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Biomedical subjects

K Wasserman

Publications and source records attributed to K Wasserman.

At least 163 records · Page 9Linked to original sources
PubMed1985

Lung function and exercise performance in smoking and nonsmoking asbestos-exposed workers.

Evaluation of impairment caused by exposure to an occupational toxin can be complicated by additional exposure to other injurious agents. Because cigarette smoking is common and cigarettes are implicated in obstructive lung disease and cardiovascular diseases, we assessed the contribution of smoking to functional abnormalities in a group of asbestos-exposed shipyard workers. Seventy-three workers who never smoked were paired with 73 current smokers by age and asbestos exposure. Pulmonary function and performance during cycle incremental exercise were compared between the 2 groups. Nonsmokers had significantly higher VC, FEV1, FEV1/VC, and diffusing capacity for carbon monoxide than did smokers. Only 3 of the 73 nonsmokers but 23 of the 73 smokers had a FEV1/VC below the 95% confidence limit of predicted value. The FEF25-75%, on the other hand, failed to identify additional subjects with obstruction not found by the FEV1/VC. During exercise, despite no difference in maximal heart rate, the maximal O2 uptake (VO2max) and oxygen-pulse were lower among smokers. In addition, smokers more frequently had abnormal AaPO2 at maximal exercise. Of 33 smokers who had a VO2max less than 80% of predicted, 16 were judged to have cardiac disease, whereas only 2 appeared to be limited by obstruction. Only 15 of the 73 nonsmokers had a VO2max less than 80%. We conclude that cigarette smoking was the major contributing factor to the obstructive lung disease observed in asbestos workers, and it also had a strong influence on the occurrence, nature, and magnitude of exercise limitation. The history of cigarette smoking has an important effect on the assessment of impairment from asbestos.

Aged↗
PubMed1985

Gas exchange during exercise in children with thalassemia major and Diamond-Blackfan anemia.

The two main goals of this study were: to determine how O2 uptake, ventilation, and CO2 production during exercise were acutely affected by transfusion in children with congenital anemia (thalassemia major and Diamond-Blackfan syndrome) requiring hypertransfusion and chelation therapy and to compare gas exchange responses to exercise of the anemic patients to normal values. Thirteen patients (age range 7-27) performed cycle ergometry with a progressively increasing work rate. Gas exchange was measured breath-by-breath. Tests were done before and after routine transfusion (mean increase in hematocrit 22%). The results were compared to 10 age-matched normal children who performed the same protocol on two occasions separated by a 2-day interval, and to the results of 109 normal children studied in this laboratory. Transfusion resulted in: a small, but significant increase in the anaerobic threshold (9%) and an increase in the slope of the relationship between O2-uptake and heart rates. Despite these improvements, the majority of the patients had abnormally low values of maximal O2 uptake, anaerobic threshold, and slope of the O2 uptake-heart rate relationship. The abnormalities were more marked in the older patients. Measurement of gas exchange during exercise may be helpful in determining an optimal hematocrit for patients on hypertransfusion regimens.

Adolescent↗
PubMed1985

A subpopulation of allospecific cytotoxic T-cell precursors with phenotypic characteristics of natural killer cells.

We have proposed that natural killer (NK) cells are germ-line V-gene encoded prothymocytes specific for either self or non-self histocompatibility antigens. This hypothesis predicts that at least some precursors of allospecific cytotoxic T cells (allo-CTL) are NK cells. To test this we examined the effect of depleting NK cells and/or T cells (by complement lysis with anti-asialo GM1 and/or anti-Thy 1) on the development of allo-CTL induced during mixed lymphocyte culture (MLC). Removal of Thy 1+ cells from MLC responder populations prevented development of allo-CTL. This was partially reversed by addition of concanavalin A-conditioned medium (Con A-CM) to the MLC at day 0. Removal of asialo GM1+ cells eliminated NK activity measured at day 0, but failed to prevent development of allo-CTL of otherwise intact responder cells. However, removal of asialo GM1+ cells did prevent the Con A-CM dependent development of allo-CTL by responder cells depleted of Thy 1+ cells. These findings indicate that a subpopulation of allo-CTL precursors has the phenotypic characteristics of NK cells: absence or low density of Thy 1, and susceptibility to complement lysis by anti-asialo GM1.

Animals↗
PubMed1984

Aerobic parameters of exercise as a function of body size during growth in children.

To examine the relationship between body weight in children and aerobic parameters of exercise, we determined the anaerobic threshold (AT), maximum O2 uptake (VO2max), work efficiency, and response time for O2 uptake (RT-VO2) in 109 healthy children (51 girls and 58 boys, range 6-17 yr old) using a cross-sectional study design. Gas exchange during exercise was measured breath by breath. The protocol consisted of cycle ergometry and a linearly increasing work rate (ramp) to the limit of the subject's tolerance. Both AT and VO2max increased systematically with body weight, whereas work efficiency and RT-VO2 were virtually independent of body size. The ratio of AT to VO2max decreased slightly with age, and its mean value was 60%. AT scaled to body weight to the power of 0.92, not significantly different from the power of 1.01 for VO2max. Thus both the AT and the VO2max increase in a highly ordered manner with increasing size, and as judged by AT/VO2max, the onset of anaerobic metabolism during exercise occurred at a relatively constant proportion of the overall limit of the gas transport system. We conclude that in children cardiorespiratory responses to exercise are regulated at optimized values despite overall change in body size during growth.

Adolescent↗
PubMed1984

Coupling of external to internal respiration.

Oxygen is required to generate chemical energy (ATP) to allow muscle contraction. The amount of chemical energy required is directly proportional to the work rate performed. Early in exercise, the muscle creatine phosphate and oxygen stores, primarily in the form of oxymyoglobin and oxyhemoglobin (oxygen content of venous blood decreases), are used for energy. This allows time for cardiac output and ventilation to increase to satisfy the total O2 requirement. Steady-state time depends on the level of work relative to the anaerobic threshold (AT). For work rates below the AT, steady-state for VO2 is achieved by 3 min and by 4 min for VCO2 and VE. For work rates above the AT, steady-states are considerably delayed or not achieved. For purposes of description of the pattern of external respiration (gas exchange at the lungs), three phases are defined. Phase I is the initial increase in VO2 and VCO2 at the start of exercise, lasting approximately 15 s. Because the gas exchange ratio (R) typically doesn't change during Phase I, the initial increase in VO2 and VCO2 must be due primarily to an increase in pulmonary blood flow and proportional increase in ventilation (cardiodynamic phase). Phase II is the exponential-like increase in VO2 and VCO2, which follow Phase I and terminates in a steady-state or asymptotic value (Phase III). At moderate work, VO2 increases more rapidly than VCO2 during Phase II (CO2 stores increase). Therefore, R decreases before it increases to the steady-state. Below the AT, the rate of external respiration equals the rate of internal respiration during Phase III.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbon Dioxide↗
PubMed1984

The anaerobic threshold measurement to evaluate exercise performance.

During exercise, the oxygen consumption above which aerobic energy production is supplemented by anaerobic mechanisms, and which results in a significant increase in lactate, is termed the anaerobic threshold (AT). This power output has important functional implications because it is a demarcation of the work rate above which metabolic acidosis accelerates the stimulation to breathing, and exercise endurance becomes reduced. The justification for relating lactate increase to tissue anaerobiosis during exercise is presented, and the gas exchange methods for measuring the AT are described. The form of work affects the AT, treadmill being about 10% greater than cycling in sedentary subjects. It is useful for predicting the ability of the subject to sustain a given work rate for a prolonged period and for determining the VO2 above which there is cardiovascular insufficiency in meeting tissue O2 requirements.

Acidosis↗
PubMed1984

Predicted values for clinical exercise testing.

Following thorough evaluation at rest, 265 of 400 current or ex-shipyard workers rode a cycle ergometer with equal work increments each minute to exhaustion while continuous multiple noninvasive cardiorespiratory measures and intermittent intra-arterial blood pressure and blood gas measures were made. Seventy-seven men, with a mean age of 54, including some who were smokers, obese, or hypertensive, were judged to have normal cardiorespiratory systems based on history, physical, electrocardiogram during rest and exercise, chest X-ray, pulmonary function tests, and exercise performance. Their responses to exercise are given. It was unusual to find at maximal exercise a breathing reserve less than 11 L/min, arterial PO2 less than 80 mm Hg, alveolar-arterial PO2 difference greater than 38 mm Hg, arterial-end tidal PCO2 difference greater than 1 mm Hg, respiratory frequency greater than 60, or a dead space/tidal volume ratio greater than 0.28. The normal anaerobic threshold/maximal O2 uptake ratio exceeded 40%. With maximal exercise, the intra-arterial systolic and diastolic pressures rose an average of 68 and 13 mm Hg, respectively. For predicting maximal oxygen uptake and oxygen pulse in an overweight man, we find it preferable to use age and height rather than age and weight.

Adult↗
PubMed1984

Growth-related changes in oxygen uptake and heart rate during progressive exercise in children.

Although body size and muscle mass increase considerably during growth in children, certain aerobic responses to exercise appear to be regulated so that the delivery of oxygen to muscle is maintained at optimized levels. We proposed that the relationship between oxygen uptake, (VO2) and heart rate (HR) was one of the regulated responses. We further hypothesized that the increase in VO2 per increase in HR during progressive exercise would differ in subjects of different size, but when normalized to body weight would be constant since changes in muscle mass are highly correlated to changes in body mass. To test this, we performed a cross-sectional study of 107 normal children, 50 girls and 57 boys ranging in age from 6 to 17 years. The protocol consisted of a continuously increasing work rate on a cycle ergometer, to the limit of the child's tolerance (ramp forcing function). Gas exchange was measured breath-by-breath for the determination of VO2, and heart rate was measured beat-by-beat. We used linear regression techniques to determine M, the slope, and B, the y intercept of the equation: VO2 = M X HR - B. In both boys and girls, M increased significantly with body weight, but when normalized for body weight (M/kg), there was no systematic change with increasing weight or age, the mean value being 0.33 +/- 0.10 ml/min/kg (SD). The mean value for the boys was 0.37 +/- 0.10 which was significantly greater than that of the girls (0.29 +/- 0.08, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

The anaerobic threshold measurement in exercise testing.

The exercise intensity (VO2) above which aerobic energy production starts to be supplemented by anaerobic mechanisms is termed the anaerobic threshold (AT). Lactic acid is produced at an increased rate above this work level. Since this acid is almost completely buffered by HCO-3, the rate of CO2 production increases in excess of that being derived from oxidative metabolism. Thus measurement of this excess CO2, or some reflection of it, can be used during exercise to measure the AT noninvasively. The AT has great physiologic significance, as it demarcates the work rate that the subject can perform for a prolonged period and above which a metabolic acid occurs.

Acid-Base Equilibrium↗
PubMed1983

Effects of beta-adrenergic blockade on ventilation and gas exchange during exercise in humans.

The effects of beta-adrenergic blockade induced by intravenous propranolol hydrochloride (0.2 mg/kg) on ventilatory and gas exchange responses to exercise were studied during tests in which the work rate was either increased progressively or maintained at a constant load in six healthy young male subjects. Heart rate during exercise decreased by about 20% and cardiac output, as estimated by a modification of the method of Kim et al. (J. Appl. Physiol. 21: 1338-1344, 1966), by about 15%. The relation between work rate and O2 uptake (VO2) was unaffected by propranolol, whereas maximal O2 uptake (VO2max) decreased by 5% and the anaerobic threshold, estimated noninvasively, was lowered by 23%. The relations between CO2 output (VCO2) and end-tidal CO2 partial pressure (PCO2) and between VCO2 and minute ventilation (VE) were both unaffected. The time constants for changes of VO2, VCO2, and VE during on-transients from unloaded pedaling to either a moderate (ca. 50% VO2max) or a heavy (ca. 67% VO2max) work rate in the control studies were in agreement with previously reported values, i.e., 42, 60, and 69 s, respectively. beta-Blockade was associated with a significantly increased time constant for VO2 of 61 s but with less consistent and insignificant changes for VCO2 and VE. There was a small but significant increase of the time constant for heart rate from 40 to 45 s. It is concluded that propranolol exerts its primary influence during exercise on the cardiovascular system without any discernible effect on ventilatory control.

Adult↗
PubMed1983

Exercise gas exchange in asthmatics after beta-adrenergic blockade.

Pharmacologic beta-adrenergic blockade reduces maximal heart rate (HR) during exercise but variable results have been reported for minute ventilation (VE), CO2 output (VCO2), and O2 uptake (VO2). A total group of 19 subjects with mild asthma was studied. We studied 16 subjects from the group who received placebo or pindolol, a beta-adrenergic antagonist, during 1-min incremental exercise on a cycle ergometer. During incremental exercise, HR, VE, VCO2, and VO2 were less after beta-blockade than after placebo at the same work rate below the anaerobic threshold. Maximal HR, VE, VO2, VCO2, and work rate were significantly less after beta-blockade. In addition, we studied six subjects from the group, including three who had also performed incremental exercise, during the steady state of constant-work cycling exercise. We found no difference in VE, VCO2, or VO2 although HR was less after beta-blockade. We conclude that beta-adrenergic blockade affects gas exchange by delaying the normal cardiovascular response to exercise. Decreased VE during incremental exercise is due to slowed delivery of CO2 load to the lungs rather than alterations in substrate, lung function, or ventilatory control.

Adolescent↗
PubMed1983

Influence of body CO2 stores on ventilatory dynamics during exercise.

Pulmonary CO2 flow (the product of cardiac output and mixed venous CO2 content) is purported to be an important determinant of ventilatory dynamics in moderate exercise. Depletion of body CO2 stores prior to exercise should thus slow these dynamics. We investigated, therefore, the effects of reducing the CO2 stores by controlled volitional hyperventilation on cardiorespiratory and gas exchange response dynamics to 100 W cycling in six healthy adults. The control responses of ventilation (VE), CO2 output (VCO2), O2 uptake (VO2), and heart rate were comprised of an abrupt increase at exercise onset, followed by a slower rise to the new steady state (t1/2 = 48, 43, 31, and 33 s, respectively). Following volitional hyperventilation (9 min, PETCO2 = 25 Torr), the steady-state exercise responses were unchanged. However, VE and VCO2 dynamics were slowed considerably (t1/2 = 76, 71 s) as PETCO2 rose to achieve the control exercise value. VO2 dynamics were slowed only slightly (t1/2 = 39 s), and heart rate dynamics were unaffected. We conclude that pulmonary CO2 flow provides a significant stimulus to the dynamics of the exercise hyperpnea in man.

Carbon Dioxide↗
PubMed1983

Control of breathing at the start of exercise as influenced by posture.

It has been suggested that the initial phase of the ventilatory response to exercise is governed by a mechanism which responds to the increase in pulmonary blood flow (Q)--cardiodynamic hyperpnea. Because the initial change in stroke volume and Q is less in the supine (S) than in the upright (U) position at the start of exercise, we hypothesized that the increase in ventilation would also be less in the first 20 s (phase I) of S exercise. Ten normal subjects performed cycle ergometry in the U and S positions. Inspired ventilation (VI), O2 uptake (VO2), CO2 output (VCO2), corrected for changes in lung gas stores, and end-tidal O2 and CO2 tensions were measured breath by breath. Heart rate (HR) was determined beat by beat. The phase I ventilatory response was markedly different in the two positions. In the U position, VI increased abruptly by 81 +/- 8% (mean +/- SE) above base line. In the S position, the phase I response was significantly attenuated (P less than 0.001), the increase in VI being 50 +/- 6%. Similarly, the phase I VO2 and VO2/HR responses reflecting the initial increase in Q and stroke volume, were attenuated (P less than 0.001) in the S posture, compared with that for U; VO2 increased 49 +/- 5.3 and 113 +/- 14.7% in S and U, respectively, and VO2/HR increased 16 +/- 3.0 and 76 +/- 7.1% in the S and U, respectively. The increase in VI correlated well with the increase in VO2, (r = 0.80, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Optimizing the exercise protocol for cardiopulmonary assessment.

Twelve normal men performed 1-min incremental exercise tests to exhaustion in approximately 10 min on both treadmill and cycle ergometer. The maximal O2 uptake (VO2 max) and anaerobic threshold (AT) were higher (6 and 13%, respectively) on the treadmill than the cycle; the AT was reached at about 50% of VO2 max on both ergometers. Maximal CO2 output, heart rate, and O2 pulse were also slightly, but significantly higher on the treadmill. Maximal ventilation, gas exchange ratio, and ventilatory equivalents for O2 and CO2 for both forms of exercise were not significantly different. To determine the optimum exercise test for both treadmill and cycle, we exercised five of the subjects at various work rate increments on both ergometers in a randomized design. The treadmill increments were 0.8, 1.7, 2.5, and 4.2%/min at a constant speed of 3.4 mph, and 1.7 and 4.2%/min at 4.5 mph. Cycle increments were 15, 30, and 60 W/min. The VO2 max was significantly higher on tests where the increment magnitude was large enough to induce test durations of 8-17 min, but the AT was independent of test duration. Thus, for evaluating cardiopulmonary function with incremental exercise testing by either treadmill or cycle, we suggest selecting a work rate increment to bring the subject to the limit of his tolerance in about 10 min.

Adult↗
PubMed1983

Effects of obesity on respiratory function.

Obesity, because it alters the relationship between the lungs, chest wall, and diaphragm, has been expected to alter respiratory function. We studied 43 massively obese but otherwise normal, nonsmoking, young adults with spirometry, lung volume measurement by nitrogen washout, and single-breath diffusing capacity for carbon monoxide (DLCO). Changes in respiratory function were of two types, those that changed in proportion to degree of obesity--expiratory reserve volume (ERV) and DLCO--and those that changed only with extreme obesity--vital capacity, total lung capacity, and maximal voluntary ventilation. When compared with commonly used predicting equations, we found that mean values of subjects grouped by degree of obesity were very close to predicted values, except in those with extreme obesity in whom weight (kg)/height (cm) exceeded 1.0. In 29 subjects who lost a mean of 56 kg, significant increases in vital capacity, ERV, and maximal voluntary ventilation were found, along with a significant decrease in DLCO. Because most subjects fell within the generally accepted 95% confidence limits for the predicted values, we concluded that obesity does not usually preclude use of usual predictors. An abnormal pulmonary function test value should be considered as caused by intrinsic lung disease and not by obesity, except in those with extreme obesity.

Adult↗
PubMed1983

Contrasting cardiovascular and respiratory responses to exercise in mitral valve and chronic obstructive pulmonary diseases.

The role of cardiovascular and pulmonary limitation in performing maximal exercise is contrasted in patients with mitral valve disease (MVD) and chronic obstructive pulmonary disease (COPD). The ventilatory (VE) gas exchange (VO2 and VCO2) and heart rate (HR) responses to an incremental cycle ergometer exercise were measured in six patients with MVD, seven patients with COPD, and six normal subjects. The VE requirement for the work (VE-VO2 relationship) was increased in both COPD and MVD groups compared with control subjects, but the breathing reserve was significantly lower in COPD (13 percent) compared with MVD (49 percent) and control groups (44 percent). In contrast, the VO2 at the anaerobic threshold was significantly lower in MVD (12.2 +/- .5 ml/kg) compared with COPD (15.7 +/- 1.2 ml/kg) and control subjects (16.6 +/- .9 ml/kg). Also, the heart rate reserve and the VO2-HR slope were significantly reduced in MVD (9 +/- 6 percent and 6.9 +/- 1.0 ml/min/beat, respectively) compared with COPD patients (44 +/- 7 percent and 2.0 ml/min/beat, respectively). Both patient groups experienced an acidosis in their terminal work rate, but the acidosis was primarily respiratory in the COPD and totally metabolic in the MVD group. These studies indicate that at maximal work rate, MVD but not COPD patients, manifest compromised O2 delivery to the muscles, while COPD but not MVD patients were unable to increase VE sufficiently to match the exercise-induced CO2 production.

Acid-Base Equilibrium↗