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Biomedical subjects

R Casaburi

Publications and source records attributed to R Casaburi.

At least 19 recordsLinked to original sources
PubMed1992

Acid-base regulation during exercise and recovery in humans.

Arterial pH, PCO2, standard bicarbonate, lactate, and ventilation were measured with a high sampling density during rest, exercise, and recovery in normal subjects performing upright cycle ergometer exercise. Three 6-min constant-work exercise tests (moderate, heavy, and very heavy) were performed by each subject. We found a small respiratory acidosis during the moderate-intensity exercise and an early respiratory acidosis followed by a metabolic acidosis for the heavy- and very-heavy-intensity exercise. During recovery, arterial pH rapidly returned to the preexercise value for the moderate-intensity work. However, arterial pH decreased further during the first 2 min of recovery for the heavy- and very-heavy-intensity work, before a slower return toward the resting values. We conclude that arterial acidosis is the consistent arterial pH reaction for moderate-, heavy-, and very-heavy-intensity cycle ergometer exercise in humans and that this acidosis is blunted but not eliminated by the ventilatory response. During recovery, the return to resting arterial pH and PCO2 and standard bicarbonate appears to be determined by the rate of lactate decline.

Acid-Base Equilibrium↗
PubMed1992

Evidence that circulatory oscillations accompany ventilatory oscillations during exercise in patients with heart failure.

Periodic breathing (PB) during exercise in patients with congestive heart failure (CHF) is associated with prominent oscillations (OSC) of O2 uptake (VO2). We hypothesized that the VO2 OSC represent OSC in true O2 exchange, resulting from concomitant cardiac output fluctuations and are not merely due to OSC of lung O2 stores. We compared the amplitude of the OSC of VO2, ventilation (VE), and end-expiratory lung volume (EELV) in 17 patients with CHF and PB and in seven healthy control subjects who volitionally simulated PB. Subjects underwent an incremental and/or a constant work-rate exercise test. VE and VO2 were measured breath by breath. EELV change was estimated by summing the difference between inspiratory and expiratory tidal volumes for each breath. The amplitude of the OSC, delta, is expressed as the ratio of the difference between the peak and nadir of the oscillating variable divided by its mean [delta = (peak - nadir)/mean]. In CHF, during incremental testing, the amplitude of the VE OSC was smaller than that of the VO2 OSC (delta VE = 49 +/- 15% [SD], delta VO2 = 63 +/- 25%, p less than 0.01). In contrast, during volitional PB in the control subjects, VE OSC were larger than VO2 OSC (delta VE = 48 +/- 12%, delta VO2 = 25 +/- 11%, p less than 0.01). This suggests that changing VE itself cannot account for the marked VO2 OSC seen in CHF. In the patients, EELV showed no systematic OSC, did not correlate with delta VO2, and was not significantly different from zero.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Dynamic and steady-state ventilatory and gas exchange responses to arm exercise.

Previous studies have suggested that, for the same power output, arm exercise requires higher oxygen uptake (VO2), carbon dioxide output (VCO2), and ventilation (VE) than leg exercise and that response kinetics are slower. To evaluate these differences, four healthy subjects performed a total of 95 arm cranking tests. Each subject performed several tests at each of three or four power outputs spaced evenly below the maximum the subject could sustain (average = 53 W). Breath-by-breath responses to identical stimuli were averaged. End-exercise blood lactate was determined at each power output. Responses were compared to leg exercise responses in these subjects (J. Appl. Physiol. 67:547-555, 1989). For power outputs unassociated with lactic acidosis, differences between steady-state VO2, VCO2, and VE responses for arm and leg exercise were not significant. At higher power outputs, the higher VO2, VCO2, and VE during arm exercise were well correlated with higher lactate. For power outputs not engendering lactic acidosis, the time constants (tau) for VO2, VCO2 and VE were not greatly different for arm than for leg exercise. For each variable, at higher power outputs tau became longer by an amount correlated with higher lactate level. Like leg exercise, the slower kinetics of VO2 and VE (but not VCO2) at higher power outputs were well described as a superimposed slower component. We conclude that both dynamic and steady-state responses of VE and gas exchange to arm exercise do not differ substantially from those to leg exercise so long as the power output does not elevate blood lactate.

Adult↗
PubMed1992

Principles of exercise training.

Design of exercise programs that are part of pulmonary rehabilitation programs should be founded on an appreciation of the principles of exercise training of healthy subjects. Training produces structural and biochemical changes in the muscles that exercise which increase the ability of the trained muscle to perform aerobic exercise. After training, a given level of heavy exercise engenders lower levels of blood lactate. This is associated with a lower requirement for oxygen uptake, carbon dioxide output, and ventilation. Although the precise mechanism by which training produces changes in the exercising muscles is unknown, characteristics of an effective training program have been defined. Healthy subjects must train for at least 30 min per day, 3 to 5 days per week for 4 to 8 weeks to achieve a physiologic training effect. More controversial is whether a critical training intensity exists. Further, it is not clear which yardstick to apply to quantitate training intensity. Finally, after a training effect has been achieved, regular exercise must be continued or the gains will be lost.

Exercise↗
PubMed1991

Reductions in exercise lactic acidosis and ventilation as a result of exercise training in patients with obstructive lung disease.

Though exercise training is part of most pulmonary rehabilitation programs, whether there is a physiologic basis for increased exercise tolerance is unclear. We sought to determine whether patients with chronic obstructive pulmonary disease (COPD) are capable of obtaining a physiologic training effect, as manifested by a reduction in blood lactate and ventilation (VE) at a given level of exercise. We also sought to determine whether training work rate determines the size of the training effect. Nineteen participants with COPD of predominantly moderate severity in an inpatient rehabilitation program performed two cycle ergometer exercise tests at a low and a high work rate for 15 min or to tolerance and also an incremental exercise test to tolerance. Arterial blood was sampled for blood gas and lactate analyses. Identical tests were performed before and after 5-day-per-week cycle ergometer training for 8 wk either for 45 min/day at a high work rate (average, 71 W) or for a proportionally longer time at a low work rate (average, 30 W). Average FEV1 was 56 +/- 12% predicted and did not change with training. Peak exercise lactate (average, 6.5 mEq/L) was not correlated with FEV1. For the high work rate training group, identical work rates engendered less lactate (4.5 versus 7.2 mEq/L) and less VE (48 versus 55 L/min) after training; the low work rate training group had significantly less lactate and VE decrease (p less than 0.01). Further, endurance time for the high constant work rate increased 73% in the high work rate training group but only 9% in the low work rate training group. At identical work rates, VE decrease average 2.5 L/min per mEq/L decrease in lactate (r = 0.75). We conclude that most COPD subjects studied increased blood lactate at low work rates. Many of these patients were able to achieve a physiologic training effect. Though total work was the same, training at a high work rate was more effective than was training at a low work rate. The lower VE requirement to perform exercise was in proportion to the lower lactate level, but the VE decrease for a given decrease in lactate was smaller than that seen in normal subjects (7.2 L/min/mEq/L), apparently because patients with COPD fall to hyperventilate in response to lactic acidosis (PaCO2 does not drop). These findings provide a physiologic rationale for exercise training of patients with COPD.

Acidosis, Lactic↗
PubMed1991

Comparison of albuterol to isoproterenol as a bronchodilator for use in pulmonary function testing.

We compared the effectiveness of albuterol with isoproterenol as a bronchodilator for use in pulmonary function testing. A total of 180 patients presenting for routine pulmonary function testing were randomly assigned to receive 5 mg of either albuterol or isoproterenol by compressed air nebulizer. Forced expiratory maneuvers were performed before, 5 min after, and 10 min after bronchodilator administration. The average increase in FEV1 and FVC did not differ between drugs. Also, the fraction of patients achieving a clinically significant bronchodilator response did not differ between drugs. Importantly, there was no significant difference between average 5 and 10 min postbronchodilator values for FEV1 or FVC for either bronchodilator, suggesting that a peak response was reached by 5 min. These results show no advantage of isoproterenol over albuterol in terms of potency or speed of action. Given the well-known cardiovascular side effects of isoproterenol, albuterol is the preferable agent for use in pulmonary function testing.

Albuterol↗
PubMed1990

Relationship between right atrial and mixed venous oxygen saturation and heart rate during exercise in normal subjects and patients with cardiac disease.

An ideal sensing variable for use in rate responsive pacemakers should measure a physiological parameter that closely correlates with heart rate during various activities in a diverse group of subjects. Nineteen patients, 12 normal and 7 patients with heart disease, were studied to assess the relationship between mixed venous oxygen saturation and heart rate. In patients with heart disease right atrial oxygen saturation and heart rate were also compared. Each subject underwent pulmonary artery catheterization and performed seated cycle ergometer exercise. Gas exchange and heart rate were measured continuously and blood sampled at frequent intervals. Normal patients were studied at rest and during steady-state exercise (mean work rate 149 watts). Patients were studied at rest, steady-state exercise (mean work rate 37 watts), and during incremental exercise (5-10 watts/min) to tolerance. There were 248 paired right atrial or mixed venous oxygen saturation/heart rate observations obtained. Changes in mixed venous oxygen saturation and heart rate were not substantially altered by fitness or cardiac disease. Rate responsive pacemakers sensing changes in oxygen saturation may be a superior sensing variable for both normal and patients with heart disease.

Adult↗
PubMed1990

Assessing precision and accuracy in blood gas proficiency testing.

Blood gas proficiency testing has focused on assessing the accuracy of measurement of each analyte (pH, PCO2) independently of each other. Recently, the American Thoracic Society-California Thoracic Society Blood Gas Proficiency Testing Survey distributed the same lot of ampules of proficiency testing material (a buffered fluorocarbon-containing emulsion) on three occasions within a 1-yr period, allowing us to assess the precision (reproducibility) of measurement of each analyte. Comparing 580 instruments of 13 models, we found that the precision of measurement of each analyte was positively correlated with the precision of measurement of each other analyte, and the correlation of precision between models was much stronger than precision between the individual instruments. We also found correlation of precision of each analyte with two targets for accuracy: (1) the all-instrument mean and (2) the model-specific means. Correlations were higher with the model-specific means. These findings suggest: (1) that features unique to design of each model are important in the precision of measurement of these ampules, and (2) that it would be informative to include measurements of precision with linked and cumulative ratings of analyte accuracy in proficiency testing rating systems.

Blood Gas Analysis↗
PubMed1989

Effect of liver disease on the kinetics of lactate removal after heavy exercise.

Recovery from heavy exercise requires clearance of lactic acid from the blood and body tissues. Although it has long been felt that the liver plays the major role in lactate removal, it has more recently been asserted that skeletal muscle plays the dominant role. We felt it relevant to this controversy to determine whether patients with liver dysfunction have slowed lactate removal following heavy exercise. Eight patients with alcoholic liver disease and 5 normal subjects were studied. Liver function was measured by the 14C-aminopyrine breath test; the results were expressed as the rate of appearance of 14CO2 in the breath two hours after ingestion, as a fraction of the ingested 14C dose (%.h-1). Each participant exercised on a cycle ergometer for 7 min at a work rate which was moderately heavy for that subject (mean peak lactate is 5.3 mmol.L-1). During, and for 45 minutes after exercise, blood was drawn from a hand vein catheter. The time required for blood lactate to decrease halfway toward resting levels (t1/2 LA) was determined. Compared to the normal subjects and historical controls, seven of the patients had distinctly slowed lactate removal. The t1/2 LA was as long as 46 min (as compared to approximately 15 min seen normally). Further, among the patients the 2 h breath excretion of 14C was well correlated with the rate constant of lactate removal (r 0.82, P less than 0.01). Four of the patients with severe liver dysfunction performed a second exercise test in which, instead of resting after heavy exercise, low level exercise was continued. The t1/2 LA of the averaged responses decreased by 29%.2+

Adult↗
PubMed1989

Influence of work rate on ventilatory and gas exchange kinetics.

A linear system has the property that the kinetics of response do not depend on the stimulus amplitude. We sought to determine whether the responses of O2 uptake (VO2), CO2 output (VCO2), and ventilation (VE) in the transition between loadless pedaling and higher work rates are linear in this respect. Four healthy subjects performed a total of 158 cycle ergometer tests in which 10 min of exercise followed unloaded pedaling. Each subject performed three to nine tests at each of seven work rates, spaced evenly below the maximum the subject could sustain. VO2, VCO2, and VE were measured breath by breath, and studies at the same work rate were time aligned and averaged. Computerized nonlinear regression techniques were used to fit a single exponential and two more complex expressions to each response time course. End-exercise blood lactate was determined at each work rate. Both VE and VO2 kinetics were markedly slower at work rates associated with sustained blood lactate elevations. A tendency was also detected for VO2 (but not VE) kinetics to be slower as work rate increased for exercise intensities not associated with lactic acidosis (P less than 0.01). VO2 kinetics at high work rates were well characterized by the addition of a slower exponential component to the faster component, which was seen at lower work rates. In contrast, VCO2 kinetics did not slow at the higher exercise intensities; this may be the result of the coincident influence of several sources of CO2 related to lactic acidosis. These findings provide guidance for interpretation of ventilatory and gas exchange kinetics.

Adult↗
PubMed1989

Abrupt changes in mixed venous blood gas composition after the onset of exercise.

It has been assumed that increases in both O2 uptake and ventilation occurring within the first few seconds after the onset of exercise cannot be the result of changes in blood gas composition reaching the central circulation because of the circulatory delay from the exercising limbs (A. Krogh and J. Lindhard, J. Physiol. Lond. 42: 112-136, 1913). We sought to validate this assumption by measuring the time course of pulmonary arterial blood gases during the transition from rest to exercise. Six healthy men underwent pulmonary arterial catheterization and then performed transitions from rest to moderate cycle ergometer exercise. An anaerobic sampling manifold withdrew 19 samples of blood during the rest-to-exercise transition; sampling interval was usually 4 s. Blood gas analysis showed that, on average, from rest-to-steady-state exercise, O2 saturation (Svo2) fell from 71 to 41% and mixed venous PCO2 (PvCO2) rose from 42 to 59 Torr. Contrary to our expectations, Svo2 decreased and PvCO2 increased with no discernible latency after exercise onset (by 10% and 2 Torr, respectively, within 6 s). The half time for the Svo2 decrease was 32 s, whereas for the PvCO2 increase it was 80 s. The time course of superior vena cava blood gas composition was determined in several experiments; no rapid changes after exercise onset were found. We conclude that at exercise onset there is a rapid fall in Svo2 and rise in PvCO2 well in advance of arrival of blood produced by exercising legs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Comparison of blood gas analyzer biases in measuring tonometered blood and a fluorocarbon-containing, proficiency-testing material.

This study was designed to test whether the interinstrument differences (biases) in analyses of the PO2 and PCO2 of the commercial fluorocarbon-containing emulsion (FCE) proficiency-testing material abc were similar in magnitude and direction to analyses of the PO2 and PCO2 at four similar partial pressures in tonometered blood. There were large differences among the 13 individual instrumental mean values for both blood and FCE at the four levels: for PO2 (average range, 10.3 mm Hg for blood and 17.0 mm Hg for FCE) and PCO2 (average range, 9.4 mm Hg for blood and 6.2 mm Hg for FCE). Although the instrumental biases for blood and FCE were approximately the same, the biases were slightly higher for FCE in measuring PO2 and slightly higher for blood in measuring PCO2. Accuracy and precision in blood measurement and precision in FCE measurement were significantly correlated among instruments for PO2 and PCO2. The biases of the nine instrument models evaluated significantly correlated with those of the same models participating in national surveys. We suggest that differences in technique, maintenance, and instrumental design rather than inherent differences in PO2 and PCO2 electrodes probably account for the demonstrable differences between instruments. The fluorocarbon-containing emulsion used is of value in proficiency testing for PO2 and PCO2.

Blood Gas Analysis↗
PubMed1989

Effect of altering heart rate on oxygen uptake at exercise onset.

At the onset of exercise, both cardiac output and ventilation increase abruptly. We investigated the hypothesis that a rapid change in cardiac output, as effected by an immediate increase in heart rate at the start of exercise and a decrease in heart rate at the termination of exercise, affects the responses of oxygen uptake. Five patients in whom programmable pacemakers had been previously inserted for complete heart block were studied. Responses in ventilation and gas exchange were recorded breath by breath during studies in which each subject performed 16 transitions between rest and moderate exercise on a cycle ergometer. In a randomized fashion, in half of the transitions, heart rate was accelerated from a low rate to a high rate as exercise began; in the other half, heart rate was held constant at the low rate as exercise began. Oxygen uptake increased by 30 percent in the first 20 seconds of exercise, when heart rate was constrained, while it increased by 70 percent when heart rate was abruptly accelerated. Similarly, smaller changes were observed at the cessation of exercise when the heart rate was constrained, as compared to an abrupt decrease in heart rate. Despite this difference in the responses of oxygen uptake, at the transitions in exercise, the ventilatory responses were indistinguishable. We have demonstrated that ventilation-independent changes in oxygen uptake can be induced at the onset and cessation of exercise. These alterations in oxygen uptake are predictable from differences in blood flow which occur as a consequence of the differences in time course of the heart rate.

Adult↗
PubMed1989

Selection criteria for exercise training in pulmonary rehabilitation.

While exercise training appears to have no effect on resting respiratory function, and its effect on ventilation/perfusion relationships is uncertain, it can significantly reduce the rate of lactic acid production, carbon dioxide generated from buffering of acid and the hydrogen ion stimulus to breathe during exercise. We had two objectives in this study: 1) to determine if patients who might benefit from exercise training could be selected based on resting respiratory function measurements; 2) to determine if the work rate at which the metabolic acidosis starts to develop could be reliably determined, non-invasively, by a simple modification of the recently described V-slope method of Beaver et al. Patients with severe obstructive lung disease, all of whom experienced exertional dyspnoea, underwent incremental exercise testing to determine if they could exercise to a level causing metabolic acidosis. About two thirds of the patients with severe airflow obstruction developed a significant metabolic acidosis (arterial standard HCO3- decrease of more than 2 mEq.l-1 after two minutes recovery following an incremental exercise test to maximum). The oxygen uptake (VO2) at which the metabolic acidosis (directly measured) and that of which the increase in CO2 in the expired air attributable to buffering (V-slope method), were in close agreement. There was no significant correlation between the magnitude of the exercise metabolic acidosis and the forced expiratory volume in one second (FEV1) or the diffusing capacity for carbon monoxide (DLCO). Thus, it is necessary to perform exercise testing in order to select patients for exercise training, based on the benefits accrued from reducing the exercise metabolic acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1989

A new perspective in pulmonary rehabilitation: anaerobic threshold as a discriminant in training.

Exercise training is a mainstay of many pulmonary rehabilitation programmes. However, the physiologic basis for improved exercise tolerance is unclear. We hypothesized that since endurance training is known to reduce blood lactate at levels of work above the anaerobic threshold (AT), minute ventilation (VE) would also be lower. This might be an important benefit for the ventilatory-limited patient. We studied 10 normal subjects who performed 15 min of exercise at each of 4 work rates before and after 8 weeks of training. The lowest work rate was chosen to be below the AT; training produced a minimal decrease in VE (2.5 l.min-1). For the highest work rate, training produced a 4 mEq.l-1 decrease in lactate and a 37 l.min-1 decrease in VE. End-exercise VE reduction was well correlated with lactate reduction (r = 0.69). Seven men with chronic obstructive pulmonary disease (COPD) have also been studied. Each performed an incremental exercise test and two constant work rate tests (one above and one below AT) before and after an 8 week training period. Though responses were more variable than in normal subjects, training produced a reduced ventilatory requirement for exercise when blood lactate was reduced.

Adult↗
PubMed1988

Oxygen uptake as related to work rate increment during cycle ergometer exercise.

We postulated that the commonly observed constant linear relationship between VO2 and work rate during cycle ergometry to exhaustion is fortuitous and not due to an unchanging cost of external work. Therefore we measured VO2 continuously in 10 healthy men during such exercise while varying the rate of work incrementation and analyzed by linear regression techniques the relationship between VO2 and work rate (delta VO2/delta wr). After excluding the first and last portions of each test we found the mean +/- SD of the delta VO2/delta wr in ml.min-1.W-1 to be 11.2 +/- 0.15, 10.2 +/- 0.16, and 8.8 +/- 0.15 for the 15, 30, and 60 W.min-1 tests, respectively, expressed as ml.J-1 the values were 0.187 +/- 0.0025, 0.170 +/- 0.0027 and 0.147 +/- 0.0025. The slopes of the lower halves of the 15 and 30 W.min-1 tests were 9.9 +/- 0.2 ml.min-1.W-1 similar to the values for aerobic work reported by others. However the upper halves of the 15, 30, and 60 W.min-1 tests demonstrated significant differences: 12.4 +/- 0.36 vs 10.5 +/- 0.31 vs 8.7 +/- 0.23 ml.min-1.W-1 respectively. We postulate that these systematic differences are due to two opposing influences: 1) the fraction of energy from anaerobic sources is larger in the brief 60 W.min-1 tests and 2) the increased energy requirement per W of heavy work is evident especially in the long 15 W.min-1 tests.

Adult↗
PubMed1988

Dyspnea: physiological and pathophysiological mechanisms.

Dyspnea, the sensation of feeling breathless, is a symptom experienced under conditions in which there is an inordinately high ventilatory demand relative to the ability to breathe. Its major physical sign is tachypnea. New developments in monitoring ventilation during exercise have improved our ability to evaluate the symptom of dyspnea and to understand pathophysiological mechanisms contributing to the symptom. We briefly describe the range of mechanisms that determine exercise ventilation and their possible relationship to dyspnea. Questionnaires and psychophysical testing have been used to quantify dyspnea, but there is variability in dyspnea grade from these methods. Dyspnea-producing stimuli and the mechanisms by which they act are reviewed. Disorders producing dyspnea and the pathophysiological mechanisms underlying each are discussed. Perception of dyspnea is obviously through the central nervous system, where dyspnea-producing stimuli are integrated. The specific integration site is probably in the region of the brain stem, since occasional patients with brain stem lesions do not experience dyspnea despite the presence of a number of dyspnea-producing stimuli.

Anemia↗