Ratings of perceived exertion in individuals with varying fitness levels during walking and running

It was the purpose of this investigation to: 1) compare the ratings of perceived exertion (RPEs) in high and low fit individuals when walking and running at comparable exercise intensities and 2) to determine if ventilation (VE) provides a central signal for RPEs. Nine high fit and nine low fit male subjects completed two exercise bouts on a treadmill, one uphill walking and the other level running. Workloads for each bout were set at 90% of each subject's ventilatory threshold (VT) as determined from a graded exercise test. Oxygen consumption (Vo2), heart rate (HR), and VE were all similar between the walk and run trials for the low fit subjects (P greater than 0.05). HR were found to be significantly greater during the walk trial vs. the run trial (P less than 0.05) for the high fit subjects, whereas, VE was significantly greater during the run trial. Oxygen consumption was similar for the high fit subjects during both trials (P greater than 0.05). During the walk and run trials, central (12.1 +/- 1.6 vs. 11.4 +/- 1.5), local (14.0 +/- 1.3 vs. 13.9 +/- 1.1) and overall (12.8 +/- 1.2 vs. 12.4 +/- 1.4) RPEs were not found to be significantly different for the low fit group (P greater than 0.05). In contrast, during the walk vs. the run trial there was a significant increase in central (10.7 +/- 2.0 vs. 9.2 +/- 1.9), local (11.5 +/- 2.0 vs. 9.8 +/- 1.8) and overall (11.2 +/- 2.4 vs. 9.6 +/- 2.3) RPEs for the high fit group (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in lung volume and breathing pattern during exercise and CO2 inhalation in humans

Lung volume changes during CO2 inhalation and exercise were compared in seven human subjects. Expiratory reserve volume (ERV) normalized by vital capacity (VC) was used as an index of end-expiratory lung volume (EELV). Work loads tried were 30, 60, and 90 W and inspired CO2 concentrations were 3.5 and 5.0%. Exercise at 30 W led to a significant decrease in EELV, by 7% VC (P less than 0.005), with no further change at higher levels of exercise (P greater than 0.1). Both 3.5 and 5.0% CO2 inhalation resulted in an increase in EELV that was not statistically significant (3% VC, P greater than 0.1). A possible linkage of this different EELV behavior to breathing pattern was tested. The tidal volume-inspiratory duration curve shifted to a higher volume region during exercise compared with CO2 inhalation. Consequently, the volume-time threshold characteristic was better described by an end-inspiratory lung volume-inspiratory duration plot, resulting in a common relationship under these two different stimuli. These results suggest that the depth and rate of breathing in humans can be affected by not only phasic but also tonic components. A decrease in functional residual capacity or EELV was peculiar to exercise and should be associated with increased mechanical efficiency compared with CO2 inhalation. Theoretical predictions based on work of breathing optimization via a decreased EELV seemed to be capable of explaining isocapnic exercise hyperpnea in conjunction with proportional control of arterial CO2 tension.     

Metabolic and performance effects of raisins versus sports gel as pre-exercise feedings in cyclists

Research suggests that pre-exercise sources of dietary carbohydrate with varying glycemic indexes may differentially affect metabolism and endurance. This study was designed to examine potential differences in metabolism and cycling performance after consumption of moderate glycemic raisins vs. a high glycemic commercial sports gel. Eight endurance-trained male (n = 4) and female (n = 4) cyclists 30 +/- 5 years of age completed 2 trials in random order. Subjects were fed 1 g carbohydrate per kilogram body weight from either raisins or sports gel 45 minutes prior to exercise on a cycle ergometer at 70% V(.-)O2max. After 45 minutes of submaximal exercise, subjects completed a 15-minute performance trial. Blood was collected prior to the exercise bout, as well as after the 45th minute of exercise, to determine serum concentrations of glucose, insulin, lactate, free fatty acids (FFAs), triglycerides, and beta-hydroxybutyrate. Performance was not different (p > 0.05) between the raisin (189.5 +/- 69.9 kJ) and gel (188.0 +/- 64.8 kJ) trials. Prior to exercise, serum concentrations of glucose and other fuel substrates did not differ between trials; however, insulin was higher (p < 0.05) for the gel (110.0 +/- 70.4 microU x ml(-1)) vs. raisin trial (61.4 +/- 37.4 microU x ml(-1)). After 45 minutes of exercise, insulin decreased to 14.2 +/- 6.2 microU x ml(-1) and 13.3 +/- 18.9 microU x ml(-1) for gel and raisin trials, respectively. The FFA concentration increased (+0.2 +/- 0.1 mmol x L(-1)) significantly (p < 0.05) during the raisin trial. Overall, minor differences in metabolism and no difference in performance were detected between the trials. Raisins appear to be a cost-effective source of carbohydrate for pre-exercise feeding in comparison to sports gel for short-term exercise bouts.     

Hypohydration impairs endurance exercise performance in temperate but not cold air.

This study compared the effects of hypohydration (HYP) on endurance exercise performance in temperate and cold air environments. On four occasions, six men and two women (age = 24 +/- 6 yr, height = 170 +/- 6 cm, weight = 72.9 +/- 11.1 kg, peak O2 consumption = 48 +/- 9 ml.kg(-1).min(-1)) were exposed to 3 h of passive heat stress (45 degrees C) in the early morning with [euhydration (EUH)] or without (HYP; 3% body mass) fluid replacement. Later in the day, subjects sat in a cold (2 degrees C) or temperate (20 degrees C) environment with minimal clothing for 1 h before performing 30 min of cycle ergometry at 50% peak O2 consumption followed immediately by a 30-min performance time trial. Rectal and mean skin temperatures, heart rate, and ratings of perceived exertion measurements were made at regular intervals. Performance was assessed by the total amount of work (kJ) completed in the 30-min time trial. Skin temperature was significantly lower in the cold compared with the temperate trial, but there was no independent effect of hydration. Rectal temperature in both HYP trials was higher than EUH after 60 min of exercise, but the difference was only significant within the temperate trials (P < 0.05). Heart rate was significantly higher at 30 min within the temperate trial (HYP > EUH) and at 60 min within the cold trial (HYP > EUH) (P < 0.05). Ratings of perceived exertion increased over time with no differences among trials. Total work performed during the 30-min time trial was not influenced by environment but was less (P < 0.05) for HYP than EUH in the temperate trials. The corresponding change in performance (EUH-HYP) was greater for temperate (-8%) than for cold (-3%) (P < 0.05). These data demonstrate that 1) HYP impairs endurance exercise performance in temperate but not cold air but 2) cold stress per se does not.     

Effects of low and moderate exercise intensity on postprandial lipemia and postheparin plasma lipoprotein lipase activity in physically active men.

This study was designed to assess differences in the intensity of exercise to attenuate postprandial lipemia (PPL). Thirteen healthy men (age 23.8 +/- 0.9 yr) participated in three random-ordered trials: in low-(25% peak oxygen consumption; Low) and moderate-intensity (65% peak oxygen consumption; Mod) exercise trials, which were completed 1 h before a high-fat meal (1.3 g fat/kg body mass), and a control (Con), fat meal only, trial. Venous blood samples were obtained before the fat meal, and at 2, 4, 6, 8, and 20 h after the fat meal. PPL in the Mod trial (267 +/- 50 mg.dl-1.8 h) was lower compared with that in either Con (439 +/- 81 mg.dl-1.8 h) or Low (403 +/- 91 mg.dl-1.8 h) trials (P < 0.05), whereas there was no difference in PPL between Con and Low trials (P > 0.05). High-density lipoprotein cholesterol (HDL-C) and HDL subtype 2 cholesterol were not different between or within trials (P > 0.05). Postprandial insulinemia was lower in the Mod trial (20.5 +/- 5.7 microIU.ml-1.8 h; P < 0.05), but not in the Low trial (31.4 +/- 4.7 microIU.ml-1.8 h), compared with that in the Con trial (34.9 +/- 5.0 microIU.ml-1.8 h). Postheparin lipoprotein lipase activity at 8 h was higher in the Low trial compared with that in either Con or Mod trials, whereas there were no differences between trials at 20 h. These results suggest that, when exercise is performed 1 h before a fat meal, only exercise of moderate but not of low intensity attenuates PPL and that this effect is not associated with changes in postheparin lipoprotein lipase activity.     

Effects of pre-exercise carbohydrate feedings on muscle glycogen use during exercise in well-trained runners

The purpose of this study was to examine the effects of pre-exercise glucose and fructose feedings on muscle glycogen utilization during exercise in six well-trained runners (VO2max = 68.2 +/- 3.4 ml X kg-1 X min-1). On three separate occasions, the runners performed a 30 min treadmill run at 70% VO2max. Thirty minutes prior to exercise each runner ingested 75 g of glucose (trial G), 75 g of fructose (trial F) or 150 ml of a sweetened placebo (trial C). During exercise, no differences were observed between any of the trials for oxygen uptake, heart rate or perceived exertion. Serum glucose levels were elevated as a result of the glucose feeding (P less than 0.05) reaching peak levels at 30 min post-feeding (7.90 +/- 0.24 mmol X l-1). With the onset of exercise, glucose levels dropped to a low of 5.89 +/- 0.85 mmol X l-1 at 15 min of exercise in trial G. Serum glucose levels in trials F and C averaged 6.21 +/- 0.31 mmol X l-1 and 5.95 +/- 0.23 mmol X l-1 respectively, and were not significantly different (P less than 0.05). There were also no differences in serum glucose levels between any of the trials at 15 and 30 min of exercise.     

Ventilatory response to exercise in aged runners breathing He-O2 or inspired CO2.

The ventilatory response to exercise below ventilatory threshold (VTh) increases with aging, whereas above VTh the ventilatory response declines only slightly. We wondered whether this same ventilatory response would be observed in older runners. We also wondered whether their ventilatory response to exercise while breathing He-O(2) or inspired CO(2) would be different. To investigate, we studied 12 seniors (63 +/- 4 yr; 10 men, 2 women) who exercised regularly (5 +/- 1 days/wk, 29 +/- 11 mi/wk, 16 +/- 6 yr). Each subject performed graded cycle ergometry to exhaustion on 3 separate days, breathing either room air, 3% inspired CO(2), or a heliox mixture (79% He and 21% O(2)). The ventilatory response to exercise below VTh was 0.35 +/- 0.06 l x min(-1) x W(-1) and above VTh was 0.66 +/- 0.10 l x min(-1) x W(-1). He-O(2) breathing increased (P < 0.05) the ventilatory response to exercise both below (0.40 +/- 0.12 l x min(-1) x W(-1)) and above VTh (0.81 +/- 0.10 l x min(-1) x W(-1)). Inspired CO(2) increased (P < 0.001) the ventilatory response to exercise only below VTh (0.44 +/- 0.10 l x min(-1) x W(-1)). The ventilatory responses to exercise with room air, He-O(2), and CO(2) breathing of these fit runners were similar to those observed earlier in older sedentary individuals. These data suggest that the ventilatory response to exercise of these senior runners is adequate to support their greater exercise capacity and that exercise training does not alter the ventilatory response to exercise with He-O(2) or inspired CO(2) breathing.     

Varied and repeated atropine dosages and exercise-heat stress

Comparisons of physiological responses to 0, 0.5, 1, and 2 mg atropine (IM) were made in seven males (X +/- SD: age, 24 +/- 3 years; ht, 174 +/- 12 cm; wt, 76 +/- 3 kg) while they exercised (approximately 390 W) in a hot-dry (40 degrees C, 20% rh) environment. Responses to 4 mg, as well as repeatability of responses to 2 mg, were studied in two and six of these subjects, respectively. On 8 test days an intramuscular injection of atropine or saline control was administered 20 min before subjects walked on a treadmill for two 50-min bouts. Heart rate (HR) during exercise did not change in the control trial but by min 50 increased during all atropine trials (P less than 0.01). Rectal temperature (Tre) increased (P less than 0.01) in all trials by min 50 and continued increasing (P less than 0.01) in the 2-mg trial during the second exercise bout. For the two subjects tested with all dosages (0.5 - 4 mg atropine), the change in HR and Tre between the atropine and control trials at 50 min of exercise was regressed against the various atropine dosages. The relationship (r = 0.92) for HR was curvilinear while the relationship (r = 0.99) for Tre was linear. Mean weighted skin temperature (Tsk) was relatively constant during exercise and was warmer (P less than 0.05) with increasing atropine dosage. In a repeat 2 mg trial, HR was 6 bt . min-1 lower (P less than 0.05) on the second exposure but Tre was the same (P greater than 0.05) on both days. For subjects walking in the heat, three new observations were: 1) 0.5 mg of atropine resulted in increased HR and Tsk compared to control values; 2) HR was elevated but the magnitude of change decreased with increasing dosage, while the elevation in Tre was consistent with increasing dosage; and 3) rectal temperatures (in trials with and without atropine) were unaffected by previous days of atropine administration.     

Intramyocellular triacylglycerol in prolonged cycling with high- and low-carbohydrate availability.

Vastus lateralis intramyocellular lipid (IMCL) content was assessed by (1)H-magnetic resonance spectroscopy before and after prolonged time trial cycling bouts of approximately 3-h duration. Six highly trained male cyclists completed a double-blind, randomized, crossover design of two experimental trials after a strenuous exercise bout and 48 h of high (HC) (9.32 +/- 0.08 g. kg(-1). day(-1)) and low (LC) (0.59 +/- 0.21 g. kg(-1). day(-1)) dietary carbohydrate. Resting IMCL content was significantly higher after LC vs. HC (P < 0.01) and was reduced during exercise by 64 and 57%, respectively. IMCL was not different between conditions after exercise (P > 0.05). The approximately twofold increase in IMCL degradation in LC compared with HC suggests that higher rates of whole body lipid metabolism in LC were in part attributable to a greater IMCL utilization. Four subjects experienced reductions of IMCL in excess of 70% during exercise. To our knowledge, this is the first study to report near depletion of IMCL during prolonged cycling, indicating that IMCL, presumably the triacylglycerol component, may be exhausted by prolonged strenuous exercise.     

Effects of creatine supplementation on the energy cost of muscle contraction: a 31P-MRS study.

Five women and 3 men (29.8 +/- 1.4 yr) performed dynamic knee-extension exercise inside a magnetic resonance system (means +/- SE). Two trials were performed 7-14 days apart, consisting of a 4- to 5-min exhaustive exercise bout. To determine quadriceps cost of contraction, brief static and dynamic contractions were performed pre- and postexercise. (31)P spectra were used to determine pH and relative concentrations of P(i), phosphocreatine (PCr), and betaATP. Subjects consumed 0.3 g. kg(-1). day(-1) of a placebo (trial 1) or creatine (trial 2) for 5 days before each trial. After creatine supplementation, resting DeltaPCr increased from 40.7 +/- 1.8 to 46. 6 +/- 1.1 mmol/kg (P = 0.04) and PCr during exercise declined from -29.6 +/- 2.4 to -34.1 +/- 2.8 mmol/kg (P = 0.02). Muscle static (DeltaATP/N) and dynamic (DeltaATP/J) costs of contraction were unaffected by creatine supplementation as well as were ATP, P(i), pH, PCr resynthesis rate, and muscle strength and endurance. DeltaATP/J and DeltaATP/N were greatest at the onset of the exercise protocol (P < 0.01). In summary, creatine supplementation increased muscle PCr concentration, which did not affect muscle ATP cost of contraction.     

Hypohydration does not impair skeletal muscle glycogen resynthesis after exercise

The purpose of this investigation was to examine the effects of moderate hypohydration (HY) on skeletal muscle glycogen resynthesis after exhaustive exercise. On two occasions, eight males completed 2 h of intermittent cycle ergometer exercise (4 bouts of 17 min at 60% and 3 min at 80% of maximal O2 consumption/10 min rest) to reduce muscle glycogen concentrations (control values 711 +/- 41 mumol/g dry wt). During one trial, cycle exercise was followed by several hours of light upper body exercise in the heat without fluid replacement to induce HY (-5% body wt); in the second trial, sufficient water was ingested during the upper body exercise and heat exposure to maintain euhydration (EU). In both trials, 400 g of carbohydrate were ingested at the completion of exercise and followed by 15 h of rest while the desired hydration level was maintained. Muscle biopsy samples were obtained from the vastus lateralis immediately after intermittent cycle exercise (T1) and after 15 h of rest (T2). During the HY trial, the muscle water content was lower (P less than 0.05) at T1 and T2 (288 +/- 9 and 265 +/- 5 ml/100 g dry wt, respectively; NS) than during EU (313 +/- 8 and 301 +/- 4 ml/100 g dry wt, respectively; NS). Muscle glycogen concentration was not significantly different during EU and HY at T1 (200 +/- 35 vs. 251 +/- 50 mumol/g dry wt) or T2 (452 +/- 34 vs. 491 +/- 35 mumol/g dry wt). These data indicate that, despite reduced water content during the first 15 h after heavy exercise, skeletal muscle glycogen resynthesis is not impaired.     

A respiratory sensory reflex in response to CO2 inhibits breathing in preterm infants.

Traditionally, the increase in ventilation occurring after approximately 4 s of CO2 inhalation in preterm infants has been attributed to an action at the peripheral chemoreceptors. However, on a few occasions, we have observed a short apnea (2-3 s) in response to 3-5% CO2 in these infants. To test the hypothesis that this apnea reflects a respiratory sensory reflex to CO2, we gave nine preterm infants [birth wt 1.5 +/- 0.1 (SE) kg, gestational age 31 +/- 1 wk] 7-8% CO2 while they breathed 21% O2. To study the dose-response relationship, we also gave 2, 4, 6, and 8% CO2 to another group of seven preterm infants (birth wt 1.5 +/- 0.1 kg, gestational age 31 +/- 1 wk). In the first group of infants, minute ventilation during 21% O2 breathing (0.232 +/- 0.022 l.min-1.kg-1) decreased after CO2 administration (0.140 +/- 0.022, P < 0.01) and increased with CO2 removal (0.380 +/- 0.054, P < 0.05). This decrease in ventilation was related to an apnea (12 +/- 2.6 s) occurring 7.7 +/- 0.8 s after the beginning of CO2 inhalation. There was no significant change in tidal volume. In the second group of infants, minute ventilation increased during administration of 2, 4, and 6% CO2 but decreased during 8% CO2 because of the presence of an apnea. These findings suggest that inhalation of a high concentration of CO2 (> 6%) inhibits breathing through a respiratory sensory reflex, as described in adult cats (H. A. Boushey and P. S. Richardson. J. Physiol. Lond. 228: 181-191, 1973).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Effect of time and vascular pressure on permeability and cyclic nucleotides in ischemic lungs

We previously found that increased intravascular pressure decreased ischemic lung injury by a nitric oxide (NO)-dependent mechanism (Becker PM, Buchanan W, and Sylvester JT. J Appl Physiol 84: 803-808, 1998). To determine the role of cyclic nucleotides in this response, we measured the reflection coefficient for albumin (sigma(alb)), fluid flux (), cGMP, and cAMP in ferret lungs subjected to either 45 min ("short"; n = 7) or 180 min ("long") of ventilated ischemia. Long ischemic lungs had "low" (1-2 mmHg, n = 8) or "high" (7-8 mmHg, n = 6) vascular pressure. Other long low lungs were treated with the NO donor (Z)-1-[N-(3-ammoniopropyl)-N-(n-propyl)amino]diazen-1-ium -1, 2-diolate (PAPA-NONOate; 5 x 10(-4) M, n = 6) or 8-bromo-cGMP (5 x 10(-4) M, n = 6). Compared with short ischemia, long low ischemia decreased sigma(alb) (0.23 +/- 0.04 vs. 0.73 +/- 0.08; P < 0.05) and increased (1.93 +/- 0.26 vs. 0.58 +/- 0.22 ml. min(-1). 100 g(-1); P < 0.05). High pressure prevented these changes. Lung cGMP decreased by 66% in long compared with short ischemia. Lung cAMP did not change. PAPA-NONOate and 8-bromo-cGMP increased lung cGMP, but only 8-bromo-cGMP decreased permeability. These results suggest that ischemic vascular injury was, in part, mediated by a decrease in cGMP. Increased vascular pressure prevented injury by a cGMP-independent mechanism that could not be mimicked by administration of exogenous NO.     

Effect of carbohydrate ingestion and ambient temperature on muscle fatigue development in endurance-trained male cyclists.

The aim of the present study was to determine the effect of carbohydrate (CHO; sucrose) ingestion and environmental heat on the development of fatigue and the distribution of power output during a 16.1-km cycling time trial. Ten male cyclists (Vo(2max) = 61.7 +/- 5.0 ml.kg(-1).min(-1), mean +/- SD) performed four 90-min constant-pace cycling trials at 80% of second ventilatory threshold (220 +/- 12 W). Trials were conducted in temperate (18.1 +/- 0.4 degrees C) or hot (32.2 +/- 0.7 degrees C) conditions during which subjects ingested either CHO (0.96 g.kg(-1).h(-1)) or placebo (PLA) gels. All trials were followed by a 16.1-km time trial. Before and immediately after exercise, percent muscle activation was determined using superimposed electrical stimulation. Power output, integrated electromyography (iEMG) of vastus lateralis, rectal temperature, and skin temperature were recorded throughout the trial. Percent muscle activation significantly declined during the CHO and PLA trials in hot (6.0 and 6.9%, respectively) but not temperate conditions (1.9 and 2.2%, respectively). The decline in power output during the first 6 km was significantly greater during exercise in the heat. iEMG correlated significantly with power output during the CHO trials in hot and temperate conditions (r = 0.93 and 0.73; P < 0.05) but not during either PLA trial. In conclusion, cyclists tended to self-select an aggressive pacing strategy (initial high intensity) in the heat.     

Role of lung inflammatory mediators as a cause of exercise-induced arterial hypoxemia in young athletes.

We examined whether lung inflammatory mediators are increased during exercise and whether pharmacological blockade can prevent exercise-induced arterial hypoxemia (EIAH) in young athletes. Seventeen healthy athletes (9 men, 8 women; age 23 +/- 3 yr) with varying degrees of EIAH completed maximal incremental treadmill exercise tests after administration of fexofenadine, zileuton, and nedocromil sodium or placebo in a randomized double-blind crossover study. Lung function, arterial blood gases, and inflammatory metabolites in plasma, urine, and induced sputum were assessed. Drug administration did not improve EIAH or gas exchange during exercise. At maximal exercise, oxygen saturation fell to 91.4 +/- 2.6% (drug trial) and 91.9 +/- 2.1% (placebo trial) and alveolar-arterial oxygen difference widened to 28.1 +/- 6.3 Torr (drug trial) and 29.3 +/- 5.7 Torr (placebo trial). Oxygen consumption, ventilation, and other exercise variables were similarly unaffected by drug treatment. Although plasma histamine increased with exercise, values did not differ between trials, and urinary leukotriene E(4) and 11beta-prostaglandin F(2alpha) levels were unchanged after exercise. Postexercise sputum revealed no significant changes in markers of inflammation. These results demonstrate that EIAH in young athletes is not attenuated with acute administration of drugs targeting histamine and bioactive lipids. We conclude that airway inflammation is of insufficient magnitude to cause impairments in gas exchange and does not appear to be linked to EIAH in healthy young athletes.     

Effects of respiratory muscle work on exercise performance.

The normal respiratory muscle effort at maximal exercise requires a significant fraction of cardiac output and causes leg blood flow to fall. We questioned whether the high levels of respiratory muscle work experienced in heavy exercise would affect performance. Seven male cyclists [maximal O(2) consumption (VO(2)) 63 +/- 5 ml. kg(-1). min(-1)] each completed 11 randomized trials on a cycle ergometer at a workload requiring 90% maximal VO(2). Respiratory muscle work was either decreased (unloading), increased (loading), or unchanged (control). Time to exhaustion was increased with unloading in 76% of the trials by an average of 1.3 +/- 0.4 min or 14 +/- 5% and decreased with loading in 83% of the trials by an average of 1.0 +/- 0.6 min or 15 +/- 3% compared with control (P < 0.05). Respiratory muscle unloading during exercise reduced VO(2), caused hyperventilation, and reduced the rate of change in perceptions of respiratory and limb discomfort throughout the duration of exercise. These findings demonstrate that the work of breathing normally incurred during sustained, heavy-intensity exercise (90% VO(2)) has a significant influence on exercise performance. We speculate that this effect of the normal respiratory muscle load on performance in trained male cyclists is due to the associated reduction in leg blood flow, which enhances both the onset of leg fatigue and the intensity with which both leg and respiratory muscle efforts are perceived.     

Reversal of fatigue during prolonged exercise by carbohydrate infusion or ingestion

Seven cyclists exercised at 70% of maximal O2 uptake (VO2max) until fatigue (170 +/- 9 min) on three occasions, 1 wk apart. During these trials, plasma glucose declined from 5.0 +/- 0.1 to 3.1 +/- 0.1 mM (P less than 0.001) and respiratory exchange ratio (R) fell from 0.87 +/- 0.01 to 0.81 +/- 0.01 (P less than 0.001). After resting 20 min the subjects attempted to continue exercise either 1) after ingesting a placebo, 2) after ingesting glucose polymers (3 g/kg), or 3) when glucose was infused intravenously ("euglycemic clamp"). Placebo ingestion did not restore euglycemia or R. Plasma glucose increased (P less than 0.001) initially to approximately 5 mM and R rose (P less than 0.001) to approximately 0.83 with glucose infusion or carbohydrate ingestion. Plasma glucose and R then fell gradually to 3.9 +/- 0.3 mM and 0.81 +/- 0.01, respectively, after carbohydrate ingestion but were maintained at 5.1 +/- 0.1 mM and 0.83 +/- 0.01, respectively, by glucose infusion. Time to fatigue during this second exercise bout was significantly longer during the carbohydrate ingestion (26 +/- 4 min; P less than 0.05) or glucose infusion (43 +/- 5 min; P less than 0.01) trials compared with the placebo trial (10 +/- 1 min). Plasma insulin (approximately 10 microU/ml) and vastus lateralis muscle glycogen (approximately 40 mmol glucosyl U/kg) did not change during glucose infusion, with three-fourths of total carbohydrate oxidation during the second exercise bout accounted for by the euglycemic glucose infusion rate (1.13 +/- 0.08 g/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of reduced free fatty acid availability on skeletal muscle PDH activation during aerobic exercise. Pyruvate dehydrogenase

This study investigated the effect of reduced free fatty acid (FFA) availability on pyruvate dehydrogenase activation (PDHa) and carbohydrate metabolism during moderate aerobic exercise. Eight active male subjects cycled for 40 min at 55% Vo(2 peak) on two occasions. During one trial, subjects ingested 20 mg/kg body mass of the antilipolytic drug nicotinic acid (NA) during the hour before exercise to reduce FFA. Nothing was ingested in the control trial (CON). Blood and expired gas measurements were obtained throughout the trials, and muscle biopsy samples were obtained immediately before exercise and at 5, 20, and 40 min of exercise. Plasma FFA were lower in the NA trial (0.13 +/- 0.01 vs. 0.48 +/- 0.03 mM, P < 0.05), and the respiratory exchange ratio (RER) was increased with NA (0.93 +/- 0.01 vs. 0.89 +/- 0.01, P < 0.05), resulting in a 14.5 +/- 1.8% increase in carbohydrate oxidation compared with CON. PDHa increased rapidly in both trials at exercise onset but was approximately 15% higher (P < 0.05) throughout exercise in the NA trial (2.44 +/- 0.19 and 2.07 +/- 0.12 mmol x kg wet muscle(-1) x min(-1) for NA and CON at 40 min). Muscle glycogenolysis was 15.3 +/- 9.6% greater in the NA trial vs. the CON trial but did not reach statistical significance. Glucose 6-phosphate contents were elevated (P < 0.05) in the NA trial at 30 and 40 min of exercise, but pyruvate and lactate contents were unaffected. These data demonstrate that the reduction of exogenous FFA availability increased the activation of PDH and carbohydrate oxidation during moderate aerobic exercise in men. The increased activation of PDH was not explained by changes in muscle pyruvate or the ATP/ADP ratio but may be related to a decrease in the NADH/NAD(+) ratio or an epinephrine-induced increase in calcium concentration.     

Effect of exercise duration on postprandial hypertriglyceridemia in men with metabolic syndrome.

We examined the effect of exercise on postprandial hypertriglyceridemia (PHTG) and insulin resistance in individuals with metabolic syndrome. Subjects were 10 hypertriglyceridemic men with insulin resistance [age = 35.0 +/- 1.8 yr, body weight = 90.7 +/- 3.3 kg, fasting triglyceride (TG) = 2.6 +/- 0.4 mmol/l, peak oxygen consumption ((.)Vo(2peak)) = 36.0 +/- 1.3 ml(-1).kg(-1).min(-1), and homeostatic model assessment of insulin resistance (HOMA-IR)= 3.1 +/- 0.3]. Each participant performed a control trial (Ctr; no exercise) and three exercise trials at 60% of their (.)Vo(2peak) for 30 min (30 min-Ex), 45 min (45 min-Ex) and 60 min (60 min-Ex). All subjects had a fat meal in each trial. In the exercise trials, the subject jogged on a treadmill for a designated duration of 12 h before ingestion of a fat meal. Blood samples were taken at 0 h (before the meal) and at 2, 4, 6, and 8 h after the meal. The plasma TG, area score under TG concentration curve over an 8-h period (TG AUC) after the meal, and HOMA-IR were analyzed. The TG AUC scores in both the 45 min-Ex and 60 min-Ex were 31 and 33% lower, respectively, than Ctr (P < 0.02). There were no significant differences in TG AUC scores between the 30 min-Ex and the Ctr (P > 0.05). There were no trial differences in the fasting plasma glucose concentration (P > 0.05). HOMA-IR values in the 30 min-Ex, 45 min-Ex, and 60 min-Ex trials were lower than the Ctr (P < 0.03), but no significant differences were found in HOMA-IR among the exercise trials. The results suggest that for physically inactive individuals with metabolic syndrome, exercising at moderate intensity for 45 min effectively attenuates PHTG while exercise for 30 min is sufficient to improve insulin action.