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Biomedical subjects

K Wasserman

Publications and source records attributed to K Wasserman.

At least 145 records · Page 8Linked to original sources
PubMed1987

Determinants and detection of anaerobic threshold and consequences of exercise above it.

During exercise, the level of oxygen consumption (VO2) above which aerobic energy production is supplemented by anaerobic mechanisms causing a sustained increase in lactate and metabolic acidosis is termed the anaerobic threshold. The VO2 at which the anaerobic threshold occurs is influenced by the factors that affect oxygen delivery to the tissues, being increased when oxygen flow is enhanced and decreased when oxygen flow is diminished. The anaerobic threshold is an important functional demarcation since the physiologic responses to exercise are different above the anaerobic threshold as compared with below the anaerobic threshold. Above the anaerobic threshold, in addition to the development of metabolic acidosis, exercise endurance is reduced, VO2 kinetics are slowed so that a steady state is delayed, and minute ventilation increases disproportionately to the metabolic requirement and a progressive tachypnea develops. The anaerobic threshold can be measured directly from lactate concentration with good threshold detection from a log-log transformation of lactate and VO2. This threshold defines the VO2 at which the lactate/pyruvate ratio increases. As bicarbonate changes reciprocally with lactate, its measurement can also be used to estimate the lactate threshold. But most conveniently, changes in gas exchange caused by the physical-chemical event of buffering of lactic acid by bicarbonate can be used to detect the anaerobic threshold during exercise.

Acidosis↗
PubMed1986

Glucose turnover in response to exercise during high- and low-FIO2 breathing in man.

The purpose of this study was to assess whether breathing high or low concentrations of O2 could affect glucose turnover during exercise in man. Ten healthy subjects performed two constant work-rate exercise tests, one when the fraction of inspired O2 (FIO2) was 0.15 and the other at the same work rate but when the FIO2 was 0.80. The work rate for each subject was chosen so that blood lactate would be elevated during hypoxia, but would be lower during hyperoxia. Glucose appearance (Ra) and disappearance (Rd) were measured using the primed, constant infusion of [3-3H]glucose. Although the work rate was the same during hypoxia and hyperoxia in each subject, hypoxic exercise was accompanied by a significantly larger rest to exercise increase in Rd (delta Rd) compared with hyperoxia by 265%. Similarly, delta Ra was greater during hypoxia than during hyperoxia by 188%. Lactate to pyruvate ratios were significantly higher during hypoxic exercise suggesting a shift in the cell redox to a more reduced state. Insulin and glucagon were not affected by the FIO2, but both epinephrine and norepinephrine were increased during hypoxic exercise, which may explain the increase in Ra. The regulation of blood glucose during exercise in vivo appears to be dependent on the availability of oxygen to the working muscle cells.

Adult↗
PubMed1986

Bicarbonate buffering of lactic acid generated during exercise.

The pattern of decrease in arterial bicarbonate concentration ([HCO3-]) during progressive incremental exercise was compared with that of the rise in arterial lactate ([La-]) to determine the degree of buffering of lactic acid by bicarbonate. A mathematical model was derived for the change in [HCO3-] beyond the lactate threshold. This was based on a log-log transformation of the data, a model previously found to provide a very good fit to the [La-]-O2 consumption (VO2) relationship. The results of the analysis of incremental exercise data from 10 subjects show that the decrease in [HCO3-] very nearly matches the increase in [La-]. However, it was found by comparing regression models that the correspondence between [HCO3-] and [La-] could be improved by assuming that the [HCO3-] decrease was delayed until the arterial lactate level had increased by approximately 0.4 meq/l. This result is compatible with the existence of buffering mechanisms in the cell which buffer the initial increase of lactic acid. Beyond this initial buffering, lactic acid appears to be buffered almost entirely by the bicarbonate buffer system.

Adult↗
PubMed1986

A new method for detecting anaerobic threshold by gas exchange.

Excess CO2 is generated when lactate is increased during exercise because its [H+] is buffered primarily by HCO-3 (22 ml for each meq of lactic acid). We developed a method to detect the anaerobic threshold (AT), using computerized regression analysis of the slopes of the CO2 uptake (VCO2) vs. O2 uptake (VO2) plot, which detects the beginning of the excess CO2 output generated from the buffering of [H+], termed the V-slope method. From incremental exercise tests on 10 subjects, the point of excess CO2 output (AT) predicted closely the lactate and HCO-3 thresholds. The mean gas exchange AT was found to correspond to a small increment of lactate above the mathematically defined lactate threshold [0.50 +/- 0.34 (SD) meq/l] and not to differ significantly from the estimated HCO-3 threshold. The mean VO2 at AT computed by the V-slope analysis did not differ significantly from the mean value determined by a panel of six experienced reviewers using traditional visual methods, but the AT could be more reliably determined by the V-slope method. The respiratory compensation point, detected separately by examining the minute ventilation vs. VCO2 plot, was consistently higher than the AT (2.51 +/- 0.42 vs. 1.83 +/- 0.30 l/min of VO2). This method for determining the AT has significant advantages over others that depend on regular breathing pattern and respiratory chemosensitivity.

Adult↗
PubMed1986

Ventilatory responses to partial cardiopulmonary bypass at rest and exercise in dogs.

We determined the role of blood flow-induced changes in CO2 load to the lungs on ventilatory control, at rest and in the steady-state of electrically induced exercise, in the anesthetized dog. A portion of the vena caval blood was diverted to the descending aorta following "arterialization" through an extracorporeal gas exchanger. Ventilation typically decreased, both at rest and during exercise (i.e., at 2 different levels of mixed venous CO2), in proportion to the CO2 loss; arterial PCO2 was consequently regulated. There were concomitant increases of the pulmonary and peripheral vascular resistance. Bilateral cervical vagosympathectomy markedly attenuated the ventilatory response at rest, thus disrupting arterial PCO2 homeostasis, but not so during exercise. The results therefore provide evidence for and support the suggestion of CO2 flow-related hyperpnea both at rest and during muscular exercise.

Animals↗
PubMed1986

Dynamics of oxygen uptake during exercise in adults with cyanotic congenital heart disease.

The dynamic increase in oxygen uptake (VO2) at the start of exercise reflects the circulatory adjustments to metabolic changes induced by the exercise. Because VO2 measured at the lungs is the product of pulmonary blood flow and arteriovenous oxygen difference, pathologic conditions affecting the capacity of these factors to change would be expected to alter VO2 kinetics. To determine whether measurement of VO2 kinetics can detect conditions in which the pulmonary blood flow response to exercise is abnormal, VO2 was measured, breath-by-breath, during the transition from rest to exercise in 13 adults with cyanotic congenital heart disease (central venoarterial shunting) and in nine normal subjects. The increase in VO2 above baseline during the first 20 sec of exercise (phase I), reflecting the immediate increase in pulmonary blood flow, was diminished in the patients compared with that in normal subjects (14.8 +/- 10.9 vs. 49.8 +/- 19.2 ml of oxygen) (p less than .001). The patients' phase I responses correlated with their reported physical activity tolerance (p less than .01). In addition, the second phase of the VO2 response kinetics was prolonged in patients compared with normal subjects (half-time = 63 +/- 13 vs 15 +/- 13 sec) (p less than .001). We conclude that striking disturbances in VO2 kinetics occur in patients with cyanotic congenital heart disease and that these measurements provide a useful noninvasive means of evaluating the degree to which the increase in pulmonary blood flow is constrained in response to exercise.

Adult↗
PubMed1986

Bronchodilatation and attenuation of exercise-induced bronchospasm by PY 108-068, a new calcium antagonist.

The effect of a new dihydropyridine-derivative calcium antagonist, PY 108-068, on resting and postexercise flow rates was evaluated in 12 adult asthmatic subjects in a double-blind, randomized, placebo-controlled, cross-over study. The study consisted of 2 periods, each lasting for 3 days. For a given period a single dose of PY 108-068 (or placebo) was given orally, 75 mg on the first day and 150 mg on the second and third day. Spirometry was obtained at 30-min intervals thereafter. On Day 3, 75 min after the medication was given, a 6-min treadmill exercise test was performed breathing dry air. The mean maximal FEV1 recorded after 150 mg of PY 108-068 on Day 2 was 15 +/- 4% higher than the daily baseline (p less than 0.05), whereas after placebo the maximal FEV1 value was not different from the daily baseline. Also, the mean FEV1 values, expressed as percent of the daily predrug baseline, were significantly higher at 2 and 3 h after 150 mg of PY 108-068 than the respective values after placebo (110 +/- 4 compared with 95 +/- 1, and 106 +/- 5 compared with 91 +/- 3, respectively). Exercise-induced bronchospasm (EIB), expressed as maximal percent fall in FEV1 from preexercise baseline, was attenuated by PY 108-068 as compared with placebo (% delta FEV1 of 20 +/- 6 and 40 +/- 4, respectively; p less than 0.001). Protection against EIB did not correlate with the resting bronchodilation induced by PY 108-068, but was more likely if the patient had eosinophilia. Thus, PY 108-068 not only attenuates EIB but also causes resting bronchodilation, a unique finding for calcium channel blockers.

Adult↗
PubMed1986

Mechanisms and patterns of blood lactate increase during exercise in man.

The close balance between the O2 requirement to perform exercise and the O2 supply was analyzed. A non-uniform capillary PO2 can result in anaerobic metabolism in some muscle fibers despite an apparently adequate mean capillary PO2. The pattern of lactate increase for constant work rates and incremental exercise is described. Lactate increases without an increase in pyruvate at a threshold work rate above which the lactate/pyruvate ratio increases. The latter decreases immediately at the start to recovery. From simultaneous measurements of arterial lactate and pyruvate during exercise and recovery, we conclude that the lactate increase at the lactate threshold is consequent to a change in redox state rather than a mass action effect.

Adult↗
PubMed1986

Comparison of PY 108-068, a new calcium antagonist, with nifedipine in exercise-induced asthma.

Several calcium antagonists, each with significantly different chemical structures, have demonstrated variable attenuation of exercise-induced asthma. Quantitative comparisons have been hampered by differences in the intensity of challenge and the severity of the underlying disease between groups of patients. In 12 asthmatic adults with relatively severe exercise-induced asthma, we compared the effect of a new calcium antagonist, PY 108-068, in doses of 75 mg and 150 mg with nifedipine (30 mg) and placebo on resting flow rates and flow rates after exercise. Over a three-week period, each patient completed a four-day, randomized, double-blind Latin-square study. After receiving one of four oral drugs, spirometry was repeated every 30 minutes for two hours, followed by a six-minute treadmill exercise test breathing dry air. The exercise tests were well matched for work rate, ventilation, heart rate, and oxygen uptake. Spirometry was then repeated seven times over the next 30 minutes after exercise. Though both 150 mg of PY 108-068 and nifedipine were associated with mild bronchodilation before exercise, only the latter was significant (p less than 0.05). Exercise-induced asthma (expressed as maximal percent fall in the forced expiratory volume in one second from before baseline) was significantly attenuated only by 150 mg of PY 108-068 compared to placebo (24 +/- 13 vs 40 +/- 16; p less than 0.05). Headache, which occurred in six subjects after nifedipine, five after 150 mg of PY 108-068, one after 75 mg of PY 108-068, and none after placebo, was subjectively more severe after nifedipine. We conclude that in these patients, there was a tendency for mild bronchodilation before exercise with both 150 mg of PY 108-068 and nifedipine, but only the 150-mg dose provided significant protection against exercise-induced asthma two hours after the drug.

Adolescent↗
PubMed1986

Anaerobiosis, lactate, and gas exchange during exercise: the issues.

The lactate increase during exercise is a critically important biochemical and physiological event that leads to decreasing cell pH, an accelerated rate of glycogen depletion in the muscle, and important changes in ventilatory and gas exchange dynamics. Lactate increases only slightly at low work rates, and this increase is proportional to pyruvate increase (i.e. compatible with accelerated glycolysis without a change in redox state). At high work rates lactate increases disproportionately to pyruvate, the increased rate of lactate accumulation and lactate/pyruvate ratio appearing to occur at a threshold O2 consumption for a given individual. This symposium addresses the biochemical origin and physiological consequences of the increased lactate production during exercise.

Anaerobiosis↗
PubMed1986

Effect of anaerobiosis on the kinetics of O2 uptake during exercise.

The anaerobic threshold is an O2-related threshold of metabolic acidemia of which the chief metabolic acid is lactic acid. As such, it is a crucial parameter of aerobic function. For power outputs that are below the anaerobic threshold, the dynamics of O2 uptake (VO2) is well characterized as a linear first-order exponential process. The system time constant for leg exercise in humans has been shown to be congruent to 25-35 s with a "delay" of 15-20 s. Steady states are therefore normally achieved within 3 min at this work intensity. Above the anaerobic threshold a second, slower component of VO2 becomes evident that delays the steady state (if attainable). Consequently, the difference in VO2 between the third and the sixth minute of exercise is zero if the work rate is subthreshold and becomes progressively greater, the higher the increment above this parameter; this also correlates highly with the increment of arterial blood lactate, [L-]. This slow phase of the VO2 kinetics results in "excess" VO2, in that the VO2 rises to values above those attained by fitter subjects. This excess VO2 correlates highly with the increased [L-] (and possibly other factors), although its magnitude increases even more rapidly at work rates for which the increase in [L-] exceeds 4-5 meq/liter.

Anaerobiosis↗
PubMed1986

The anaerobic threshold: definition, physiological significance and identification.

During exercise, the oxygen consumption above which aerobic energy production is supplemented by anaerobic mechanisms, causing a sustained increase in lactate and metabolic acidosis, is termed the anaerobic threshold (AT). The oxygen consumption at the AT depends on factors that affect oxygen delivery to the tissues. It is increased when oxygen flow is enhanced and decreased when oxygen flow is diminished. Its value is quite low in patients with heart disease. The AT is an important functional demarcation since the physiological responses to exercise are different above the AT compared to below the AT. Above the AT, in addition to the development of metabolic acidosis, exercise endurance is reduced, VO2 kinetics are slowed so that a steady state is delayed, and VE increases disproportionately to the metabolic requirement and a progressive tachypnea develops. The AT can be measured directly from the lactate concentration with precise threshold detection from a log-log transformation of lactate and VO2. This threshold also defines the VO2 above which the lactate/pyruvate ratio increases. As bicarbonate changes reciprocally with lactate, its measurement can also be used to estimate the lactate threshold. But most convenient are gas exchange measurements made during exercise testing which can be used to noninvasively detect the lactate or anaerobic threshold. These methods are based on the physical-chemical event of buffering lactic acid with bicarbonate, and the increased CO2 output which occurs in association with the acute development of a metabolic acidosis.

Acidosis↗
PubMed1985

Immediate effects of cigarette smoking on cardiorespiratory responses to exercise.

To determine the acute action of cigarette smoking on cardiorespiratory function under stress, the immediate effects of cigarette smoking on the ventilatory, gas exchange, and cardiovascular responses to exercise were studied in nine healthy male subjects. Each subject performed an incremental exercise test to exhaustion on two separate days, one without smoking (control) and one after smoking 3 cigarettes/h for 5 h. The order of the two tests was randomized. Arterial blood gases and pH were measured during rest and all levels of exercise; CO blood levels confirmed the absorption of cigarette smoke. In addition, minute ventilation (VE), end-tidal PCO2 and PO2, O2 uptake (VO2), CO2 production, directly measured blood pressure, electrocardiogram, and heart rate (HR) were recorded every 30 s. The dead space-to-tidal volume ratio (VD/VT), maximal aerobic capacity (VO2max), and anaerobic threshold (AT) were determined from the gas exchange data. Cigarette smoking resulted in a significantly lower VO2max, AT, and VO2/HR (O2 pulse) and a significantly higher HR, pulse-pressure product, and pulse pressure (P less than 0.05) compared with the control. Additionally, a trend toward a higher VD/VT and arterial-end-tidal PCO2 difference was found during exercise after smoking. We conclude that cigarette smoking causes immediate detrimental effects on cardiovascular function during exercise, including tachycardia, increased pulse-pressure product, and impaired O2 delivery. The acute effects on respiratory function were less striking and primarily limited to abnormalities reflecting ventilation-perfusion mismatching.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Kinetics of oxygen uptake and heart rate at onset of exercise in children.

Requirements for cellular homeostasis appear to be unchanged between childhood and maturity. We hypothesized, therefore, that the kinetics of O2 uptake (VO2) in the transition from rest to exercise would be the same in young children as in teenagers. To test this, VO2 and heart rate kinetics from rest to constant work rate (75% of the subject's anaerobic threshold) in 10 children (5 boys and 5 girls) aged 7-10 yr were compared with values found in 10 teenagers (5 boys and 5 girls) aged 15-18 yr. Gas exchange was measured breath to breath, and phases I and II of the transition and phase III (steady-state exercise) were evaluated from multiple transitions in each child. Phase I (the VO2 at 20 s of exercise expressed as percent rest-to-steady-state exercise VO2) was not significantly correlated with age or weight [mean value 42.5 +/- 8.9% (SD)] nor was the phase II time constant for VO2 [mean 27.3 +/- 4.7 (SD) s]. The older girls had significantly slower kinetics than the other children but were also found to be less fit. When the teenagers exercised at work rates well below 75% of their anaerobic threshold, phase I VO2 represented a higher proportion of the overall response, but the phase II kinetics were unchanged. The temporal coupling between the cellular production of mechanical work at the onset of exercise and the uptake of environmental O2 appears to be controlled throughout growth in children.

Adolescent↗
PubMed1985

Lactate, pyruvate, and lactate-to-pyruvate ratio during exercise and recovery.

The pattern of lactate increase and its relation to pyruvate and lactate-to-pyruvate (L/P) ratio were studied during exercise and early recovery in 10 normal subjects for incremental exercise on a cycle ergometer. Gas exchange was measured breath by breath. Lactate and pyruvate were measured by enzymatic techniques. Lactate and log lactate changed only slightly at low levels of O2 uptake (VO2) but both began to abruptly increase at approximately 40-55% of the maximal VO2. However, the point of abrupt increase in pyruvate occurred at higher work rates and the rate of increase was not as great as that for lactate. Thus L/P ratio increased at the same VO2 as the log lactate increase. Following the exercise, pyruvate continued to increase steeply for at least the first 5 recovery min, whereas at 2 min lactate increased only slightly or decreased. Thus arterial L/P ratio reversed its direction of change and decreased toward the resting value by 2 min of recovery. Lactate, as well as L/P ratios, decreased in all subjects by 5 min. This study demonstrates that lactate and pyruvate concentrations increase slightly at low levels of exercise without a change in L/P ratio until a threshold work rate at which lactate abruptly increases without pyruvate. The resulting increase in L/P ratio is progressive as work rate is incremented and abruptly reverses when exercise stops.

Adult↗
PubMed1985

Improved detection of lactate threshold during exercise using a log-log transformation.

The pattern of arterial lactate concentration ([La-]) increase during incremental exercise was studied using a transformation defined by plotting log([La-]) vs. log(VO2), where VO2 is O2 uptake. A plot of this function exhibits a phase of very slow increase followed by a phase of rapid increase, defining a transition in the underlying relationship between [La-] and VO2. These phases were found to be linear on the log-log plot; linear regression analysis may therefore be used to locate the transition between them (lactate threshold). A transition point was found at a lower VO2 on the semilog plot of log([La-]) vs. VO2. Consideration of the data from all studies led to the conclusion that a more accurate result is provided by the log-log transformation. This analysis shows lactate to have a small, but significant, increase before the transition and to increase beyond it with a power law having an exponent of about 2.9. This result shows that, during incrementally increasing work rate tests, arterial lactate exhibits a threshold behavior, i.e., an abrupt transition from a phase of slow increase to a phase of rapidly accelerating increase.

Adult↗