Physiological responses to upper body exercise on an arm and a modified leg ergometer.

PURPOSE: The present study was undertaken to compare cardiorespiratory, metabolic, and perceptual responses to upper body exercise on an arm ergometer (AE) and a modified leg ergometer (LE). METHODS: Seventeen male and seven female subjects completed two experimental trials. During each trial, the subjects performed two successive 8-min steady-state arm crank exercises on either an AE or an LE. The crank frequency was kept constant at 50 rev x min(-1) during all exercise bouts. The two power outputs selected were 50 and 75 W for male subjects and 25 and 50 W for female subjects. To achieve these power outputs, the brake resistance was set at 1, 2, and 3 kg at a power output of 25, 50, and 75 W, respectively, for the AE and 0.5, 1, and 1.5 kg at a power output of 25, 50, and 75 W, respectively, for the LE. Oxygen uptake (VO2), heart rate (HR), respiratory exchange ratio (RER), expired ventilation (VE), gross efficiency (GE), and ratings of perceived exertion (RPE) were measured every minute during the last 2 min of each exercise bout. RESULTS: In male subjects, VO2, HR, RER, VE, and RPE were higher (P < 0.05), whereas GE was lower (P < 0.05) during arm crank exercise on an AE than an LE at power outputs of 50 and 70 W. In female subjects, similar differences in these variables between the two ergometers were also observed when exercise was performed at 50 W. However, VO2, RER, VE, and GE did not differ between the two ergometers when exercise was performed at 25 W. CONCLUSIONS: Upper body exercise elicits greater cardiorespiratory, metabolic, and perceptual responses on an AE than an LE at the same power output when power output is computed according to the manufacturer's instructions.     

Menstrual cycle: no effect on exercise cardiorespiratory variables or blood lactate concentration

PURPOSE: Numerous investigations have reported changes in metabolic and cardiorespiratory responses associated with the menstrual cycle. We examined whether variables commonly used in exercise testing are influenced by menstrual cycle phases. METHODS: Nineteen eumenorrheic women performed two incremental tests to voluntary exhaustion on a cycle ergometer during two different phases of the menstrual cycle: the follicular phase (FP) and the luteal phase (LP). Our study variables were power output, VO2, HR, VE, RER, ventilatory equivalents of oxygen (VE/VO2) and carbon dioxide (VE/VCO2), and blood lactate concentration (LA) and were measured at rest, at exhaustion, and at different thresholds of aerobic and anaerobic metabolism. The threshold determination consisted of a three-phase model with two lactate turnpoints (LTP1, LTP2) and a three-phase model with two respiratory thresholds: the anaerobic threshold (AT) and the respiratory compensation point (RCP). RESULTS: When comparing power output, VO2, LA, HR, and RER, we found no significant differences between FP and LP at rest, at maximal load, at any selected threshold, or any stage of the incremental tests. We observed higher values for VE/VO2, VE/VCO2, and VE at rest, at exhaustion, and at our AT in LP. CONCLUSION: We did not find performance changes associated with menstrual cycle. Our data do not support findings that the menstrual cycle influences lactate "thresholds" and ventilatory "thresholds." In agreement with other studies, we observed a higher ventilatory drive in the LP compared with the FP of the menstrual cycle.     

Effect of pedal rate on cardiorespiratory responses during continuous exercise.

The role of cycle ergometer pedal rate on the gradual increase in ventilation (VE), heart rate (HR), and oxygen uptake (VO2) accompanying continuous submaximal exercise is unknown. To examine this problem, five trained males (VO2peak = 4.00 +/- 0.27 l.min-1) performed 45 min of moderate intensity (MI, 127 W) and high-moderate intensity (HMI, 166 W) cycle ergometry both at pedal rates of 60 rpm and 90 rpm. Power output and pedal rate had an additive effect on the overall mean responses for VE, HR, and VO2, producing significantly higher values as power output and pedal rate increased. During continuous exercise, VE, HR, and VO2 increased progressively from the 10th to the 45th minute for all tests. However, the rates of increase and factors modifying the VE, HR, and VO2 responses were different. HR increased during all exercise tests an average of 10.8% independent of power output and pedal rate. VE increased 7.4% during MI exercise and 10% during HMI exercise independent of pedal rate. Similar power output dependent responses were observed for rectal temperature (Tr) and blood lactate. VO2 increased 4.4% for MI and HMI exercise at 60 rpm, and 8.2% for the same power outputs at 90 rpm, respectively. Increases in Tr, the oxygen cost of pulmonary ventilation and fat oxidation, and lactate removal were estimated to account for only 31-36% of the slow rise in VO2 for any single test. This suggests that 64-69% of the rise in VO2 was due to factors related to muscle use.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiorespiratory responses to arm cranking and electrical stimulation leg cycling in people with paraplegia.

PURPOSE: The purpose of this study was to assess the cardiorespiratory responses during arm exercise with and without concurrent electrical stimulation-induced leg cycling in people with paraplegia. METHODS: On separate days, 10 subjects with spinal cord injuries (T5-T12) performed either arm cranking (ACE), or simultaneous arm cranking + electrical stimulation-induced leg cycling (ACE+ES-LCE) graded exercise tests. RESULTS: During submaximal, steady-state exercise, ACE+ES-LCE elicited significantly higher VO2, (by 0.25-0.28 L x min(-1)) stroke volume (by 13 mL), and VE(BTPS) (by 9.4 L x min(-1)) compared with ACE alone. In contrast, there were no significant differences of submaximal HR, cardiac output, or power output between the exercise modes. At maximal exercise, ACE+ES-LCE elicited significantly higher VO2 (by 0.23 L x min(-1)) compared with ACE alone, but there were no differences in power output, HR, or VE(BTPS). CONCLUSIONS: These results demonstrate that during submaximal or maximal exercise there was a greater metabolic stress elicited during ACE+ES-LCE compared with during ACE alone. The higher stroke volume observed during submaximal ACE+ES-LCE, in the absence of any difference in HR, implied a reduced venous pooling and higher cardiac volume loading during ACE+ES-LCE. These results suggest that training incorporating ACE+ES-LCE may be more effective in improving aerobic fitness in people with paraplegia than ACE alone.     

Ventilatory and plasma lactate response with different exercise protocols: a comparison of methods

The purpose of this study was to compare the methods used to identify abrupt changes in ventilation or plasma lactate (LA) during exercise. Ten males randomly performed a 1-, 3-, and 5-min, 30-W incremental cycle ergometer test to fatigue. The first change in VE and VCO2 relative to VO2 (ventilation threshold, VT1) was determined from plots of VE, VE X VO2-1, and excess CO2 vs VO2. Data were also analyzed for a second change in VE (VT2) relative to both VCO2 and VO2 using plots of VE and VE X VCO2(-1) vs VO2 and semi-log plots of VE X VO2(-1) and VE X VCO2(-1) vs VO2. Arterialized blood samples were taken each 1.0, 1.5, or 2.5 min for the 1-, 3-, and 5-min tests, respectively, to determine the LA threshold (LT) and the onset of blood lactate accumulation (4 mM, OBLA) and 1, 2, 5, 7.5, and 10 min after all tests to calculate the individual anaerobic threshold (IAT). At weekly intervals, subjects also exercised for 10 min at eight different power outputs (W) to define the onset of plasma lactate accumulation (OPLA). Results showed that VO2max was significantly higher for the 1-min (3.88 l X min-1)vs the 3- or 5-min tests (3.65 l X min-1). With increasing W duration, VT1 from either VE or VE X VO2-1 vs VO2 were similar (1.77 vs 1.72 l X min-1) but significantly lower using excess CO2 (1.23 l X min-1) . VO2 at LT (1.62 l X min-1) and OPLA (1.73 l X min-1) were similar to VT1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Faster kinetics of VO2 during arm exercise with circulatory occlusion of the legs

Occlusion of the nonworking leg muscles prior to the onset of supine arm exercise was examined for an effect on the kinetics of respiratory gas exchange (VO2 and VCO2), ventilation (VE), and heart rate (HR). Seven subjects performed arm cycling at 40 W (two females) or 50 W (five males) for 8 min following 4 min of "0" W pedaling. Six repetitions of each of uncuffed and cuffed leg conditions were averaged for individual subject analysis. The VO2 kinetics were significantly faster in the cuffed than the uncuffed condition (mean response time 66.0 +/- 26.4 vs 81.2 +/- 37.5 s, P less than 0.04). The kinetics of VCO2, VE, and HR were not affected by occlusion. It is concluded that the faster VO2 kinetics with the prior occlusion of nonworking leg muscles was a consequence of increased availability of oxygen to the working arm muscles at the onset of exercise.     

Effects of training status and exercise intensity on phase II VO2 kinetics

PURPOSE: To test the hypotheses that: 1) the time constant for the fast component of .VO2 kinetics (tau1) at exercise onset would be faster in trained than in untrained subjects for both moderate and heavy exercise, and that 2) tau1 would become progressively slower in untrained subjects at higher power outputs but be invariant in trained subjects. METHODS: Eight untrained subjects (.VO2peak: 42.9 +/- 5.1 mL.kg-1.min-1) and seven trained cyclists (.VO2peak: 66.6 +/- 2.5 mL.kg-1.min-1) completed square-wave transitions to power outputs requiring 60% and 80% of gas exchange threshold (GET), and 50% of the difference between GET and .VO2 peak (50%Delta) from a baseline of "unloaded" cycling. .VO2 was measured breath-by-breath and individual responses were modeled using nonlinear regression techniques. RESULTS: A repeated measures ANOVA revealed that the tau1 was significantly smaller (i.e., the kinetics were faster) in the trained compared with the untrained subjects and that tau1 became significantly greater (i.e., the kinetics were slowed) at higher power outputs both in the untrained (60%GET: 17.8 +/- 3.8 s, 80%GET: 21.5 +/- 6.6 s, and 50%Delta: 23.5 +/- 2.8 s) and the trained (60%GET: 8.9 +/- 1.3 s, 80%GET: 11.7 +/- 2.5 s, and 50%Delta: 15.2 +/- 2.0 s) subjects (P < 0.05). CONCLUSION: Phase II .VO2 kinetics became progressively slower at higher power outputs in both trained and untrained subjects. That a greater tau1 was evident at a higher power output within the moderate exercise intensity domain (相似文献   

Influence of high-intensity exercise training on the ventilatory response to exercise in patients with reduced ventricular function.

BACKGROUND: Exercise training increases exercise capacity in patients with reduced ventricular function in part through improved skeletal muscle metabolism, but the effect training might have on abnormal ventilatory and gas exchange responses to exercise has not been clearly defined. METHODS: Twenty-five male patients with reduced ventricular function after a myocardial infarction were randomized to either a 2-month high-intensity residential exercise training program or to a control group. Before and after the study period, upright exercise testing was performed with measurements of ventilatory gas exchange, lactate, arterial blood gases, cardiac output, and pulmonary artery and wedge pressures. RESULTS: In the exercise group, peak VO2 and VO2 at the lactate threshold increased 29 and 39%, respectively, whereas no increases were observed among controls. Maximal cardiac output increased only in the exercise group (1.7 L x min(-1), P < 0.05), and no changes in rest or peak exercise pulmonary pressures were observed in either group. At baseline, modest inverse relationships were observed between pulmonary wedge pressure and peak VO2 both at rest (r = -0.56, P < 0.05) and peak exercise (r = -0.43, P < 0.05). Maximal VE/VCO2 was inversely related to maximal cardiac output (r = -0.72, P < 0.001). Training did not have a significant effect on these relationships. Training lowered VE/VO2, heart rate, and blood lactate levels at matched work rates throughout exercise and tended to lower maximal Vd/Vt. The slope of the relationship between VE and VCO2 was reduced after training in the exercise group (0.33 pre vs 0.27 post, P < 0.01), whereas control patients did not differ. CONCLUSIONS: Exercise training among patients with reduced left ventricular function results in a systematic improvement in the ventilatory response to exercise. Training increased maximal cardiac output, tended to lower Vd/Vt, and markedly improved the efficiency of ventilation. Peak VO2 and ventilatory responses to exercise were only modestly related to pulmonary vascular pressures, and training had no effect on the relationships between exercise capacity, ventilatory responses, and pulmonary pressures.     

Ventilatory and gas-exchange responses to incremental exercise performed with reduced muscle glycogen content

This study examined the relationship between minute ventilation (VE), CO2 production (VCO2), and blood lactate concentration ([La-]) during incremental exercise performed with reduced muscle glycogen stores. Nine untrained female subjects (25.3+/-4.2 year) performed incremental cycling in a normal glycogen (NG) state and under conditions of reduced muscle glycogen (RG) content. To reduce muscle glycogen stores, subjects cycled to exhaustion (124+/-33 min) at a power output corresponding to their gas-exchange anaerobic threshold. Peak oxygen uptake (VO2peak) was unchanged with glycogen reduction, even though subjects achieved a significantly lower maximal power output in the RG state (p<0.05). Peak blood [La-] decreased significantly by 37% in the RG state (p<0.001). At any percentage of VO2peak, O2 uptake and VE were similar for both treatment conditions, whereas VCO2 and respiratory exchange ratio values were lower during the RG trial than under NG conditions. Therefore, VE/VCO2 tended to be higher and end-tidal CO2 partial pressure tended to be lower during exercise performed in the RG state. VE was significantly correlated with VCO2 under both treatment conditions (NG: r=0.99, p<0.01; RG: r=0.99, p<0.01). However, the slope of the VE-VCO2 relationship was significantly elevated during the RG trial (p<0.01). VE during exercise was similar under both treatment conditions, even though VCO2 and blood [La-] were lower during the RG trial compared to the NG trial. This suggests that factors other than CO2 delivery to the lung and metabolic acidosis play an important role in regulating VE during exercise.     

Leg strength is associated with ventilatory efficiency in older women

The aim of the present study was to determine if leg function is associated with ventilatory efficiency during exercise in healthy older adults. 24 women and 18 men aged 60-80 years performed treadmill exercise to fatigue for calculation of ventilatory efficiency using the ratio of ventilation to carbon dioxide at the anaerobic threshold (VE/VCO?@AT). On a separate day, participants performed leg strength testing and graded single-leg knee extension exercise. The VE/VCO?@AT was higher in women than men (33±3 vs. 30±3; p=0.03). After adjustment for age and VO(?max), leg strength (knee extensor isometric force) was inversely associated with VE/VCO?@AT in women (r= - 0.44, p=0.03) while no relationships were found for men. Strength-matched women and men had similar VE/VCO?@AT indicating that the correlation between leg strength and VE/VCO?@AT was strength- but not sex-specific. During knee extensor exercise, women with lower leg strength had increased VE/VCO? slope across 0-15 W as compared to higher strength women (38±8 vs. 31±3; p<0.05), while no differences were found for men. These results find leg strength to be associated with ventilatory responses to exercise in healthy older women, a finding that might be related to lower leg strength in women than men.     

Exercise performance and ventilatory response in the menstrual cycle

We investigated the effects of the luteal phase of the menstrual cycle, as compared with the follicular phase, on ventilatory response (VR) and exercise performance in eight normally menstruating, non-athletic women. Subjects were studied near the predicted mid-point of each phase which was later documented by serum progesterone level. Resting VR to hypercapnia was greater, and VR to hypoxia tended to be greater in the luteal phase than in the follicular phase, but the increases in VRs were unrelated to progesterone level. There were no differences in maximal oxygen uptake, maximal duration of exercise, maximal heart rate, work efficiency, maximal ventilation (VE), anaerobic (ventilatory) threshold, gas exchange, cardiac output, or oxygen delivery. The PaCO2 was lower, and pHa tended to be higher during exercise. VE per unit CO2 output (VE/VCO2) was increased. R values (VCO2/VO2) were less, and maximal lactate values tended to be less, suggestive of increased dependence on fat for energy metabolism. At a given workload, exercise VE was unchanged due to the effect of less CO2 output at a given VO2 (lower R), balancing increased VE/VCO2. We conclude that, although ventilatory parameters are altered by the menstrual cycle, there is no overall effect on maximal exercise performance.     

Submaximal exercise quantified as percent of normoxic and hyperoxic maximum oxygen uptakes

Maximum oxygen uptake (VO2max) was measured in six college-aged males under normoxic (NVO2max) and hyperoxic (HVO2max; 70% oxygen) conditions. Subjects then randomly performed the following three 20-min submaximal exercise bouts: 75% normoxic VO2max under normoxia (NVO2N), 75% normoxic VO2max under hyperoxia (NVO2H), and 75% hyperoxic VO2max under hyperoxia (HVO2H). Metabolic parameters were obtained at 5-min intervals. Hyperoxia resulted in a 13% increase (P less than 0.01) in VO2max (NVO2max = 3.54 l X min-1 vs HVO2max = 4.00 l X min-1). Significant (P less than 0.05) decreases were observed in VE (ventilation) (13%), epinephrine (37%), norepinephrine (26%), and blood lactate (28%), with no change in oxygen uptake (VO2), carbon dioxide production (VCO2), or respiratory exchange ratio (R) during hyperoxia at the same absolute power output (NVO2N vs NVO2H). However, at the same relative power outputs (NVO2N vs HVO2H) no significant changes in VE, epinephrine, norepinephrine, or blood lactate were observed when hyperoxia and normoxia were compared.     

Influence of testing protocol on ventilatory thresholds and cycling performance

PURPOSE: To compare the ventilatory response of two incremental exercise tests and determine their predictive validity on 40-km cycle time trial (40K) mean power output (40Kavgwatts). METHODS: Fifteen male cyclists performed two incremental exercise tests (T50x3:100 W +50 W x 3(-1) min, T25x1:20 W + 25 W x min(-1)) and a 40K over an 8-d period. Key variable was power at ventilatory threshold (VT). For VT determination during each test we used: VE/VO2 method, first clear breakpoint on the VE/VCO2 plot, V-slope method, RER = 1, and RER = 0.95. RESULTS: VO2max during T50x3 and T25x1 was not different (66.6 vs 67.6 mL x kg(-1) x min(-1)), although T25x1 peak power output (MaxT25x1; 402 W) was significantly higher than MaxT50x3 (363 W). T50x3 and T25x1 VT power outputs indicated that the power output at T25x1:RER = 1 and T25x1:RER = 0.95 were significantly higher compared with T50x3 (324 vs 304 W and 282 vs 264 W, respectively). Regression analyses between T50x3 variables and 40Kavgwatts were significant for T50x3:V-slope (R2 = 0.37; SEE 20.2 W), T50x3:VE/VO2 (R2 = 0.64; SEE 15.3 W), T50x3:RER = 0.95 (R2 = 0.42; SEE 19.4 W), T50x3:RER = 1 (R2 = 0.45; SEE 18.8 W), and MaxT50x3 (R2 = 0.51; SEE 17.8 W). Regression analyses between T25x1 variables and 40Kavgwatts were significant for T25x1:V-slope (R2 = 0.63; SEE 15.4 W), T25x1:VE/VO2 (R2 = 0.64; SEE 15.2 W), T25x1:RER = 0.95 (R2 = 0.53; SEE 17.4 W), T25x1:RER = 1 (R2 = 0.57; SEE 16.7 W), and MaxT25x1 (R2 = 0.65; SEE 15.0 W). There was no significant difference between 40Kavgwatts (282 W) and power outputs at T50x3:VE/VO2 (277 W), T50x3:V-slope (289 W), T25x1:VE/VO2 (276 W), and T25x1:RER = 0.95 (282 W). CONCLUSION: Generally, T25x1 based VT variables were superior to T50x3 variables regarding the prediction of 40Kavgwatts. We conclude that the VE/VO2 method is protocol independent and a valid 40Kavgwatts predictor.     

Influence of light additional arm cranking exercise on the kinetics of VO2 in severe cycling exercise

This study examined the influence of light additional arm cranking exercise on the VO2 slow component observed during severe cycling exercise. During incremental tests, eleven triathletes exercised to exhaustion cycling with leg, cranking with arm and combined arm and leg cranking and cycling (arm work-rates being set at the third of leg work rates) to determine arm, leg and combined arm and leg lactate threshold and VO2max. After these incremental tests subjects performed in random order severe exercises until exhaustion at work-rates corresponding to the lactate threshold + 50% of the difference to the work rate associated with VO2max and the lactate threshold, i.e., delta50: 1) with legs only (leg delta50) 2) leg delta50 plus a very light arm cranking exercise at 25 % of the arm lactate threshold (Ldelta50 + A25). VO2 slow component was the increase of VO2 (in ml x min(-1)) between the third and the sixth minute of exercise (deltaVO2 63 min). Results showed 1) Nine of the eleven triathletes had a VO2 slow component in arm delta50; 2) a light cycle arm exercise (25% of lactate threshold) added to a severe leg cycle exercise did not decrease time to exhaustion in severe exercise (493 +/- 154s vs 418 +/- 84, P=0.4); 3) For the five subjects who had a VO2 slow component in leg cycling, the addition of a light arm exercise (25% of arm LT) decreased the VO2 slow component significantly (from 457 +/- 173 ml x min(-1) for leg delta50 to 111 +/- 150 ml x min(-1) for Ldelta50 + A25, Z = -2.0, P = 0.04). In conclusion, light additional arm cranking decreases the VO2 slow component in severe cycling. Further studies are needed to confirm the hypothesis that extra work due to an increasing handgrip on the handlebars may contribute to the VO2 slow component in cycling.     

Effects of beta-adrenergic blockade on ventilation and gas exchange during the rest to work transition

The purpose of these experiments was to determine the effects of acute beta-blockade on the kinetics of oxygen uptake (VO2), expired carbon dioxide (VCO2), and expired ventilation (VE) in the transition from rest to submaximal exercise. Six male subjects exercised for 6 min on a cycle ergometer (60 W) initiated as a square wave from rest on two occasions. The beta-blockade experiment began 60 min after the subject ingested propranolol hydrochloride (1 mg.kg-1 BW) while the second experiment served as control with the treatment order counterbalanced. Ventilation and gas exchange were monitored by open circuit techniques and the data were modeled with a single-component exponential function using a time delay. No differences existed (p greater than 0.05) in the steady state VO2, VCO2, or VE nor the kinetics of VCO2 and VE between treatments. However, the rate of adaptation of VO2 toward steady state was significantly slowed (p less than 0.05) with beta-blockade. These data suggest that acute beta blockade results in diminished VO2 kinetics in the transition from rest to steady-state exercise. We hypothesize that the mechanism to explain this finding is a slowed time course of cardiac output adjustment at the beginning of exercise.     

An evaluation of the predictive validity and reliability of ventilatory threshold

PURPOSE: To identify a valid and reliable method to determine 40-km time trial (40K) performance in a laboratory setting. METHODS: Part 1: Ventilatory threshold (VT) and 40K performance were determined on two occasions (February/September) using two subsets of cyclists (N = 15 each; VO(2max) 67.6 +/- 4.2/71.5 +/- 3.0 mL x kg(-1) x min(-1)) to determine the predictive validity of VT assessments. Variables of interest were power output at VT, peak power output (MaxVT(w)), and average power output during 40K (40K(avgwatts)). For VT determination we used: breakpoint of VE/VO2; breakpoint of VE/VCO2; V-slope; RER = 1; and RER = 0.95. In part 2, test-retest reliability of VT and MaxVT(w) were examined in 20 subjects (VO(2max) 64.8 +/- 8.0 mL x kg(-1) x min(-1)) on two occasions, separated by 48 h. RESULTS: Regression analyses between power outputs at VTs and 40K(avgwatts) showed significant predictive validity for (February/September): V-slope (r = 0.79/0.84; SEE 155/13.3W), VE/VO2 (r = 0.80/0.81; SEE 15.2/14.2W), RER0.95 (r = 0.73/0.58; SEE 17.4/21.2W), RER1 (r = 0.75/0.74; SEE 16.8/16.7W), and MaxVT(w) (r = 0.81/0.73; SEE 15.0/17.1W). Paired t-tests between power outputs at VTs and the 40K(avgwatts) indicated that mean power outputs at VE/O2 (261 +/- 29W; P = 0.33) and RER0.95 (274 +/- 55W; P = 0.93) in February and VE/VO2 (274 +/- 37W; P = 0.79) in September were not significantly different from the respective 40K(avgwatts) (277 +/- 30W/281 +/- 30W). Test-retest reliability analysis yielded the following intraclass correlation and relative test-retest errors: V-slope: 0.98, 2.6%; VE/VO2: 0.95, 5.3%; RER0.95: 0.87, 9.8%; RER1: 0.94, 5.7%; VE/VCO2: 0.87, 12.1%; MaxVT(w): 0.98, 2.6%. CONCLUSION: The high test-retest reliability and consistent ability to accurately predict athletes' 40K(avgwatts) across a competitive season indicated that VE/VO2 was superior to the other evaluated methods.     

Breathlessness predicts perceived exertion in young women with mild asthma.

We examined ratings of breathlessness (BRE) as a predictor of perceived exertion (RPE) during incremental cycling at power outputs of 50, 75, and 100 W. Young females (21 yr +/- 1.9) diagnosed with mild asthma (N = 25) were compared with females having normal lung function (N = 25) matched for age, VO2peak, trait anxiety, activity history (7-d recall), and BMI (kg.m-2). Relative oxygen consumption (%VO2peak), blood lactate concentration, VE.VO2(-1), and state anxiety were statistically controlled in hierarchical multiple linear regression analyses. For each group, %VO2peak explained 60% of the variance in RPE across power outputs (P less than 0.001); R2 was unchanged (P greater than 0.10) with the addition of blood lactate, VE.VO2(-1), and state anxiety. Absolute RPE and BRE did not differ between groups at any power output, but partial standardized (beta) and unstandardized (b) regression coefficients and increases in R2 showed that BRE had a greater effect (P less than 0.01) on RPE for asthmatics [adjusted R2 increased to 0.89; (beta) = 0.75; (b) = 0.79 +/- 0.06] than for controls [adjusted R2 increased to 0.74; (beta) = 0.52; (b) = 0.51 +/- 0.09]. The standard error of the prediction was 0.79 for asthmatics and 1.16 for controls. The prediction of RPE by BRE was not moderated by variation in forced expiratory volume for 1 s (FEV1), forced vital capacity (FVC) or peak inspiratory flow (VI). Physiological responses were similar for the groups, but blood lactate was higher in asthmatics at rest, at each power output, and at VO2peak.(ABSTRACT TRUNCATED AT 250 WORDS)     

The slow component of VO2 in professional cyclists

OBJECTIVES: To analyse the slow component of oxygen uptake (VO2) in professional cyclists and to determine whether this phenomenon is due to altered neuromuscular activity, as assessed by surface electromyography (EMG). METHODS: The following variables were measured during 20 minute cycle ergometer tests performed at about 80% of VO2MAX in nine professional road cyclists (mean (SD) age 26 (2) years; VO2max 72.6 (2.2) ml/kg/min): heart rate (HR), gas exchange variables (VO2, ventilation (VE), tidal volume (VT), breathing frequency (fb), ventilatory equivalents for oxygen and carbon dioxide (VE/VO2 and VE/VCO2 respectively), respiratory exchange ratio (RER), and end tidal PO2 and PCO2 (PETO2 and PETCO2 respectively)), blood variables (lactate, pH, and [HCO3-]) and EMG data (root mean from square voltage (rms-EMG) and mean power frequency (MPF)) from the vastus lateralis muscle. RESULTS: The mean magnitude of the slow component (from the end of the third minute to the end of exercise) was 130 (0.04) ml in 17 minutes or 7.6 ml/min. Significant increases from three minute to end of exercise values were found for the following variables: VO2 (p<0.01), HR (p<0.01), VE (p<0.05), fb (p<0.01), VE/VO2 (p<0.05), VE/VCO2 (p<0.01), PETO2 (p<0.05), and blood lactate (p<0.05). In contrast, rms-EMG and MPF showed no change (p>0.05) throughout the exercise tests. CONCLUSIONS: A significant but small VO2 slow component was shown in professional cyclists during constant load heavy exercise. The results suggest that the primary origin of the slow component is not neuromuscular factors in these subjects, at least for exercise intensities up to 80% of VO2MAX.     

Effect of simulated weightlessness on exercise-induced anaerobic threshold

Ventilation (VE), CO2 output (VCO2), oxygen uptake (VO2), respiratory exchange ratio (R), and the ventilatory equivalents for VO2 and VCO2 were measured during graded exercise before and after 10 d of continuous bed rest (BR) in the -6 degrees head-down position to determine the effect of deconditioning on the anaerobic threshold (AT), i.e., the highest workrate or VO2 which was achieved without evidence of lactic acidosis, as judged from the profile of ventilatory and gas exchange responses. Ten healthy male subjects performed a supine graded cycle ergometer test before (pre) and after (post) BR which consisted of 4 min of unloaded pedaling at 60 rpm followed by an increased workrate of 15 W X min-1 until volitional fatigue (max). VE, VCO2, VO2, R, VE/VO2 and VE/VCO2 were measured every 30 s and used collectively to identify the AT. Plasma (PV) and blood (BV) volumes were measured pre- and post-BR by T-1824. Following BR, VO2max decreased from 2.42 +/- 0.17 to 2.25 +/- 0.13 L X min-1 (7.0%, p less than 0.05). BR significantly (p less than 0.05) reduced the AT from 1.26 +/- 0.09 to 0.95 +/- 0.05 L X min-1 VO2; from 52.2 +/- 2.0 to 42.6 +/- 1.6% VO2max; and from 93 +/- 9 to 65 +/- 6 W. A correlation coefficient (r) of -0.11 (NS) was found between the change in VO2max and change in AT. A decrease in BV of 8.8% (p less than 0.05) was due to the 11.0% reduction in PV; red cell volume remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thermoregulation of exercising men in the morning rise and evening fall phases of internal temperature.

The purpose of this study was to compare the thermoregulatory responses during exercise in the morning rise (0900 h) and evening fall phases (2000 h) in circadian variation of body temperature. Five healthy volunteers performed bicycle exercises at 30% and 60% of maximal aerobic power (VO2max) at 26 degrees C with a relative humidity of 50%. Whole-body sweat rate (SR), rectal (Tre), mean skin (Tsk) and mean body (Tb) temperature, pulmonary ventilation (VE), oxygen uptake (VO2), and carbon dioxide output (VCO2) and heart rate (HR) were measured during the experimental period. SR during exercise at 30% VO2max was significantly higher at 2000 h than at 0900 h. However, the circadian variation of SR during exercise was not observed at 60% VO2max. At the two experimental times, there were also no significant differences in VO2, VCO2, VE and Tsk in both workloads. In HR, Tb and Tre circadian effects were demonstrated as well as in workload levels. As Tb was plotted against SR during exercise, positive correlations were observed. The data showed that there was a parallel shift in the SR to Tb relationship during exercise in the morning and evening. This rightward shift indicated that there was an increased Tb threshold for the onset of sweating in the evening. Resting Tb at 2000 h was significantly higher when compared with Tb at 0900 h. The present results suggest that the circadian influence on the thermoregulatory response to exercise may be evident only at low workloads.