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Biomedical subjects

K Wasserman

Publications and source records attributed to K Wasserman.

At least 127 records · Page 7Linked to original sources
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

Evidence that maturation of the peripheral chemoreceptors is not complete in childhood.

We examined the hypothesis that the peripheral chemoreceptors contribute a different degree of tone to respiration during exercise in normal young children as compared to adults. To improve resolution of the peripheral chemoreceptor contribution, the studies were conducted during controlled levels of exercise. Peripheral chemoreceptor function was assessed by the hyperoxic (FIO2 = 0.80) switch technique during steady-state, sub-anaerobic threshold exercise during air (FIO2 = 0.21) and midly hypoxic gas (FIO2 = 0.15) breathing in 9 healthy children (mean +/- 1 SD age (years) = 8.2 +/- 1.4) and 10 healthy adults (28.2 +/- 6.5). Ventilation during exercise was significantly greater under hypoxic conditions in both children and adults. During air breathing exercise the mean ventilatory decrease in response to the hyperoxic switch was similar in the two groups (27.9 +/- 10.7% in children and 23.3 +/- 6.3% in adults). In contrast, during hypoxic gas breathing exercise the children demonstrated a much greater decrease in ventilation following the hyperoxic switch (57.9 +/- 3.6%) compared to adults (38.9 +/- 5.5%) (P less than 0.0001). Thus, the peripheral chemoreceptors have a greater role in the exercise hyperpnea during hypoxic exercise in young children as compared to adults, suggesting attenuation of peripheral chemoreceptor function during maturation.

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↗
PubMed1988

Control of ventilation during exercise in patients with central venous-to-systemic arterial shunts.

The diversion of systemic venous blood into the arterial circulation in patients with intracardiac right-to-left shunts represents a pathophysiological condition in which there are alterations in some of the potential stimuli for the exercise hyperpnea. We therefore studied 18 adult patients with congenital (16) or noncongenital (2) right-to-left shunts and a group of normal control subjects during constant work rate and progressive work rate exercise to assess the effects of these alterations on the dynamics of exercise ventilation and gas exchange. Minute ventilation (VE) was significantly higher in the patients than in the controls, both at rest (10.7 +/- 2.4 vs. 7.5 +/- 1.2 l/min, respectively) and during constant-load exercise (24.9 +/- 4.8 vs. 12.7 +/- 2.61 l/min, respectively). When beginning constant work rate exercise from rest, the ventilatory response of the patients followed a pattern that was distinct from that of the normal subjects. At the onset of exercise, the patients' end-tidal PCO2 decreased, end-tidal PO2 increased, and gas exchange ratio increased, indicating that pulmonary blood was hyperventilated relative to the resting state. However, arterial blood gases, in six patients in which they were measured, revealed that despite the large VE response to exercise, arterial pH and PCO2 were not significantly different from resting values when sampled during the first 2 min of moderate-intensity exercise. Arterial PCO2 changed by an average of only 1.4 Torr after 4.5-6 min of exercise. Thus the exercise-induced alveolar and pulmonary capillary hypocapnia was of an appropriate degree to compensate for the shunting of CO2-rich venous blood into the systemic arterial circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Assessing cardiac function by gas exchange.

Exercise stresses the primary function of the cardiovascular system, which is the supply of O2 and removal of CO2 from the cells of the body. Even ordinary walking requires an increase in O2 consumption and CO2 production by the exercising muscles of 20 times the resting level. While pulmonary dysfunction may affect arterial blood gas tensions, the dynamics of O2 uptake and CO2 output by the lungs depend on the circulatory responses to exercise. Thus, measurement of the dynamics of O2 uptake in response to exercise has been shown to reflect cardiovascular function. Inability of the circulatory responses to meet an increased O2 requirement may be reflected in abnormalities in O2 uptake dynamics, and an early increase in CO2 output relative to O2 uptake consequent to bicarbonate buffering of lactic acid. Application of currently available technology for the continuous measurement and analysis of pulmonary gas exchange can afford the practicing or investigative cardiologist with a noninvasive and inexpensive means for assessing cardiovascular function.

Animals↗
PubMed1988

The Dickinson W. Richards lecture. New concepts in assessing cardiovascular function.

The primary role of the heart is to provide energy for the circulatory transport of oxygen (O2) to cells at rates commensurate with their metabolic activity. At rest, even a "sick" heart may be capable of transporting O2 adequately. But during exercise, the increase in O2 required by muscle cells demands that their blood flow be increased. The supply of O2 needed to meet the O2 requirement for muscle mitochondrial high-energy phosphate generation during exercise is a critical function of the circulation. Thus, the adequacy of cardiovascular function can be estimated, noninvasively, from the pattern of O2 uptake in response to an exercise stimulus. While arterial O2 tension (PaO2) is dependent on pulmonary function (except for intracardiac right-to-left shunt), the mass transfer of O2 (VO2) between the cells and lungs depends on pulmonary blood flow (i.e., cardiac output) and O2 concentration difference between the pulmonary arterial and pulmonary venous blood, C(a-v)O2 (Fick principle). Thus, VO2 in the first 15 seconds of exercise can be used to describe the initial increase in pulmonary blood flow and stroke volume, while the subsequent rise in VO2 results from the further increase in VO2 in response to work rate increase are used to detect circulatory disturbances. Also, the rate of CO2 output (VCO2) has been valuable in the assessment of cardiovascular function when related to VO2. Inadequate O2 availability results in anaerobic metabolism, causing increased muscle lactic acid production. At the pH of cell water, most of the hydrogen ions produced with lactate are buffered by bicarbonate. The CO2 generated by the buffering reaction (22 ml for each milliequivalent) causes a net increase in VCO2 relative to VO2 at the work rate at which buffering begins. This provides a useful estimate of the anaerobic threshold. Thus, study of the dynamic coupling of external to cellular respiration during a work rate stimulus provides valuable, direct, and noninvasive information about cardiovascular mechanisms in health and disease.

Anaerobic Threshold↗
PubMed1988

Metabolic acidosis during exercise in patients with chronic obstructive pulmonary disease. Use of the V-slope method for anaerobic threshold determination.

Patients with chronic obstructive pulmonary disease (COPD) usually have limited exercise tolerance owing to low ventilatory capacity. Because metabolic acidosis induced by exercise increases ventilatory drive, decreasing the hydrogen ion stimulus may improve exercise capacity. However, in those with mechanical limitation to ventilation or chemoreceptor insensitivity, identifying metabolic acidosis may be difficult using gas exchange methods that depend on the ventilatory response to the acidosis. We compared a modification of a gas exchange method (V-slope) for determining the lactate (anaerobic) threshold (AT), which is independent of ventilatory response with a method using the change in blood standard bicarbonate (HCO3-) level in COPD and normal subjects during cycle incremental exercise. In 43 normal subjects, the VO2 at which metabolic acidosis was identified using the two method correlated (r = 0.75), although mean values differed. In 22 patients with moderately severe to severe COPD, eight who had a change in standard HCO3- less than 2.0 mEq/L between rest and 2 min of recovery from exercise (group 1) were contrasted with 14 whose blood standard HCO3- fell by greater than 2.5 mEq/L (group 2). Mean VC was higher and FEV1/VC was lower in group 2, but mean FEV1, maximal voluntary ventilation, and diffusing capacity for carbon monoxide were not different. The degree of obstruction did not correlate strongly with the degree of exercise metabolic acidosis. The AT determined by the V-slope method was compared with that from standard HCO3-; good correlation between these methods was found (r = 0.98), although mean values were different. The V-slope method predicted metabolic acidosis in 10/14 who had a fall in HCO3- more than 2.5 mEq/L. A significant proportion of patients with COPD seem to develop metabolic acidosis during exercise. The V-slope gas exchange method may be useful in selecting those patients with COPD who develop exercise metabolic acidosis and might therefore benefit from exercise training.

Acidosis↗
PubMed1987

Diffusing capacity for carbon monoxide as a predictor of gas exchange during exercise.

In patients with pulmonary disease, the diffusing capacity for carbon monoxide has been used to predict abnormal gas exchange in the lung. However, abnormal values for arterial blood gases during exercise are likely to be the most sensitive manifestations of lung disease. We compared the single-breath diffusing capacity for carbon monoxide at rest with measurements of gas exchange during exercise, including arterial oxygen tension, the alveolar-arterial difference in oxygen tension, the arterial-end-tidal difference in carbon dioxide tension, and the dead-space/tidal-volume ratio in 276 current and former shipyard workers. Sixteen workers had a diffusing capacity for carbon monoxide below 70 percent of predicted; one or more measurements of gas exchange during exercise were abnormal in 14. In contrast, of 96 men who had abnormal gas exchange during exercise, only 14 had a diffusing capacity for carbon monoxide below 70 percent of predicted. Neither the type nor the degree of abnormality in gas exchange could be predicted from the diffusing capacity. We conclude that diffusing capacity for carbon monoxide at rest is a specific but insensitive predictor of abnormal gas exchange during exercise and that, if indicated, measurements of arterial blood gases should be obtained during exercise.

Asbestosis↗
PubMed1987

Relation of oxygen uptake to work rate in normal men and men with circulatory disorders.

The relation between the increase in oxygen uptake (VO2) and increase in work rate (WR) between unloaded pedaling and maximal work during incremental cycle ergometer exercise was studied in normal men, men with uncomplicated systemic hypertension and ambulatory men with various cardiovascular diseases. The postulation was that impaired peripheral oxygen delivery would reduce the ratio of the oxygen utilized relative to work performed. The ratio of increase in VO2 to increase in WR (delta VO2/delta WR) was relatively constant: 10.29 +/- 1.01 ml/min/W in normal men (n = 54) for exercise 6 to 14 minutes in duration with uniform work increments of 15, 20, 25 or 30 W/min, regardless of age. The value in men with uncomplicated systemic hypertension (n = 24) was not significantly different from that of normal men. However, more than half of the men with peripheral vascular disease (n = 7) or pulmonary vascular disease (n = 5) or men who had electrocardiographic abnormalities during exercise (n = 39) had a significantly lower delta VO2/delta WR, 8.29 +/- 1.17 ml/min/W (p less than 0.05) especially evident as maximal work rates were approached. Thus, delta VO2/delta WR during incremental exercise testing is predictable for normal men and a reduction in this ratio indicates cardiovascular dysfunction.

Adult↗
PubMed1987

Effect of endurance training on possible determinants of VO2 during heavy exercise.

When moderate exercise begins, O2 uptake (VO2) reaches a steady state within 3 min. However, with heavy exercise, VO2 continues to rise beyond 3 min (VO2 drift). We sought to identify factors contributing to VO2 drift. Ten young subjects performed cycle ergometer tests of 15 min duration for each of four constant work rates, corresponding to 90% of the anaerobic threshold (AT) and 25, 50, and 75% of the difference between maximum VO2 (VO2 max) and AT for that subject. Time courses of VO2, minute ventilation (VE), and rectal temperature were recorded. Blood lactate, norepinephrine, and epinephrine were measured at the end of exercise. Eight weeks of cycle ergometer endurance training improved average VO2 max by 15%. Subjects then performed four tests identical to pretraining studies. For the above AT tests, training reduced VO2 drift substantially; reduction in each of the possible mediators we measured was also demonstrated. The training-induced decrease in VO2 drift was well correlated with decreases in end exercise lactate and less well correlated with the drift in VE seen at above AT work rates. The training-induced reduction in VO2 drift was not significantly correlated with attenuation of rectal temperature rise or decrease in end-exercise level of the catecholamines. Thus the slow rise in VO2 during heavy exercise seems linked to lactate, though a component dictated by the work of breathing cannot be ruled out.

Adult↗
PubMed1987

Effect of interbreath fluctuations on characterizing exercise gas exchange kinetics.

Breathing has inherent irregularities that produce breath-to-breath fluctuations ("noise") in pulmonary gas exchange. These impair the precision of characterizing nonsteady-state gas exchange kinetics during exercise. We quantified the effects of this noise on the confidence of estimating kinetic parameters of the underlying physiological responses and hence of model discrimination. Five subjects each performed eight transitions from 0 to 100 W on a cycle ergometer. Ventilation, CO2 output, and O2 uptake were computed breath by breath. The eight responses were interpolated uniformly, time aligned, and averaged for each subject; and the kinetic parameters of a first-order model (i.e., the time constant and time delay) were then estimated using three methods: linear least squares, nonlinear least squares, and maximum likelihood. The breath-by-breath noise approximated an uncorrelated Gaussian stochastic process, with a standard deviation that was largely independent of metabolic rate. An expression has therefore been derived for the number of square-wave repetitions required for a specified parameter confidence using methods b and c; method a being less appropriate for parameter estimation of noisy gas exchange kinetics.

Adult↗
PubMed1987

Mediation of reduced ventilatory response to exercise after endurance training.

To investigate the mechanism by which ventilatory (VE) demand is modulated by endurance training, 10 normal subjects performed cycle ergometer exercise of 15 min duration at each of four constant work rates. These work rates represented 90% of the anaerobic threshold (AT) work rate and 25, 50, and 75% of the difference between maximum O2 consumption and AT work rates for that subject (as determined from previous incremental exercise tests). Subjects then underwent 8 wk of strenuous cycle ergometer exercise for 45 min/day. They then repeated the four constant work rate tests at work rates identical to those used before training. During tests before and after training, VE and gas exchange were measured breath by breath and rectal temperature (Tre) was measured continuously. A venous blood sample was drawn at the end of each test and assayed for lactate (La), epinephrine (EPI), and norepinephrine (NE). We found that the VE for below AT work was reduced minimally by training (averaging 3 l/min). For the above AT tests, however, training reduced VE markedly, by an average of 7, 23, and 37 l/min for progressively higher work rates. End-exercise La, NE, EPI, and Tre were all lower for identical work rates after training. Importantly, the magnitude of the reduction in VE was well correlated with the reduction in end-exercise La (r = 0.69) with an average decrease of 5.8 l/min of VE per milliequivalent per liter decrease in La. Correlations of VE with NE, EPI, and Tre were much less strong (r = 0.49, 0.43, and 0.15, respectively).

Adult↗
PubMed1987

The role of exercise testing in impairment evaluation.

To examine the usefulness of exercise testing in impairment evaluation, we reviewed the evaluation of 348 asbestos-exposed shipyard workers. We compared work capacity predicted from history, physical examination, chest roentgenogram, resting electrocardiogram, and resting pulmonary function tests with measured work capacity during an incremental cycle exercise test. The predicted work capacity was often incorrect when compared with measured maximal oxygen uptake (VO2). One third (22 of 66) of those predicted to have reduced work capacity had normal measured work capacity, and 46 of 148 workers (31%) predicted to have normal work capacity were found to have low maximal VO2 during exercise. Of 134 men for whom predicted work capacity was uncertain, maximal VO2 during exercise was low in 49 (37%), normal in 81 (60%), and remained indeterminate in 4 (3%). Thus, of the 138 workers who had low measured VO2, 43 were correctly predicted to have normal work capacity, 46 were incorrectly predicted, and the prediction was uncertain in 49. Only a few were limited by respiratory disease, and cardiovascular disorders limited 69% of those with a low maximal VO2 during exercise. Accordingly, resting VC, FEV1, and DLCO had a poor correlation with exercise performance. Finally, we found that resting DLCO was a poor predictor of abnormal exercise AaPO2, dead-space/tidal volume ratio, or arterial end-tidal PCO2 difference. We conclude that exercise testing is needed for accurate work capacity assessment in impairment evaluation. Exercise testing also facilitates the identification of the major limiting system in those with low work capacity.

Asbestosis↗
PubMed1987

Oxygen uptake kinetics and lactate concentration during exercise in humans.

For constant-load exercise of moderate intensity, oxygen uptake (VO2) increases monoexponentially, reaching a constant value within 3 min, i.e., steady state. However, at work rates associated with increased blood lactate, i.e., above the lactate threshold (LT), VO2 continues to increase slowly beyond 3 min; this delays or precludes steady state. We therefore correlated the characteristics of this slow phase of the VO2 kinetics with the increase in blood lactate during 6 randomized, constant-load cycle exercise tests in 6 normal men. One test was below and the others were at various levels above our gas exchange estimate of LT. The slow kinetic phase of VO2, characterized as the increase between the third and the sixth minute of exercise [delta VO2 (6-3)] or the third minute and termination of exercise [delta VO2 (term-3)], was linearly correlated with the blood lactate increase. The VO2 at termination of a given work rate above LT was greater than predicted from the sub-LT VO2 versus work-rate relationship. Work rates less than approximately 50% of the difference between VO2max and LT resulted in lactate and VO2 curves that reached recognizable asymptotes. At the higher work rates, both the lactate and VO2 curves continued to rise to the point of fatigue. We conclude that positive values for delta VO2 (6-3) and delta VO2(term-3) during constant-load exercise only occur at work rates above the LT, and the magnitudes of which are highly correlated with the increase in blood lactate.

Adult↗
PubMed1987

Coupling of ventilation and CO2 production during exercise in children.

The purpose of this study was to determine how ventilation (VE) and CO2 production (VCO2) in response to exercise change during the growth process in children and teenagers. Dynamic gas exchange responses were measured in two types of studies: 128 healthy children ranging in age from 6 to 18 yr performed progressive exercise tests ("ramp" type protocol) for measurement of the slope of the relationship between VE and VCO2--delta VE/delta VCO2; and the response characteristics of VE and VCO2 in the transition between rest and exercise were measured in 11 teenagers and 11 younger children. Gas exchange was measured breath by breath. We found a small but significant decrease in delta VE/delta VCO2 with increasing body weight (r = -0.46, p less than 0.05), height, or age (mean slope of 27 in the youngest in 21 in the oldest subjects). The response characteristics of VE and VCO2 (measured as the time constant of the best-fit exponential response) were longer than for VO2 in both younger children and teenagers; but the time constants for VE and VCO2 were each approximately 30% faster in younger children compared to teenagers. In addition, end-tidal PCO2 during exercise was significantly lower in the younger subjects (mean value of 39.6 torr) compared to the teenagers (mean value of 43.5 torr). The results suggest that the process of respiratory control in exercise matures to a small degree during childhood in that PCO2 may be regulated at lower levels in younger children and there may be growth-related differences in the relative amounts of CO2 that can be stored in tissues.

Adolescent↗