Changes in cardiac output during sustained maximal ventilation in humans

To determine the increment in cardiac output and in O2 consumption (Vo2) from quiet breathing to maximal sustained ventilation, Vo2 and cardiac output were measured using an acetylene rebreathing technique in five subjects. Cardiac output and Vo2 were measured multiple times in each subject at rest and during sustained maximal ventilation. During maximal ventilation subjects breathed 5% CO2 to prevent hypocapnia. The increase in cardiac output from rest to maximal breathing was taken as an estimate of respiratory muscle blood flow and was used to calculate the arteriovenous O2 content difference across the respiratory muscles from the Fick equation. Cardiac output increased by 4.3 +/- 1.0 l/min (mean +/- SD), from 5.6 +/- 0.7 l/min at rest to 9.9 +/- 1.1 l/min, during maximal ventilations ranging from 127 to 193 l/min. Vo2 increased from 312 +/- 29 to 723 +/- 69 ml/min during maximal ventilation. O2 extraction across the respiratory muscles during maximal breathing was 9.6 +/- 1.0 vol% (range 8.5 to 10.7 vol%). These values suggest an upper limit of respiratory muscle blood flow of 3-5 l/min during unloaded maximal sustained ventilation.     

Cardiovascular response to cycle exercise during and after pregnancy

Our purpose was to determine if pregnancy alters the cardiovascular response to exercise. Thirty-nine women [29 +/- 4 (SD) yr], performed submaximal and maximal exercise cycle ergometry during pregnancy (antepartum, AP, 26 +/- 3 wk of gestation) and postpartum (PP, 8 +/- 2 wk). Neither maximal O2 uptake (VO2max) nor maximal heart rate (HR) was different AP and PP (VO2 = 1.91 +/- 0.32 and 1.83 +/- 0.31 l/min; HR = 182 +/- 8 and 184 +/- 7 beats/min, P greater than 0.05 for both). Cardiac output (Q, acetylene rebreathing technique) averaged 2.2 to 2.8 l/min higher AP (P less than 0.01) at rest and at each exercise work load. Increases in both HR and stroke volume (SV) contributed to the elevated Q at the lower exercise work loads, whereas an increased SV was primarily responsible for the higher Q at higher levels. The slope of the Q vs. VO2 relationship was not different AP and PP (6.15 +/- 1.32 and 6.18 +/- 1.34 l/min Q/l/min VO2, P greater than 0.05). In contrast, the arteriovenous O2 difference (a-vO2 difference) was lower at each exercise work load AP, suggesting that the higher Q AP was distributed to nonexercising vascular beds. We conclude that Q is greater and a-vO2 difference is less at all levels of exercise in pregnant subjects than in the same women postpartum but that the coupling of the increase in Q to the increase in systemic O2 demand (VO2) is not different.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of two noninvasive techniques for estimating cardiac output during exercise

This study presents the comparison of two different noninvasive techniques for the estimation of cardiac output (Q). The two techniques used were transthoracic impedance plethysmography (Z) and the indirect Fick CO2 rebreathing (RB) method. Paired estimates of Q were made on 60 different male subjects at rest and during graded increments of work on a cycle ergometer. The mean resting Q as measured by the Z technique (COZ) was 7.46 +/- 0.35 and 5.96 +/- 0.43 l/min using the RB (CORB) technique. At 200 W the mean COZ was 18.67 +/- 0.72 l/min and the CORB was 23.73 +/- 0.84 l/min. Both the techniques were linearly correlated (R) with O2 consumption; i.e., RZ = 0.752, RRB = 0.855. The difference between these two R values is statistically significant (P less than 0.001). A linear relationship was found between the Z and RB techniques at all work loads (R = 0.75). This study suggests that both techniques are equally as reliable over a large range of work loads, with the Z technique being the simplest and most efficient to implement. It was also found that lung volume had no effect on the calculated COZ.     

Comparison of cardiac output during exercise by single-breath and CO2-rebreathing methods

Cardiac output (Q) was estimated in supine rest and in upright cycling at several work rates up to 200 W in five male and one female subjects. At least four repetitions of both the CO2-rebreathing plateau method (Collier, J. Appl. Physiol. 9:25-29, 1956) and the Kim et al. (J. Appl. Physiol. 21: 1338-1344, 1966) single-breath method were performed at each work rate, in a steady state of O2 consumption and heart rate. At supine rest and low work rates, estimates of Q were similar by the two methods. However, at higher work rates, the single-breath method significantly (P less than 0.05) underestimated the value obtained by CO2 rebreathing. The reason for the difference in estimates of Q by the two methods was traced to the determination of arterial partial pressure of CO2 (PaCO2) and mixed venous partial pressure of CO2 (PvCO2). The estimate of PaCO2 from the single-breath method was approximately 88.5% of the estimate from end-tidal PCO2 used with the rebreathing method (P less than 0.001). The oxygenated PvCO2 calculated from the single-breath Q averaged approximately 92.5% of the PvCO2 from CO2 rebreathing (P less than 0.0001). The difference in estimates of Q was not eliminated by using a logarithmic form of the CO2 dissociation curve with the single-breath method.     

Non-invasive assessment of cardiac output and stroke volume in patients during exercise. Evaluation of a CO2-rebreathing method

A one-step CO2 rebreathing method for the determination of cardiac output and stroke volume (SV) has been evaluated by comparison with the direct Fick technique during recumbent exercise (10-90 W) in 13 patients. In an initial analysis, the influence of different rebreathing times and of correction for haemoglobin concentration was studied. The best correlation with the direct Fick technique was obtained with the longest analysis time, i.e. 21 s, and correction for variations in haemoglobin concentration further improved the correlation. Consequently, an analysis time of 21 s and correction for haemoglobin have been used. At low cardiac outputs, the CO2-rebreathing method overestimated the flow compared to the Fick technique. The correlation between the methods, however, was so good that a valid estimate of cardiac output could be obtained from the CO2 rebreathing method with appropriate corrections (Cardiac output, CO2 method = 2.7 + 0.77. Cardiac output, Fick; r = 0.91; Residual Standard deviation (SD res) = 0.77 l X min-1). Stroke volumes measured with the CO2 rebreathing method did not differ significantly from those obtained with the direct Fick technique, although there was a tendency to overestimate stroke volume with the CO2 rebreathing method (SV, CO2 method = 12 + 0.89 X SV, Fick; r = 0.82; SD res = 11 ml).     

Alveolar dead space does not affect indirect Fick cardiac output determinations

We examined the influence of three variables (different breathing circuits, breath selected for analysis, and alveolar dead space ventilation) on the accuracy of noninvasive cardiac output determinations with the Fick CO2 (indirect) equation. We compared noninvasive determinations with invasive thermodilution measurements over a wide range of cardiac outputs in 17 2-mo-old pigs anesthetized with halothane and nitrous oxide and paralyzed with either pancuronium or d-tubocurare. We found that rebreathing and nonrebreathing circuits provide accurate cardiac output determinations and that the optimal breath for analysis with either the rebreathing or nonrebreathing technique appears to depend on the cardiac output. When alveolar dead space was increased by using positional changes and the intracardiac administration of glass beads, there was still a good correlation between noninvasive and invasive cardiac output determinations. We conclude that both rebreathing and nonrebreathing techniques of indirect Fick cardiac output determinations correlate well with thermodilution measures over a wide range of cardiac outputs and alveolar dead space/tidal volume fractions.     

Measurement of cardiac output during exercise by open-circuit acetylene uptake.

Noninvasive measurement of cardiac output (QT) is problematic during heavy exercise. We report a new approach that avoids unpleasant rebreathing and resultant changes in alveolar PO(2) or PCO(2) by measuring short-term acetylene (C(2)H(2)) uptake by an open-circuit technique, with application of mass balance for the calculation of QT. The method assumes that alveolar and arterial C(2)H(2) pressures are the same, and we account for C(2)H(2) recirculation by extrapolating end-tidal C(2)H(2) back to breath 1 of the maneuver. We correct for incomplete gas mixing by using He in the inspired mixture. The maneuver involves switching the subject to air containing trace amounts of C(2)H(2) and He; ventilation and pressures of He, C(2)H(2), and CO(2) are measured continuously (the latter by mass spectrometer) for 20-25 breaths. Data from three subjects for whom multiple Fick O(2) measurements of QT were available showed that measurement of QT by the Fick method and by the C(2)H(2) technique was statistically similar from rest to 90% of maximal O(2) consumption (VO(2 max)). Data from 12 active women and 12 elite male athletes at rest and 90% of VO(2 max) fell on a single linear relationship, with O(2) consumption (VO(2)) predicting QT values of 9.13, 15.9, 22.6, and 29.4 l/min at VO(2) of 1, 2, 3, and 4 l/min. Mixed venous PO(2) predicted from C(2)H(2)-determined QT, measured VO(2), and arterial O(2) concentration was approximately 20-25 Torr at 90% of VO(2 max) during air breathing and 10-15 Torr during 13% O(2) breathing. This modification of previous gas uptake methods, to avoid rebreathing, produces reasonable data from rest to heavy exercise in normal subjects.     

High-intensity endurance training in 20- to 30- and 60- to 70-yr-old healthy men

Factors contributing to maximal incremental and short-term exercise capacity were measured before and after 12 wk of high-intensity endurance training in 12 old (60-70 yr) and 10 young (20-30 yr) sedentary healthy males. Peak O2 uptake in incremental cycle ergometer exercise increased from 1.60 +/- 0.073 to 2.21 +/- 0.073 (SE) l/min (38% increase) in the old subjects and from 2.54 +/- 0.141 to 3.26 +/- 0.181 l/min (29%) in the young subjects. Peak cardiac output, estimated by extrapolation from a series of submaximal measurements by the CO2 rebreathing method, increased by 30% (from 12.7 to 16.5 l/min) in the old subjects, associated with a 6% increase (from 126 to 135 ml/l) in arteriovenous O2 difference; in the young subjects there were equal 14% increases in both variables (18.0 to 20.5 l/min and 140 to 159 ml/l, respectively). Submaximal mean arterial pressure and cardiac output were lower posttraining in the old subjects; total vascular conductance and cardiac stroke volume increased. Although peak power at the start of a short-term maximal isokinetic test did not change, total work accomplished in 30 s at a pedaling frequency of 110 revolutions/min increased in both groups, from 11.2 to 12.6 kJ and from 15.7 to 16.9 kJ in the old and young, respectively; fatigue during the 30-s test was less, and postexercise plasma lactate concentrations were lower. In older subjects, increases in aerobic power after high-intensity endurance training are at least as large as in younger subjects and are associated with increases in vascular conductance, maximal cardiac output, and stroke volume.     

Maximal aerobic exercise in pregnant women: heart rate, O2 consumption, CO2 production, and ventilation

This study was to determine whether pregnancy affects maximal aerobic power. We measured heart rate, O2 uptake (VO2), CO2 production (VCO2), and ventilation at rest and during bicycle (BE) and treadmill exercise (TE) tests with rapidly increasing exercise intensities at 16, 25, and 35 wk gestation and 7 wk after delivery. Maximal heart rate was slightly lower throughout pregnancy compared with the nonpregnant state during both BE [174 +/- 2 vs. 178 +/- 2 (SE) beats/min] and TE (178 +/- 2 vs. 183 +/- 2 beats/min). Maximal VO2 was unaffected by pregnancy during BE and TE (2.20 +/- 0.08, 2.16 +/- 0.08, 2.15 +/- 0.08, and 2.19 +/- 0.08 l/min for BE and 2.45 +/- 0.08, 2.38 +/- 0.09, 2.33 +/- 0.09, and 2.39 +/- 0.08 l/min for TE at 16, 25, and 35 wk gestation and 7 wk postpartum, respectively). As a result of increased VO2 at rest, the amount of O2 available for exercise (exercise minus rest) tended to decrease with advancing gestation, reaching statistical significance only during TE at 35 wk gestation (1.99 +/- 0.08 l/min vs. 2.10 +/- 0.08 l/min postpartum). Power showed a positive linear correlation with O2 availability during BE as well as TE, and the relationship was unaffected by pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of exercise training on plasma catecholamines and blood pressure in labile hypertensive subjects

Plasma catecholamine concentrations (norepinephrine, NE; epinephrine, E) were measured along with heart rate (HR) and blood pressure (BP) at rest in supine (20 min) and standing (10 min) positions and in response to cycle ergometer exercise (5 min; 60% estimated maximal aerobic power) in 12 hypertensive patients before and after 20 weeks of aerobic training on cycle ergometer (six males, one female) or by jogging (five males). In a control group of labile hypertensive patients (five males, two females), estimated maximal aerobic power as well as HR and BP at rest in the supine and standing positions and in response to exercise were not modified from the first to the second evaluation (43 +/- 4 vs 43 +/- 5 ml.kg-1.min-1). In comparison estimated maximal aerobic power significantly increased in both training groups (cycle: 38 +/- 4 to 43 +/- 4; jogging: 38 +/- 3 to 46 +/- 4 ml.kg-1.min-1). However HR and BP were not modified following training, except for small reductions in systolic (18.9 to 18 kPa: 142 to 135 mmHg) and diastolic pressures (13.3 to 12 kPa: 100 to 90 mmHg) (p less than 0.05) at standing rest in the cycle group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of respiratory muscle work on VO(2) and leg blood flow during submaximal exercise.

The work of breathing (W(b)) normally incurred during maximal exercise not only requires substantial cardiac output and O(2) consumption (VO(2)) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q(leg)). We wondered whether the W(b) normally incurred during submaximal exercise would also reduce Q(leg). Therefore, we investigated the effects of changing the W(b) on Q(leg) via thermodilution in 10 healthy trained male cyclists [maximal VO(2) (VO(2 max)) = 59 +/- 9 ml. kg(-1). min(-1)] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% of VO(2 max). Inspiratory muscle work was 1) reduced 40 +/- 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 +/- 8% by addition of inspiratory resistive loads. Increasing the W(b) during submaximal exercise caused VO(2) to increase; decreasing the W(b) was associated with lower VO(2) (DeltaVO(2) = 0.12 and 0.21 l/min at 50 and 75% of VO(2 max), respectively, for approximately 100% change in W(b)). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, or Q(leg) when W(b) was reduced or increased. Why are LVR, norepinephrine spillover, and Q(leg) influenced by the W(b) at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal W(b) required makes insufficient demands for VO(2) and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50-70% increase in W(b) during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR or Q(leg).     

Does fitness level modulate the cardiovascular hemodynamic response to exercise?

Subjects with greater aerobic fitness demonstrate better diastolic compliance at rest, but whether fitness modulates exercise cardiac compliance and cardiac filling pressures remains to be determined. On the basis of maximal oxygen consumption (VO2max), healthy male subjects were categorized into either low (LO: VO2max=43+/-6 ml.kg-1.min-1; n=3) or high (HI: VO2max=60+/-3 ml.kg-1.min-1; n=5) aerobic power. Subjects performed incremental cycle exercise to 90% Vo(2max). Right atrial (RAP) and pulmonary artery wedge (PAWP) pressures were measured, and left ventricular (LV) transmural filling pressure (TMFP=PAWP-RAP) was calculated. Cardiac output (CO) and stroke volume (SV) were determined by direct Fick, and LV end-diastolic volume (EDV) was estimated from echocardiographic fractional area change and Fick SV. There were no between-group differences for any measure at rest. At a submaximal workload of 150 W, PAWP and TMFP were higher (P<0.05) in LO compared with HI (12 vs. 8 mmHg, and 9 vs. 4 mmHg, respectively). At peak exercise, CO, SV, and EDV were lower in LO (P<0.05). RAP was not different at peak exercise, but PAWP (23 vs. 15 mmHg) and TMFP (12 vs. 6 mmHg) were higher in LO (P<0.05). Compared with less fit subjects, subjects with greater aerobic fitness demonstrated lower LV filling pressures during exercise, whereas SV and EDV were either similar (submaximal exercise) or higher (peak exercise), suggesting superior diastolic function and compliance.     

Interactive effects of body posture and exercise training on maximal oxygen uptake

To determine the effect of posture on maximal O2 uptake (VO2 max) and other cardiorespiratory adaptations to exercise training, 16 male subjects were trained using high-intensity interval and prolonged continuous cycling in either the supine or upright posture 40 min/day 4 days/wk for 8 wk and 7 male subjects served as non-training controls. VO2 max measured during upright cycling and supine cycling, respectively, increased significantly (P less than 0.05) by 16.1 +/- 3.4 and 22.9 +/- 3.4% in the supine training group (STG) and by 14.6 +/- 2.0 and 6.0 +/- 2.0% in the upright training group (UTG). The increase in VO2 max measured during supine cycling was significantly greater (P less than 0.05) in the STG than in the UTG. The increase in VO2 max in the UTG was significantly greater (P less than 0.05) when measured during upright exercise than during supine exercise. However, there was no significant difference in posture-specific VO2 max adaptations in the STG. A postural specificity was also evident in other maximal cardiorespiratory variables (ventilation, CO2 production, and respiratory exchange ratio). In the UTG, maximal heart rate decreased significantly (P less than 0.05) only during supine cycling; there was no significant difference in maximal heart rate after training in the STG. We conclude that posture affects maximal cardiorespiratory adaptations to cycle training. Additionally, supine training is more effective than upright training in increasing maximal cardiorespiratory responses measured during supine exercise, and the effects of supine training generalize to the upright posture to a greater extent than the effects of upright training generalize to the supine posture.(ABSTRACT TRUNCATED AT 250 WORDS)     

Respiratory muscle blood flows during physiological and chemical hyperpnea in the rat.

Whether the diaphragm retains a vasodilator reserve at maximal exercise is controversial. To address this issue, we measured respiratory and hindlimb muscle blood flows and vascular conductances using radiolabeled microspheres in rats running at their maximal attainable treadmill speed (96 +/- 5 m/min; range 71-116 m/min) and at rest while breathing either room air or 10% O(2)-8% CO(2) (balance N(2)). All hindlimb and respiratory muscle blood flows measured increased during exercise (P < 0.001), whereas increases in blood flow while breathing 10% O(2)-8% CO(2) were restricted to the diaphragm only. During exercise, muscle blood flow increased up to 18-fold above rest values, with the greatest mass specific flows (in ml. min(-1). 100 g(-1)) found in the vastus intermedius (680 +/- 44), red vastus lateralis (536 +/- 18), red gastrocnemius (565 +/- 47), and red tibialis anterior (602 +/- 44). During exercise, blood flow was higher (P < 0.05) in the costal diaphragm (395 +/- 31 ml. min(-1). 100 g(-1)) than in the crural diaphragm (286 +/- 17 ml. min(-1). 100 g(-1)). During hypoxia+hypercapnia, blood flows in both the costal and crural diaphragms (550 +/- 70 and 423 +/- 53 ml. min(-1). 100 g(-1), respectively) were elevated (P < 0.05) above those found during maximal exercise. These data demonstrate that there is a substantial functional vasodilator reserve in the rat diaphragm at maximal exercise and that hypoxia + hypercapnia-induced hyperpnea is necessary to elevate diaphragm blood flow to a level commensurate with its high oxidative capacity.     

Cardiac output during exercise by the open circuit acetylene washin method: comparison with direct Fick.

An open-circuit (OpCirc) acetylene uptake cardiac output (QT) method was modified for use during exercise. Two computational techniques were used. OpCirc1 was based on the integrated uptake vs. end-tidal change in acetylene, and OpCirc2 was based on an iterative finite difference modeling method. Six subjects [28-44 yr, peak oxygen consumption (VO(2)) = 120% predicted] performed cycle ergometry exercise to compare QT using OpCirc and direct Fick methods. An incremental protocol was repeated twice, separated by a 10-min rest, and subsequently subjects exercised at 85-90% of their peak work rate. Coefficient of variation of the OpCirc methods and Fick were highest at rest (OpCirc1, 7%, OpCirc2, 12%, Fick, 10%) but were lower at moderate to high exercise intensities (OpCirc1, 3%, OpCirc2, 3%, Fick, 5%). OpCirc1 and OpCirc2 QT correlated highly with Fick QT (R(2) = 0.90 and 0.89, respectively). There were minimal differences between OpCirc1 and OpCirc2 compared with Fick up to moderate-intensity exercise (<70% peak VO(2)); however, both techniques tended to underestimate Fick at >70% peak VO(2). These differences became significant for OpCirc1 only. Part of the differences between Fick and OpCirc methods at the higher exercise intensities are likely related to inhomogeneities in ventilation and perfusion matching (R(2) = 0.36 for Fick - OpCirc1 vs. alveolar-to-arterial oxygen tension difference). In conclusion, both OpCirc methods provided reproducible, reliable measurements of QT during mild to moderate exercise. However, only OpCirc2 appeared to approximate Fick QT at the higher work intensities.     

Gastrointestinal transit during mild exercise

Although exercise is often recommended as therapy for constipation, almost nothing is known of the effects of exercise on rates of movement of material in the gastrointestinal tract. In this study we investigated the influence of mild exercise on transit of a liquid meal from the mouth to the large intestine. Orocecal transit time was determined by a consistent elevation of H2 concentration in a rebreathing apparatus after ingestion of 30 g lactulose; the lactulose was part of a 360-kcal, 350-ml liquid meal. Comparison of transit time was made, in 12 young healthy subjects, between seated rest and a treadmill walk at 5.6 km/h up a 2% grade. The walk elevated heart rate from 64 +/- 4 to 109 +/- 5 beats/min, O2 uptake (VO2) from 0.29 +/- 0.02 to 1.20 +/- 0.07 l/min STPD, and final rectal temperature from 37.0 +/- 0.1 to 38.3 +/- 0.1 degrees C (all P less than 0.01). Exercise speeded transit of the liquid meal, with mean rises in H2 concentration taking place 66 +/- 10 min after ingestion at rest, compared with 44 +/- 6 min after food intake during exercise (P less than 0.02). H2 concentrations in the rebreathing apparatus showed similar base lines in the two experiments, and quantitative increases in H2 concentration, although shifted in time by exercise, were otherwise identical. Subjects with the slowest resting transit rates showed the largest exercise effects (r = 0.79, P less than 0.05). These results indicate that mouth-to-cecum transit of at least the first portion of a liquid meal-based nonabsorbable carbohydrate marker is significantly accelerated during mild exercise.     

Blood pressure and plasma catecholamine responses to various challenges during exercise-recovery in man

The purpose of this study was to assess the effects of a 2 h cycle exercise (50% VO2max) on heart rate (HR) and blood pressure (BP), and on plasma epinephrine (E) and norepinephrine (NE) concentrations, during the recovery period in seven normotensive subjects. Measurements were made at rest in supine (20 min) and standing (10 min) positions, during isometric exercise (hand-grip, 3 min, 25% maximal voluntary, contraction), in response to a mild psychosocial challenge (Stroop conflicting color word task) and during a 5-min period of light exercise (42 +/- 3% VO2max). Data were compared to measurements taken on another occasion under similar experimental conditions, without a previous exercise bout (control). The results showed HR to be slightly elevated in all conditions following the exercise bout. However, diastolic and systolic BP during the recovery period following exercise were not significantly different from the values observed in the control situation. Plasma NE concentrations in supine position and in response to the various physiological and/or psychosocial challenges were similar in the control situation and during the recovery period following exercise. On the other hand plasma E (nmol.1-1) was about 50% lower at rest (0.11 +/- 0.03 vs 0.23 +/- 0.04) as well as in response to hand-grip (0.21 +/- 0.04 vs 0.41 +/- 0.20) and the Stroop-test (0.21 +/- 0.05 vs 0.41 +/- 0.15) following the exercise bout.(ABSTRACT TRUNCATED AT 250 WORDS)     

Estimation of cardiac output by the CO2 rebreathing method during tethered swimming

The reproducibility of cardiac output (Q) estimated by the CO2 rebreathing method during tethered swimming was studied in five highly trained college swimmers. The reproducibility of the CO2 rebreathing method for estimations of Q during tethered swimming was similar to the reproducibility reported for the CO2 rebreathing method, direct Fick method, or dye-dilution method during either cycling or treadmill walking. All duplicate estimates of Q by the CO2 rebreathing method were within 15% of one another. A comparison was made between the Q's estimated by the CO2 rebreathing method during tethered swimming and previously published data on Q determined by the dye-dilution method during free swimming in a flune. At any given oxygen uptake, Q obtained by the CO2 rebreathing method during tethered swimming was not significantly different from the Q obtained by the dye-dilution method during flume swimming. Estimates of Q by the CO2 rebreathing method made during high intensities of tethered swimming were reproducible and appear to be valid.     

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.     

Volumetric responses of right and left ventricles during upright exercise in normal subjects

We evaluated the volumetric responses of the right and left ventricles to upright exercise using two noninvasive methods, first-pass radionuclide angiocardiography and the CO2 rebreathing technique, in nine normal subjects. Right (RV) and left (LV) ventricular ejection fractions, heart rate, and cardiac index were determined at rest and during steady-state exercise on the bicycle ergometer at 50% of maximal O2 consumption. From these data, stroke volume index (SVI), end-diastolic volume index (EDVI), and end-systolic volume index (ESVI) were derived. SVI increased from 40 +/- 7 ml/m2 at rest to 59 +/- 13 ml/m2 with exercise (P less than 0.001). RVEDVI increased significantly from 82 +/- 16 ml/m2 at rest to 95 +/- 21 ml/m2 during exercise (P = 0.008), while there was no significant change in RVESVI with exercise. Changes in LVEDVI and LVESVI during upright exercise were similar to the right ventricle. The increase in systolic blood pressure during exercise, along with no change in LVESVI, indicated enhanced ventricular contractility. The normal augmentation in SVI during submaximal exercise was due to both the Frank-Starling mechanism and an increased contractile state. Application of these or similar techniques may be useful in evaluating ventricular performance in patients with cardiorespiratory dysfunction.