Ineffective ventilation during exercise in patients with chronic congestive heart failure.

The pathophysiologic mechanisms causing exertional breathlessness in patients with chronic congestive heart failure (CHF) are not fully understood. Therefore, we have studied whether the ventilation in such patients is ineffective during exercise. Thirteen patients with treated chronic CHF (New York Heart Association class II-IV) and eight healthy controls underwent a maximal bicycle ergometer test with continuous analysis of expired air and frequent arterial blood sampling for gas and lactate analysis. All subjects were non-smokers and none had any signs of a pulmonary disease. Peak O2 consumption of the patients was 14.9 +/- 5.3 ml min-1 kg-1 and that of controls 33.6 +/- 7.5 ml min-1 kg-1. In patients with CHF the ratio of pulmonary dead space to tidal volume was significantly elevated at peak exercise compared with that of the controls (0.36 +/- 0.08 vs. 0.20 +/- 0.07, P less than 0.05). The ventilatory equivalent for CO2 (VE:VCO2) was also significantly higher in patients than in controls during exercise (P less than 0.05). Furthermore, both the ventilatory equivalents for CO2 and O2 (VE:VO2) had a significant inverse correlation with peak O2 consumption (P less than 0.001 for VE:VCO2 and P less than 0.05 for VE:VO2), O2 consumption at anaerobic threshold (P less than 0.01) and O2-pulse (P less than 0.001) among the patients. During exercise the arterial PO2 and PCO2 remained normal in patients and controls. These data indicate that in patients with chronic CHF wasted ventilation is pathologically increased during exercise, and this is related to the severity of the disease. Chronic CHF is not associated with decreased ventilatory reserve, hypoxaemia or alveolar hyperventilation. The ineffectiveness of ventilation is probably an important cause of exertional breathlessness in patients with CHF.     

Time courses of pulmonary gas exchange and heart rate changes in supine exercise.

The time courses of ventilation (VE), O2 uptake (VO2), CO2 elimination (VCO2), respiratory exchange ratio (R), end-tidal PO2 and PCO2 and heart rate (HR) were studied in seven subjects performing light dynamic leg exercise in the supine position. Individual and group mean time courses in response to step changes in work load were computed and displayed graphically. A computer-based method was also used to fit mono- or bi-exponential mathematical functions to the recorded responses. The over-all rate of HR change in response to the transition from 0-load pedalling to exercise (on-response) was faster (mean response time, MRT = 31 s) than the corresponding VO2 response (MRT = 45 s) while VE responded considerably slower (MRT = 86 s). During the reverse transition (off-response), VO2 and VE changed with the same rate as in the on-response, while the HR-change was slower than during the on-response (MRT = 50 s). During the initial 15-sec period, VO2 changed only slightly, which contrasts to previous results in the sitting position, where 50% of the final change in VO2 has been reported to occur within the first 15-sec period, and where changes in blood distribution and stroke volume are known to be more pronounced than in the supine position. Our results emphasize the importance of central circulatory changes for the time course of VO2 at the start and end of exercise.     

The Effects of Caffeine on the Kinetics of O2Uptake, CO2Production and Expiratory Ventilation in Humans During the On-Transient of Moderate and Heavy Intensity Exercise

In order to test the hypothesis that glycogen sparing observed early during exercise following caffeine ingestion was a consequence of tighter metabolic control reflected in faster VO2 kinetics, we examined the effect of caffeine ingestion on oxygen uptake (VO2), carbon dioxide production (VCO2) and expiratory ventilation (VE) kinetics at the onset of both moderate (MOD) and heavy (HVY) intensity exercise. Male subjects (n = 10) were assigned to either a MOD (50% VO2,max, n = 5) or HVY (80% VO2,max, n = 5) exercise condition. Constant-load cycle ergometer exercise was performed as a step function from loadless cycling 1 h after ingestion of either dextrose (placebo, PLAC) or caffeine (CAFF; 6 mg (kg body mass)-1). Alveolar gas exchange was measured breath-by-breath. A 2- or 3-component exponential model, fitted through the entire exercise transient, was used to analyse gas exchange and ventilatory data for the determination of total lag time (TLT: the time taken to attain 63% of the total exponential increase). Caffeine had no effect on TLT for VO2 kinetics at either exercise intensity (MOD: 36 +/- 14 s (PLAC) and 41 +/- 10 s (CAFF); HVY: 99 +/- 30 s (PLAC) and 103 +/- 26 (CAFF) (mean +/- S.D.)). TLT for VE was increased with caffeine at both exercise intensities (MOD: 50 +/- 20 s (PLAC) and 59 +/- 21 s (CAFF); HVY: 168 +/- 35 s (PLAC) and 203 +/- 48 s (CAFF)) and for VCO2 during MOD only (MOD: 47 +/- 14 s (PLAC) and 53 +/- 17 s (CAFF); HVY: 65 +/- 13 s (PLAC) and 69 +/- 17 s (CAFF)). Contrary to our hypothesis, the metabolic effects of caffeine did not alter the on-transient VO2 kinetics in moderate or heavy exercise. VCO2 kinetics were slowed by a reduction in CO2 stores reflected in pre-exercise and exercise endtidal CO2 pressure (PET,CO2) and plasma PCO2 which, we propose, contributed to slowed VE kinetics.     

Cardiodynamic factors affecting hyperpnea during steady-state exercise in man

In order to know the role of cardiodynamic factors for exercise hyperpnea, ventilation and several cardiorespiratory variables were measured simultaneously in human subjects during exercise. Cardiac output (Q) and mixed venous CO2 content (CVCO2) were determined by a rebreathing method. The correlation coefficients (r) for the relationships between minute expiratory ventilation (VE) and each of end-tidal CO2 tension (PETCO2), Q, CVCO2, CO2 flow into the lung (QCO2, the product of Q and CVCO2), oxygen consumption (VO2), and CO2 output (VCO2) were determined during the steady-state exercise up to 90 W. The correlation was highly significant (r = 0.84-0.99, p less than 0.001) in each case except for PETCO2 (r = 0.13, N.S.). The highest correlation was observed in the VE-VCO2 relationship. It was assume that VCO2 released from the pulmonary capillaries into the alveoli is the most likely stimulus leading to exercise hyperpnea. Arterial CO2 oscillation may be regarded as a potential linkage between VCO2 and VE.     

Cardiorespiratory dynamics in men in response to passive work

Dynamic characteristics of ventilation, cardiac output, and gas exchange in response to passive limb movements were studied in four healthy men in an upright position. Passive exercise was performed on a motor-driven bicycle ergometer, of which pedaling rate was varied from control (30 rpm) to stimulus (90 rpm) level in a stepwise fashion. Stroke volume (SV), heart rate (HR), and cardiac output (Q) were determined continuously during the exercise by using an automated impedance cardiograph. Minute ventilation (VE), respiratory frequency (f), tidal volume (VT), oxygen consumption (VO2), carbon dioxide output (VCO2), end-tidal pressure of oxygen and carbon dioxide (PETO2 and PETCO2), and the gas exchange ratio (R) were also determined at each breath. When the pedaling rate was increased, Q and VE rose in excess of metabolic need with a half response time of about 10 sec, and remained elevated for the duration of the stimulus. VO2 and VCO2 rose transiently, then recovered to the initial control level after a few min. PETCO2 remained at the control level for about one min, then decreased by 1 Torr. PETO2 and R rose transiently. These results suggest that hyperpnea during passive exercise is not induced by chemical stimuli to known chemoreceptors, but is due to reflexes mediated either by moving limbs or the right heart.     

VE response to VCO2 during exercise is unaffected by exercise training and different exercise limbs

We designed two experiments to investigate the relationship between ventilation (VE) and CO2 output (VCO2) during exercise under the conditions of exercising different limbs, the arms as opposed to the legs (experiment 1), and of different physical training states after undergoing standard exercise training for 90 d (experiment 2). Six healthy young subjects underwent submaximal ramp exercise at an incremental work rate of 15 W/min for the arm and leg, and 11 healthy middle-aged subjects underwent an incremental exercise test at the rate of 30 W/3 min before and after exercise training. We measured pulmonary breath-by-breath VE, VCO2, oxygen uptake (VO2), tidal volume (VT), breathing frequency (bf), and end-tidal O2 and CO2 pressures (PETO2, PETCO2) via a computerized metabolic cart. In experiment 1, arm exercise produced significantly greater VE than did leg exercise at the same work rates, as well as significantly higher VO2, VCO2, and bf. The slopes of the regression lines in the VE-VCO2 relationship were not significantly different: the values were 27.8 +/- 2.1 (SD) during the arm exercise, and 25.3 +/- 3.9 during the leg exercise, with no differences in their intercepts. In experiment 2, the VO2, VCO2, and VE responses at the same work rates were similar in both before and after the 90-d exercise training, whereas the heart rate (HR) and mean blood pressure (MBP) were significantly reduced after training. Exercise training did not alter the VE-VCO2 relationship, the slope of which was 31.9 +/- 4.9 before exercise training and 34.2 +/- 4.4 after exercise training. We concluded that the VE-VCO2 relationship during exercise is unaltered, independent of not only working muscle regions but also exercise training states.     

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

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

Comparison of objective methods for determining ventilatory threshold

This study was undertaken to compare and re-examine the relation of lactate threshold (LT) and ventilatory threshold (VT), using six objective determination methods proposed previously. Twenty-one young male subjects performed a cycle exercise test in which the work rate was increased by 150 kg.m every 2 min up to his limit of volitional fatigue. Through each test, gas exchange parameter measurements were made every 1 min (every 30 s at nearly maximal level), and the venous blood samples were taken from a warmed ear lobe at each work rate for determining blood lactate concentration. LT and its variance were determined by the intersecting straight lines regression. LT ranged from 0.72 to 1.40 l/min in terms of VO2, and the mean value of S.D. for each LT was about 0.1 l/min. Each objective method for determining VT used in this study was based on the simple modelling of the criterion for visual detection of VT, that is the non-linear increase in VE or the systematic increase in VE/VO2. When the relationship between LT and VT was examined, VT by the objective methods based on determining minimum value of VE/VO2 showed relatively high consistency with LT. Of 16-20 individuals out of all 21 subjects, there were VT within LT +/- 0.2 in VO2. It is concluded that VE/VO2 is a more sensitive index for detecting VT than VE in the gas exchange parameters, and the objective VT determination method based on minimum value of VE/VO2 could facilitate estimation of LT within an error of +/- 0.2 l/min VO2 in most normal individuals.     

Ventilatory response and arterial potassium concentration during incremental exercise in patients with chronic airways obstruction

The relationship of ventilation response (VE) to arterial potassium concentration (K+) during ramp incremental exercise was assessed in nine patients with chronic obstructive pulmonary disease (COPD), and in 10 healthy subjects. For COPD patients the maximum oxygen uptake (VOmax) was 19.6 +/- 3.8 ml kg-1 min-1 (+/- SD), and percentage of forced expired volume at 1 s (% FEV1) was 47.8 +/- 10.4%. In healthy subjects, VO2max was 44.4 +/- 7.0 ml kg-1 min-1 and FEV1 was 89.7 +/- 7.4%. Breath-by-breath determinations for VE, oxygen uptake (VO2) and carbon dioxide output (VCO2), as well as determinations for K+, partial pressure of oxygen (PO2), partial pressure of carbon dioxide (PCO2), pH and lactate in arterial blood were performed during a workout on an exercise bicycle at a ramp function work rate of 20 W min-1, preceded by a 40 min warm-up period. The major findings in the present study are: (1) that there is a linear relation between ventilation and arterial K+ concentration during ramp exercise in both healthy subjects and COPD patients; (2) that the slope of the VE-K+ relationship is significantly lower in COPD patients (16.2 +/- 7.3 l min-1 mM-1) than in normal subjects (37.4 +/- 6.9 l min-1 mM-1, P less than 0.01); and, (3) that the slope of the VE-K+ relationship is significantly related to the ability to ventilate during maximal exercise in both healthy subjects and COPD patients (P less than 0.05). It is thought that the significantly reduced slope of the VE-K+ relationship in the COPD patients could be interpreted as a reduced sensitivity to the stimulus and/or as a mechanical impairment of the ventilation.     

Hypercapnia during maximal exercise in patients with chronic airflow obstruction

The pattern of breathing during maximal oxygen uptake (Vo2max) was studied in 26 patients with chronic airflow obstruction (CAO), in whom the vital capacity (VC), forced expiratory volume in 1 s (FEV1) and residual volume (RV) were measured. The patients performed, on a cycle ergometer, in a sitting position, a submaximal (A) and a maximal (B) exercise in a single session during which three arterial blood samples (pH, PaCO2, PaO2, lactate) were taken: the first at rest, the second at the 10th min of steady-state 40 W exercise, and the third at maximal VO2. VE, VCO2, VO2, respiratory rate (RR) and VT were measured with an open circuit. Physiological dead space (VD) and alveolar to arterial O2 pressure differences (A-aPO2) were computed. According to the measured value of PaCO2 at maximal exercise, the patients were divided in non-hypercapnic (NH; PaCO2 less than 44 mmHg; n = 17) and hypercapnic (H; PaCO2 greater than 44 mmHg; n = 9) groups, and were compared with a group of normal subjects (N; n = 11). At rest, VC, FEV1, FEV1/VC ratio, TLC and PaO2 were more decreased in H than in NH patients. However, RV, VE, RR and VT did not differ between H and NH patients. PaCO2 at rest was comparable in N and H subjects but was significantly lower in NH patients. During B exercise, VE, VO2 and PaO2 were lower in H patients. With both A and B exercises, the H patients showed a lower VT and VT/VC ratio with a higher VD/VT ratio, while A-aPO2 were the same in NH and H patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolic control of pulmonary ventilation in the developing chick embryo

In birds, during the period from the breaking of the air cell by the beak (internal pipping) to hatching, pulmonary ventilation (VE) begins and gas exchange is jointly provided by the lungs and the chorioallantoic membrane (CAM). We asked to what extent, during this phase of two concurrent gas exchange organs, changes in the embryo's metabolic needs were accompanied by changes in VE. The carbon dioxide and oxygen exchange rates (VCO2, VO2) through lungs and CAM were separately, but simultaneously, measured in chicken embryos at 20-21 days of incubation, while VE was calculated from the measurements of pressure oscillations in the air cell during breathing. During the last 24 h of incubation, lung VO2 and VCO2 gradually progressed as the corresponding CAM values declined. An increase in egg temperature (T) from 33 to 39 degrees C increased the embryo's total metabolic rate, especially when the lungs were the predominant gas exchange route. Whether metabolism increased because of the embryo's development or because of the increase in T, VE was linearly proportional to lung VO2 and VCO2, and not to the embryo's total metabolic rate. Hence, in the developing chick embryo, VE control mechanisms sense the peripheral tissue requirements via the gaseous component of cellular metabolism.     

Respiratory and cardiac responses to dynamic exercise in man

Ventilation (VE), cardiac output (Q), oxygen consumption (VO2), carbon dioxide production (VCO2), and end tidal gas tensions (PETO2 and PETCO2) were measured in four healthy men during stepwise, steady state increases in work rate on a bicycle ergometer (25, 50, 75, 100, 125, and 150 W). Both the ventilation equivalent (VE/VCO2) and the cardiac equivalent (Q/VCO2) for carbon dioxide, fell during a steady state exercise at 150 W to 2/3 and to 1/3 of the initial levels, respectively. This stepwise reduction in the carbon dioxide production with increasing work rate was compatible with a non-chemical stimulus increasing in proportion to work rate, and governing both ventilation and circulation. These observations do not support the cardio-dynamic hypothesis.     

The differences in CO2 kinetics during incremental exercise among sprinters, middle, and long distance runners

The purpose of this study was to investigate the differences in kinetics of CO2 output (VCO2) during incremental exercise in sprinters (S), middle (MD), and long distance runners (LD). In the steady state exercise, the VCO2 was linearly related to the O2 uptake (VO2). In the incremental exercise below anaerobic threshold (AT), the VCO2 was also linearly related to the VO2. The difference between the VCO2 estimates from the regression lines obtained in steady state and incremental exercise was added from the start of exercise up to a given time. The added values were defined as CO2 stores. The CO2 stores per body weight were significantly related to mixed venous CO2 pressure (PVCO2) determined by the CO2 rebreathing method. The slopes of the regression lines between PVCO2 and CO2 stores per body weight were not different among three groups. If VCO2 above AT is estimated from the VO2 using the regression line obtained in incremental exercise below AT, the estimated VCO2 is lower than the measured VCO2. The sum of the differences in VCO2 up to a given time was defined as CO2 excess. The CO2 excess per body weight was significantly related to delta LA (the difference between blood lactates at 5 min after exercise and at rest). The ratios of CO2 excess per body weight to delta LA were 3.30 +/- 1.49, 4.16 +/- 2.33, and 5.55 +/- 2.05 for sprinters, middle, and long distance runners, respectively. This ratio obtained in sprinters was significantly lower than that in long distance runners (p less than 0.01).     

Cardiorespiratory dynamics during sinusoidal and impulse exercise in man

Dynamic characteristics of ventilation, cardiac output, and gas exchange during sinusoidally varying work rates for the periods from 1 to 12 min and impulse work rate with a duration of 10 sec were studied on five healthy men in an upright position. Changes in work rate were given by controlling externally the electromagnetic braking system of a bicycle ergometer. Stroke volume, heart rate, and cardiac output during exercise were determined continuously by using an automated impedance cardiograph. Breath by breath determination in minute ventilation, respiratory frequency, tidal volume, oxygen consumption, carbon dioxide output, end-tidal pressures of oxygen and carbon dioxide, and gas exchange ratio were conducted. From these and steady-state response data amplitude and phase relations between each variable and the input work loads were obtained utilizing the frequency analysis techniques. The response characteristics to sinusoidal stimuli were well represented by first-order models with time constants for VE, VCO2, VO2, and Q averaging 75, 67, 52, and 36 sec, respectively. The kinetics of HR closely resembled that of Q. There was a close link between both the dynamics of VE and VCO2. On the other hand, the responses to impulse stimuli were better described by second-order models in which fast and slow response components were connected in parallel. However, the contribution of the fast component to total response was small. Although this response may support in its form the neuro-humoral concept to explain exercise hyperpnea, a tight linkage was observed between VE and VCO2 responses to impulse stimuli. Thus, hyperpnea during the unsteady-state of exercise may be explained by the cardiodynamic hypothesis.     

Time course study on the stability of the electrode in the oxygen consumption analyzer RM-200

We investigated the stability of the polarographic electrode, the CO2 electrode and the expired minute ventilation value (VE value) in the oxygen consumption analyzer RM-200 over a 6-month duration. A total of analyses 363 were performed on 71 normal subjects. Two methods were used; one is the gas response curve which directly shows the property of the polarographic electrode and the CO2 electrode, and the other is the Douglas bag method which is considered to be a standard method of O2 consumption (VO2) and CO2 output (VCO2) measurement. The gas response curve analyses were performed just after setting a new polarographic electrode, at the third month and at the sixth month. Measurement by the Douglas bag method was usually done once a week. The effects of respiratory rate on the values of VE, VO2 and VCO2 were evaluated from the ratio of each value measured by RM-200 to that obtained by the Douglas bag method. Evaluation by the gas response curve, revealed that the polarographic electrode was stable for 3 months, but not at the six month. The Douglas bag method revealed that a decrease in VO2 value had already occurred after a 4-month use of the polarographic electrode. However, a definite correction of the time constant allowed the use of the electrode up to six months. The VCO2 value and the VE value were stable for 6 months. Increase in the respiratory rate caused a slight but significant difference between VO2 and VCO2 values measured by RM-200 and those obtained by the Douglas bag method, but did not influence the VE values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute physiological effects of exhaustive whole-body vibration exercise in man.

Vibration exercise (VE) is a new neuromuscular training method which is applied in athletes as well as in prevention and therapy of osteoporosis. The present study explored the physiological mechanisms of fatigue by VE in 37 young healthy subjects. Exercise and cardiovascular data were compared to progressive bicycle ergometry until exhaustion. VE was performed in two sessions, with a 26 Hz vibration on a ground plate, in combination with squatting plus additional load (40% of body weight). After VE, subjectively perceived exertion on Borg's scale was 18, and thus as high as after bicycle ergometry. Heart rate after VE increased to 128 min-1, blood pressure to 132/52 mmHg, and lactate to 3.5 mM. Oxygen uptake in VE was 48.8% of VO2max in bicycle ergometry. After VE, voluntary force in knee extension was reduced by 9.2%, jump height by 9.1%, and the decrease of EMG median frequency during maximal voluntary contraction was attenuated. The reproducibility in the two VE sessions was quite good: for heart rate, oxygen uptake and reduction in jump height, correlation coefficients of values from session 1 and from session 2 were between 0.67 and 0.7. Thus, VE can be well controlled in terms of these parameters. Surprisingly, an itching erythema was found in about half of the individuals, and an increase in cutaneous blood flow. It follows that exhaustive whole-body VE elicits a mild cardiovascular exertion, and that neural as well as muscular mechanisms of fatigue may play a role.     

Modulating effects of the menstrual cycle on cardiorespiratory responses to exercise under acute hypobaric hypoxia

The purpose of this study was to examine the hypothesis that the menstrual cycle-induced modulation of the cardiorespiratory response to exercise might be altered by acute exposure to altitude. During both the luteal and follicular phases, 9 moderately trained female subjects with normal menstrual cycles performed incremental exercise to maximal effort on a cycle ergometer at sea level (SL) and under hypobaric hypoxia (HH) at the equivalent of 3,000 m altitude. Both at rest and during exercise, minute ventilation (.VE) and oxygen uptake (.VO(2)) did not differ between the luteal and follicular phases (either at SL or HH). However, the ratio of .VE to .VO(2) (.VE /.VO(2)), both at rest and during peak exercise, was greater in the luteal phase than in the follicular phase under HH conditions. Furthermore, the partial pressure of end-tidal carbon dioxide (PETCO(2)) during exercise was lower in the luteal phase than in the follicular phase in HH. These results suggest that the menstrual cycle-induced modulation of the ventilatory response to exercise may be altered under acute hypobaric-hypoxic conditions.     

Training profile counts for time-to-exhaustion performance.

The objective of this study was to compare the time to exhaustion (Tlim) at maximal aerobic speed (v.VO2max) in middle- and long-distance runners. Five middle-distance (MDR) and 5 long-distance (LDR) male runners, ages 28 +/- 7 years, were tested running on a treadmill, with the Université de Montréal Track Test (UMTT), on maximal velocity and on time-to-exhaustion track tests. During the laboratory test, cardiorespiratory variables (e.g., HR, .VO2max, .VCO2, .VE) were assessed. Second, running velocity at .VO2max (v.VO2max) during the UMTT was determined and HR values were recorded; also, maximal velocity on a 30-m sprint (V30) and maximal heart rate (HR max) and time to exhaustion were determined on the track. No significant difference was observed between groups during the multistage treadmill test. Significant differences were found between groups for V30 and Tlim, with MDR showing a 23% longer running time than LDR. The results of the present study demonstrated that the training profile of middle-distance and long-distance runners plays a significant role in Tlim performance when v.VO2max is obtained during a test with short-duration stages.     

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

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