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).     

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.     

Kinetics of excess CO2 output during and after intensive exercise.

In order to clarify the kinetics of excess CO2 output during and after intensive exercise, six male subjects were each instructed to perform 40-, 60- and 80-s cycle ergometer exercises (282 +/- 9 W, 90 rpm). Ventilation and gas exchange parameters were recorded breath-by-breath, and lactate concentration (La) was repeatedly measured with blood samples from a finger tip. The increase in La from the resting value to peak value and the duration of exercise showed a significant linear relationship (r = 0.91, p<0.01) passing through zero, indicating that lactic acid was produced at a constant rate in working muscles from the beginning of exercise. However, in contrast to this increase in La, excess V.CO2, defined as the difference between V.CO2 and V.O2, showed a temporary negative value after the start of exercise. Subsequently, excess V.CO2 became positive, reaching a peak at 60 s post-exercise, and then decreased down to zero at about 9 min after the end of the 80-s exercise. End-tidal CO2 rose above the pre-exercise level during exercise and at about 3 min post-exercise, and thereafter remained below the pre-exercise level. Excess CO2, calculated by the sum of excess V. CO2 from the start of exercise to the 10th min after the end of exercise, was significantly COrrelated with the increase in La from resting to 10 min post-exercise (r = 0.88, p<0.01). These results suggest that although excessive CO2 output (excess CO2) in response to intensive exercise is related to the increase in lactic acid, the time course of excessive CO2 output (excess V.CO2) is delayed, relative to the production of lactic acid, and is affected by hyperventilation.     

Ventilatory response to the onset of passive and active exercise in human subjects.

Ventilatory responses at the onset of passive and active exercise with different amount of exercising muscle mass were studied in 10 healthy male subjects. Four exercise tests were performed for each subject with appropriate intervals on the same day, i.e., two voluntary exercises of one leg or both legs and two passive exercises of one leg or both legs. Inspiratory minute volume (VI), end-tidal CO2 and O2 partial pressures (PETCO2, PETO2) were measured breath-by-breath using a hot-wire flowmeter, infrared CO2 analyzer, and a rapid O2 analyzer. Average values of VI were obtained from 5 breaths at rest preceding exercise and the first and second breaths after the onset of exercise. The ventilatory response to exercise was calculated as the difference (delta) between the mean of exercise VI and mean of resting VI. In this study, the PETCO2 decreased by about 0.5 Torr in four exercise tests, though the decrement of PETCO2 was not statistically significant. The average values and standard deviation of delta VI were 4.22 +/- 1.63 l/min for the one leg and 6.46 +/- 1.80 l/min for the two legs in the active exercise, and were 2.46 +/- 1.12 l/min for the one leg and 3.44 +/- 1.55 l/min for the two legs in the passive exercise, respectively. These results suggest that in awake conditions, the ventilatory response at the onset of passive or active exercise does not increase additively with the increasing amount of muscle mass being exercised.     

A constant flux of carbon dioxide injected into the airways mimics metabolic carbon dioxide in exercise

This paper reports the expired minute-ventilation (VE) responses of 5 subjects to three step levels in a) work rate on a bicycle ergometer (30, 50, and 70 W), b) inhaled constant fraction (CF) of CO2 (3, 5, and 7%), and c) inhaled constant flux (CFlux) of CO2 (0.3, 0.4, and 0.5 l/min (STPD) injected in the inspired air-stream). Both exercise (isocapnic with regulated PETCO2) and CFlux provoke larger and similar steady-state responses in VE, than CF. Both the CF and CFlux responses are hypercapnic, but the CFlux responses show evidence of "hypercapnic regulation." VE and total CO2 input into the alveoli (i.e., VCO2 plus inhaled CO2) are excellently correlated in both the CF and the CFlux cases. However, the CFlux delivery provokes a far greater VE for a given total input of CO2 than CF, and the CFlux response resembles the VE/VCO2 plot of exercise. We conclude that CFlux inhalation of CO2 simulates the metabolic CO2 production rate of exercise, and thus the humoral aspects of exercise hyperpnea in the steady state.     

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.     

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.     

Oxygen consumption following exercise of moderate intensity and duration

Summary To study the effects of exercise intensity and duration on excess postexercise oxygen consumption (EPOC), 8 men [age= 27.6 (SD 3.8) years, VO_2max = 46.1 (SD 8.5) ml min^–1 kg^–1] performed four randomly assigned cycle-ergometer tests (20 min at 60% VO_2max, 40 min at 60% VO_2max, 20 min at 70% VO_2max, and 40 min at 70% VO_2max). O₂ uptake, heart rate and rectal temperature were measured before, during, and for 1 h following the exercise tests. Blood for plasma lactate measurements was obtained via cannulae before, and at selected times, during and following exercise. VO₂ rapidly declined to preexercise levels following each of the four testing sessions, and there were no differences in EPOC between the sessions. Blood lactate and rectal temperature increased (P<0.05) with exercise, but had returned to preexercise levels by 40 min of recovery. The results indicate that VO₂ returned to resting levels within 40 min after the end of exercise, regardless of the intensity (60% and 70% VO_2max or duration (20 min and 40 min) of the exercise, in men with a moderate aerobic fitness level.     

Analysis of end-tidal and arterial PCO2 gradients using a breathing model

The aim of this paper was to analyse the difference between end-tidal carbon dioxide tension (PETCO2) and arterial carbon dioxide tension (PaCO2) at rest and during exercise using a homogeneous lung model that simulates the cyclic feature of breathing. The model was a catenary two-compartment model that generated five non-linear first-order differential equations and two equations for gas exchange. The implemented mathematical modelling described variations in CO2 and O2 compartmental fractions and alveolar volume. The model also included pulmonary capillary gas exchange. Ventilatory experimental data were obtained from measurements performed on a subject at rest and during four 5-min bouts of exercise on a cycle ergometer at 50, 100, 150 and 200 W, respectively. Analysis of the PETCO2-PaCO2 difference between experimental and sinusoidally adjusted ventilatory flow profiles at rest and during exercise showed that the model produced similar values in PETCO2-PaCO2 for different respiratory flow dynamics (P approximately equal to 0.75). The model simulations allowed us to study the effects of metabolic, circulatory and respiratory parameters on PETCO2-PaCO2 at rest and during exercise. During exercise, metabolic CO2 production, O2 uptake and cardiac output affected significantly the PETCO2-PaCO2 difference from the 150-W workload (P < 0.001). The pattern of breathing had a significant effect on the PETCO2-PaCO2 difference. The mean (SD) PETCO2-PaCO2 differences simulated using experimental profiles were 0.80 (0.95), 1.65 (0.40), 2.40 (0.20), 3.30 (0.30) and 4.90 (0.20) mmHg, at rest and during exercise at 50, 100, 150 and 200 W, respectively. The relationship between PETCO2-PaCO2 and tidal volume was similar to data published by Jones et al. (J Appl Physiol 47: 954-960, 1979).     

Effect of hypoxia and hyperoxia on cardiorespiratory responses during exercise in man

To clarify the role of the carotid body in the mechanism governing exercise hyperpnea, the effect of hypoxia and hyperoxia on ventilation and cardiac output was studied in four healthy men. The VE increased 10.7% in hypoxia and decreased 10.1% in hyperoxia from normoxia as judged from the steady-state values during exercise. On the contrary, Q showed only a slight reduction of -3.2% in hyperoxia. The hypoxic hyperpnea and hyperoxic hypopnea led to a concomitant alteration in PETCO2. An overshoot following the onset of exercise was observed during the first 30s of VE response in hypoxia, which damped progressively in normoxia and hyperoxia. No remarkable difference was observed in the early transient responses of Q between hypoxia and hyperoxia. The discrepancy in the dynamics between VE and Q led to a phasic deviation in PETCO2; an isocapnic transition from the control to stimulus period in normoxia, hypocapnic in hypoxia and hypercapnic in hyperoxia. The time constant representing the kinetics of VE and that for VCO2 prolonged significantly in hyperoxia. These results support the cardiodynamic consequence of exercise hyperpnea, i.e., the carotid body is the first to respond to the increase in CO2 flow into the lungs.     

Respiratory compensation point during incremental exercise as related to hypoxic ventilatory chemosensitivity and lactate increase in man

The pulmonary ventilation-O2 uptake (VE-VO2) relationship during incremental exercise has two inflection points: one at a lower VO2, termed the ventilatory threshold (VT); and another at a higher VO2, the respiratory compensation point (RCP). The individuality of RCP was studied in relation to those of the chemosensitivities of the central and peripheral chemoreceptors, which were assessed by resting estimates of hypercapnic ventilatory response (HCVR) and hypoxic ventilatory response (HVR), respectively, and the rate of lactic acid increase during exercise, which was estimated as a slope difference (delta slope) between a lower slope of VCO2-VO2 relationship (VCO2:CO2 output) obtained at work rates below VT and a higher slope at work rates between VT and RCP. Twenty-two male and sixteen female subjects underwent a 1 min incremental exercise test until exhaustion, in which VT, RCP and delta slope were determined. All measures were normalized for body surface area. In the males, the individual difference in RCP was inversely correlated with those of HVR and delta slope (p < 0.05), and in the females, similar tendencies persisted, while the correlation did not reach statistically significant levels (0.05 < p < 0.1). There was no significant correlation between RCP and HCVR in either sex. A multiple linear regression analysis showed that 40 to 50% of the variance of RCP was accounted for by those of HVR and delta slope, both of which were related linearly and additively to RCP, this relation being manifested in the males but not in the females without consideration of the menstrual cycle. These results suggest that the individuality of RCP depends partly on the chemosensitivity of the carotid bodies and the rate of lactic acid increase during incremental exercise.     

The effect of thymoxamine and cromolyn sodium on postexercise bronchoconstriction in asthma.

Of the 22 patients with extrinsic bronchial asthma, 13 patients developed post-exercise bronchoconstriction after treadmill exercise, whereas in 9 patients treadmill exercise had no effect on the ventilatory capacity. No statistical difference in the resting lung volumes and CO transfer factor was found between the two groups. A significant inhibition of postexercise bronchoconstriction was observed in 12 of 13 patients following thymoxamine or cromolyn sodium inhalation. Inhibition of postexercise bronchoconstriction by alpha blockade with thymoxamine suggests that increased alpha adrenergic activity in the presence of diminished beta receptor responsiveness to catecholamines, norepinephrine released during exercise could have a marked alpha agonistic effect giving rise to bronchoconstriction. It has been suggested that cromolyn sodium has a cyclic phosphodiesterase inhibiting action. This might increase levels of AMP and restore the beta receptor responsiveness to catecholamines.     

Effect of airway anaesthesia on the ventilatory and heart rate responses to isocapnic progressive hypoxia

The effect of airway anaesthesia by lidocaine inhalation on the hypoxic ventilatory response was examined together with the heart rate response by the isocapnic progressive hypoxia test in human subjects. During the test, end-tidal PCO2 (PETCO2) was maintained at the resting level. However, because resting PETCO2 tends to decrease by airway anaesthesia, we conducted the test at the resting PETCO2 determined both before (normocapnic) and after lidocaine (hypocapnic). Ventilatory and heart rate response were evaluated as a linear function of oxygen saturation of the arterial blood (SaO2). In the "hypocapnic" runs, ventilatory responses tended to be depressed, while the slope of heart rate response-PETCO2 relationship increased after lidocaine. However, when PETCO2 was restored to the normocapnic level, ventilation apparently increased from the control, and the augmented slope in the heart rate response disappeared. Although the elevated ventilation in normocapnic hypoxia might be due simply to the increased ventilatory response to CO2, we suggested that the augmented slope in the heart rate response in hypocapnic hypoxia might be related not only to PETCO2 level itself but also to the direct effect of airway anaesthesia.     

The pulmonary vascular response to the sustained activation of the muscle metaboreflex in man

The pulmonary circulation is influenced by the autonomic nervous system, yet whether this is physiologically important during exercise in man is not known. The aim of this study was to assess the pulmonary vascular response to sympathoexcitation induced by the maintained activation of the muscle metaboreflex in the postexercise period. Nine healthy subjects performed isometric handgrip exercise at 50% of their maximal voluntary contraction force for 2 min. Exercise was followed by circulatory occlusion so as to maintain the muscle metaboreflex activated for 2 min (postexercise circulatory occlusion; PECO). Blood pressure measurements and echocardiographically determined estimates of systolic pulmonary artery pressure (SPAP) and cardiac output were obtained at various intervals throughout the two protocols. Compared with baseline values, elevations in SPAP (by 20.06 +/- 2.08%), cardiac output (by 36.04 +/- 4.97%) and mean arterial pressure (MAP; by 25.62 +/- 3.54%) were noted during isometric exercise (means +/- s.e.m., all P < 0.05). Increases in SPAP and MAP persisted during PECO (all P < 0.05), whereas cardiac output returned to resting levels. Our findings suggest that the sympathoexcitation induced by isometric exercise affects the pulmonary circulation, possibly by inducing vasoconstriction and/or stiffening the large conduit arteries. The exaggerated activation of the sympathetic nervous system that has been evidenced in cardiopulmonary patients could therefore be implicated in their abnormal pulmonary haemodynamic responses and intolerance of exercise.     

Effects of epinephrine and lactate on the increase in oxygen consumption of nonexercising skeletal muscle after aerobic exercise

The purpose of this study was to measure O2 consumption of nonexercising skeletal muscles (VO2nonex) at rest and after aerobic exercise and to investigate the stimulant factors of O2 consumption. In experiment 1, we measured the resting metabolic rate of the finger flexor muscles in seven healthy males by 31P-magnetic resonance spectroscopy during a 15 min arterial occlusion. In experiment 2, the VO2nonex of the finger flexor muscles was measured using near infrared continuous wave spectroscopy at rest, immediate postexercise, and 3, 5, 10, 15, and 20 min following a cycling exercise at a workload corresponding to 50% of peak pulmonary O2 uptake for 20 min. We also monitored deep tissue temperature in the VO2nonex measurement area and determined catecholamines and lactate concentrations in the blood at rest and immediate postexercise. VO2nonex at rest was 1.1 +/- 0.1 microM O2/S (mean +/- standard error) and VO2nonex after exercise increased 59.6 +/- 7.2% (p < 0.001) from the resting values. There were significant correlations between the increase in VO2nonex and the increase in epinephrine concentration (p < 0.01), and between the increase in VO2nonex and the increase in lactate concentration (p < 0.05). These results suggest that epinephrine and lactate concentrations are important VO2nonex stimulant factors.     

Arterial to end-tidal PCO2 difference varies with different ventilatory conditions during steady state hypercapnia in the rat

To estimate the influence of ventilatory conditions on the CO2 equilibration between the alveolar gas and arterial blood during steady state hypercapnia, we measured arterial and end-tidal PCO2 (PaCO2, PETCO2) of the anesthetized rat under the following three conditions: spontaneously breathing with CO2 inhalation, artificial respiration with gas mixture containing CO2, and artificial respiration with reduced ventilatory volume (hypoventilation). In each ventilatory condition, PaCO2 correlated linearly with PETCO2. However, in spontaneously breathing animals, the PaCO2-PETCO2 difference which was positive in a control condition (without CO2 inhalation) became negative during CO2 inhalation. The mean (+/- S.D.) difference was -3.6 +/- 1.5 mmHg (n = 9, p less than 0.001) at the PETCO2 range from 72 to 77 mmHg. During artificial respiration with constant ventilatory volume, initial positive PaCO2-PETCO2 difference approached zero when CO2 was administered into inspiratory gas. In both ventilatory conditions the slope of the PETCO2-PaCO2 relation line was less than 1.0, whereas the PaCO2-PETCO2 difference remained positive when PCO2 level was increased with reducing the ventilatory volume (accumulation of endogenous CO2). These observations suggest that for a given increase in PCO2 by administration of exogenous CO2, the extent to which PaCO2 increases is smaller than that of PETCO2. This peculiar relationship together with changes in breathing pattern during CO2 inhalation likely results in "negative" PaCO2-PETCO2 difference in the spontaneously breathing animal. We conclude that the PaCO2-PETCO2 difference, either as positive or negative values, depends upon both the level of PCO2 and the ventilatory condition to increase PCO2.     

Effects of exercise and alkalosis on serum insulin-like growth factor I and IGF-binding protein-3.

This investigation examines the effects of orally induced alkalosis on serum IGF-I and IGFBP3 concentrations in response to an acute 90-s bout of high intensity cycle exercise. Ten healthy, active men, ages 24.60 +/- 4.90 years, participated in a randomized, double-blind, counterbalanced trial order with a cross-over design. Subjects ingested an experimental bicarbonate solution or a placebo solution. Blood was sampled at baseline; pre-exercise; and 0, 5, 10, and 30 min postexercise. The pH between groups for pre-exercise and postexercise time points differed significantly (p < or = .05) in the experimental condition (from 7.42 +/- 0.01 to 7.35 +/- 0.02) versus the placebo condition (from 7.36 +/- 0.01 to 7.25 +/- 0.03). Increases in IGF-I over resting conditions occurred with placebo conditions at 5 and 10 min postexercise and in the experimental condition at 5 min postexercise. Concentrations of IGFBP3 were elevated above baseline at IP in both experimental and placebo conditions.     

Resting mechanomyography after aerobic exercise.

A number of mechanisms have been proposed for the elevation in oxygen consumption following exercise. Biochemical processes that return muscle to its preexercise state do not account for all the oxygen consumed after exercise. It is possible that mechanical activity in resting muscle, which produces low frequency vibrations (i.e., muscle sounds: mechano-myographic [MMG] activity), could contribute to the excess postexercise oxygen consumption. Therefore the purpose of this study was to determine whether the resting MMG amplitude changes after exercise, and whether the change is related to the elevation in oxygen consumption (VO2). Ten young male subjects (22.9 yrs) performed 30 minutes of exercise on a cycle ergometer at an intensity corresponding to 70% peak VO2. Oxygen consumption was measured by indirect calorimetry, and MMG by an accelerometer placed over the mid-quadriceps before exercise and for 5.5 hours after exercise. MMG activity, expressed as mean absolute acceleration, was significantly elevated for the 5.5 hours of measurement after exercise (p < 0.05). MMG and VO2 decayed exponentially after exercise with time constants of 7.2 minutes and 7.4 minutes, respectively. We conclude that muscle is mechanically active following exercise and that this may contribute to an elevated VO2.     

Preload maintenance and the left ventricular response to prolonged exercise in men

This study examined whether left ventricular function was reduced during 3 h of semi-recumbent ergometer cycling at 70% of maximal oxygen uptake while preload to the heart was maintained via saline infusion. Indices of left ventricular systolic function (end-systolic blood pressure-volume relationship, SBP/ESV) and diastolic filling (ratio of early to late peak filling velocities into the left ventricle, E:A) were calculated during recovery and compared with baseline resting data. During exercise in seven healthy, trained male subjects, an arterial catheter allowed continuous assessment of arterial pressure, stroke volume (SV), cardiac output ( ) and an index of contractility (dP/dt(max)). A venous catheter assessed that central venous pressure (CVP) was maintained throughout rest, exercise and 10 min into recovery. Both systolic blood pressure and heart rate (HR) increased with the onset of exercise (from 132 +/- 5 to 185 +/- 19 mmHg and from 66 +/- 9 to 135 +/- 23 beats min(-1); increases from rest to the end of the first 5 min of exercise in SBP and HR, respectively) but systolic blood pressure did not change from 30 to 180 min of exercise ( approximately 150 mmHg), while heart rate only increased by 8 +/- 9 beats min(-1) (means +/- s.d.; P > 0.05). The attenuated increase in HR compared with other studies suggests that the maintained CVP ( approximately 5 mmHg) helped to prevent cardiovascular drift in this protocol. Stroke volume, and dP/dt(max) were all increased with the onset of exercise (from 85 +/- 8 to 120 +/- 18 ml, from 5.4 +/- 1.3 to 16.5 +/- 3.3 l min(-1) and from 14.4 +/- 4 to 28 +/- 8 mmHg s(-1); values from rest to the end of the first 5 min of exercise for SV, and dP/dt(max), respectively) and were maintained during exercise. There was no difference in the SBP/ESV ratio from pre- to postexercise. Conversely, E:A was reduced from 2.0 +/- 0.4 to 1.6 +/- 0.5 postexercise (P < 0.05), returning to normal values at 24 h postexercise. This change in diastolic filling could not be fully explained (r(2) = 0.39) by an increased heart rate and, with CVP unchanged, it is likely to represent some depression of intrinsic relaxation properties of left ventricular myocytes. Three hours of semi-supine cycling resulted in no evidence of a depression in left ventricular systolic function, while left ventricular diastolic function declined postexercise.     

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.