Stimulation of ventilation by normobaric hyperoxia in exercising dogs

Philippe Haouzi, E. M. Allioui, J. P. Gille, Y. Bedez, B. Tousseul, B. Chalon

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

In order to describe the factors which, during hyperoxic exercise, can counteract the chemoreceptor-mediated inhibition of ventilation by O2, minute ventilation (V̇) and the pulmonary gas exchange were studied breath-by-breath in four dogs running on a treadmill (5 km h-1) for 10 min during and following exposure to O2 of different durations. We found that a brief inhalation of O2 applied during the steady state of the V̇ response provoked a reduction in V̇ by 6.5±0.9 l min-1 whereas hyperoxia applied 2 min before the onset of exercise and maintained for 2.5 min during the running tests had a significantly weaker effect on V̇ (-1.8±0.2 l min-1, P<0.05). The rise in pulmonary CO2 output (V̇(CO2)) during the prolonged O2 exposure was less than in normoxic exercise leading to a deficit of CO2 eliminated by the lungs of 181 ml. The return to air breathing provoked a rise in V̇, which reached within 73 s a much higher level than the control tests (22.9 ± 3.6 vs. 19.5 ± 2.21 min-1, P<0.05); V̇ then subsided to control levels with a long exponential decline. The CO2 deficit during O2 breathing, was fully compensated after recovery in air within 6 min. No stimulatory effect on ventilation was observed at rest at the cessation of a similar exposure to O2 despite a higher end-tidal P(CO2) (+4 ± 1 mmHg) than in exercise. In conclusion, the stimulatory effect of O2 during exercise can be clearly revealed after recovery in air and seems to operate through a more complex mechanism than that thought to be involved at rest. We propose that the changes in CO2 stores in the exercising muscles could contribute to O2-induced stimulation during exercise, possibly through stimulation of muscle afferents responding to local circulatory changes. Finally, the observation that during continuous dopamine (DA) infusion (5 μg kg-1 min-1) the V(E) response to recovery in air was only a slow decrease, suggests that the arterial chemoreceptors potentiate O2-induced hyperventilation, or that the vascular actions of DA counteract part of the effects provoked by CO2 accumulation in the exercising muscles.

Original languageEnglish (US)
Pages (from-to)829-838
Number of pages10
JournalExperimental Physiology
Volume85
Issue number6
DOIs
StatePublished - Jan 1 2000

Fingerprint

Hyperoxia
Ventilation
Air
Dogs
Muscles
Dopamine
Respiration
Pulmonary Gas Exchange
Lung
Hyperventilation
Running
Inhalation
Blood Vessels

All Science Journal Classification (ASJC) codes

  • Physiology

Cite this

Haouzi, Philippe ; Allioui, E. M. ; Gille, J. P. ; Bedez, Y. ; Tousseul, B. ; Chalon, B. / Stimulation of ventilation by normobaric hyperoxia in exercising dogs. In: Experimental Physiology. 2000 ; Vol. 85, No. 6. pp. 829-838.
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abstract = "In order to describe the factors which, during hyperoxic exercise, can counteract the chemoreceptor-mediated inhibition of ventilation by O2, minute ventilation (V̇) and the pulmonary gas exchange were studied breath-by-breath in four dogs running on a treadmill (5 km h-1) for 10 min during and following exposure to O2 of different durations. We found that a brief inhalation of O2 applied during the steady state of the V̇ response provoked a reduction in V̇ by 6.5±0.9 l min-1 whereas hyperoxia applied 2 min before the onset of exercise and maintained for 2.5 min during the running tests had a significantly weaker effect on V̇ (-1.8±0.2 l min-1, P<0.05). The rise in pulmonary CO2 output (V̇(CO2)) during the prolonged O2 exposure was less than in normoxic exercise leading to a deficit of CO2 eliminated by the lungs of 181 ml. The return to air breathing provoked a rise in V̇, which reached within 73 s a much higher level than the control tests (22.9 ± 3.6 vs. 19.5 ± 2.21 min-1, P<0.05); V̇ then subsided to control levels with a long exponential decline. The CO2 deficit during O2 breathing, was fully compensated after recovery in air within 6 min. No stimulatory effect on ventilation was observed at rest at the cessation of a similar exposure to O2 despite a higher end-tidal P(CO2) (+4 ± 1 mmHg) than in exercise. In conclusion, the stimulatory effect of O2 during exercise can be clearly revealed after recovery in air and seems to operate through a more complex mechanism than that thought to be involved at rest. We propose that the changes in CO2 stores in the exercising muscles could contribute to O2-induced stimulation during exercise, possibly through stimulation of muscle afferents responding to local circulatory changes. Finally, the observation that during continuous dopamine (DA) infusion (5 μg kg-1 min-1) the V(E) response to recovery in air was only a slow decrease, suggests that the arterial chemoreceptors potentiate O2-induced hyperventilation, or that the vascular actions of DA counteract part of the effects provoked by CO2 accumulation in the exercising muscles.",
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Haouzi, P, Allioui, EM, Gille, JP, Bedez, Y, Tousseul, B & Chalon, B 2000, 'Stimulation of ventilation by normobaric hyperoxia in exercising dogs', Experimental Physiology, vol. 85, no. 6, pp. 829-838. https://doi.org/10.1111/j.1469-445X.2000.02035.x

Stimulation of ventilation by normobaric hyperoxia in exercising dogs. / Haouzi, Philippe; Allioui, E. M.; Gille, J. P.; Bedez, Y.; Tousseul, B.; Chalon, B.

In: Experimental Physiology, Vol. 85, No. 6, 01.01.2000, p. 829-838.

Research output: Contribution to journalArticle

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T1 - Stimulation of ventilation by normobaric hyperoxia in exercising dogs

AU - Haouzi, Philippe

AU - Allioui, E. M.

AU - Gille, J. P.

AU - Bedez, Y.

AU - Tousseul, B.

AU - Chalon, B.

PY - 2000/1/1

Y1 - 2000/1/1

N2 - In order to describe the factors which, during hyperoxic exercise, can counteract the chemoreceptor-mediated inhibition of ventilation by O2, minute ventilation (V̇) and the pulmonary gas exchange were studied breath-by-breath in four dogs running on a treadmill (5 km h-1) for 10 min during and following exposure to O2 of different durations. We found that a brief inhalation of O2 applied during the steady state of the V̇ response provoked a reduction in V̇ by 6.5±0.9 l min-1 whereas hyperoxia applied 2 min before the onset of exercise and maintained for 2.5 min during the running tests had a significantly weaker effect on V̇ (-1.8±0.2 l min-1, P<0.05). The rise in pulmonary CO2 output (V̇(CO2)) during the prolonged O2 exposure was less than in normoxic exercise leading to a deficit of CO2 eliminated by the lungs of 181 ml. The return to air breathing provoked a rise in V̇, which reached within 73 s a much higher level than the control tests (22.9 ± 3.6 vs. 19.5 ± 2.21 min-1, P<0.05); V̇ then subsided to control levels with a long exponential decline. The CO2 deficit during O2 breathing, was fully compensated after recovery in air within 6 min. No stimulatory effect on ventilation was observed at rest at the cessation of a similar exposure to O2 despite a higher end-tidal P(CO2) (+4 ± 1 mmHg) than in exercise. In conclusion, the stimulatory effect of O2 during exercise can be clearly revealed after recovery in air and seems to operate through a more complex mechanism than that thought to be involved at rest. We propose that the changes in CO2 stores in the exercising muscles could contribute to O2-induced stimulation during exercise, possibly through stimulation of muscle afferents responding to local circulatory changes. Finally, the observation that during continuous dopamine (DA) infusion (5 μg kg-1 min-1) the V(E) response to recovery in air was only a slow decrease, suggests that the arterial chemoreceptors potentiate O2-induced hyperventilation, or that the vascular actions of DA counteract part of the effects provoked by CO2 accumulation in the exercising muscles.

AB - In order to describe the factors which, during hyperoxic exercise, can counteract the chemoreceptor-mediated inhibition of ventilation by O2, minute ventilation (V̇) and the pulmonary gas exchange were studied breath-by-breath in four dogs running on a treadmill (5 km h-1) for 10 min during and following exposure to O2 of different durations. We found that a brief inhalation of O2 applied during the steady state of the V̇ response provoked a reduction in V̇ by 6.5±0.9 l min-1 whereas hyperoxia applied 2 min before the onset of exercise and maintained for 2.5 min during the running tests had a significantly weaker effect on V̇ (-1.8±0.2 l min-1, P<0.05). The rise in pulmonary CO2 output (V̇(CO2)) during the prolonged O2 exposure was less than in normoxic exercise leading to a deficit of CO2 eliminated by the lungs of 181 ml. The return to air breathing provoked a rise in V̇, which reached within 73 s a much higher level than the control tests (22.9 ± 3.6 vs. 19.5 ± 2.21 min-1, P<0.05); V̇ then subsided to control levels with a long exponential decline. The CO2 deficit during O2 breathing, was fully compensated after recovery in air within 6 min. No stimulatory effect on ventilation was observed at rest at the cessation of a similar exposure to O2 despite a higher end-tidal P(CO2) (+4 ± 1 mmHg) than in exercise. In conclusion, the stimulatory effect of O2 during exercise can be clearly revealed after recovery in air and seems to operate through a more complex mechanism than that thought to be involved at rest. We propose that the changes in CO2 stores in the exercising muscles could contribute to O2-induced stimulation during exercise, possibly through stimulation of muscle afferents responding to local circulatory changes. Finally, the observation that during continuous dopamine (DA) infusion (5 μg kg-1 min-1) the V(E) response to recovery in air was only a slow decrease, suggests that the arterial chemoreceptors potentiate O2-induced hyperventilation, or that the vascular actions of DA counteract part of the effects provoked by CO2 accumulation in the exercising muscles.

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