Ventilatory responses to the metabolic acidosis of treadmill and cycle ergometry

1976 ◽  
Vol 40 (6) ◽  
pp. 864-867 ◽  
Author(s):  
S. N. Koyal ◽  
B. J. Whipp ◽  
D. Huntsman ◽  
G. A. Bray ◽  
K. Wasserman
Keyword(s):  
Metabolic Acidosis ◽  
Treadmill Exercise ◽  
Cycle Ergometer ◽  
Cycle Ergometry ◽  
O2 Uptake ◽  
Ventilatory Responses ◽  
Arterial Ph ◽  
Ergometer Exercise ◽  
Type Of Exercise ◽  
Relationship Of

Ventilation and acid-base responses were studied at comparable levels of O2 uptake during cycle ergometer and treadmill exercise, to determine the extent to which the type of exercise affects these responses. Twenty male subjects performed 50-, 100-, and 150-W cycle ergometer exercise and three work rates of similar O2 uptake on a treadmill. At comparable oxygen uptakes, arterial lactate and VE were higher and arterial pH and bicarbonate were lower for cycle ergometer than treadmill exercise. These differences could be accounted for by the greater degree of metabolic acidosis during cycle ergometer work. The increment in VE over that predicted (from an extrapolation of the linear relationship of the VE-VO2 relationship for low work rates) was linearly related to the decrease in arterial bicarbonate; VE was increased by approximately 4 1/min for each meq/1 of bicarbonate decrease for both treadmill and cycle ergometry.

scholarly journals Oxygen cost and oxygen uptake dynamics and recovery with 1 min of exercise in children and adults

1991 ◽  
Vol 71 (3) ◽  
pp. 993-998 ◽  
Author(s):  
S. Zanconato ◽  
D. M. Cooper ◽  
Y. Armon
Keyword(s):  
Time Course ◽  
Significant Degree ◽  
Cycle Ergometer ◽  
Work Intensity ◽  
O2 Uptake ◽  
Ergometer Exercise ◽  
Adults And Children ◽  
The Difference ◽  
Recovery Dynamics ◽  
Best Fit

To test the hypothesis that O2 uptake (VO2) dynamics are different in adults and children, we examined the response to and recovery from short bursts of exercise in 10 children (7–11 yr) and 13 adults (26–42 yr). Each subject performed 1 min of cycle ergometer exercise at 50% of the anaerobic threshold (AT), 80% AT, and 50% of the difference between the AT and the maximal O2 uptake (VO2max) and 100 and 125% VO2max. Gas exchange was measured breath by breath. The cumulative O2 cost [the integral of VO2 (over baseline) through exercise and 10 min of recovery (ml O2/J)] was independent of work intensity in both children and adults. In above-AT exercise, O2 cost was significantly higher in children [0.25 +/- 0.05 (SD) ml/J] than in adults (0.18 +/- 0.02 ml/J, P less than 0.01). Recovery dynamics of VO2 in above-AT exercise [measured as the time constant (tau VO2) of the best-fit single exponential] were independent of work intensity in children and adults. Recovery tau VO2 was the same in both groups except at 125% VO2max, where tau VO2 was significantly smaller in children (35.5 +/- 5.9 s) than in adults (46.3 +/- 4 s, P less than 0.001). VO2 responses (i.e., time course, kinetics) to short bursts of exercise are, surprisingly, largely independent of work rate (power output) in both adults and children. In children, certain features of the VO2 response to high-intensity exercise are, to a small but significant degree, different from those in adults, indicating an underlying process of physiological maturation.

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

1993 ◽  
Vol 75 (2) ◽  
pp. 755-762 ◽  
Author(s):  
T. J. Barstow ◽  
R. Casaburi ◽  
K. Wasserman
Keyword(s):  
Blood Lactate ◽  
Time Constant ◽  
Exercise Intensity ◽  
Power Output ◽  
Cycle Ergometer ◽  
O2 Uptake ◽  
Ergometer Exercise ◽  
Lactate Levels ◽  
Power Outputs ◽  
O2 Deficit

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)

Accuracy and Reproducibility of an Exercise Prescription Based on Ratings of Perceived Exertion for Treadmill and Cycle Ergometer Exercise

1994 ◽  
Vol 78 (3_suppl) ◽  
pp. 1335-1344 ◽  
Author(s):  
Christopher C. Dunbar ◽  
Carole Goris ◽  
Donald W. Michielli ◽  
Michael I. Kalinski
Keyword(s):  
Heart Rate ◽  
Exercise Intensity ◽  
Perceived Exertion ◽  
Exercise Prescription ◽  
Treadmill Exercise ◽  
Cycle Ergometer ◽  
Ratings Of Perceived Exertion ◽  
Cycle Ergometer Exercise ◽  
Ergometer Exercise ◽  
Target Intensity

The accuracy of regularing exercise intensity by Ratings of Perceived Exertion (RPE) was examined. Subjects underwent 4 production trials, 2 on a treadmill (PIA, P1B) and 2 on a cycle ergometer (P2A, P2B). 9 untrained subjects used only their perceptions of effort to regulate exercise intensity. Target intensity was the RPE equivalent to 60% VO2mx. Exercise intensity (VO2) during P1A, P1B, and P2A did not differ from the target, but during P2B was lower than target. During P1A and P1B heart rate did not differ from the target but was lower than target during P2A and P2B. RPE seems a valid means of regulating exercise intensity during repeated bouts of treadmill exercise at 60% VO2max; however, exercise intensity during repeated bouts on the cycle ergometer may be lower than target.

Control of breathing during prolonged exercise

1981 ◽  
Vol 50 (1) ◽  
pp. 27-31 ◽  
Author(s):  
B. J. Martin ◽  
E. J. Morgan ◽  
C. W. Zwillich ◽  
J. V. Weil
Keyword(s):  
Core Temperature ◽  
Cycle Ergometer ◽  
Body Core Temperature ◽  
Heavy Exercise ◽  
Arterial Lactate ◽  
Arterial Ph ◽  
Ergometer Exercise ◽  
Constant Work Rate ◽  
Body Core

Ventilation (VE) climbs steadily throughout prolonged heavy exercise. While this VE "drift" has implications for the adequacy of gas exchange in long-term exercise, its mechanism remains unknown. We examined the behavior of previously proposed mediators of VE drift during one hour of cycle ergometer exercise at constant work rate requiring 2/3 VO2 max in 10 subjects. VE increased 13% from 12 to 61 min of exercise (P less than 0.05). Although body core temperature rose as VE rose, equal elevation of core temperature by passive means failed to increase exercise VE. Rising VE during the hour of exercise occurred despite unchanged arterial pH, PCO2, and lactate and despite unchanged VCO2. Thus, all of the VE increase was calculated to be due to increased dead space ventilation (VD). Tidal volume (VT) was unchanged, while VD/VT rose from 0.16 to 0.24 from 12 to 61 min of work (P less than 0.05). These results show that increased body core temperature does not mediate VE drift, and that changes in previously proposed mediators (arterial pH, arterial lactate, and VCO2) are not necessary for a slow VE rise to occur in prolonged heavy exercise.

Variation in cardiac output with acid-base changes in the anesthetized dog

1965 ◽  
Vol 20 (5) ◽  
pp. 948-953 ◽  
Author(s):  
S. A. Allan Carson ◽  
Gordon E. Chorley ◽  
F. Norman Hamilton ◽  
Do Chil Lee ◽  
Lucien E. Morris
Keyword(s):  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Combined Effects ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Relationship Of ◽  
The Relationship

Studies were performed in dogs anesthetized with pentobarbital, 30 mg/kg, and ventilated mechanically during succinylcholine apnea in order to ascertain the variation in cardiac output under various acid-base conditions. The findings were: 1) metabolic acidosis decreases cardiac output; 2) increasing respiratory acidosis in the absence of severe metabolic acidosis causes increase in cardiac output; 3) increasing respiratory acidosis in the presence of severe metabolic acidosis causes depression of cardiac output. The effect on cardiac output of changing arterial pH at steady PaCOCO2 is shown quantitatively. The relationship of PaCOCO2 to “pH adjusted” cardiac output is determined. From these data a nomogram is presented from which the combined effects of arterial pH and PaCOCO2 on cardiac output can be estimated. cardiac output and anesthesia; acid-base status and cardiac output; pH and cardiac output; PaCOCO2 and cardiac output Submitted on June 29, 1964

Acid-base regulation during exercise and recovery in humans

1992 ◽  
Vol 72 (3) ◽  
pp. 954-961 ◽  
Author(s):  
W. Stringer ◽  
R. Casaburi ◽  
K. Wasserman
Keyword(s):  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Exercise Tests ◽  
Cycle Ergometer Exercise ◽  
Arterial Ph ◽  
Ergometer Exercise ◽  
Exercise In Humans

Arterial pH, PCO2, standard bicarbonate, lactate, and ventilation were measured with a high sampling density during rest, exercise, and recovery in normal subjects performing upright cycle ergometer exercise. Three 6-min constant-work exercise tests (moderate, heavy, and very heavy) were performed by each subject. We found a small respiratory acidosis during the moderate-intensity exercise and an early respiratory acidosis followed by a metabolic acidosis for the heavy- and very-heavy-intensity exercise. During recovery, arterial pH rapidly returned to the preexercise value for the moderate-intensity work. However, arterial pH decreased further during the first 2 min of recovery for the heavy- and very-heavy-intensity work, before a slower return toward the resting values. We conclude that arterial acidosis is the consistent arterial pH reaction for moderate-, heavy-, and very-heavy-intensity cycle ergometer exercise in humans and that this acidosis is blunted but not eliminated by the ventilatory response. During recovery, the return to resting arterial pH and PCO2 and standard bicarbonate appears to be determined by the rate of lactate decline.

Ventilatory responses of the horse to exercise: effect of gas collection systems

1987 ◽  
Vol 63 (3) ◽  
pp. 1210-1217 ◽  
Author(s):  
W. M. Bayly ◽  
D. A. Schultz ◽  
D. R. Hodgson ◽  
P. D. Gollnick
Keyword(s):  
Treadmill Exercise ◽  
O2 Uptake ◽  
Exercise Tests ◽  
Arterial Blood Gas ◽  
Warm Up ◽  
Ventilatory Responses ◽  
Exercise Condition ◽  
Arterial Blood ◽  
Exercise Effect ◽  
Flow Through

Experiments were undertaken to determine whether respiratory masks worn by horses exercising strenuously on a treadmill may interfere with normal gas exchange. Four collection systems, two flow-through systems and two incorporating one-way valve systems with subject-generated airflow were studied. Six horses performed standard treadmill exercise tests consisting of a 2-min warm up followed by galloping 1 min each at 8,9, and 10 m/s. Each horse exercised six times while wearing each of the four respiratory masks. Each flow-through system was used twice with flow rates of 2,360 and 3,840 l/min for one system, and 3,840 and 6,300 l/min for the other. Arterial blood gas tensions were measured during exercise at each speed for each system and were compared with values measured when the horses performed the same test without wearing a mask. Hypercapnia developed during exercise with each of the respiratory masks except with the 6,300–l/min flow-through system. All horses became hypoxemic during every exercise test, but it was most severe when systems incorporating one-way valves were used. This, plus the degree of hypercapnia observed and a suboptimal heart rate-O2 uptake relationship, indicated that such systems severely impede ventilation and suggest that experiments performed while utilizing them do not represent the normal exercise condition.

Effect of positive-pressure breathing on cardiovascular and thermoregulatory responses to exercise

1985 ◽  
Vol 58 (3) ◽  
pp. 876-881 ◽  
Author(s):  
N. B. Vroman ◽  
W. S. Beckett ◽  
S. Permutt ◽  
S. Fortney
Keyword(s):  
Airway Pressure ◽  
Forearm Blood Flow ◽  
Positive Airway Pressure ◽  
Cycle Ergometer ◽  
Positive Pressure ◽  
Esophageal Temperature ◽  
Healthy Male ◽  
O2 Uptake ◽  
Warm Environment ◽  
Ergometer Exercise

Five healthy male volunteers performed 20 min of both seated and supine cycle-ergometer exercise (intensity, 50% maximal O2 uptake) in a warm environment (Tdb = 30 degrees C, relative humidity = 40–50%) with and without breathing 10 cmH2O of continuous positive airway pressure (CPAP). The final esophageal temperature (Tes) at the end of 20 min of seated exercise was significantly higher during CPAP (mean difference = 0.18 +/- 0.04 degree C, P less than 0.05) compared with control breathing (C). The Tes threshold for forearm vasodilation was significantly higher (P less than 0.05) during seated CPAP exercise than C (C = 37.16 +/- 0.13 degrees C, CPAP = 37.38 + 0.12 degree C). The highest forearm blood flow (FBF) at the end of exercise was significantly lower (P less than 0.05) during seated exercise with CPAP (mean +/- SE % difference from C = -30.8 +/- 5.8%). During supine exercise, there were no significant differences in the Tes threshold, highest FBF, or final Tes with CPAP compared with C. The added strain on the cardiovascular system produced by CPAP during seated exercise in the heat interacts with body thermoregulation as evidenced by elevated vasodilation thresholds, reduced peak FBF, and slightly higher final esophageal temperatures.

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