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K Wasserman

Publications and source records attributed to K Wasserman.

At least 37 records · Page 2Linked to original sources
PubMed1990

Evidence supporting the existence of an exercise anaerobic threshold.

In this paper, we provided evidence to support the concept that work above the anaerobic threshold, measured by the V-slope method, is, in fact, performed partially anaerobically. In contrast, work performed below the anaerobic threshold is totally aerobic (Figure 2, 4 and 5). The VO2 at the transition from aerobic to partial anaerobic metabolism must depend on cardiovascular performance since it regulates the capillary PO2 level needed for O2 diffusion transport into the mitochondria (Figure 1). At high work rates, the capillary PO2 needed for the oxygen requirement might not be met by the cardiovascular oxygen supply. This would result in the oxygen consumed being less than the oxygen required by the working tissue (Figure 2), with the oxygen equivalent difference necessarily coming from anaerobic metabolism. The consequences are increased lactate formation and metabolic acidosis, and the physiological and biochemical disturbances which result from the latter.

Adolescent↗
PubMed1990

Evidence that the metabolic acidosis threshold is the anaerobic threshold.

We evaluated maximal O2 uptake (VO2max), the metabolic acidosis threshold determined by the V-slope analysis [plot of CO2 output (VCO2) as a function of oxygen uptake (VO2)], the ratio of increase in VO2 to work rate increment (delta VO2/delta WR), the upper slope (S2) of the V-slope analysis, and the VO2 for work below and above the metabolic acidosis threshold to determine whether the changes in O2 transport caused by increased carboxyhemoglobin (HbCO) affected these parameters and variables. Ten normal subjects (aged 32.8 +/- 7.1 yr) performed symptom-limited incremental exercise tests in a ramp pattern on a cycle ergometer while breathing air and air with added carbon monoxide to cause HbCO to be approximately 11% and 20%. VO2max decreased by 11.6 and 19.3%, the metabolic acidosis threshold decreased by 11.9 and 19.6%, delta VO2/delta WR decreased by 8.9 and 14.0%, and S2 increased by 13.6 and 21.8% when HbCO was increased to 11 and 20%, respectively. Most importantly, VO2 was unchanged related to work rate below the metabolic acidosis threshold during the tests with increased HbCO but was reduced at the work rates above the metabolic acidosis threshold. These findings are consistent with the concept that the metabolic acidosis threshold is synonymous with an anaerobic threshold, i.e., the latter demarcating the VO2 above which the contracting muscles are not adequately supplied with O2 but below which they are.

Acidosis↗
PubMed1990

Ventilatory control during exercise in calves with artificial hearts.

To determine the role of cardiac reflexes in mediating exercise hyperpnea, we investigated ventilatory responses to treadmill exercise in seven calves with artificial hearts and seven controls. In both groups, the ventilatory responses were adequate for the metabolic demands of the exercise; this resulted in regulation of arterial PCO2 and pH despite the absence of cardiac output increase in the implanted group. In this group, there was a small but significant reduction of arterial PO2 by 4 +/- 3 Torr and a rise of blood lactate by 1.1 +/- 1 mmol/l. When cardiac output was experimentally increased in the implanted calves to a level commensurate with that spontaneously occurring in the control calves, ventilation was not affected. However, experimental reductions of cardiac output led to an immediate augmentation of exercise hyperpnea by 4.56 +/- 4.3 l/min and a further significant lactate increase of 1.2 +/- 1.22 mmol/l that was associated with a significant decrease in the exercise O2 consumption (0.32 +/- 0.13 l/min). These observations indicate that neither cardiac nor hemodynamic effects of increased cardiac output constitute an obligatory cause of exercise hyperpnea in the calf.

Animals↗
PubMed1990

Evidence that diffusion limitation determines oxygen uptake kinetics during exercise in humans.

To determine the role of arterial O2 content on the mechanism of muscle O2 utilization, we studied the effect of 2, 11, and 20% carboxyhemoglobin (COHb) on O2 uptake (VO2), and CO2 output (VCO2) kinetics in response to 6 min of constant moderate- and heavy-intensity cycle exercise in 10 subjects. Increased COHb did not affect resting heart rate, VO2 or VCO2. Also, the COHb did not affect the asymptotic VO2 in response to exercise. However, VO2 and VCO2 kinetics were affected differently. The time constant (TC) of VO2 significantly increased with increased COHb for both moderate and heavy work intensities. VO2 TC was positively correlated with blood lactate. In contrast, VCO2 TC was negatively correlated with increased COHb for the moderate but unchanged for the heavy work intensity. The gas exchange ratio reflected a smaller increase in CO2 stores and faster VCO2 kinetics relative to VO2 with increased COHb. These changes can be explained by compensatory cardiac output (heart rate) increase in response to reduced arterial O2 content. The selective slowing of VO2 kinetics, with decreased blood O2 content and increased cardiac output, suggests that O2 is diffusion limited at the levels of exercise studied.

Adolescent↗
PubMed1990

A respiratory gas exchange simulator for routine calibration in metabolic studies.

We have developed a method for simulating respiratory gas exchange for on-line calibration of metabolic measurement systems. It utilizes a pump which intakes a mixture of atmospheric air and a known flow of precision-analysed calibration gas (21% CO2, 79% N2). It expels the resulting mixture with flow wave form and profiles of gas concentration which closely resemble those of normal expiration. Control of the calibration mixture's inflow allows the investigator to set any desired metabolic rate regardless of the minute ventilatory rate. This separation of metabolic from ventilatory rates provides a stringent test of the computational performance of the respiratory gas exchange measurement systems. The apparatus can reproduce any range of respiratory and metabolic performance (currently ranging from 0.2-5 l.min-1 O2 uptake and CO2 output) with accuracy +/- 2%.

Calibration↗
PubMed1990

Gas exchange theory and the lactic acidosis (anaerobic) threshold.

The physiological requirements of performing exercise above the anaerobic threshold are considerably more demanding than for lower work rates. Lactic acidosis develops at a metabolic rate that is specific to the individual and the task being performed. Although numerous pyruvate-dependent mechanisms can lead to an elevated blood lactate, the increase in lactate during muscular exercise is accompanied by an increase in lactate/pyruvate ratio (i.e., increased NADH/NAD ratio). This is typically caused by an inadequate O2 supply to the mitochondria. Thus, the anaerobic threshold can be considered to be an important assessment of the ability of the cardiovascular system to supply O2 at a rate adequate to prevent muscle anaerobiosis during exercise testing. In this paper, we demonstrate, with statistical justification, that the pattern of arterial lactate and lactate/pyruvate ratio increase during exercise evidences threshold dynamics rather than the continuous exponential increase proposed by some investigators. The pattern of change in arterial bicarbonate (HCO3-) and pulmonary gas exchange supports this threshold concept. To estimate the anaerobic threshold by gas exchange methods, we measure CO2 output (VCO2) as a continuous function of O2 uptake (VO2) (V-slope analysis) as work rate is increased. The break-point in this plot reflects the obligate buffering of increasing lactic acid production by HCO3-. The anaerobic threshold measured by the V-slope analysis appears to be a sensitive index of the development of metabolic acidosis even in subjects in whom other gas exchange indexes are insensitive, owing to irregular breathing, reduced chemoreceptor sensitivity, impaired respiratory mechanics, or all of these occurrences.

Acidosis, Lactic↗
PubMed1989

Breathing-valve encumbrance and arterial blood gas and acid-base status in exercise in man.

It has been suggested that the mouth-piece-breathing valve assemblies commonly used in laboratory investigations of ventilatory control may influence regulation of arterial blood gas and acid-base status during exercise. To examine this hypothesis, 10 healthy males each underwent two incremental cycle-ergometer tests (15 W min-1) to the limit of tolerance: one was conducted free of breathing apparatus; the other utilized a mouth-piece (with noseclip) connected to a low-resistance turbine volume sensor. The order was randomly assigned and tests were separated by a 2 h recovery. Blood sampled from an indwelling brachial artery catheter at rest and every 30 W during exercise was analyzed for PCO2, PO2, pH and HCO-3. Maximum power was not different between the two tests. Furthermore, no systematic effect of the assembly could be discerned on PaCO2, PaO2 or pHa over the entire range of power. We therefore conclude that although ventilation and its pattern may be affected by laboratory breathing apparatus, such encumbrance (if of low resistance and dead space) does not influence blood gas and acid-base regulation during exercise.

Acid-Base Equilibrium↗
PubMed1989

Ventilatory control of the 'isocapnic buffering' region in rapidly-incremental exercise.

During incremental exercise PCO2 does not fall for several work rates ('isocapnic buffering') above the anaerobic threshold (theta an). We explored this apparent lack of compensatory hyperventilation in 24 normal subjects who underwent incremental cycling (15 W/min) to exhaustion. Ventilation, pulmonary gas exchange, and end-tidal gas tensions were computed breath-by-breath. In 10 subjects, arterial blood was sampled every 2 min throughout the test. Our findings confirmed the 'isocapnic' supra-theta an region, but it consistently followed a progressive increase of PETCO2 in the sub-theta an region. A similar pattern was evident for PaCO2. The leveling-out of PETCO2 and PaCO2 was a result of breathing frequency increasing at theta an, thereby shortening expiratory time, i.e., progressively truncating the continued increase in the alveolar PCO2 slope. Consequently 'isocapnic buffering' during incremental exercise does not reflect PCO2 which continues to be regulated at a constant sub-theta an value. Rather it reflects a ventilatory response to the metabolic acidosis which levels a systematically-rising phase of PETCO2 and PaCO2, largely through a change in breathing pattern. Respiratory compensation, as reflected by a declining PETCO2 and PaCO2, does not occur typically for a subsequent 2 or more minutes.

Acid-Base Equilibrium↗
PubMed1989

Psychosocial responses to the threat of HIV exposure among people with bleeding disorders.

The findings of a state-wide needs assessment of people with bleeding disorders at risk of human immunodeficiency virus (HIV) infection are reported. The effects of the threat of HIV exposure on the psychosocial functioning of respondents is assessed. A total of 394 of 796 (49 percent) persons aged 14 years and older responded to a questionnaire. Psychological distress, marital distress, AIDS-related dating problems, and AIDS-related sexual problems were examined. Potential predictors were illness-related indicators, subjective assessments of sources and consequences of vulnerability to HIV, social sources of distress such as AIDS-related isolation and discrimination, and behaviors respondents engaged in to assess or reduce their risk of infection. The implications of these findings for service provision are discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Changes in breath 13CO2/12CO2 consequent to exercise and hypoxia.

Because the natural enrichment of carbohydrate with 13C is greater than that of lipid, we hypothesized that the natural enrichment of exhaled CO2 with 13C (EN) could be used to gauge endogenous substrate utilization in exercising human subjects. To test this, EN and the respiratory exchange ratio (R) which equals the respiratory quotient (RQ) in the steady state, were measured simultaneously in seven subjects. Rest and exercise protocols, performed under conditions of room air (sea level) and hypoxic (inspired O2 fraction = 0.15) breathing, were chosen to cause a variety of patterns of oxidative substrate utilization. Work rates were performed both below and above the subject's lactate threshold (LT). Work above the LT was expected to cause the greatest increase in EN reflecting greater utilization of glucose. There was significant intersubject (P less than 0.05) but not intrasubject variability in resting EN. By 40 min of exercise, EN increased significantly (P less than 0.05) over resting values in all exercise protocols during both room air and hypoxia conditions. In the room air studies, we found no difference in EN during the below-LT work, even though there were significant increases in O2 uptake (VO2). In contrast, above-LT work resulted in significantly greater increases in EN by 20 and 40 min of exercise (P less than 0.05). Contrary to our expectations, we observed no separate effect by hypoxia on the EN during exercise. Both EN and R tended to increase from rest to exercise, but during exercise there was no overall correlation between R and the EN. EN reflects changes in endogenous substrate utilization over relatively long periods of time such as at rest, but delays in the appearance of 13CO2 at the mouth due to dilution in body CO2 pools, and possibly isotopic fractionation, preclude the usefulness of EN as an indicator of endogenous fuel mix during short-term exercise.

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

Early dynamics of O2 uptake and heart rate as affected by exercise work rate.

The kinetics of O2 uptake (Vo2) and heart rate (HR) in response to constant work rate exercise have been characterized as two phases, an immediate response as the result largely of abrupt hemodynamic changes and a slower response as the result of increases in both blood flow and arteriovenous O2 difference (avDo2). There are few data reported concerning Vo2 and HR during phase I or the relationship between their kinetics and work rate or intensity. Because phase I responses depend on abrupt cardiovascular adjustments, it was hypothesized that phase I increases in Vo2 and HR would be greater the more "fit" the subject and would be relatively independent of work rate. To test this, 10 normal subjects exercised from rest to each of five work rates ranging from unloaded cycling to 150 W. The phase I increases of Vo2, HR, and Vo2/HR had small but significant correlations with work rate but not with fitness. At very low work rates (unloaded cycling and 25 W), Vo2 and HR often exceeded their steady-state levels in phase I. There was therefore no phase II increase for Vo2 or HR at these work rates, the entire O2 requirement having been met by phase I circulatory adjustments. For all other work rates, mean response times for Vo2 and HR were related to fitness and were slower than those for Vo2/HR, suggesting that avDo2 reached a steady state before cardiac output did.

Adult↗
PubMed1989

Respiration during recovery from exercise: effects of trapping and release of femoral blood flow.

To investigate the contribution of vascular and metabolic stimuli to the sustained hyperpnea after exercise, the respiratory effects of obstructing and then releasing the femoral blood flow were recorded in 15 normal volunteers during recovery from steady-state cycle exercise (80 W). Obstruction was achieved using cuffs around the upper thighs, inflated for the first 2 min of recovery to a pressure of 200 mmHg. Cuff inflation significantly reduced ventilation during recovery compared with control (P less than 0.001); the subsequent release of pressure was accompanied by an increase in ventilation (averaging 3.2 l/min), which began on the first breath after release. This preceded a rise in end-tidal CO2 (maximum 8.3 Torr increase), which first became significant on the fourth breath after release and led to a further rise in ventilation. The first-breath increase in ventilation after cuff release persisted, although slightly attenuated (averaging 2.5 l/min), in additional experiments with inspired O2 fraction of 1.0. The pattern of ventilatory response was also similar when the experiments were performed with 5% CO2 in air as the inspirate. The immediate rise in ventilation on cuff release, together with the persistent response on 100% O2, suggests that the vascular changes resulting from cuff release exert an influence on ventilation independent of the effects of released metabolites on the known chemoreceptors. The persistence of the response on 5% CO2 indicates that CO2-sensitive lung afferents do not have a major role in these responses.

Adolescent↗
PubMed1989

Effect of altering the proportion of dietary fat and carbohydrate on exercise gas exchange in normal subjects.

A low proportion of dietary calories as carbohydrate has been suggested for patients with chronic obstructive pulmonary disease, because oxidation of carbohydrate (CHO) compared to fat results in greater CO2 production (VCO2) and, at the same arterial PCO2 (PaCO2), higher alveolar and minute ventilation (VE) and increased dyspnea. We hypothesized that a low CHO-high fat diet, although reducing VCO2 and VE at rest, might result in only a small change in VCO2 and VE during exercise. Eight healthy volunteers were randomized to receive for 24 h either isocaloric diets containing 10% or 70% of total calories from CHO (remainder of nonprotein calories from fat). Measurements of VCO2, VE, and respiratory gas exchange ratio (R) were made at rest and during constant work rate cycle exercise below the anaerobic threshold. Five to seven days later, the alternate diet was given and the studies were repeated. At rest, mean VCO2 and R were significantly lower after the low CHO diet compared to the high CHO diet. Mean resting VE was less but not significantly (high CHO 9.6 [0.7] versus low CHO 8.7 [0.8] L/min, mean [SEM]). During exercise, mean VCO2 and R were significantly less after the low CHO diet, but mean VE was only slightly smaller and not significantly different between diets (high CHO 25.4 [1.1] versus low CHO 24.0 [1.0] L/min). The increase in VCO2 from rest to exercise was relatively independent of the substrate mix recently consumed, suggesting that the exercising muscles use stored muscle glycogen as substrate during short bouts of low-intensity exercise despite changes in substrate utilization by nonmuscle tissues at rest.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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↗