Physiological responses of skilled players during a competitive wheelchair tennis match

The purpose of this study was to determine heart rate (HR, b.min(-1)) response during competitive match play of 6 men who were skilled wheelchair (WC) tennis players. Each participant completed an arm crank ergometer test that measured HR via a telemetry device and O2 via open circuit spirometry from rest until fatigue (.V(O2)peak). Each athlete participated in 2 competitive singles matches during which HRs were recorded in 5-second intervals and O2 was estimated using the corresponding HR values recorded during the arm ergometer tests. Data analysis revealed an average playing intensity of 69.4 +/- 8.9% of HRpeak and 49.9 +/-14.5% of .V(O2)peak. In conclusion, it is recommended that skilled adult WC tennis players perform off-court aerobic conditioning as part of their training program, because the intensity of a competitive WC tennis match is sufficiently high enough to stress the cardiovascular system.     

Relation between maximal aerobic power and the ability to repeat sprints in young basketball players

The aim of this study was to examine the effects of maximal aerobic power (V(.-)O2max peak) level on the ability to repeat sprints (calculated as performance decrement and total sprinting time) in young basketball players. Subjects were 18 junior, well-trained basketball players (age, 16.8 +/- 1.2 years; height, 181.3 +/- 5.7 cm; body mass, 73 +/- 10 kg; V(.-)O2max peak, 59.6 +/- 6.9 ml x kg(-1) x min(-1)). Match analysis and time-motion analysis of competitive basketball games was used to devise a basketball-specific repeated-sprint ability protocol consisting of ten 15-m shuttle run sprints with 30 s of passive recovery. Pre, post, and post plus 3-minute blood lactate concentrations were 2.5 +/- 0.7, 13.6 +/- 3.1, and 14.2 +/- 3.5 mmol x L(-1), respectively. The mean fatigue index (FI) value was 3.4 +/- 2.3% (range, 1.1-9.1%). No significant correlations were found between V(.-)O2max peak and either FI or total sprint time. A negative correlation (r = -0.75, p = 0.01) was found between first-sprint time and FI. The results of this study showed that V(.-)O2max peak is not a predictor of repeated-sprint ability in young basketball players. The high blood lactate concentrations found at the end of the repeated-sprint ability protocol suggest its use for building lactate tolerance in conditioned basketball players.     

Comparison of cardiorespiratory responses of moderately trained men and women using two different treadmill protocols

In practice, the Bruce protocol is the most commonly used treadmill protocol to assess maximal oxygen consumption (V(.-)O2max). It has been suggested that a running protocol (e.g., Astrand) may elicit a comparatively higher V(.-)O2max and different cardiorespiratory responses when applied to moderately trained runners. Thus, the purpose of this study was to compare V(.-)O2max and other cardiorespiratory responses as elicited by the standard Bruce and a modified Astrand treadmill protocol in moderately trained runners. Fifteen women (age = 21 years, height = 171.5 cm, weight = 63 kg, and body fat = 18%) and 15 men (age = 26 years, height = 177 cm, weight = 72 kg, and body fat = 9%) who were moderately trained runners completed a standard Bruce and modified Astrand protocol (random order), separated by approximately 7 days. Heart rate, Borg ratings of perceived exertion, blood pressure, and pulmonary gas exchange variables were measured during the exercise tests using standard laboratory procedures. This study revealed V(.-)O2max values between the Bruce protocol (51.3 +/- 11.6 ml x kg(-1) x min(-1)) and modified Astrand (51.5 +/- 10.9 ml x kg(-1) x min(-1)) were not significantly different in either the men or the women. However, the Bruce protocol elicited significantly higher maximum treadmill time in men and maximum respiratory exchange ratio (RERmax) and maximum minute ventilation (VEmax) values in both genders. Conversely, the modified Astrand elicited a higher HRmax. These data suggest that V(.-)O2max in both moderately trained men and women runners is independent of treadmill protocol despite differences in HRmax, RERmax, and VEmax.     

Torque-velocity relationship in isokinetic cycling exercise

Seven healthy female subjects performed brief (less than 10 s) periods of maximal exercise on a constant-velocity cycle ergometer, over the functional range of pedaling velocities, and an isometric contraction with each leg. There was an inverse relationship between peak torque and pedal crank velocity in all subjects; isometric torque was (mean +/- SE) 19.8 +/- 8.3% greater than the torque recorded at the slowest velocity of 11 rpm. The torque-velocity relationship was described best by a single exponential equation: y = 189.6 X e-0.0834x, where y is peak torque in Newton . meters and x is crank velocity in revolutions per minute. Peak power was a parabolic function of crank velocity; the data were fitted suitably by a second-order polynomial equation: y = -0.0589x2 + 14.504x + 47.092, where y is peak power in watts and x is crank velocity in revolutions per minute. Maximal peak power occurred at crank velocities ranging from 120 to 160 rpm, when the torque was 0.36 +/- 0.06 of the maximal isometric tension. These results demonstrate the importance of recording velocity in measurements of dynamic maximal power.     

Plasma glucose kinetics during prolonged exercise in trained humans when fed carbohydrate

Nine endurance-trained men exercised on a cycle ergometer at approximately 68% peak O2 uptake to the point of volitional fatigue [232 +/- 14 (SE) min] while ingesting an 8% carbohydrate solution to determine how high glucose disposal could increase under physiological conditions. Plasma glucose kinetics were measured using a primed, continuous infusion of [6,6-2H]glucose and the appearance of ingested glucose, assessed from [3-3H]glucose that had been added to the carbohydrate drink. Plasma glucose was increased (P < 0.05) after 30 min of exercise but thereafter remained at the preexercise level. Glucose appearance rate (R(a)) increased throughout exercise, reaching its peak value of 118 +/- 7 micromol. kg(-1). min(-1) at fatigue, whereas gut R(a) increased continuously during exercise, peaking at 105 +/- 10 micromol. kg(-1). min(-1) at the point of fatigue. In contrast, liver glucose output never rose above resting levels at any time during exercise. Glucose disposal (R(d)) increased throughout exercise, reaching a peak value of 118 +/- 7 micromol. kg(-1). min(-1) at fatigue. If we assume 95% oxidation of glucose R(d), estimated exogenous glucose oxidation at fatigue was 1.36 +/- 0.08 g/min. The results of this study demonstrate that glucose uptake increases continuously during prolonged, strenuous exercise when carbohydrate is ingested and does not appear to limit exercise performance.     

Acute effect of two aerobic exercise modes on maximum strength and strength endurance

The purpose of this study was to evaluate the effects of 2 modes of aerobic exercise (continuous or intermittent) on maximum strength (1 repetition maximum, 1RM) and strength endurance (maximum repetitions at 80% of 1RM) for lower- and upper-body exercises to test the acute hypothesis in concurrent training (CT) interference. Eight physically active men (age: 26.9 +/- 4.2 years; body mass: 82.1 +/- 7.5 kg; height: 178.9 +/- 6.0 cm) were submitted to: (a) a graded exercise test to determine V(.-)O2max (39.26 +/- 6.95 ml x kg(-1) x min(-1)) and anaerobic threshold velocity (3.5 mmol x L(-1)) (9.3 +/- 1.27 km x h(-1)); (b) strength tests in a rested state (control); and (c) 4 experimental sessions, at least 7 days apart. The experimental sessions consisted of a 5-kilometer run on a treadmill continuously (90% of the anaerobic threshold velocity) or intermittently (1:1 minute at V(.-)O2max). Ten minutes after the aerobic exercise, either a maximum strength or a strength endurance test was performed (leg press and bench press exercises). The order of aerobic and strength exercises followed a William's square distribution to avoid carryover effects. Results showed that only the intermittent aerobic exercise produced an acute interference effect on leg strength endurance, decreasing significantly (p < 0.05) the number of repetitions from 10.8 +/- 2.5 to 8.1 +/- 2.2. Maximum strength was not affected by the aerobic exercise mode. In conclusion, the acute interference hypothesis in concurrent training seems to occur when both aerobic and strength exercises produce significant peripheral fatigue in the same muscle group.     

Effects of previous exercise on the ventilatory determination of the aerobic threshold

To study the effects of previous submaximal exercise on the ventilatory determination of the Aerobic Threshold (AeT), 16 men were subjected to three maximal exercise tests (standard test = ST, retest = RT, and test with previous exercise = TPE ) on a cycle ergometer. The protocol for the three tests consisted of 3 min pedalling against 25 W, followed by increments of 25 W every minute until volitional fatigue. TPE was preceded by 10 min cycling at a power output corresponding to the AeT as determined in ST, followed by a recovery period pedalling against 25 W until VO2 returned to values consistent with the initial VO2 response to 25 W. AeT was determined from the gas exchange curves (ventilatory equivalent for O2, fraction of expired O2, excess of VCO2, ventilation, and respiratory gas exchange ratio) printed every 30 s. The results showed good ST X RT reliability (r = 0.89). TPE showed significantly higher AeT values (2.548 +/- 0.44 1 X min-1) when compared with ST (2.049 +/- 0.331 X min-1) and RT (2.083 +/- 0.30 1 X min-1). There were no significant differences for the sub-threshold respiratory gas exchange ratios among the trials. The sub-threshold VO2 response showed significantly higher values for TPE at power outputs above 50 W. It was concluded that the performance of previous exercise can increase the value for the ventilatory determination of the AeT due to a faster sub-threshold VO2 response.     

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O2 uptake (VO2 peak) = 56.4 +/- 2.8 ml x kg(-1) x min(-1); mean +/- SE]. Subjects exercised on a cycle ergometer at >or=90% VO2 peak) to exhaustion (13.2 +/- 0.8 min), during which time arterial O2 saturation (Sa(O2)) fell from 97.7 +/- 0.1% at rest to 91.9 +/- 0.9% (range 84-94%) at end exercise, primarily because of changes in blood pH (7.183 +/- 0.017) and body temperature (38.9 +/- 0.2 degrees C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired O2 fraction (Fi(O2)) = 0.25-0.31] that prevented EIAH (Sa(O2) = 97-99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1-100 Hz). Immediately after exercise at Fi(O2) 0.21, the mean force response across 1-100 Hz decreased 33 +/- 5% compared with only 15 +/- 5% when EIAH was prevented (P < 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at Fi(O2) 0.21 (Sa(O2) = 95.3 +/- 0.7%), the decrease in evoked force was exacerbated by 35% (P < 0.05) in response to further desaturation induced via Fi(O2) 0.17 (Sa(O2) = 87.8 +/- 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (-6 +/- 1% DeltaSa(O2) from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism.     

Energy expenditure and influence of physiologic factors during marathon running

This study examined energy expenditure and physiologic determinants for marathon performance in recreational runners. Twenty recreational marathon runners participated (10 males aged 41 +/- 11.3 years, 10 females aged 42.7 +/- 11.7 years). Each subject completed a V(.-)O2max and a 1-hour treadmill run at recent marathon pace, and body composition was indirectly determined via dual energy X-ray absorptiometry. The male runners exhibited higher V(.-)O2max (ml x kg(-1) x min(-1)) values (52.6 +/- 5.5) than their female counterparts (41.9 +/- 6.6), although ventilatory threshold (T-vent) values were similar between groups (males: 76.2 +/- 6.1 % of V(.-)O2max, females: 75.1 +/- 5.1%). The male runners expended more energy (2,792 +/- 235 kcal) for their most recent marathon as calculated from the 1-hour treadmill run at marathon pace than the female runners (2,436 +/- 297 kcal). Body composition parameters correlated moderately to highly (r ranging from 0.50 to 0.87) with marathon run time. Also, V(.-)O2max (r = -0.73) and ventilatory threshold (r = -0.73) moderately correlated with marathon run time. As a group, the participants ran near their ventilatory threshold for their most recent marathon (r = 0.74). These results indicate the influence of body size on marathon run performance. In general, the larger male and female runners ran slower and expended more kilocalories than smaller runners. Regardless of marathon finishing time, the runners maintained a pace near their T-vent, and as T-vent or V(.-)O2max increased, marathon performance time decreased.     

The relationship of the heart rate deflection point to the ventilatory threshold in trained cyclists

The purpose of this study was to assess the relationship of the heart rate deflection point (HRDP) to the ventilatory threshold (VT) in trained cyclists. Twenty-one endurance-trained cyclists (mean +/- SD: Vo(2)max = 67.6 +/- 4.7 ml x kg x min(-1)) completed a maximal cycle ergometer test of volitional fatigue using a ramped protocol. Ventilatory variables (Ve, Vo(2), Vco(2)) and power were measured online with averages reported every 20 seconds. Heart rate (HR) was recorded every 20 seconds using a Polar monitor. VT was calculated using the excess CO(2) elimination curve. The first derivative of a logistic growth curve fit to the HR-power data produced the HRDP. No significant differences (p > 0.01) existed between HR values at HRDP (171.7 +/- 9.6 b x min(-1)) and VT (169.8 +/- 9.9 b x min(-1)) or between Vo(2) values at HRDP (53.6 +/- 4.2 ml x kg x min(-1)) and VT (52.2 +/- 4.8 ml x kg x min(-1)). But power values at HRDP (318.7 +/- 30.7 W) were significantly different (p < 0.01) from those at VT (334.8 +/- 36.7 W). There were significant relationships between HRDP and VT for the physiological variables of HR (r = 0.92, p < 0.001), Vo(2) (r = 0.72, p < 0.001), and power (r = 0.77, p < 0.001). These findings indicate that HR and Vo(2) at HRDP are not significantly different from the values at VT in trained cyclists. HR values derived from HRDP may be used to set parameters for training intensity. Variability in the speed/power-HRDP relationship across detrained/trained states may be used to evaluate training programs.     

Hypohydration adversely affects lactate threshold in endurance athletes

The purpose of this investigation was to observe the effect of hypohydration (-4% body mass) on lactate threshold (LAT) in 14 collegiate athletes (8 men and 6 women; age, 20.9 +/- 0.5 years; height, 171.1 +/- 2.4 cm; weight, 64.8 +/- 2.3 kg; V(O)2 max, 62.8 +/- 1.9 ml x kg(-1) x min(-1); percentage of fat, 11.4 +/- 1.5%). Subjects performed 2 randomized, discontinuous treadmill bouts at a dry bulb temperature (T(db)) of 22 degrees C to volitional exhaustion in 2 states of hydration, euhydrated and hypohydrated. The hypohydrated condition was achieved in a thermally neutral environment (T(db), 22 degrees C; humidity, 45%), with exercise conducted at a moderate intensity as defined by rating of perceived exertion (RPE, approximately 12) 12-16 hours before testing. On average, subjects decreased 3.9% of their body mass before the hypohydration test. Blood lactate, hematocrit, V(O)2, minute ventilation (VE), R value, heart rate (HR), and RPE were measured during each 4-minute stage of testing. In the hypohydrated condition, LAT occurred significantly earlier during exercise and at a lower absolute V(O)2, VE, respiratory exchange ratio, RPE, and blood lactate concentration. Also, the blood lactate concentration was significantly lower in the hypohydrated condition (6.7 +/- 0.8 mmol) compared with the euhydrated condition (10.2 +/- 0.9 mmol) at peak exercise. There were no differences in HR or percentage of maximum HR at LAT nor did plots of V(CO2):V(O)2 reveal differences in bicarbonate buffering during exercise between the 2 conditions. From these results, we speculate that hypohydration did not significantly alter cardiovascular function or buffering capacity but did cause LAT to occur at a lower absolute exercise intensity.     

Aerobic run training improves brachial artery flow-mediated dilation

The purpose of this study was to assess the relationship between aerobic exercise training and brachial artery flow-mediated dilation (FMD) in healthy subjects. Healthy controls (HC) and aerobically-trained (T) subjects were studied with high-resolution vascular ultrasound at baseline, and during a 5-minute period of hyperemia following forearm cuff occlusion. Training was defined by self-reported participation in recreational or competitive run training. Forearm cuff occlusion was held at 200 mm Hg for 5 minutes. At baseline, both brachial artery flow and diameter were greater in T than in HC (p < 0.05). Resting heart rate was lower in T than in HC (p < 0.05). Peak hyperemic flow (15 seconds postocclusion) was significantly greater in T than in HC (HC; 539 +/- 75 ml x min(-1) vs. T; 832 +/- 103 ml x min(-1), p < 0.05) and correlated well with V(.-)O2peak (r = 0.67, p = 0.008). Flow-mediated dilation was significantly greater in T vs. HC throughout the 5-minute postocclusion phase (p < 0.05). Maximal brachial artery dilation was greater in T than in HC (HC; 3 +/- 1% of baseline vs. T; 8 +/- 3% of baseline; p < 0.05) and moderately correlated with V(.-)O2peak (r = 0.55, p < 0.05). These data suggest that the greater FMD observed in trained subjects may be due, in part, to an augmentation of peak hyperemic flow.     

Peak oxygen uptake during arm cranking for men and women

To determine upper body peak O2 uptake (VO2) in a group of young females and to obtain information on possible sex differences, 40 subjects, 20 females and 20 males, mean age 26 +/- 4 (SD) and 31 +/- 6 yr, respectively, were studied during maximal arm-cranking exercise. Peak values for power output, VO2, minute ventilation (VE), and heart rate (HR) were determined for each subject. In addition, arm-shoulder volume (A-SV) was measured before exercise. Significant differences between males and females (P less than 0.05) were found for peak power output (134 +/- 18 vs. 86 +/- 13 W), peak VO2 expressed in liters per minute (2.55 +/- 0.45 vs. 1.81 +/- 0.36) and milliliters per kilogram per minute (34.2 +/- 5.3 vs. 29.2 +/- 4.9), peak VE (95.4 +/- 14.5 vs. 70.1 +/- 19.2 1 X min-1), and A-SV (3,126 +/- 550 vs. 2,234 +/- 349 ml), whereas peak HR was not significantly different between the two groups (174 +/- 14 vs. 174 +/- 36 beats X min-1). However, when peak VO2 was corrected for arm and shoulder size there was no significant difference between the groups (0.82 +/- 0.13 vs. 0.78 +/- 0.13 ml X ml A-SV-1 X min-1). These results suggest that the observed differences between men and women for peak VO2 elicited during arm cranking when expressed in traditional terms (1 X min-1 and ml X kg-1 X min-1) are a function of the size of the contracting muscle mass and are not due to sex-related differences in either O2 delivery or the O2 utilization capacity of the muscle itself.     

Work capacity during 30 days of bed rest with isotonic and isokinetic exercise training

The purpose was to test the hypothesis that twice daily, short-term, variable intensity isotonic and intermittent high-intensity isokinetic leg exercise would maintain peak O2 uptake (VO2) and muscular strength and endurance, respectively, at or near ambulatory control levels during 30 days of -6 degrees head-down bed rest (BR) deconditioning. Nineteen men (aged 32-42 yr) were divided into no exercise control (peak VO2 once/wk, n = 5), isokinetic (Lido ergometer, n = 7), and isotonic (Quinton ergometer, n = 7) groups. Exercise training was conducted in the supine position for two 30-min periods/day for 5 days/wk. Isotonic training was at 60-90% of peak VO2, and isokinetic training (knee flexion-extension) was at 100 degrees/s. Mean (+/- SE) changes (P less than 0.05) in peak VO2 (ml.m-1.kg-1) from ambulatory control to BR day 28 were 44 +/- 4 to 36 +/- 3, -18.2% (3.27-2.60 l/m) for no exercise, 39 +/- 4 to 40 +/- 3, +2.6% (3.13-3.14 l/min) for isotonic, and 44 +/- 3 to 40 +/- 2, -9.1% (3.24-2.90 l/min) for isokinetic. There were no significant changes in any groups in leg peak torque (right knee flexion or extension), leg mean total work, arm total peak torque, or arm mean total work. Mean energy costs for the isotonic and isokinetic exercise training were 446 kcal/h (18.8 +/- 1.6 ml.min-1.kg-1) and 214 kcal/h (8.9 +/- 0.5 ml.m-1.kg-1), respectively. Thus near-peak, variable intensity, isotonic leg exercise maintains peak VO2 during 30 days of BR, while this peak, intermittent, isokinetic leg exercise protocol does not.     

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.     

Effects of oral propranolol and exercise protocol on indices of aerobic function in normal man

The exercise responses to two different progressive, upright cycle ergometer tests were studied in nine healthy, young subjects either with no drug (ND) or following 48 h or oral propranolol (P) (40 mg q.i.d.). The ergometer tests increased work rate by 30 W either every 30 s or every 4 min. Propranolol caused a significant (p less than 0.05) reduction in peak oxygen uptake (VO2) during both the 30-s and 4-min tests (30-s ND, 3949 +/- 718 mL X min-1 (means +/- SD); 30-s P, 3408 +/- 778 mL X min-1; 4-min ND, 4058 +/- 409 mL X min-1; 4-min P, 3725 +/- 573 mL X min-1). There was no difference between 30-s ND and 4-min ND for peak VO2. The ventilatory anaerobic threshold was not significantly different between any test (30-s ND, 2337 +/- 434 mL O2 X min-1; 30-s P, 2174 +/- 406 mL O2 X min-1; ND, 2433 +/- 685 mL O2 X min-1; 4-min P, 2296 +/- 604 mL O2 X min-1). The VO2 at which blood lactate had increased by 0.5 mM above resting levels was significantly lower than the ventilatory anaerobic threshold for the 4-min ND (1917 +/- 489) and the 4-min P (1978 +/- 412) tests, but was not different for the 30-s ND and 30-s P tests. At exhaustion in the progressive tests, the blood PCO2 was higher (p less than 0.05) in both 30-s tests than 4-min tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lactate, fructose and glucose oxidation profiles in sports drinks and the effect on exercise performance

Exogenous carbohydrate oxidation was assessed in 6 male Category 1 and 2 cyclists who consumed CytoMax (C) or a leading sports drink (G) before and during continuous exercise (CE). C contained lactate-polymer, fructose, glucose and glucose polymer, while G contained fructose and glucose. Peak power output and VO2 on a cycle ergometer were 408+/-13 W and 67.4+/-3.2 mlO2 x kg(-1) x min(-1). Subjects performed 3 bouts of CE with C, and 2 with G at 62% VO2peak for 90 min, followed by high intensity (HI) exercise (86% VO(2)peak) to volitional fatigue. Subjects consumed 250 ml fluid immediately before (-2 min) and every 15 min of cycling. Drinks at -2 and 45 min contained 100 mg of [U-(13)C]-lactate, -glucose or -fructose. Blood, pulmonary gas samples and 13CO2 excretion were taken prior to fluid ingestion and at 5,10,15,30,45,60,75, and 90 min of CE, at the end of HI, and 15 min of recovery. HI after CE was 25% longer with C than G (6.5+/-0.8 vs. 5.2+/-1.0 min, P<0.05). 13CO2 from the -2 min lactate tracer was significantly elevated above rest at 5 min of exercise, and peaked at 15 min. 13CO2 from the -2 min glucose tracer peaked at 45 min for C and G. 13CO2 increased rapidly from the 45 min lactate dose, and by 60 min of exercise was 33% greater than glucose in C or G, and 36% greater than fructose in G. 13CO2 production following tracer fructose ingestion was greater than glucose in the first 45 minutes in C and G. Cumulative recoveries of tracer during exercise were: 92%+/-5.3% for lactate in C and 25+/-4.0% for glucose in C or G. Recoveries for fructose in C and G were 75+/-5.9% and 26+/-6.6%, respectively. Lactate was used more rapidly and to a greater extent than fructose or glucose. CytoMax significantly enhanced HI.     

Exercise-induced abdominal muscle fatigue in healthy humans.

The abdominal muscles have been shown to fatigue in response to voluntary isocapnic hyperpnea using direct nerve stimulation techniques. We investigated whether the abdominal muscles fatigue in response to dynamic lower limb exercise using such techniques. Eleven male subjects [peak oxygen uptake (VO2 peak) = 50.0 +/- 1.9 (SE) ml.kg(-1).min(-1)] cycled at >90% VO2 peak to exhaustion (14.2 +/- 4.2 min). Abdominal muscle function was assessed before and up to 30 min after exercise by measuring the changes in gastric pressure (Pga) after the nerve roots supplying the abdominal muscles were magnetically stimulated at 1-25 Hz. Immediately after exercise there was a decrease in Pga at all stimulation frequencies (mean -25 +/- 4%; P < 0.001) that persisted up to 30 min postexercise (-12 +/- 4%; P = 0.001). These reductions were unlikely due to changes in membrane excitability because amplitude, duration, and area of the rectus abdominis M wave were unaffected. Declines in the Pga response to maximal voluntary expiratory efforts occurred after exercise (158 +/- 13 before vs. 145 +/- 10 cmH2O after exercise; P = 0.005). Voluntary activation, assessed using twitch interpolation, did not change (67 +/- 6 before vs. 64 +/- 2% after exercise; P = 0.20), and electromyographic activity of the rectus abdominis and external oblique increased during these volitional maneuvers. These data provide new evidence that the abdominal muscles fatigue after sustained, high-intensity exercise and that the fatigue is primarily due to peripheral mechanisms.     

Determinants of skin sympathetic nerve responses to isometric exercise.

Exercise-induced increases in skin sympathetic nerve activity (SSNA) are similar between isometric handgrip (IHG) and leg extension (IKE) performed at 30% of maximal voluntary contraction (MVC). However, the precise effect of exercise intensity and level of fatigue on this relationship is unclear. This study tested the following hypotheses: 1) exercise intensity and fatigue level would not affect the magnitude of exercise-induced increase in SSNA between IHG and IKE, and 2) altering IHG muscle mass would also not affect the magnitude of exercise-induced increase in SSNA. In protocol 1, SSNA (peroneal microneurography) was measured during baseline and during the initial and last 30 s of isometric exercise to volitional fatigue in 12 subjects who randomly performed IHG and IKE bouts at 15, 30, and 45% MVC. In protocol 2, SSNA was measured in eight subjects who performed one-arm IHG at 30% MVC with the addition of IHG of the contralateral arm in 10-s intervals for 1 min. Exercise intensity significantly increased SSNA responses during the first 30 s of IHG (34+/-13, 70+/-11, and 92+/-13% change from baseline) and IKE (30+/-17, 69+/-12, and 76+/-13% change from baseline) for 15, 30, and 45% MVC. During the last 30 s of exercise to volitional fatigue, there were no significant differences in SSNA between exercise intensities or limb. SSNA did not significantly change between one-arm and two-arm IHG. Combined, these data indicate that exercise-induced increases in SSNA are intensity dependent in the initial portion of isometric exercise, but these differences are eliminated with the development of fatigue. Moreover, the magnitude of exercise-induced increase in SSNA responses is not dependent on either muscle mass involved or exercising limb.     

Deciphering the metabolic and mechanical contributions to the exercise-induced circulatory response: insights from eccentric cycling

Metabolic demand and muscle mechanical tension are closely coupled during exercise, making their respective drives to the circulatory response difficult to establish. This coupling being altered in eccentric cycling, we implemented an experimental design featuring eccentric vs. concentric constant-load cycling bouts to gain insights into the control of the exercise-induced circulatory response in humans. Heart rate (HR), stroke volume (SV), cardiac output (Q), oxygen uptake (V(.-)(O(2))), and electromyographic (EMG) activity of quadriceps muscles were measured in 11 subjects during heavy concentric (heavy CON: 270 +/- 13 W; V(.-)(O(2)) = 3.59 +/- 0.20 l/min), heavy eccentric (heavy ECC: 270 +/- 13 W, V(.-)(O(2)) = 1.17 +/- 0.15 l/min), and light concentric (light CON: 70 +/- 9 W, V(.-)(O(2)) = 1.14 +/- 0.12 l/min) cycle bouts. Using a reductionist approach, the circulatory responses observed between heavy CON vs. light CON (difference in V(.-)(O(2)) and power output) was ascribed either to metabolic demand, as estimated from heavy CON vs. heavy ECC (similar power output, different V(.-)(O(2))), or to muscle mechanical tension, as estimated from heavy ECC vs. light CON (similar V(.-)(O(2)), different power output). 74% of the Q response was determined by the metabolic demand, also accounting for 65% and 84% of HR and SV responses, respectively. Consequently, muscle mechanical tension determined 26%, 35%, and 16% of the Q, HR, and SV responses, respectively. Q was significantly related to V(.-)(O(2)) (r(2) = 0.83) and EMG activity (r(2) = 0.82; both P < 0.001). These results suggest that the exercise-induced circulatory response is mainly under metabolic control and support the idea that the level of muscle activation plays a role in the cardiovascular regulation during cycle exercise in humans.