Cardiac Output Kinetics Research Articles

Abstract 13282: Oxygen Uptake and Cardiac Output Exhibit Delayed Recovery After Maximum Incremental Ramp Exercise in Patients With Exercise Pulmonary Hypertension

Introduction: In individuals with dyspnea on exertion (DOE) and suspected exercise pulmonary hypertension (exPH), oxygen uptake (VO 2 ), cardiac output (CO), peripheral oxygen extraction (Ca-vO 2 ), and mean pulmonary artery pressure (mPAP) have been well characterized during incremental exercise but less is known about the kinetics of post-exercise recovery patterns. Hypothesis: Exercise recovery cardiac output kinetics are slowed in patients with exPH. Methods: Upright maximum incremental ramp cycle ergometry cardiopulmonary exercise testing with invasive hemodynamic monitoring and serial blood gas measurements during exercise and recovery was performed in 50 consecutive patients referred for evaluation of DOE of unclear etiology. VO 2 , arterial and venous oxygen content (Ca-vO 2 ), Fick cardiac output, and mPAP were analyzed from rest, peak exercise, and 2 minutes post-exercise. ExPH was defined in a consistent manner with recent consensus statements (ΔmPAP/ΔCO >3.0 mmHg/L/min) from rest to peak exercise. Results: Among 50 patients with DOE, [62% female, Age 61.7±11.8, BMI 30.7±8.2] 2-min post-exercise VO 2 was -56±11%, CO: -22±19%, Ca-vO 2 :-42±15% compared to peak exercise values. The % fall in CO at 2min was significantly lower in the 26 patients with exPH compared to the 24 patients without exPH (Table). The average mPAP remained elevated at 2 min post-exercise (>20mmHg) in exPH despite normal average resting values. Conclusions: Patients with exPH demonstrate slowed CO recovery kinetics in conjunction with persistent PAP elevation 2-min post-exercise. Persistent elevation in blood flow through the pulmonary circuit at a time conducive to non-invasive assessment of PAP (i.e. by echocardiography) may lend itself to non-invasive detection of exercise-PH in patients undergoing evaluation of dyspnea on exertion.

Effects of high-intensity interval training on central haemodynamics and skeletal muscle oxygenation during exercise in patients with chronic heart failure.

Background High-intensity interval training (HIT) improves exercise capacity in patients with chronic heart failure (CHF). Moreover, HIT was associated with improved resting cardiac function. However, the extent to which these improvements actually contribute to training-induced changes in exercise capacity remains to be elucidated. Therefore, we evaluated the effects of HIT on exercising central haemodynamics and skeletal muscle oxygenation. Methods Twenty-six CHF patients were randomised to a 12-week 4 × 4 minute HIT program at 85-95% of peak VO2 or usual care. Patients performed maximal and submaximal cardiopulmonary exercise testing with simultaneous assessment of cardiac output and skeletal muscle oxygenation by near infrared spectroscopy, using the amplitude of the tissue saturation index (TSIamp). Results Peak workload increased by 11% after HIT ( p between group = 0.01) with a non-significant increase in peak VO2 (+7%, p between group = 0.19). Cardiac reserve increased by 37% after HIT ( p within group = 0.03, p between group = 0.08); this increase was not related to improvements in peak workload. Oxygen uptake recovery kinetics after submaximal exercise were accelerated by 20% ( p between group = 0.02); this improvement was related to a decrease in TSIamp ( r = 0.71, p = 0.03), but not to changes in cardiac output kinetics. Conclusion HIT induced improvements in maximal exercise capacity and exercising haemodynamics at peak exercise. Improvements in recovery after submaximal exercise were associated with attenuated skeletal muscle deoxygenation during submaximal exercise, but not with changes in cardiac output kinetics, suggesting that the effect of HIT on submaximal exercise capacity is mediated by improved microvascular oxygen delivery-to-utilisation matching.

The relation between cardiac output kinetics and skeletal muscle oxygenation during moderate exercise in moderately impaired patients with chronic heart failure.

Oxygen uptake (V̇o2) kinetics are prolonged in patients with chronic heart failure (CHF). This may be caused by impaired oxygen delivery or skeletal muscle derangements. We investigated whether impaired cardiac output (Q̇) kinetics limit skeletal muscle oxygen delivery relative to the metabolic demands at submaximal exercise in CHF patients by evaluating the relation between Q̇ kinetics and skeletal muscle deoxygenation. Forty-three CHF patients, NYHA II-III, performed a constant-load exercise test at 80% of the ventilatory aerobic threshold (VAT) to assess V̇o2 kinetics (τV̇o2). Q̇ kinetics (τQ̇) were assessed by a radial artery pulse contour analysis method. Skeletal muscle deoxygenation was assessed by near infrared spectroscopy at the m. vastus lateralis, using the minimal value of the tissue saturation index during onset of exercise (TSImin). Patients were categorized in slow and normal Q̇ responders relative to metabolic demands (τQ̇/V̇o2 ≥1 and τQ̇/V̇o2 <1, respectively), τQ̇ (62 ± 29 s), and τV̇o2 (60 ± 21 s) were significantly related (r = 0.66, P = 0.001). There was a significant correlation between τQ̇ and TSImin in the slow Q̇ responders [rs= -0.57, P = 0.005, n = 22 (51%)]. In conclusion, in moderately impaired CHF patients with relatively slow Q̇ kinetics, central hemodynamics may limit skeletal muscle oxygenation during moderate-intensity exercise.

Kinetics of Cardiac Output at the Onset of Exercise in Precapillary Pulmonary Hypertension.

Purpose. Cardiac output (CO) is a cornerstone parameter in precapillary pulmonary hypertension (PH). The Modelflow (MF) method offers a reliable noninvasive determination of its beat-by-beat changes. So MF allows exploration of CO adjustment with the best temporal resolution. Methods. Fifteen subjects (5 PH patients, 10 healthy controls) performed a submaximal supine exercise on a cycle ergometer after 5 min of rest. CO was continuously determined by MF (COMF). Kinetics of heart rate (HR), stroke volume (SV), and CO were determined with 3 monoexponential models. Results. In PH patients, we observed a sudden and transitory drop of SV upon exercise onset. This implied a transitory drop of CO whose adjustment to a new steady state depended on HR increase. The kinetics of HR and CO for PH patients was slower than that of controls for all models and for SV in model 1. SV kinetics was faster for PH patients in models 2 and 3. Conclusion. This is the first description of beat-by-beat cardiovascular adjustments upon exercise onset in PH. The kinetics of HR and CO appeared slower than those of healthy controls and there was a transitory drop of CO upon exercise onset in PH due to a sudden drop of SV.

On- and off-exercise kinetics of cardiac output in response to cycling and walking in COPD patients with GOLD Stages I–IV

Exercise-induced dynamic hyperinflation and large intrathoracic pressure swings may compromise the normal increase in cardiac output (Q) in Chronic Obstructive Pulmonary Disease (COPD). Therefore, it is anticipated that the greater the disease severity, the greater would be the impairment in cardiac output during exercise. Eighty COPD patients (20 at each GOLD Stage) and 10 healthy age-matched individuals undertook a constant-load test on a cycle-ergometer (75% WRpeak) and a 6min walking test (6MWT). Cardiac output was measured by bioimpedance (PhysioFlow, Enduro) to determine the mean response time at the onset of exercise (MRTon) and during recovery (MRToff). Whilst cardiac output mean response time was not different between the two exercise protocols, MRT responses during cycling were slower in GOLD Stages III and IV compared to Stages I and II (MRTon: Stage I: 45±2, Stage II: 65±3, Stage III: 90±3, Stage IV: 106±3s; MRToff: Stage I: 42±2, Stage II: 68±3, Stage III: 87±3, Stage IV: 104±3s, respectively). In conclusion, the more advanced the disease severity the more impaired is the hemodynamic response to constant-load exercise and the 6MWT, possibly reflecting greater cardiovascular impairment and/or greater physical deconditioning.

Effects of priming exercise on the speed of adjustment of muscle oxidative metabolism at the onset of moderate-intensity step transitions in older adults

Aging is associated with a functional decline of the oxidative metabolism due to progressive limitations of both O(2) delivery and utilization. Priming exercise (PE) increases the speed of adjustment of oxidative metabolism during successive moderate-intensity transitions. We tested the hypothesis that such improvement is due to a better matching of O(2) delivery to utilization within the working muscles. In 21 healthy older adults (65.7 ± 5 yr), we measured contemporaneously noninvasive indexes of the overall speed of adjustment of the oxidative metabolism (i.e., pulmonary Vo(2) kinetics), of the bulk O(2) delivery (i.e., cardiac output), and of the rate of muscle deoxygenation (i.e., deoxygenated hemoglobin, HHb) during moderate-intensity step transitions, either with (ModB) or without (ModA) prior PE. The local matching of O(2) delivery to utilization was evaluated by the ΔHHb/ΔVo(2) ratio index. The overall speed of adjustment of the Vo(2) kinetics was significantly increased in ModB compared with ModA (P < 0.05). On the contrary, the kinetics of cardiac output was unaffected by PE. At the muscle level, ModB was associated with a significant reduction of the "overshoot" in the ΔHHb/ΔVo(2) ratio compared with ModA (P < 0.05), suggesting an improved O(2) delivery. Our data are compatible with the hypothesis that, in older adults, PE, prior to moderate-intensity exercise, beneficially affects the speed of adjustment of oxidative metabolism due to an acute improvement of the local matching of O(2) delivery to utilization.

Comment on “On the method of fitting cardiac output kinetics in severe exercise” by Richard L. Hughson and Azmy Faisal in Eur J Appl Physiol DOI 10.1007/s00421-010-1787-x

Dr. Hughson and Dr. Faisal in their original article ‘‘On themethod of fitting cardiac output kinetics in severe exer-cise’’, published on the European Journal of AppliedPhysiology, commented on the approach applied to fit thekinetics of the cardiac output during supra maximal exer-cise (i.e. above V_O

On the method of fitting cardiac output kinetics in severe exercise

The kinetic responses of oxygen uptake (VO₂) and cardiac output (Q) describe the rate at which these physiological variables approach the required steady state value with work rate transitions. In this issue of the Journal, Adami and colleagues examined the kinetic responses during the transition to severe intensity exercise (metabolic demands exceeding maximal VO₂). Two methods were described for fitting VO₂ kinetics: one was an exponential model that referenced the time course of VO₂ relative to an apparent plateau while the second examined the rate of change with respect to the value predicted to be 120% of maximal VO₂. The rate of change of the primary adaptive component described by the time constant (tau2) was considerably slower when referenced to the predicted VO₂ (62.5 s) than when fit by the exponential model (20.3 s). For the description of Q kinetics Adami and colleagues fitted only the exponential model. We investigated the impact of fitting the kinetics of Q relative to a predicted value for this severe work rate as was done for VO₂. The time course for Q was reconstructed from their group mean fitting parameters then referenced to values for the required Q based on the literature. The estimate for the time constant (tau2) exceeded the value determined from the exponential model in which the curve fit was referenced to an apparent plateau by more than sixfold (86.4 s vs. 13.5 s). This outcome suggests that future investigations should explore further the dynamic interactions of metabolic regulatory factors and the limitations of the O₂ supply system when describing the system kinetics.

Prior moderate and heavy exercise accelerate oxygen uptake and cardiac output kinetics in endurance athletes

Cardiorespiratory interactions at the onset of dynamic cycling exercise are modified by warm-up exercises. We tested the hypotheses that oxygen uptake (Vo(2)) and cardiac output (Q) kinetics would be accelerated at the onset of heavy and moderate cycling exercise by warm-up. Nine male endurance athletes (peak Vo(2): 60.5 +/- 3.2 ml.min(-1).kg(-1)) performed multiple rides of two different 36-min cycling protocols, involving 6-min bouts at moderate and heavy intensities. Breath-by-breath Vo(2) and beat-by-beat stroke volume (SV) and Q, estimated by Modelflow from the finger pulse, were measured simultaneously with kinetics quantified from the phase II time constant (tau(2)). One novel finding was that both moderate (M) and heavy (H) warm-up bouts accelerated phase II Vo(2) kinetics during a subsequent bout of heavy exercise (tau(2): after M = 22.5 +/- 2.7 s, after H = 22.1 +/- 2.9 vs. 26.2 +/- 3.2 s; P < 0.01). Q kinetics in heavy exercise were accelerated by both warm-up intensities (tau(2): M = 22.0 +/- 4.1 s, H = 23.8 +/- 5.6 s vs. 27.4 +/- 7.2 s; P < 0.05). During moderate exercise, prior heavy-intensity warm-up (one or two bouts) accelerated Vo(2) kinetics and elevated Q at exercise onset, with no changes in Q kinetics. A second novel finding was a significant overshoot in the estimate of SV from Modelflow in the first minutes of each moderate and heavy exercise bout. These findings suggest that the acceleration of Vo(2) kinetics during heavy exercise was enabled by the acceleration of Q kinetics, and that rapid increases in Q at the onset of moderate and heavy exercise might result, in part, from an overshoot of SV.

Are oxygen uptake kinetics in chronic heart failure limited by oxygen delivery or oxygen utilization?

Background The delay in O 2 uptake kinetics during and after submaximal physical activity (O 2 onset and recovery kinetics, respectively) correlates well with the functional capacity of patients with chronic heart failure (CHF). This study examined the physiological background of this delay in moderately impaired CHF patients by comparing kinetics of cardiac output ( Q̇) and O 2 uptake ( V̇ O 2 ). Methods Fourteen stable CHF patients (New York Heart Association class II–III) and 8 healthy subjects, matched for age and body mass index, were included. All subjects performed a submaximal constant-load exercise test to assess O 2 uptake kinetics. Furthermore, in 10 CHF patients Q̇ was measured by a radial artery pulse contour analysis method, which enabled the simultaneous modelling of exercise-related kinetics of Q̇ and V̇ O 2 . Results Both O 2 onset and recovery kinetics were delayed in the patient group. There were no significant differences between the time constants of Q̇ and V̇ O 2 during exercise-onset (62 ± 25 s versus 59 ± 28 s, p = 0.51) or recovery (61 ± 25 s versus 57 ± 20 s, p = 0.38) in the patient group, indicating that O 2 delivery was not in excess of the metabolic demands in these patients. Conclusion The delay in O 2 onset and recovery kinetics in moderately impaired CHF patients is suggested to be due to limitations in O 2 delivery. Therefore, strategies aimed at improving exercise performance of these patients should focus more on improvements of O 2 delivery than on O 2 utilization.

Last Word on Point:Counterpoint: The major limitation to exercise performance in COPD is 1) inadequate energy supply to the respiratory and locomotor muscles, 2) lower limb muscle dysfunction, 3) dynamic hyperinflation

to the editor: The clear and resounding conclusion of the correspondents who weighed in on this debate is that exercise limitation in COPD is multifactorial . Protagonists who advance a single dominant mechanism of activity limitation in this phenotypically heterogeneous population do so at their

The major limitation to exercise performance in COPD is inadequate energy supply to the respiratory and locomotor muscles

No doubt dynamic hyperinflation and lack of oxidative capacity of skeletal muscles are important causes of exercise limitation in COPD. O'Donnell and Webb and Debigare and Maltais will convince the reader of this by the elegant experiments they have performed. The thesis we will put forward is that

Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics

Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O(2) uptake (Vo(2)(p)) kinetics during exercise, which may stem from inadequate muscle O(2) delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O(2) delivery to uptake during exercise. We tested the hypothesis that, along with slowed Vo(2)(p) kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Qt) following the onset of heavy-intensity exercise. We measured Vo(2)(p), Qt (impedance cardiography), and muscle deoxygenation (near-infrared spectroscopy) during heavy-intensity exercise performed to the limit of tolerance by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. Time to exercise intolerance was significantly (P < 0.05) lower in patients and related to the kinetics of Vo(2)(p) (r = -0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of Vo(2)(p) (42 +/- 13 vs. 73 +/- 24 s) and Qt (67 +/- 11 vs. 96 +/- 32 s), and faster overall kinetics of muscle deoxy-Hb (19.9 +/- 2.4 vs. 16.5 +/- 3.4 s). Consequently, the time constant ratio of O(2) uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O(2) delivery. In conclusion, our data show that patients with moderate-to-severe COPD have impaired central and peripheral cardiovascular adjustments following the onset of heavy-intensity exercise. These cardiocirculatory disturbances negatively impact the dynamic matching of O(2) delivery and utilization and may contribute to the slower Vo(2)(p) kinetics compared with age-matched controls.

Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men

We tested whether the kinetics of systemic O(2) delivery (QaO(2)) at exercise start was faster than that of lung O(2) uptake (Vo(2)), being dictated by that of cardiac output (Q), and whether changes in Q would explain the postulated rapid phase of the Vo(2) increase. Simultaneous determinations of beat-by-beat (BBB) Q and QaO(2), and breath-by-breath Vo(2) at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/- 3.2 years, maximal aerobic power 333 +/- 61 W). Vo(2) was determined using Grønlund's algorithm. Q was computed from BBB stroke volume (Q(st), from arterial pulse pressure profiles) and heart rate (f(h), electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O(2) saturation (infrared oximetry) allowed computation of BBB QaO(2). The Q, QaO(2) and Vo(2) kinetics were analyzed with single and double exponential models. f(h), Q(st), Q, and Vo(2) increased upon exercise onset to reach a new steady state. The kinetics of QaO(2) had the same time constants as that of Q. The latter was twofold faster than that of Vo(2). The Vo(2) kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q changes fully explained the phase I of Vo(2) increase. We suggest that in unsteady states, lung Vo(2) is dissociated from muscle O(2) consumption. The two components of Q and QaO(2) kinetics may reflect vagal withdrawal and sympathetic activation.

Prolonged recovery of cardiac output after maximal exercise in patients with chronic heart failure

OBJECTIVESThe aim of this study was to characterize the kinetics of cardiac output during recovery from maximal exercise in patients with chronic heart failure (CHF).BACKGROUNDRecent studies have shown that oxygen uptake kinetics during recovery from exercise are delayed in patients with CHF. However, the kinetics of cardiac output during recovery from maximal exercise in CHF has not been examined.METHODSThirty patients with CHF performed maximal upright ergometer exercise with respiratory gas analysis. Kinetics of oxygen uptake (VO2) and carbon dioxide output (VCO2) during recovery were characterized by T1/2, the time to reach 50% of the peak values. Cardiac output was measured at 1-min intervals during exercise and recovery. Kinetics of cardiac output during recovery were characterized by the ratios of cardiac output during the first 4 min of recovery to cardiac output at peak exercise. Overshoot of cardiac output was defined as a further increase in cardiac output at 1 min of recovery above the cardiac output at peak exercise.RESULTSBoth T1/2 VO2 and T1/2 VCO2 increased as CHF worsened. The ratios of cardiac output during recovery to cardiac output at peak exercise were significantly correlated with T1/2 VO2 (r = 0.47 to 0.62, p < 0.05) and T1/2 VCO2 (r = 0.40 to 0.70, p < 0.05). There was a negative correlation between cardiac index at peak exercise and both T1/2 VO2 (r = −0.65, p < 0.001) and T1/2 VCO2 (r = −0.60, p < 0.001). Overshoot of cardiac output was recognized in 11 of 30 patients. Cardiac index at peak exercise was significantly lower in patients with overshoot (4.5 ± 0.9 L/min/m2) than in those without overshoot (6.1 ± 2.1 L/min/m2, p < 0.05). However, because of a continued increase in cardiac output at 1 min of recovery in patients with overshoot, there were no differences in cardiac index after the first minute of recovery. Heart rate at peak exercise and recovery of heart rate did not differ between these groups. Overshoot of cardiac output was caused by a rebound increase in stroke volume which was due to a reduction in systemic vascular resistance.CONCLUSIONSProlonged kinetics of VO2 or VCO2 during recovery from maximal exercise represent impairment of circulatory response to exercise and delayed recovery of cardiac output after exercise. Overshoot of cardiac output at 1 min of recovery was characteristic of severe CHF with poor cardiac output response to exercise.

Dynamic asymmetries of cardiac output transients in response to muscular exercise in man.

1. We determined the kinetics of cardiac output (Q) with respect to oxygen uptake (VO2) at the on- and off-transients of constant-load exercise. Six subjects performed constant-load exercise which consisted of 5 min rest, 5 min one-legged pedalling at 50 W and a 5 min recovery period. 2. The transient responses were characterized by first-order kinetics. There was no significant difference between the time constants for VO2 (tau VO2) at the on- (33.9 +/- 3.5 s, mean +/- S.E.M.) and off-transient (37.2 +/- 2.9 s). The time constant for Q (tau Q, 29.4 +/- 3.2 s) was consistently shorter than tau VO2 at the on-transient. However, tau Q was appreciably longer at the off-transient (44.3 +/- 3.6 s) than the on-transient. 3. The results support the contention that the time constant for the on-transient of Q is appreciably faster than that for VO2 and hence there seems little justification for the notion that the time constants for the kinetics of VO2 are determined by the limitations of blood flow in the transient. The asymmetry of Q kinetics, with the off-transient tau Q being appreciably slower than the on-transient tau Q, serves to maintain a sufficiently high oxygen flow to the muscle during recovery from exercise at a time when the muscle oxygen uptake remains high.

Postural effect on cardiac output, oxygen uptake and lactate during cycle exercise of varying intensity

Owing to changes in cardiac output, blood volume distribution and the efficacy of the muscle pump, oxygen supply may differ during upright and supine cycle exercise. In the present study we measured, in parallel, circulatory (heart rate, stroke volume, blood pressure) and metabolic parameters (oxygen uptake, lactic acid concentration [la]) during incremental-exercise tests and at constant power levels ranging from mild to severe exercise. In supine position, cardiac output exceeded the upright values by 1.0-1.5 l.min-1 during rest, light ([la] < 2 mmol.l-1) and moderate ([la] = 2-4 mmol.l-1) exercise. At higher exercise intensities the cardiac output in an upright subject approached and eventually slightly exceeded the supine values. For both rest-exercise transitions and large-amplitude steps (delta W > or = 140 W) the cardiac output kinetics was significantly faster in upright cycling. The metabolic parameters (VO2 and [la]) showed no simple relationship to the circulatory data. In light to moderate exercise they were unaffected by body position. Only in severe exercise, when cardiac output differences became minimal, could significant influences be observed: with supine body posture, [la] started to rise earlier and maximal power (delta W = 23 W) and exercise duration (64 s) were significantly reduced. However, the maximal [la] value after exercise was identical in both positions. The present findings generally show advantages of upright cycling only for severe exercise. With lower workloads the less effective muscle pump in the supine position appears to be compensated for by the improved central circulatory conditions and local vasodilatation.

Continuous noninvasive measurements of cardiac output during exercise by impedance cardiography--application to evaluation of cardiac output kinetics

The purpose of the present study was to compare the impedance derivate waveforms using spot and band electrode array and to assess applicability of automated signal processing system for cardiac output kinetics. Five healthy male subjects were tested. Cardiac output (Q) were measured using spot electrode array. Each subject performed rest-exercise transitions in leg and arm exercise on an electrically braked ergometer. The intensities of leg exercise were 25, 50, and 100 W for 5 min and those of arm exercise were 25 and 50 W. Comparisons between spot and band electrodes were made for the absolute magnitude of Q and stroke volume (SV), as well as for impedance derivative waveforms. The waveforms for spot electrodes showed less fluctuation by breathing and movement artifacts than for band electrodes. Q for spot electrodes were larger than those for band electrodes. There was a significant correlationship between oxygen uptake (Vo2) and Q. There was a significant correlationship between Q using spot electrode and Q measured by CO2 rebreathing method. Nonlinear correlation coefficient to exponential curve of Q kinetics for leg exercise was more than 0.7 and for arm exercise more than 0.4 in spite of large movement of upper body. It is suggested that the present system using spot electrodes is superior in signal processing to those for band electrodes and able to evaluate Q kinetics without multiple repetition of exercise tests.

Computer simulation of O2 transport and utilization mechanisms at the onset of exercise.

During transitions in work rate, O2 uptake (VO2) kinetics at the working tissue level might be rate limited by O2 transport and/or by O2 utilization. A computer model with parallel working and non-working tissue compartments, connected to an ideal lung by a variable-sized venous blood volume, was developed to study this. The time constant for working tissue O2 demand (tau T) was set by a first-order linear metabolic response. The model attempted to replicate the VO2 response at the alveolar level of a single subject performing step transitions on a cycle ergometer from 25 to 105 W [total lag time (equivalent to 63% increase above baseline) = 40.2 s]. Measured cardiac output kinetics (total lag time = 44.1 s) were used as a model parameter. Blood flow to the nonworking tissue (QNW) was kept constant at 4.5 or 5.0 l/min. A critical PO2 of 20 Torr was set, and the Bohr effect on the O2-hemoglobin dissociation curve was included. The "best" simulation had tau T = 36 s, QNW = 4.5 l/min, and venous blood volume = 2 liters and was not O2 transport limited. The approximation to the real data was good in all but the phase 1 response, where the model underpredicted the measured response. However, when QNW was increased to 5.0 l/min, the model was O2 transport limited; yet the predicted VO2 response at the alveolar level was not notably different from the subject's data.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of body position and pre-exercise activity on cardiac output and oxygen uptake following step changes in exercise intensity.

Parallel measurements of breath-by-breath oxygen uptake, cardiac output (Doppler technique), blood pressure (Finapres technique) and heart rate were performed in nine subjects during cycle ergometer exercise in the upright and supine positions. Transients were monitored during power steps starting from and leading to either rest or lower levels of exercise intensity. Oxygen uptake (VO2) and cardiac output kinetics were markedly faster than in all other conditions when exercise was started from rest. In contrast to exercise-exercise on steps, the computed arteriovenous difference in O2 content increased almost immediately in this situation, indicating that not only the additional energy expenditure due to the acceleration of the flywheel but also an increased venous admixture from non-exercising parts of the body contributed to the early kinetics. The off kinetics generally showed a more uniform pattern and did not simply mirror the on transients. The present findings indicate that transitions from rest should be avoided when muscle VO2 kinetics are to be assessed on the basis of VO2 measurements at the mouth.