Effect of dopamine on transient ventilatory response to exercise

1986 ◽  
Vol 61 (6) ◽  
pp. 2102-2107 ◽  
Author(s):  
C. L. Boetger ◽  
D. S. Ward

The effect of exogenous dopamine on the development of exercise hyperpnea was studied. Using a bicycle ergometer, five subjects performed repetitive square-wave work-load testing from unloaded pedaling to 80% of each subject's estimated anaerobic threshold. The breath-by-breath ventilation (VE), CO2 production (VCO2), and O2 consumption (VO2) responses were analyzed by curve fitting a first-order exponential model. Comparisons were made between control experiments and experiments with a 3-micrograms X kg-1 X min-1 intravenous infusion of dopamine. Steady-state VE, VCO2 and VO2 were unchanged by the dopamine infusion, both during unloaded pedaling and at the heavier work load. The time constants for the increase in VE (tau VE) and VCO2 (tau CO2) were significantly (P less than 0.05) slowed (tau VE = 56.5 +/- 16.4 s for control, and tau VE = 76.4 +/- 26.6 s for dopamine; tau CO2 = 51.5 +/- 10.6 s for control, and tau CO2 = 64.8 +/- 17.4 s for dopamine) (mean +/- SD), but the time constant for VO2 (tau O2) was not significantly affected (tau O2 = 27.5 +/- 11.7 s for control, and tau O2 = 31.0 +/- 10.1 s for dopamine). We conclude that ablation of carotid body chemosensitivity with dopamine slows the transient ventilatory response to exercise while leaving the steady-state response unaffected.

1988 ◽  
Vol 65 (2) ◽  
pp. 921-927 ◽  
Author(s):  
C. A. Smith ◽  
L. C. Jameson ◽  
J. A. Dempsey

We investigated the effects of selective large changes in the acid-base environment of medullary chemoreceptors on the control of exercise hyperpnea in unanesthetized goats. Four intact and two carotid body-denervated goats underwent cisternal perfusion with mock cerebrospinal fluid (CSF) of markedly varying [HCO-3] (CSF [H+] = 21-95 neq/l; pH 7.68-7.02) until a new steady state of alveolar hypo- or hyperventilation was reached [arterial PCO2 (PaCO2) = 31-54 Torr]. Perfusion continued as the goats completed two levels of steady-state treadmill walking [2 to 4-fold increase in CO2 production (VCO2)]. With normal acid-base status in CSF, goats usually hyperventilated slightly from rest through exercise (-3 Torr PaCO2, rest to VCO2 = 1.1 l/min). Changing CSF perfusate [H+] changed the level of resting PaCO2 (+6 and -4 Torr), but with few exceptions, the regulation of PaCO2 during exercise (delta PaCO2/delta VCO2) remained similar regardless of the new ventilatory steady state imposed by changing CSF [H+]. Thus the gain (slope) of the ventilatory response to exercise (ratio of change in alveolar ventilation to change in VCO2) must have increased approximately 15% with decreased resting PaCO2 (acidic CSF) and decreased approximately 9% with increased resting PaCO2 (alkaline CSF). A similar effect of CSF [H+] on resting PaCO2 and on delta PaCO2/VCO2 during exercise also occurred in two carotid body-denervated goats. Our results show that alteration of the gain of the ventilatory response to exercise occurs on acute alterations in resting PaCO2 set point (via changing CSF [H+]) and that the primary stimuli to exercise hyperpnea can operate independently of central or peripheral chemoreception.


1984 ◽  
Vol 56 (5) ◽  
pp. 1143-1150 ◽  
Author(s):  
M. J. Brischetto ◽  
R. P. Millman ◽  
D. D. Peterson ◽  
D. A. Silage ◽  
A. I. Pack

Studies were performed to determine the effects of aging on the ventilatory responsiveness to two known respiratory stimulants, inhaled CO2 and exercise. Although explanation of the physiological mechanisms underlying development of exercise hyperpnea remains elusive, there is much circumstantial evidence that during exercise, however mediated, ventilation is coupled to CO2 production. Thus matched groups of young and elderly subjects were studied to determine the relationship between increasing ventilation and increasing CO2 production (VCO2) during steady-state exercise and the change in their minute ventilation in response to progressive hypercapnia during CO2 rebreathing. We found that the slope of the ventilatory response to hypercapnia was depressed in elderly subjects when compared with the younger control group (delta VE/delta PCO2 = 1.64 +/- 0.21 vs. 2.44 +/- 0.40 l X min-1 X mmHg-1, means +/- SE, respectively). In contrast, the slope of the relationship between ventilation and CO2 production during exercise in the elderly was greater than that of younger subjects (delta VE/delta VCO2 = 29.7 +/- 1.19 vs. 25.3 +/- 1.54, means +/- SE, respectively), as was minute ventilation at a single work load (50 W) (32.4 +/- 2.3 vs. 25.7 +/- 1.54 l/min, means +/- SE, respectively). This increased ventilation during exercise in the elderly was not produced by arterial O2 desaturation, and increased anaerobiasis did not play a role. Instead, the increased ventilation during exercise seems to compensate for increased inefficiency of gas exchange such that exercise remains essentially isocapnic. In conclusion, in the elderly the ventilatory response to hypercapnia is less than in young subjects, whereas the ventilatory response to exercise is greater.


1975 ◽  
Vol 39 (5) ◽  
pp. 697-701 ◽  
Author(s):  
I. Goldstein ◽  
S. Goldstein ◽  
J. A. Urbanetti ◽  
N. R. Anthonisen

Increases in functional residual capacity (FRC) decrease inspiratory muscle efficiency; the present experiments were designed to determine the effect of FRC change on the ventilatory response to exercise. Six well-trained adults were exposed to expiratory threshold loads (ETL) ranging from 5 to 40 cmH2O during steady-state exercise on a bicycle ergometer at 40–95% VO2max. Inspiratory capacity (IC) was measured and changes of IC interpreted as changes of FRC. ETL did not consistently limit exercise performance. At heavy work (greater than 92% VO2max) minute ventilation decreased with increasing ETL; at moderate work (less than 58% VO2max) it did not. Decreases in ventilation were due to decreases in respiratory frequency with prolongation of the duration of expiration being the most consistent change in breathing pattern. At moderate work levels, FRC increased with ETL; at maximum work it did not. Changes in FRC were dictated by constancy of tidal volume and a fixed maximum end-inspiratory volume of 80–90% of the inspiratory capacity. When tidal volume was such that end-inspiratory volume was less than this value, FRC increased with ETL. Mouth pressure measured during the first 0–1 s of inspiratory effort against an occluded airway (P0-1) was increased by ETL equals 30 cmH2O, in spite of the fact that ventilation was decreased. We concluded that changes in FRC due to ETL had no effect on the ventilatory response to exercise and that changes in P0-1 induced by ETL did not reflect changes of inspiratory drive so much as changes of the pattern of inspiration.


1981 ◽  
Vol 51 (1) ◽  
pp. 194-203 ◽  
Author(s):  
F. M. Bennett ◽  
P. Reischl ◽  
F. S. Grodins ◽  
S. M. Yamashiro ◽  
W. E. Fordyce

The dynamics of the ventilatory response to moderate exercise on a bicycle ergometer have been studied in humans. The work load was varied between 25 and 100 W as a pseudorandom binary sequence (PRBS) that enabled the impulse responses to be calculated by cross-correlation techniques. The response of all five subjects exhibited a bimodal response, i.e., a fast component that was followed after a delay by a slow component. The fast component accounted for a relatively small proportion of the total response. Also, it was demonstrated that to identify the rapid component it was necessary to excite the respiratory system with an input containing highfrequency components; this result was used to reconcile the findings from this study with those of previous investigation.


1984 ◽  
Vol 57 (6) ◽  
pp. 1796-1802 ◽  
Author(s):  
T. Chonan ◽  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
H. Inoue ◽  
...  

We examined the relationship between response to hypercapnia and ventilatory response to exercise under graded anesthesia in eight dogs. The response to hypercapnia was measured by the CO2 rebreathing method under three grades of chloralose-urethan anesthesia. The degrees of response to hypercapnia (delta VE/delta PETCO2, 1 X min-1 X Torr-1) in light (L), moderate (M), and deep (D) anesthesia were 0.40 +/- 0.05 (mean +/- SE), 0.24 +/- 0.03, and 0.10 +/- 0.02, respectively, and were significantly different from each other. Under each grade of anesthesia, exercise was performed by electrically stimulating the bilateral femoral and sciatic nerves for 4 min. The time to reach 63% of full response of the increase in ventilation (tauVE) after beginning of exercise was 28.3 +/- 1.5, 38.1 +/- 5.2, and 56.0 +/- 6.1 s in L, M, and D, respectively. During steady-state exercise, minute ventilation (VE) in L, M, and D significantly increased to 6.17 +/- 0.39, 5.14 +/- 0.30, and 3.41 +/- 0.16 1 X min-1, from resting values of 3.93 +/- 0.34, 2.97 +/- 0.17, and 1.69 +/- 0.14 1 X min-1, respectively, while end-tidal CO2 tension (PETCO2) in L decreased significantly to 34.8 +/- 0.9 from 35.7 +/- 0.9, did not change in M (38.9 +/- 1.1 from 38.9 +/- 0.8), and increased significantly in D to 47.3 +/- 1.9 from 45.1 +/- 1.7 Torr.(ABSTRACT TRUNCATED AT 250 WORDS)


1980 ◽  
Vol 48 (1) ◽  
pp. 109-113 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
G. Peres

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.


1962 ◽  
Vol 17 (2) ◽  
pp. 239-242 ◽  
Author(s):  
Thomas F. Hornbein ◽  
Albert Roos

Hypoxia of mild degree (PaOO2 above 60 mm Hg) produces little or no ventilatory response in resting man during the steady state. To evaluate the possibility that the effectiveness of a hypoxic chemoreceptor drive might be enhanced by exercise, the ventilatory response to mild hypoxia was measured in two human subjects during rest and exercise. Though no significant increase in ventilation occurred at rest above a PaOO2 of 60 mm Hg, a decrease in PaOO2from 100 to 94 mm Hg produced a statistically significant increase in steady state ventilation during moderate exercise. In addition, temporary block of the sympathetic innervation to the carotid and aortic bodies in one subject resulted in a diminution of work hyperpnea. This suggests that increased sympathetic tone during exercise, by reducing blood flow through the chemoreceptors, might result in increased neural discharge and hence increased ventilation even though arterial POO2 is the same as at rest. Thus, activity of the chemoreceptors as modified by sympathetic control of their blood supply may be an important determinant of the ventilatory response to exercise. Since work hyperpnea is enhanced by even mild hypoxia, this ventilatory response may be sufficient to initiate respiratory acclimatization to altitudes so low that resting ventilation on acute exposure is unaffected. Submitted on July 31, 1961


1979 ◽  
Vol 47 (3) ◽  
pp. 514-521 ◽  
Author(s):  
S. S. Segal ◽  
G. A. Brooks

To study a possible relationship between blood lactate and O2 consumption (VO2) after exercise, 11 male subjects exercised on a bicycle ergometer at moderate and heavy work loads in both normal glycogen and glycogen-depleted states. At rest, glycogen depletion resulted in significantly lowered blood glucose and lactate concentrations, CO2 production (VCO2), respiratory exchange ratio (R), and minute ventilation (VE). With the exception of glucose, these variables changed more in response to heavy exercise (HE: 2 min at a mean of 1,750 kg.m/min) than to moderate exercise (ME: 2 min at a mean of 1,000 kg.m/min). At either work load, VCO2, R, and lactate showed consistently greater responses in the normal glycogen state. The slope of the initial component of the postexercise VO2 curve was unaffected by either work load or lactate. Although the slope of the slow component of the postexercise VO2 curve became significantly more negative after HE, it was unaffected by the level of lactate. These results are inconsistent with the hypothesis of a “lactacid O2 debt.” Exercise intensity was the predominant factor influencing the magnitude and kinetics of postexercise VO2. Glycogen depletion resulted in lower VCO2, R, and blood lactate, but higher VE during heavy exercise. The results suggest that factors, in addition to CO2 flux to the lungs, influence VE during exercise.


1987 ◽  
Vol 73 (6) ◽  
pp. 617-625 ◽  
Author(s):  
K. Murphy ◽  
R. P. Stidwill ◽  
Brenda A. Cross ◽  
Kathryn D. Leaver ◽  
E. Anastassiades ◽  
...  

1. Continuous recordings of arterial pH, ventilation, airway CO2 and heart rate were made during rest and during 3–4 min periods of rhythmic leg exercise in four renal patients with arteriovenous shunts. 2. The patients were anaemic (haemoglobin 6.5–9.0 g/dl) but had a normal ventilatory response to exercise as judged by the ratio of the change in ventilation to the change in CO2 production. 3. Breath-by-breath oscillations in arterial pH disappeared for the majority of the exercise period in each patient. 4. Changes in mean arterial pH and end-tidal CO2 tension with exercise were inconsistent between subjects but consistent within a given subject. On average, mean arterial pH rose by 0.011 pH unit. Changes in end-tidal CO2 tension reflected changes in mean pHa by falling on average by 1 mmHg (0.13 kPa). 5. Hypercapnia and acidaemia were not found to be necessary for the ventilatory response to moderate exercise.


1980 ◽  
Vol 48 (6) ◽  
pp. 1065-1076 ◽  
Author(s):  
J. M. Clark ◽  
R. D. Sinclair ◽  
J. B. Lenox

Nine young athletes performed treadmill exercise at average VO2 levels of 1.08, 1.78, 3.00, and 3.57 l/min while exposed to inspired PCO2 levels of 0, 10, 20, 30, and 40 Torr. The average slope of the VE-PACO2 relationship increased significantly from 3.59 to 4.70 l.min-1.Torr-1 in the transition from rest to light exercise and then decreased progressively and significantly to 1.34 l.min-1.Torr-1 at the highest work load. A similar pattern of initial increased steepness followed by progressive flattening was found in the VT-PACO2, curves, whereas slopes of the f-PACO2 relationships continuously decreased in the transition from rest through light to heavy exercise. These data are consistent both with an increased ventilatory response to PACO2--[H+]a increments during light exercise and with progressive reduction of that response during the transition from light to heavy exercise in parallel with increasingly severe mechanical influences on VE as maximal limits are approached. They are not consistent with simple addition of chemical and nonchemical components of exercise hyperpnea at all levels of exercise.


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