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T J Barstow

Publications and source records attributed to T J Barstow.

At least 55 records · Page 3Linked to original sources
PubMed1994

Evaluation of a symmetrically disposed Pitot tube flowmeter for measuring gas flow during exercise.

We evaluated the effect of airflow and gas composition on the linearity of measurement of airflow by a new disposable flowmeter. The flowmeter is based on the principle of differential pressure measurement across two symmetrically disposed Pitot tubes. Nonlinearities arising from the pressure-to-airflow relationship and sensitivity to changes in gas density were linearized with appropriate software and monitoring of the gas composition. With room air used as the respired gas, the measured tidal volume from a piston pump assembly was consistently within 1-2% of the target tidal volume for each of five flowmeters tested across physiological ranges of flow. Changing gas densities by varying concentrations of O2, CO2, and N2 led to errors in tidal volume measurement that ranged up to 6-8%. However, because the errors were predictable, they were corrected by software to within 0.6% of the target volume. Measurement of minute ventilation during exercise was within 1-2% of that determined from bag collections. We conclude that this type of flowmeter can accurately measure exercise minute ventilation and has advantages over some other flowmeters because of its ruggedness, reproducibility, and ease of sterilization or replacement compared with other flowmeters.

Equipment Design↗
PubMed1994

Characterization of VO2 kinetics during heavy exercise.

Characterizing oxygen uptake (VO2) kinetics yields valuable information regarding both a) the effectiveness of the coupling of O2 delivery to tissue metabolic demands, and b) the ability of the muscle itself to utilize O2 for oxidative phosphorylation. During moderate exercise VO2 reaches a new steady state within 3 min in normal subjects, with little or no sustained rise in blood lactate. The steady state VO2 increases linearly with work rate. The time constant for VO2 in Phase 2 (after first 15-20 s) is constant across work intensities, and appears to reflect muscle oxygen utilization kinetics. However, when heavier exercise is performed, which elevates blood lactate throughout the exercise, the VO2 response becomes more complex. The predominant, Phase 2 response continues to rise exponentially with about the same time constant as for moderate exercise, and the amplitude continues to be linearly related to work rate. However, an additional, slowly developing rise in VO2 is also usually observed, beginning 100-200 s into exercise. This additional VO2 delays attainment of a steady state, increases the overall O2 "cost" of the exercise, and is statistically associated with the rate and magnitude of increase in blood lactate. Interestingly, in children, neither the slow component nor blood lactate rise as much during heavy exercise.

Exercise↗
PubMed1994

VO2 slow component: physiological and functional significance.

This paper offers a brief synopsis of the five preceding papers which constitute the proceedings of the symposium "Mechanistic basis of the slow component of VO2 kinetics during heavy exercise." The key features have been taken from each paper and a coherent position regarding the site and potential underlying mechanisms for the "excess" VO2 is presented. The hypothesis is developed that some aspect of fiber type recruitment patterns might be responsible for this phenomenon. Elucidation of the precise determinants of VO2 during heavy exercise is fundamental to our understanding of muscle energetics. Furthermore, certain patient populations, whose exercise tolerance is limited by impaired cardiovascular and/or respiratory capacity, may benefit from interventions designed to constrain the magnitude of the VO2 slow component.

Exercise↗
PubMed1993

31P-magnetic resonance spectroscopy of leg muscle metabolism during exercise in children and adults.

Gas exchange response to high-intensity exercise differs in children and adults. We hypothesized that these findings are related to a lower anaerobic ATP supply in children. We predicted therefore a maturation of muscle high-energy phosphate metabolism during exercise. To test this hypothesis, we measured calf muscle Pi, phosphocreatine (PCr), and pH with 31P-nuclear magnetic resonance spectroscopy during rest and progressive exercise in 10 children and 8 adults. No differences were found at rest in pH and Pi/PCr between children and adults. Exercise resulted in a greater increase in Pi/PCr (P < 0.001) and decrease in pH (P < 0.0001) in adults than in children. Six adults and five children exhibited a transition from a slow to a faster rate of Pi/PCr increase and pH decrease during exercise. No significant differences were found between the two groups in the initial slow-phase slopes of Pi/PCr and pH as a function of work rate. In contrast, during the fast phase, Pi/PCr increased (slope: adults 23.6 +/- 9.8, children 10.7 +/- 2.5; P < 0.05) and pH decreased (slope: adults -6.0 +/- 1.9, children -3.7 +/- 1.2; P < 0.05) more rapidly in adults than in children. In conclusion, high-intensity exercise results in different kinetics of Pi/PCr and pH between children and adults. These results suggest that children are less able than adults to affect ATP rephosphorylation by anaerobic metabolic pathways during high-intensity exercise.

Adenosine Triphosphate↗
PubMed1993

O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate.

The dynamic responses of O2 uptake (VO2) to a range of constant power output levels were related to exercise intensity [as percent maximal VO2 and as below vs. above lactic acid threshold (LAT)] and to the associated end-exercise lactate in three groups of subjects: group I, untrained subjects performing leg cycle ergometer exercise; group II, the same subjects performing arm cycle exercise; and group III, trained cyclists performing leg cycle ergometer exercise. Responses were described by a double-exponential equation, with each component having an independent time delay, which reduced to a monoexponential description for moderate (below-LAT) exercise. When a second exponential component to the VO2 response was present, it did not become evident until approximately 80-100 s into exercise. An overall time constant (tau T, determined as O2 deficit for the total response divided by net end-exercise VO2) and a primary time constant (tau P, determined from the O2 deficit and the amplitude for the early primary VO2 response) were compared. The tau T rose with power output and end-exercise lactate levels, but tau P was virtually invariant, even at high end-exercise lactate levels. Moreover the gain of the primary exponential component (as delta VO2/delta W) was constant across power outputs and blood lactate levels, suggesting that the primary VO2 response reflects a linear system, even at higher power outputs. These results suggest that elevated end-exercise lactate is not associated with any discernible slowing of the primary rise in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

O2 uptake kinetics in response to exercise. A measure of tissue anaerobiosis in heart failure.

Oxygen uptake (VO2) reflects the rate of aerobic regeneration of high-energy phosphate compounds (primarily adenosine triphosphate [ATP]). Since lactate increase is thought to result from an inadequate rate of aerobic ATP regeneration, it might be expected that lactate increase would be associated with a delayed attainment of steady state for VO2 in response to constant load exercise. Similarly if mitochondrial ATP regeneration during exercise is inadequately supported by O2 transport mechanisms, adenosine diphosphate (ADP) and purine nucleotide by-products, such as hypoxanthine, should increase. This study investigated the relationship between VO2 kinetics during exercise and accompanying changes in blood lactate and hypoxanthine values in heart failure patients, as a model of compromised O2 transport. Twenty-five patients with chronic heart failure performed cycle ergometry for 6 min at 25 W and at a work rate midway (50 percent delta) between their lactic acidosis threshold (LAT) and peak VO2. Ventilation and gas exchange were measured breath by breath, and venous lactate, hypoxanthine, norepinephrine, and epinephrine were determined at rest and 2 min after each test. The slow component of VO2 kinetics was quantified as the rise in VO2 from the third to the sixth minute of exercise (delta VO2 [6-3]). Ten age- and size-matched normal subjects served as control subjects. delta VO2 (6-3) was correlated with the increase in lactate (r = 0.71, p < 0.001), hypoxanthine (r = 0.61, p < 0.001), and norepinephrine (r = 0.41, p < 0.01) but not epinephrine in response to exercise in the heart failure patients. The delta VO2 (6-3) and delta lactate were both greater in the patients than in the control subjects at similar absolute work rates (54 +/- 20 and 60 W, respectively). However, the slope of the relationship between delta La and delta VO2 (6-3) for the patient and normal groups was indistinguishable. The lactate increase was correlated with hypoxanthine increase (r = 0.66, p < 0.001), but not norepinephrine or epinephrine. In summary, VO2 kinetics in response to exercise reflects delayed attainment of the steady state in heart failure patients, which is correlated with increases in lactate and hypoxanthine, markers of increased anaerobic metabolism.

Acidosis, Lactic↗
PubMed1992

Increase in bicarbonate stores with exercise.

We previously described bicarbonate exchange dynamics in humans at rest and during exercise using a three-compartment model. In the present study we tested the effect of certain assumptions of this model on the prediction of the change in exchangeable bicarbonate with the increased metabolic rate of exercise. We compared this prediction with a measurement of CO2 retention after exercise onset determined from gas exchange data. The change in tissue bicarbonate stores was estimated from differences in the kinetics of adjustment of VO2 and VCO2, and this was added to an estimate of the changes in venous blood gas stores to estimate the total change in bicarbonate. When the commonly held assumption that endogenous CO2 production, thought to occur in a rapidly equilibrating peripheral compartment at rest, was also applied to the exercise condition, the three-compartment bicarbonate model predicted an unphysiologically large increase in bicarbonate stores (700 mmol, or over 15 L). In contrast, the 'gas exchange' approach predicted a relatively small increase in bicarbonate (26 mmol), consistent with other reports. The incompatibility of these findings with the assumption about the source of endogenous CO2 production in the bicarbonate model requires that the underlying physiological correlates of the three compartments change from rest to exercise.

Bicarbonates↗
PubMed1992

13CO2 washout dynamics during intermittent exercise in children and adults.

To test the hypothesis that children store less CO2 than adults during exercise, we measured breath 13CO2 washout dynamics after oral bolus of [13C]bicarbonate in nine children [8 +/- 1 (SD) yr, 4 boys] and nine (28 +/- 6 yr, 5 males) adults. Gas exchange [O2 uptake and CO2 production (Vco2)] was measured breath by breath during rest and during light (80% of the anaerobic threshold) intermittent exercise. Breath samples were obtained for subsequent analysis of 13CO2 by isotope ratio mass spectrometry. The tracer estimate of Vco2 was highly correlated to Vco2 measured by gas exchange (r = 0.97, P < 0.0001). The mean residence time was shorter in children (50 +/- 5 min) compared with adults (69 +/- 7 min, P < 0.0001) at rest and during exercise (children, 35 +/- 7 min; adults, 50 +/- 11 min, P < 0.001). The estimate of stored CO2 (using mean Vco2 measured by gas exchange and mean residence time derived from tracer washout) was not statistically different at rest between children (254 +/- 36 ml/kg) and adults (232 +/- 37 ml/kg). During exercise, CO2 stores in the adults (304 +/- 46 ml/kg) were significantly increased over rest (P < 0.001), but there was no increase in children (mean exercise value, 254 +/- 38 ml/kg). These data support the hypothesis that CO2 distribution in response to exercise changes during the growth period.

Adult↗
PubMed1992

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

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

Adult↗
PubMed1991

Cardiac output, oxygen consumption and arteriovenous oxygen difference following a sudden rise in exercise level in humans.

1. To investigate the relative contributions of increases in cardiac output and arteriovenous oxygen difference to the increase in oxygen consumption during exercise, the ventilatory and cardiovascular responses to a sudden transition from unloaded cycling to 70 or 80 W were measured in six normal healthy subjects. 2. Oxygen consumption (VO2) was measured breath-by-breath and corrected for changes in lung gas stores. Cardiac output (Q) was measured beat-by-beat using pulsed Doppler ultrasound, and blood pressure was measured beat-by-beat using a non-invasive finger cuff (Finapres). All data were calculated off-line, second-by-second. 3. Arteriovenous oxygen difference (A-VO2) was calculated from Q and VO2 using the Fick Principle. Left ventricular afterload was calculated by dividing Q by mean blood pressure. 4. The data for Q and VO2 were closely fitted by single exponential curves (mean r2 0.84 and 0.90 respectively; r is the correlation coefficient). These curves yielded mean time constants for the increases in Q and VO2 of 28 and 55 s respectively following the increase in exercise level. In each individual subject, the time course of adjustment of Q was faster than that of VO2. There was a mean lag of 15 s from the start of the new exercise level before the derived A-V O2 began to increase; the mean time constant for A-V O2 was 57 s. 5. If A-V O2 had remained constant, the observed rise in Q alone would have resulted in an average of 87% of the increase in VO2 which was observed after 5 s. If Q had remained constant, the observed increase in A-V O2 would have led to only 8% of the actual increase in VO2 after 5 s. 6. Mean and systolic blood pressure rose and afterload fell immediately after the onset of the increased workload. The time constants of the systolic blood pressure and afterload responses to exercise varied widely and ranged from 37 to 81 and 10 to 26 s respectively (n = 4). 7. We conclude that Q is responsible for most of the early increase in VO2 following a sudden increase in exercise workload. Blood pressure responses to exercise are slower than Q and VO2 responses, probably due to the rapid decrease in afterload. 8. The dominant contribution of Q to adaptation to changing workload may be physiologically important particularly in heart disease, where decreased ability to increase cardiac output may limit the capacity to cope with changing metabolic needs during everyday activities.

Adaptation, Physiological↗
PubMed1991

Oxygen uptake dynamics during high-intensity exercise in children and adults.

We hypothesized that the O2 uptake (Vo2) response to high-intensity exercise would be different in children than in adults. To test this hypothesis, 22 children (6-12 yr old) and 7 adults (27-40 yr old) performed 6 min of constant-work-rate cycle-ergometer exercise. Sixteen children performed a single test above their anaerobic threshold (AT). In a separate protocol, six children and all adults exercised at low and high intensity. Low-intensity exercise corresponded to the work rate at 80% of each subject's AT. High-intensity exercise (above the AT) was determined first by calculating the difference in work rate between the AT and the maximal Vo2 (delta). Twenty-five, 50, and 75% of this difference were added to the work rate at the subject's AT, and these work rates were referred to as 25% delta, 50% delta, and 75% delta. For exercise at 50% delta and 75% delta, Vo2 increased throughout exercise (O2 drift, linear regression slope of Vo2 as a function of time from 3 to 6 min) in all the adults, and the magnitude of the drift was correlated with increasing work rates in the above-AT range (r = 0.91, P less than 0.0001). In contrast, no O2 drift was observed in over half of the children during above-AT exercise. The O2 drifts were much higher in adults (1.76 +/- 0.63 ml O2.kg-1.min-2 at 75% delta) than in children (0.20 +/- 0.42, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise.

We assessed the linearity of oxygen uptake (VO2) kinetics for several work intensities in four trained cyclists. VO2 was measured breath by breath during transitions from 33 W (baseline) to work rates requiring 38, 54, 85, and 100% of maximal aerobic capacity (VO2max). Each subject repeated each work rate four times over 8 test days. In every case, three phases (phases 1, 2, and 3) of the VO2 response could be identified. VO2 during phase 2 was fit by one of two models: model 1, a double exponential where both terms begin together close to the start of phase 2, and model 2, a double exponential where each of the exponential terms begins independently with separate time delays. VO2 rose linearly for the two lower work rates (slope 11 ml.min-1 W-1) but increased to a greater asymptote for the two heavier work rates. In all four subjects, for the two lighter work rates the double-exponential regression reduced to a single value for the time constant (average across subjects 16.1 +/- 7.7 s), indicating a truly monoexponential response. In addition, one of the responses to the heaviest work rate was monoexponential. For the remaining seven biexponential responses to the two heaviest work rates, model 2 produced a significantly better fit to the responses (P less than 0.05), with a mean time delay for the slow component of 105 +/- 46 s.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Oxygen uptake and heart rate responses during hypoxic exercise in children and adults.

Control of ventilation and heart rate during exercise appears to undergo maturation, while aerobic metabolism (VO2) may not. Since we had previously found that hypoxia during exercise produced different ventilatory responses in children (C) compared to adults (A), we hypothesized that VO2 and heart rate kinetics during exercise would show similar maturational responses to hypoxia. To test this hypothesis, we examined the responses during progressive (ramp) and constant work rate tests in children and adults breathing either room air or hypoxic gas (FiO2 = 0.15). When corrected for body weight, children and adults had similar values for lactic acidosis threshold (LAT) (C: 29.1 +/- 5.0 ml.min-1.kg-1; A: 27.9 +/- 4.3) and VO2max (C: 40.7 +/- 8.6 ml.min-1.kg-1; A: 45.2 +/- 6.7) during normoxia. Hypoxia significantly lowered LAT (C: 27.5 +/- 5.4 ml.min-1.kg-1; A: 23.2 +/- 3.8; both P less than 0.05) and VO2max (C: 37.7 +/- 8.3 ml.min-1.kg-1; A: 40.1 +/- 5.3; both P less than 0.05) in both children and adults. Metabolic efficiency (delta VO2/delta work rate) and the VO2-heart rate relationship (delta VO2/delta HR/kg) were similar in the two groups and unaffected by hypoxia. During the constant work rate exercise, VO2 kinetics (time constant during phase 2 of the response (pi 1) and the O2 deficit) were similar between children and adults and were significantly slowed by hypoxia, consistent with current understanding of the control of oxidative metabolism. Finally, heart rate was increased at rest and during exercise with hypoxia, while the time to reach 75% of the end-exercise response was delayed significantly, in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Are obese children truly unfit? Minimizing the confounding effect of body size on the exercise response.

To test the hypothesis that obese children are unfit (i.e., have abnormal responses to exercise testing consistent with reduced levels of habitual physical activity), we used new analytic strategies in studies of 18 obese children performing cycle ergometry. The subject's weight (mean +/- SD) was 168 +/- 24% that predicted by height, and the age range was 9 to 17 years. Size-independent measures of exercise (e.g., the ratio of oxygen uptake (VO2) to work rate during progressive exercise and the temporal response of VO2, carbon dioxide output (VCO2), and minute ventilation (VE) at the onset of exercise) were used. The ability to perform external mechanical work was corrected for VO2 at unloaded pedaling (change in maximum oxygen uptake (delta VO2max) and in anaerobic threshold (delta AT). On average, obese children's responses were in the normal range: delta VO2max, 104 +/- 41% (+/- SD) predicted (by age); delta AT, 85 +/- 51%; ratio of change in VE to change in VCO2, 111 +/- 21% and ratio of change in VO2 to change in work rate, 100 +/- 24%, but six of the obese children had values of delta VO2max or delta AT that were more than 2 SD below normal. In addition, obese children did not have increased delta VO2max or delta AT with age as observed in nonobese children. Although the response time of VO2 was normal (99 +/- 32% of predicted), those for both VCO2 and VE were prolonged. We conclude that the finding of obesity in a child is not a reliable indicator of poor fitness but that testing cardiorespiratory responses to exercise can be used to identify subjects with serious impairment and to individualize therapy.

Adolescent↗
PubMed1990

Influence of increased metabolic rate on [13C]bicarbonate washout kinetics.

The effect of changes in metabolic rate on the dynamics of CO2 exchange among its various compartments in the human body is not well understood. We examined CO2 dynamics in six healthy male subjects using an intravenous bolus of [13C]bicarbonate. Subjects were studied while resting, during light exercise [50% of the lactate threshold (LT), 3-4 times resting O2 uptake (VO2)], and during moderate exercise (95% of the LT, 6 times resting VO2). The sum of three exponential terms well described the washout of 13CO2 in exhaled breath both at rest and during each exercise level despite substantial increases in metabolic rate accompanying the exercise studies. Average recovery of 13C label rose from 67% during rest to 80% during light and moderate exercise (P less than 0.01). The estimate of CO2 elimination (VCO2) calculated from the washout parameters and corrected for recovery was in very good agreement with the VCO2 directly measured simultaneously breath by breath (r = 0.993, SE for VCO2 = 0.079 l/min). By use of a three-compartment mammillary model, the quantity of CO2 in the central pool (Q1) doubled from rest to light exercise (233 +/- 60 to 479 +/- 76 mmol, P less than 0.01) but did not change further with moderate exercise (458 +/- 74 mmol). Rate constants for exchange between pools and for irreversible loss from the system tended to increase with metabolic rate, but there was large variation in the responses. We conclude that the compartmental dynamics of CO2 transport and storage are very sensitive to changes in metabolic rate induced by exercise.

Adult↗
PubMed1990

Modulation of muscle and pulmonary O2 uptakes by circulatory dynamics during exercise.

The effect of cardiovascular adjustments on the coupling of cellular to pulmonary gas exchange during unsteady states of exercise remains controversial. Computer simulations were performed to assess these influences on O2 delivery and pulmonary O2 uptake (pVO2). Algorithms were developed representing muscle and "rest-of-body" compartments, connected in parallel by arterial and venous circulations to a pump-and-lungs compartment. Exercise-induced increases in VO2 and cardiac output went to the muscle compartment. Model parameters [e.g., time constants for blood flow and muscle O2 uptake (mVO2)] could be varied independently. Simulation results demonstrated that 1) the rise in pVO2 during exercise contains three phases; 2) the contribution of changes in venous O2 stores to pVO2 kinetics and the O2 deficit occur almost entirely in phase 1; 3) under a wide variety of manipulations, the kinetics of pVO2 in phase 2 were within a couple of seconds of that assigned to mVO2 (i.e., there is not an obligatory slowing of VO2 kinetics at the lungs relative to those at the muscles; 4) by use of available estimates of blood flow adjustment, O2 delivery would not limit mVO2 after exercise onset; and 5) blood flow could limit O2 delivery in recovery, if blood flow returned to base-line levels at rates similar to those during the on-transient phase.

Cardiac Output↗
PubMed1990

Oral [13C]bicarbonate measurement of CO2 stores and dynamics in children and adults.

During exercise, less additional CO2 is stored per kilogram body weight in children than in adults, suggesting that children have a smaller capacity to store metabolically produced CO2. To examine this, tracer doses of [13C]bicarbonate were administered orally to 10 children (8-12 yr) and 12 adults (25-40 yr) at rest. Washout of 13CO2 in breath was analyzed to estimate recovery of tracer, mean residence time (MRT), and size of CO2 stores. CO2 production (VCO2) was also measured breath by breath using gas exchange techniques. Recovery did not differ significantly between children [73 +/- 13% (SD)] and adults (71 +/- 9%). MRT was shorter in children (42 +/- 7 min) compared with adults (66 +/- 15 min, P less than 0.001). VCO2 per kilogram was higher in the children (5.4 +/- 0.9 ml.min-1.kg-1) compared with adults (3.1 +/- 0.5, P less than 0.0001). Tracer estimate of CO2 production was correlated to VCO2 (r = 0.86, P less than 0.0001) and when corrected for mean recovery accurately predicted the VCO2 to within 3 +/- 14%. There was no difference in the estimate of resting CO2 stores between children (222 +/- 52 ml CO2/kg) and adults (203 +/- 42 ml CO2/kg). We conclude that orally administered [13C]bicarbonate can be used to assess CO2 transport dynamics. The data do not support the hypothesis of lower CO2 stores under resting conditions in children.

Adult↗