Arterial CO2 Pressure Drives Ventilation with a Time Delay during Recovery from an Impulse-like Exercise without Metabolic Acidosis
We investigated this hypothesis that arterial CO2 pressure (PaCO2) drives ventilation (V.E) with a time delay duringrecovery from short impulse-like exercise (10 s) with work load of 200 watts. V.E and end tidal CO2 pressure (PETCO2) were measured continuously during rest, warming up, exercise and recovery periods. PaCO2 was predicted (PaCO2 pre) from PETCO2 and tidal volume (VT). PETCO2 and PaCO2 pre peaked at 20 s of recovery. V.E increased and peaked at the end of exercise and then decreased during recovery; however, it peaked again at 30 s of recovery, which was 10 s later than the peak of PaCO2 pre. The relationship between V. E and PaCO2pre was not significant by using data of them obtained at the same time but was significant by using data of V.E obtained 10 s later for data of PaCO2 pre. The results support our hypothesis that PaCO2 drives V.E with a time delay.
[1] J.A. Dempsey, ÔÇÿÔÇÿChallenges for future research in exercise physiology as applied to the respiratory system,-- Exerc. Sport. Sci. Rev, vol. 34, pp.
92-98, 2006.
[2] T.G. Waldrop, G.A. Iwamoto, and P. Haouzi, ÔÇÿÔÇÿPoint: Counterpoint:
supraspinal locomotor centers do/do not contribute significantly to the
hyperpnea of dynamic exercise,-- J. Appl. Physiol, vol. 100, pp. 1077-1083, 2006.
[3] D.M. Band, I.R. Cameron, and S.J. Semple, ÔÇÿÔÇÿOscillations in arterial pH with breathing in the cat,-- J. Appl. Physiol, vol. 26, pp. 261-267, 1969.
[4] D.M. Band, C.B. Wolff, J. Ward, G.M. Cohrane, and J. Prior, ÔÇÿÔÇÿRespiratory oscillations in arterial carbon dioxide tension as a control
signal in exercise,-- Nature, vol. 283, pp. 84-85, 1980.
[5] B.A. Cross, B.J. Grant, A. Guz, P.W. Jones, S.J. Semple, and R.P.
Stidwill, ÔÇÿÔÇÿDependence of phrenic motoneurone output on the oscillatory
component of arterial blood gas composition,-- J. Physiol, vol. 290, pp. 163-84, 1979.
[6] A. Oren, K. Wasserman, J.A. Davis, and B.J. Whipp, ÔÇÿÔÇÿEffect of CO2 set
point on ventilatory response to exercise,-- J. Appl. Physiol, vol. 51, pp. 185-189, 1981.
[7] K. Wasserman, A.L. Van Kessel, and G.G. Burton, ÔÇÿÔÇÿInteraction of physiological mechanisms during exercise,-- J. Appl. Physiol, vol. 22,
pp. 71-85, 1967.
[8] J.M. Kowalchuk, G.J. Heigenhauser, M.I. Lindinger, J.R. Sutton, and N.L. Jones, ÔÇÿÔÇÿFactors influencing hydrogen ion concentration in muscle after intense exercise,-- J. Appl. Physiol, vol. 65, pp. 2080-2089, 1988.
[9] W. Stringer, R. Casaburi, and K. Wasserman, ÔÇÿÔÇÿAcid-base regulation
during exercise and recovery in humans,-- J. Appl. Physiol, vol. 72, pp. 954-961, 1992.
[10] J. Duffin, ÔÇÿÔÇÿThe role of the central chemoreceptors: A modeling perspective,-- Respir. Physiol. Neurobiol, vol. 173, pp. 230-243, 2010.
[11] P.A. Stewart, ÔÇÿÔÇÿModern quantitative acid-base chemistry,-- Can. J.
Physiol. Pharmacol, vol. 61, pp. 1444-1461, 1983.
[12] G.S. Zavorsky, J. Cao, N.E. Mayo, R. Gabbay, and J.M. Murias, ÔÇÿÔÇÿArterial versus capillary blood gases: a meta-analysis,-- Respir.
Physiol. Neurobiol, vol. 155, pp. 268-279, 2007.
[13] N.L. Jones, D.G. Robertson, and J.W. Kane, ÔÇÿÔÇÿDifference between endtidal
and arterial PCO2 in exercise,-- J. Appl. Physiol. Vol. 47, pp. 954-960, 1979.
[14] D.L. Turner, ‘‘Cardiovascular and respiratory control mechanisms
during exercise: An integrated view,’’ J. Exp. Biol, vol. 160, pp. 309-
340, 1991.
[15] C. Eyzaquirre, and P. Zapata, ‘‘Perspectives in carotid body research,’’
J. Appl. Physiol, vol. 57, pp. 931-957, 1984.
[16] I.D. Clement, D.A. Bascom, J. Conway, K.L. Dorrington, D.F.
O’Connor, R. Painter, D.J. Paterson, and P.A. Robbins, ‘‘An assessment
of central-peripheral ventilatory chemoreflex interaction in humans,’’
Respir. Physiol, vol. 88, pp. 87-100, 1992.
[17] I.D. Clement, J.J. Pandit, D.A. Bascom, and P.A. Robbins, ‘‘Ventilatory
chemoreflexes at rest following a brief period of heavy exercise in
man,’’ J. Physiol, vol. 495, pp. 875-884, 1996.
[18] M.P. Kaufman, J.C. Longhurst, K.J. Rybicki, J.H. Wallach, and J.H.
Mitchhell, ‘‘Effects of static muscular contraction on impulse activity of
tests III and IV afferents in cats,’’ J. Appl. Physiol, vol. 100, pp. 105-
112, 1983.
[19] D.I. McCloskey, and J.H. Mitchell, ‘‘Reflex cardiovascular and
respiratory responses originating in exercising muscle,’’ J. Physiol, vol.
224, pp. 173-186, 1972.
[20] P. Haouzi, B. Chenuel, B. Chalon, and A. Huszczuk, ‘‘Distension of
venous structures in muscles as a controller of respiration. Frontiers in
modeling and control of breathing: integration at molecular, cellular, and
systems levels,’’ Adv. Exp. Med. Biol, vol. 499, pp. 349-356, 2001.
[21] Y. Fukuba, A. Kitano, N. Hayashi, T. Yoshida, H. Ueoka, M.Y. Endo,
and A. Miura, ‘‘Effects of femoral vascular occlusion on ventilatory
responses during recovery from exercise in human,’’ Respir. Physiol &
Neurobiol, vol. 155, pp. 29-34, 2007.
[22] P. Haouzi, B. Chenuel, and B. Chalon, ‘‘Effects of body position on the
ventilatory response following an impulse exercise in humans,’’ J. Appl.
Physiol, vol. 92, pp. 1423-1433, 2002.
[1] J.A. Dempsey, ÔÇÿÔÇÿChallenges for future research in exercise physiology as applied to the respiratory system,-- Exerc. Sport. Sci. Rev, vol. 34, pp.
92-98, 2006.
[2] T.G. Waldrop, G.A. Iwamoto, and P. Haouzi, ÔÇÿÔÇÿPoint: Counterpoint:
supraspinal locomotor centers do/do not contribute significantly to the
hyperpnea of dynamic exercise,-- J. Appl. Physiol, vol. 100, pp. 1077-1083, 2006.
[3] D.M. Band, I.R. Cameron, and S.J. Semple, ÔÇÿÔÇÿOscillations in arterial pH with breathing in the cat,-- J. Appl. Physiol, vol. 26, pp. 261-267, 1969.
[4] D.M. Band, C.B. Wolff, J. Ward, G.M. Cohrane, and J. Prior, ÔÇÿÔÇÿRespiratory oscillations in arterial carbon dioxide tension as a control
signal in exercise,-- Nature, vol. 283, pp. 84-85, 1980.
[5] B.A. Cross, B.J. Grant, A. Guz, P.W. Jones, S.J. Semple, and R.P.
Stidwill, ÔÇÿÔÇÿDependence of phrenic motoneurone output on the oscillatory
component of arterial blood gas composition,-- J. Physiol, vol. 290, pp. 163-84, 1979.
[6] A. Oren, K. Wasserman, J.A. Davis, and B.J. Whipp, ÔÇÿÔÇÿEffect of CO2 set
point on ventilatory response to exercise,-- J. Appl. Physiol, vol. 51, pp. 185-189, 1981.
[7] K. Wasserman, A.L. Van Kessel, and G.G. Burton, ÔÇÿÔÇÿInteraction of physiological mechanisms during exercise,-- J. Appl. Physiol, vol. 22,
pp. 71-85, 1967.
[8] J.M. Kowalchuk, G.J. Heigenhauser, M.I. Lindinger, J.R. Sutton, and N.L. Jones, ÔÇÿÔÇÿFactors influencing hydrogen ion concentration in muscle after intense exercise,-- J. Appl. Physiol, vol. 65, pp. 2080-2089, 1988.
[9] W. Stringer, R. Casaburi, and K. Wasserman, ÔÇÿÔÇÿAcid-base regulation
during exercise and recovery in humans,-- J. Appl. Physiol, vol. 72, pp. 954-961, 1992.
[10] J. Duffin, ÔÇÿÔÇÿThe role of the central chemoreceptors: A modeling perspective,-- Respir. Physiol. Neurobiol, vol. 173, pp. 230-243, 2010.
[11] P.A. Stewart, ÔÇÿÔÇÿModern quantitative acid-base chemistry,-- Can. J.
Physiol. Pharmacol, vol. 61, pp. 1444-1461, 1983.
[12] G.S. Zavorsky, J. Cao, N.E. Mayo, R. Gabbay, and J.M. Murias, ÔÇÿÔÇÿArterial versus capillary blood gases: a meta-analysis,-- Respir.
Physiol. Neurobiol, vol. 155, pp. 268-279, 2007.
[13] N.L. Jones, D.G. Robertson, and J.W. Kane, ÔÇÿÔÇÿDifference between endtidal
and arterial PCO2 in exercise,-- J. Appl. Physiol. Vol. 47, pp. 954-960, 1979.
[14] D.L. Turner, ‘‘Cardiovascular and respiratory control mechanisms
during exercise: An integrated view,’’ J. Exp. Biol, vol. 160, pp. 309-
340, 1991.
[15] C. Eyzaquirre, and P. Zapata, ‘‘Perspectives in carotid body research,’’
J. Appl. Physiol, vol. 57, pp. 931-957, 1984.
[16] I.D. Clement, D.A. Bascom, J. Conway, K.L. Dorrington, D.F.
O’Connor, R. Painter, D.J. Paterson, and P.A. Robbins, ‘‘An assessment
of central-peripheral ventilatory chemoreflex interaction in humans,’’
Respir. Physiol, vol. 88, pp. 87-100, 1992.
[17] I.D. Clement, J.J. Pandit, D.A. Bascom, and P.A. Robbins, ‘‘Ventilatory
chemoreflexes at rest following a brief period of heavy exercise in
man,’’ J. Physiol, vol. 495, pp. 875-884, 1996.
[18] M.P. Kaufman, J.C. Longhurst, K.J. Rybicki, J.H. Wallach, and J.H.
Mitchhell, ‘‘Effects of static muscular contraction on impulse activity of
tests III and IV afferents in cats,’’ J. Appl. Physiol, vol. 100, pp. 105-
112, 1983.
[19] D.I. McCloskey, and J.H. Mitchell, ‘‘Reflex cardiovascular and
respiratory responses originating in exercising muscle,’’ J. Physiol, vol.
224, pp. 173-186, 1972.
[20] P. Haouzi, B. Chenuel, B. Chalon, and A. Huszczuk, ‘‘Distension of
venous structures in muscles as a controller of respiration. Frontiers in
modeling and control of breathing: integration at molecular, cellular, and
systems levels,’’ Adv. Exp. Med. Biol, vol. 499, pp. 349-356, 2001.
[21] Y. Fukuba, A. Kitano, N. Hayashi, T. Yoshida, H. Ueoka, M.Y. Endo,
and A. Miura, ‘‘Effects of femoral vascular occlusion on ventilatory
responses during recovery from exercise in human,’’ Respir. Physiol &
Neurobiol, vol. 155, pp. 29-34, 2007.
[22] P. Haouzi, B. Chenuel, and B. Chalon, ‘‘Effects of body position on the
ventilatory response following an impulse exercise in humans,’’ J. Appl.
Physiol, vol. 92, pp. 1423-1433, 2002.
@article{"International Journal of Medical, Medicine and Health Sciences:60440", author = "R. Afroundeh and T. Arimitsu and R. Yamanaka and C. S. Lian and T. Yunoki and T. Yano and K. Shirakawa", title = "Arterial CO2 Pressure Drives Ventilation with a Time Delay during Recovery from an Impulse-like Exercise without Metabolic Acidosis", abstract = "We investigated this hypothesis that arterial CO2 pressure (PaCO2) drives ventilation (V.E) with a time delay duringrecovery from short impulse-like exercise (10 s) with work load of 200 watts. V.E and end tidal CO2 pressure (PETCO2) were measured continuously during rest, warming up, exercise and recovery periods. PaCO2 was predicted (PaCO2 pre) from PETCO2 and tidal volume (VT). PETCO2 and PaCO2 pre peaked at 20 s of recovery. V.E increased and peaked at the end of exercise and then decreased during recovery; however, it peaked again at 30 s of recovery, which was 10 s later than the peak of PaCO2 pre. The relationship between V. E and PaCO2pre was not significant by using data of them obtained at the same time but was significant by using data of V.E obtained 10 s later for data of PaCO2 pre. The results support our hypothesis that PaCO2 drives V.E with a time delay.
", keywords = "Arterial CO2 pressure, impulse-like exercise, time delay, ventilation.", volume = "6", number = "11", pages = "598-4", }
