM (mean +/- S.E.) for the C study, and 7.41 +/- 0.01 and 28.6 +/- 1.3 mM for the E study (p less than 0.001 and p less than 0.01, respectively). Exercise was continuous and maintained for 10 min at 40% of maximal oxygen uptake (40% VO2max), followed by 15 min at 12 W above the respiratory compensation threshold ([+RCT]) which was determined by the increase of the ventilatory equivalent for carbon dioxide (VE.VCO2(-1)), and for as long as possible at 95% VO2max. Endurance time at 95% VO2max was significantly longer in E than in C (2.98 +/- 0.64 min vs. 2.00 +/- 0.44 min, p less than 0.05). The rate of increase in arterialized venous lactate (LA) was higher in E than in C from rest to exercise at [+RCT], while there was no significant difference in the hydrogen ions ([H+]). Consequently, [H+].LA-1 (nM.mM-1) was significantly lower in E than in C. The change of VE.VCO2(-1) was shifted downward in E compared to C during exercise with the lowest value being observed at the same exercise stage. These results suggest that the respiratory responses to exercise are not affected by the higher level of [HCO3-] induced by NaHCO3 ingestion, and appear to reflect the net change of plasma [HCO3-] or [H+]. Also, induced metabolic acidosis has little effect on [H+] appearance in blood.     

Oxygen deficit is not affected by the rate of transition from rest to submaximal exercise

Five subjects cycled on an ergometer at power outputs corresponding to 20, 40, 60 and 80% of their maximal oxygen uptake (VO2 max). On one occasion the transition from rest to work was direct (D), while on the other occasion the power output was increased slowly (S) in a stepwise manner for 6-15 min prior to exercise at the predetermined intensity. Oxygen uptake (VO2) was measured, and O2 deficit and O2 debt were calculated. Oxygen deficit increased with the exercise intensities, the peak values being 2.1 +/- 0.2 and 1.9 +/- 0.1 litres (mean +/- SEM) at 80% of VO2 max after D and S respectively. No significant difference was observed in O2 deficit or O2 debt between D and S at any exercise intensity (P less than 0.05). The O2 debt was similar to the O2 deficit at 20, 40 and 60% of VO2 max but lower than the O2 deficit (P less than 0.05) at 80% of VO2 max. Femoral venous blood lactate remained unchanged at 20% of VO2 max but increased at the higher exercise intensities, reaching peak values of 7.6 +/- 0.6 and 7.4 +/- 1.1 mmol l-1 at 80% of VO2 max after D and S respectively. Blood lactate was not significantly different between D and S at any exercise intensity (P greater than 0.05). It is concluded that O2 deficit, O2 debt and blood lactate are not affected by the rate of transition from rest to submaximal exercise. The data contradict the hypothesis that O2 deficit is caused by an inadequate O2 transport at the onset of exercise.     

Cardiac output decline in prolonged dynamic exercise is affected by the exercise mode

The aim of this study was to compare the cardiovascular responses to prolonged submaximal cycling and running. Eleven males [maximal oxygen uptake (VO(2max)): 3.58+/-0.15 l min(-1) for running and 3.84+/-0.16 l min(-1) for cycling; mean+/-SE] either cycled (C) or ran (R) for 90 min at 60% of mode-specific VO(2max), on two randomly assigned occasions. Cardiac output declined after 85 min of exercise in C (-1.9+/-0.5 l min(-1), P<0.01) but not in R, as a result of a more pronounced decrease in stroke volume in the former exercise mode (-22.7+/-3.8 ml beat(-1) vs -14.3+/-1.9 ml beat(-1), P<0.01) since heart rate did not differ between trials. Stroke volume responses were despite a higher level of dehydration (-3.3+/-0.2% in R vs -2.8+/-0.2% in C, P<0.05) and hyperthermia in R (39.6+/-0.1 vs 38.8+/-0.1 degrees C in C at 90 min, P<0.01). Finally, mean skin blood flow was lower in R than C (72+/-8 vs 89+/-10%; P<0.05). In conclusion, stroke volume and cardiac output decline was more pronounced in cycling than in running despite lower dehydration and rectal temperature in the former exercise mode.     

Independence of exercise-induced diaphragmatic fatigue from ventilatory demands

Exercise-induced diaphragmatic fatigue (DF) manifests after - rather than during - exercise. This suggests that DF reflects post-exercise diaphragm-shielding. This study tested the physiological hypothesis that diaphragmatic force-generation undergoes similar regulations during either whole-body-exercise or controlled hyperventilation, but differs during recovery. Ten trained subjects (VO2(max) 60.3+/-6.4 ml/kg/min) performed: I, cycling exercise (maximal workload: 85% VO2(max)); II, controlled hyperventilation (exercise breathing pattern) followed by recovery. Ergospirometric data and twitch transdiaphragmatic pressure (TwPdi) were consecutively assessed. DF occurred following exercise, while hyperventilation enhanced diaphragmatic force-generation (TwPdi-rest 2.28+/-0.58 vs. 2.52+/-0.54, TwPdi-end-recovery: 1.94+/-0.32 kPa vs. 2.81+/-0.49 kPa, both p<0.05). TwPdi was comparable between the two protocols until recovery (p>0.05, RM-ANOVA) whereby it underwent a progressive increase. In conclusion, TwPdi progressively increases and is subject to similar regulations during exercise versus controlled hyperventilation, but differs markedly during recovery. Here, DF occurred after exercise while TwPdi increased subsequent to hyperventilation. Therefore, ventilatory demands regulate diaphragmatic force-generation during exercise, whereas DF must be attributed to non-ventilatory controlled feedback mechanisms.     

Beta-endorphin and adrenocorticotropin response to supramaximal treadmill exercise in trained and untrained males

The response of plasma beta-endorphin (beta-EP) and adrenocorticotropin (ACTH) was studied in seven well-trained (T) young endurance athletes and seven untrained (UT) age- and weight-matched males during treadmill exercise. Subjects ran continuously for 7 min at 60% VO2max, 3 min at 100% VO2max and 2 min at 110% VO2max. Arterialized blood was obtained periodically from a cannulated heated (41 degrees C) hand vein. Plasma beta-EP was measured by radio-immunoassay (RIA) which incorporated an antibody that did not cross-react (less than 1.5%) with beta-lipotropin. Plasma beta-EP was similar between groups at rest (T = 4.3 +/- 0.8 fmol ml-1, mean +/- SE, UT = 3.3 +/- 0.6 fmol ml-1) and did not change at the 60% VO2max stage. Beta-endorphin significantly increased at 100% VO2max with both groups responding similarly. A further increase occurred at 110% VO2max (T = 10.8 + 2.0 and UT = 6.6 + 1.0 fmol ml-1, P less than 0.05 for between group differences). This between group difference persisted 1 min after exercise when the highest beta-EP levels were reached (T = 18.7 +/- 4.7 and UT = 12.8 +/- 3.1 fmol ml-1, P less than 0.05). Plasma ACTH responses were similar to beta-EP with the highest values (T = 61.5 +/- 7.2, UT = 45.7 +/- 6.8 fmol ml-1, P less than 0.05 for between group differences) occurring at 1 min post-exercise. A positive correlation, r = 0.85, P less than 0.05, was found between beta-EP and ACTH using the 1 min post-exercise values. The enhanced response of beta-EP and ACTH in T may indicate a training-induced adaptation which increases the response capacity to extreme levels of stress.     

Oxygen kinetics and debt during recovery from expiratory flow-limited exercise in healthy humans

In healthy subjects expiratory flow limitation (EFL) during exercise can lower O(2) delivery to the working muscles. We hypothesized that if this affects exercise performance it should influence O(2) kinetics at the end of exercise when the O(2) debt is repaid. We performed an incremental exercise test on six healthy males with a Starling resistor in the expiratory line limiting expiratory flow to approximately 1 l s(-1) to determine maximal EFL exercise workload (W (max)). In two more square-wave exercise runs subjects exercised with and without EFL at W (max) for 6 min, while measuring arterial O(2) saturation (% SaO(2)), end-tidal pressure of CO(2) (P (ET)CO(2)) and breath-by-breath O(2) consumption VO2 taking into account changes in O(2) stored in the lungs. Over the last minute of EFL exercise, mean P (ET)CO(2) (54.7 +/- 9.9 mmHg) was significantly higher (P < 0.05) compared to control (41.4 +/- 3.9 mmHg). At the end of EFL exercise %SaO(2) fell significantly by 4 +/- 3%. When exercise stopped, EFL was removed, and we continued to measure VO2. During recovery, there was an immediate step increase in [Formula: see text] so that repayment of EFL O(2) debt started at a higher VO2 than control. Recovery VO2 kinetics after EFL exercise was best characterized by a double-exponential function with fundamental and slow time constants of 27 +/- 11 and 1,020 +/- 305 s, compared to control values of 41 +/- 10 and 1,358 +/- 320 s, respectively. EFL O(2) debt was 52 +/- 22% greater than control (2.19 +/- 0.58 vs. 1.49 +/- 0.38 l). We conclude that EFL exercise increases the O(2) debt and leads to hypoxemia in part due to hypercapnia.     

Determinants of repeated-sprint ability in females matched for single-sprint performance

This study investigated the relationship between VO2max and repeated-sprint ability (RSA), while controlling for the effects of initial sprint performance on sprint decrement. This was achieved via two methods: (1) matching females of low and moderate aerobic fitness (VO2max: 36.4 +/- 4.7 vs 49.6 +/- 5.5 ml kg(-1) min(-1) ; p < 0.05) for initial sprint performance and then comparing RSA, and (2) semi-partial correlations to adjust for the influence of initial sprint performance on RSA. Tests consisted of a RSA cycle test (5 x 6-s max sprints every 30 s) and a VO2max test. Muscle biopsies were taken before and after the RSA test. There was no significant difference between groups for work (W1, 3.44 +/- 0.57 vs 3.58 +/- 0.49 kJ; p = 0.59) or power (P1, 788.1 +/- 99.2 vs 835.2 +/- 127.2 W; p = 0.66) on the first sprint, or for total work (W(tot), 15.2 +/- 2.2 vs 16.6 +/- 2.2 kJ; p = 0.25). However, the moderate VO2max group recorded a smaller work decrement across the five sprints (W(dec), 11.1 +/- 2.5 vs 7.6 +/- 3.4%; p = 0.045). There were no significant differences between the two groups for muscle buffer capacity, muscle lactate or pH at any time point. When a semi-partial correlation was performed, to control for the contribution of W1 to W(dec), the correlation between VO2max and W(dec) increased from r = -0.41 (p > 0.05) to r = -0.50 (p < 0.05). These results indicate that VO2max does contribute to performance during repeated-sprint efforts. However, the small variance in W(dec) explained by VO2max suggests that other factors also play a role.     

Diet induced changes in sympatho-adrenal activity during submaximal exercise in relation to substrate utilization in man

In order to study how the diet may influence sympatho-adrenal activity during exercise, 7 subjects were examined at rest and during submaximal exercise (25 min at 65% of VO2 max) on two occasions. The first occasion was preceded by 5 days on a carbohydrate poor diet (5% carbohydrate, 72% fat and 23% protein) and the second one by 5 days on a carbohydrate rich diet (78% carbohydrate, 8% fat and 14% protein) with the same energy content. Oxygen uptake, respiratory exchange ratio (R), heart rate and arterial plasma concentrations of adrenaline, noradrenaline, dopamine, insulin, glucose, lactate, free fatty acids (FFA), glycerol and beta-hydroxybutyrate were measured at rest and during exercise. Oxygen uptake and heart rate during exercise were higher and R was lower after the carbohydrate poor than after the carbohydrate rich diet. During exercise the arterial plasma concentrations of FFA, glycerol and beta-hydroxybutyrate were higher after the carbohydrate poor than after the carbohydrate rich diet whereas concentrations of insulin and lactate were lower. At rest arterial plasma noradrenaline and adrenaline levels were similar on the two diets (0.70 +/- 0.31 nM noradrenaline and 0.35 +/- 0.32 nM adrenaline one the carbohydrate rich diet, mean values +/- SD). Exercise induced increases in noradrenaline were more pronounced after the carbohydrate poor than after the carbohydrate rich diet (12.42 +/- 3.41 vs. 7.45 +/- 2.68 at 25 min of exercise, p less than 0.001). A similar, although more variable accentuation of exercise induced increases in adrenaline was found. It is concluded that, when compared to a carbohydrate rich diet, a carbohydrate poor diet increases the relative contribution of fat to oxidative metabolism and increases the sympatho-adrenal response to exercise. Stimulation of lipolysis by sympatho-adrenal mechanisms might be of importance for the substrate availability when carbohydrate intake in low.     

Glycogen breakdown in different human muscle fibre types during exhaustive exercise of short duration.

The rates of glycogen breakdown during exhaustive intense exercise of three different intensities were determined in type I and subgroups of type II fibres. The exercise intensity corresponded to 122 +/- 2, 150 +/- 7 and 194 +/- 7% of VO2max. Muscle biopsies were taken from both legs before and immediately after exhaustion. Muscle lactate concentration increased by 27 +/- 1, 27 +/- 1 and 20 +/- 2 mmol kg-1 wet wt during the exercise at 122, 150 and 194% VO2max, respectively. The rates of glycogen depletion increased in all fibre types with increasing intensity, and the decline in type I fibres was 30-35% less than in type II fibres at all intensities. No differences were observed between the glycogen depletion rates in subgroups of type II fibres (IIA, IIAB and IIB). During the exercise at 194% VO2max, the rates of glycogen breakdown were 0.35 +/- 0.03 and 0.52 +/- 0.05 mmol s-1 kg-1 wet wt in type I and type II fibres, respectively. For both fibre types, the rates were 32 and 69% lower during the exercise at 150 and 122% VO2max. These data indicate that the glycolytic capacity of type I fibres is 30-35% lower than the capacity of type II fibres, in good agreement with the differences in phosphorylase and phosphofructokinase activities (Essén et al. 1975, Harris et al. 1976). The data also indicate that both fibre types contribute significantly to the anaerobic energy release at powers up till almost 200% VO2max.     

New physiological insights into exercise-induced diaphragmatic fatigue

Data on the dynamic process and time-point of manifestation of exercise-induced diaphragmatic fatigue (DF) are lacking. Therefore, this study was aimed assessing dynamic changes of diaphragmatic strength during exercise and determining the time-point of DF manifestation. Fourteen trained subjects (maximal oxygen uptake (VO2(max)) 59.3+/-5.5 ml/min/kg) performed standardized exercise protocols (maximal workload: 85% VO2(max)) followed by recovery (6 min). Ergospirometric data and twitch transdiaphragmatic pressure (TwPdi) were consecutively assessed. DF was induced (TwPdi-rest: 2.34+/-0.26 versus TwPdi-end-recovery 2.01+/-0.21 kPa, p<0.01). TwPdi progressively increased during exercise (TwPdi-rest: 2.34+/-0.26 versus TwPdi-maximal-workload: 3.28+/-0.38 kPa, p<0.001). DF was detectable immediately after exercise-termination (TwPdi-maximal-workload: 3.28+/-0.38 versus TwPdi-early-recovery 2.55+/-0.34 kPa, p<0.001). TwPdi during exercise was highly correlated to workload, VO2(max) and dyspnea (r=0.96/r=0.92/r=0.97; all p<0.0001). In conclusion, diaphragmatic strength progressively increases with increasing workload, and DF manifests after - rather than during - exercise. In addition, TwPdi is highly correlated to key-measures of ergospirometry, approving the physiological thesis that muscle strength is progressively enhanced and escapes fatiguing failure during high-intensity exercise performance.     

Effect of 4 weeks of training on the limit time at VO2 max]

The purpose of this study was to examine the effect of 4 weeks training in running on the time spent at VO2max (tlim VO2max). Eight athletes carried out, before and after an aerobic training, an incremental and five exhaustive tests at 90, 95, 100, 115% vVO2max and at the critical power at VO2max (CV'; slope of the linear relation between the tlim VO2max and the distance limit at VO2max). This training did not significantly improve VO2max (p = 0.17) or tlim VO2max (p = 0.72). However, the "tlim VO2max-intensity" curve was shifted toward the right, meaning that the athlete had to run at a higher intensity after training to obtain the same tlim VO2max. Tlim VO2max at CV' before training was significantly higher than tlim VO2max at 90, 95, 100, and 115% vVO2max (p < 0.05). This training increased CV' in absolute value (13.9 +/- 1.3 vs. 14.9 +/- 1.2 km.h-1, p < 0.05; n = 6) but not in relative value (86 +/- 4 vs. 86 +/- 5% vVO2max; p = 0.9). In conclusion, in spite of the shift of the "tlim VO2max-intensity" curve, tlim VO2max was not significantly increased by this training. Furthermore, CV' allowed subjects to spend the longest time of exercise at VO2max during a continuous exercise with constant speed, but CV', expressed in % vVO2max, did not improve with this training.     

Carbohydrate ingestion prior to exercise augments the exercise-induced activation of the pyruvate dehydrogenase complex in human skeletal muscle

This study examined the effect of pre-exercise carbohydrate (CHO) ingestion on pyruvate dehydrogenase complex (PDC) activation, acetyl group availability and substrate level phosphorylation (glycogenolysis and phosphocreatine (PCr) hydrolysis) in human skeletal muscle during the transition from rest to steady-state exercise. Seven male subjects performed two 10 min treadmill runs at 70 % maximum oxygen uptake (VO2,max), 1 week apart. Each subject ingested 8 ml (kg body mass (BM))-1 of either a placebo solution (CON trial) or a 5.5 % CHO solution (CHO trial) 10 min before each run. Muscle biopsy samples were obtained from the vastus lateralis at rest and immediately after each trial. Muscle PDC activity was higher at the end of exercise in the CHO trial compared with the CON trial (1.78+/-0.18 and 1.27+/-0.16 mmol min(-1) (kg wet matter (WM))(-1), respectively; P 0.05) and this was accompanied by lower acetylcarnitine (7.1+/-1.2 and 9.1+/-1.1 mmol kg(-1) (dry matter (DM))(-1) in CHO and CON, respectively; P<0.05) and citrate concentrations (0.73+/-0.05 and 0.91+/-0.10 mmol (kg DM)(-1) in CHO and CON, respectively; P<0.05). No difference was observed between trials in the rates of muscle glycogen and PCr breakdown and lactate accumulation. This is the first study to demonstrate that CHO ingestion prior to exercise augments the exercise-induced activation of muscle PDC and reduces acetylcarnitine accumulation during the transition from rest to steady-state exercise. However, those changes did not affect the contribution of substrate level phosphorylation to ATP resynthesis.     

Respiratory factors do not limit maximal symptom-limited exercise in patients with mild cystic fibrosis lung disease

To evaluate whether respiratory factors limit exercise capacity in patients with mild cystic fibrosis (CF) lung disease (mean FEV(1) = 76 +/- 7.7% predicted) we stressed the respiratory system of seven patients using added dead space (V(D)). Primary outcomes were exercise duration (Ex(dur)) and maximal oxygen uptake (VO(2max)). Dyspnoea/leg-discomfort were assessed at end-exercise. Ex(dur) was identical between control and V(D) studies (520 +/- 152 versus 511 +/ -166 s, p = NS) as was VO(2max)(1.6 +/- 0.5 versus 1.6 +/- 0.6 L/min, p = NS). Significant resting, sub-maximal and maximal workload increases in minute ventilation (V(E)) were detected (70.8 +/- 13.7 versus 79.5 +/- 16.9 L/min, p < 0.05). Analysis of breathing pattern revealed increases in V(E) were attributable to increases in tidal volume (2.0 +/- 0.5 versus 2.2 +/- 0.6 L, p < 0.05) with no change in respiratory frequency. There was no difference in dyspnoea/leg discomfort between tests. The increase in V(E) in response to V(D), with no change in [Exdur/VO(2max) suggests maximal symptom-limited exercise limitation is not primarily limited by respiratory factors in mild CF lung disease. Focused investigation and treatment of non-respiratory factors contributing to exercise limitation may improve exercise rehabilitation in this patient group.     

Brain activity and fatigue during prolonged exercise in the heat

We hypothesized that fatigue due to hyperthermia during prolonged exercise in the heat is in part related to alterations in frontal cortical brain activity. The electroencephalographic activity (EEG) of the frontal cortex of the brain was measured in seven cyclists [maximal O2 uptake (VO2max) 4.8 +/- 0.1 (SE) 1 min-1] cycling at 60% VO2max in a hot (H, 42 degrees C) and a cool (C, 19 degrees C) environment. Fast Fourier transformation of the EEG was used to obtain power spectrum areas in the alpha (8-13 Hz) and beta (13-30 Hz) frequencies. The ratio alpha/beta was calculated as an index of arousal level; an elevated alpha/beta index reflects suppressed arousal. In H, subjects fatigued after 34.4 +/- 1.4 min coinciding with an oesophageal temperature (Toes) of 39.8 +/- 0.1 degrees C, an almost maximal heart rate (HR 192 +/- 3 beats.min-1), a rating of perceived exertion (RPE) of 19.0 +/- 0.8 and significantly elevated alpha/beta index (188 +/- 71% of the value after 2 min of exercise; P < 0.05). In C, subjects cycled for a similar period while Toes was below 38 degrees C, HR and RPE were low, and the alpha/beta index was not significantly elevated (59 +/- 27% of 2 min value; P = NS). Increases in the alpha/beta index were strongly correlated to increases in Toes (r2 = 0.98; P = 0.0001).     

Formation of inosine monophosphate (IMP) in human skeletal muscle during incremental dynamic exercise

The influence of exercise intensity on the accumulation of inosine monophosphate (IMP) in human skeletal muscle has been investigated. Ten men cycled at workloads corresponding to 40%, 75% and 100% of their maximal oxygen uptake (VO2 max). Muscle IMP was below the detection limit (less than 0.01 mmol kg-1 dry wt) at rest and after exercise at 40% of VO2 max, but increased to 0.26 +/- 0.06 (mean +/- SEM) and 3.50 +/- 0.51 mmol kg-1 dry wt after exercise at 75% and 100% of VO2 max respectively. Accumulation of IMP corresponded to a similar decrease in the total adenine nucleotide content. The muscle content of IMP was positively related to lactate and negatively related to phosphocreatine (PCr). IMP was formed in both fibre types, but the IMP content at fatigue was about twice as high in type II fibres as in type I fibres. It was concluded that the IMP content of human skeletal muscle is very low at rest and after low-intensity exercise, but increases after moderate and high-intensity exercise. In contrast to rat muscle, where deamination of AMP predominantly occurs in the fast-twitch muscle fibres, IMP is formed during exercise in both fibre types in human muscle. Accumulation of IMP appears to reflect an imbalance between the rate of utilization and the rate of regeneration of ATP.     

Physiological responses to cycling for 60 minutes at maximal lactate steady state.

Changes in physiological variables during a 60-min continuous test at maximal lactate steady state (MLSS) were studied using highly conditioned cyclists (1 female and 9 males, aged 28.3 +/- 8.1 years). To determine power at MLSS, we tested at 8-min increments and interpolated the power corresponding to a blood lactate value of 4 mmol/L. During the subsequent 60-min exercise at MLSS, we observed a sequential increase of physiological parameters, in contrast to stable blood lactate. Heart rate drifted upward from beginning to end of exercise. This became statistically significant after 30 min. From 10-60 min of exercise, a change of +12.6 +/- 3.2 bpm was noted. Significant drift was seen after 30 min for the respiratory exchange ratio, after 40 min for the rate of perceived exertion using the Borg scale, and after 50 min for % VO(2)max/kg and minute ventilation. This slow component of VO(2)max may be the result of higher recruitment of type II fibers.