Document Type : original article


Department of Physical Education and sport Sciences, Faculty of Education and Psychology, University of Mohaghegh Ardabili, Ardabil, Iran


Purpose: Arterial CO2 pressure (PaCO2) is one of important factors in Chemical mechanism of ventilation (VE) control that its direct or indirect effect on VE or its lack of influence is still under discussion. The purpose of the present study was to investigate the effect of PaCO2 on VE during short-term intermittent activity and during recovery after this activity and to investigate time lag in stimulation of VE by PaCO2. Methods: Ten inactive male subjects performed a short-term intermittent activity (10 sec) with work load of 200 watts that induces condition in which only PaCO2 among all chemical factors is changed. VE and gas exchange data were measured continuously during rest, warming up, activity and recovery periods. PaCO2 was predicted from PETCO2 and tidal volume (VT). Cross correlation was obtained for showing correlation coefficient between VE and predicted PaCO2considering various time lags. Results: The amount of Predicted PaCO2 was significantly higher than warming up levels from 14 sec to 28 sec during recovery and the amount of VE was significantly higher than warming up levels from 14 sec to 90 sec during recovery (p < 0.05) and the highest correlation coefficient between VE and predicted PaCO2 was obtained in time lag of 7s (r=0.854). Conclusion: The results of this study indicate that in inactive males PaCO2 stimulate VE during short-term intermittent activity and during recovery after that and there is a time lag of 7 sec in stimulation of VE by PaCO2.


[1] Dempsey JA. Challenges for future research in exercise physiology as applied to the respiratory system. Exerc.Sport. Sci. Rev. 2006; 34: 92-98.
[2] Waldrop TG, Iwamoto GA, Haouzi P. Point: Counterpoint: supraspinal locomotor centers do/do not contribute significantly to the hyperpnea of dynamic exercise. J. Appl. Physiol. 2006; 100: 1077-1083.
[3] Guyenet PG, and Bayliss DA. Neural control of breathing and CO2 homeostasis. Neuron. 2015; 87(5): 946-961.
[4] Dempsey JA, Smith CA, Blain GM, Xie A, Gong Y, Teodorescu M. Role of central/peripheral chemoreceptors and their interdependence in the pathophysiology of sleep apnea.
Adv Exp Med Biol. 2012; 758:343-9.
[5] Darabi SH, Kamaneh S, Heydari A. Relationship between potassium and lactate concentration with ventilation during exercise. IJBMS. 2006; 3:167-171. [In Persian].
[6] Cunningham DJC, Robbins PA, Wolff CB. Integration of respiratory responses to changes in alveolar partial pressures of CO2 and O2 and in arterial pH. In: Fishman AP, Cherniack NS, Widdicombe JG: Handbook of Physiology, American Physiological Society, Bethesda. 1986; vol II: 475-528.
[7] Bruce RM. The control of ventilation during exercise: a lesson in critical thinking. Adv Physiol Educ. 2017; 41: 539-547. [8] Tsuji B, Hayashi K, Kondo N and Nishiyasu T. Characteristics of hyperthermia-induced hyperventilation in humans, Temperature. 2016; 3(1): 146-160.
[9] Moradi E, Asadi B, Shahedi A. Assessment of arterial blood gases in hypobaric and comparison with normal Raptor fighter pilots. J Army Uni Med Sci, 2014, 9(1):16-23
[10] Meyer T, Faude O, Scharhag J, Urhausen A, Kindermann W. Is lactic acidosis a cause of exercise-induced hyperventilation at the respiratory compensation point? Br. J. Sports. Med, 2004; 38, 622-625.
[11] Peronnet F, Meyer T, Aguilaniu B, Juneau CE, Faude O, Kindermann W. Bicarbonate infusion and pH clamp moderately reduce hyperventilation during ramp exercise in humans. J. Appl. Physiol. 2007; 102, 426-428.
[12] Ward SA. Ventilatory control in humans: constraints and limitations. Exp. Physiol. 2007; 92, 357-366.
[13] Yamanaka R, Yunoki T, Arimitsu T, Lian CS, Yano T. Effects of sodium bicarbonate ingestion on EMG, effort sense and ventilatory response during intense exercise and subsequent active recovery. Eur. J. Appl. Physiol. 111, 851-858 (2011)
[14] Duffin J. The role of the central chemoreceptors: A modeling perspective. Respir. Physiol. Neurobiol. 2010; 173: 230-243.
[15] Stewart PA. Modern quantitative acid-base chemistry. Can. J. Physiol. Pharmacol. 1983; 61: 1444-1461.
[16] Poon CS. Evolving paradigms in H+ control of breathing: From homeostatic regulation to homeostatic competition. Respir. Physiol. Neurobiol. 2011; 179, 122-126.
[17] Duffin J. Role of acid-base balance in the chemoreflex control of breathing. J. Appl. Physiol. 2005; 99, 2255-2265.
[18] Afroundeh R, Arimitsu T, Yamanaka R, Lian CS, Yunoki T, Yano T. Effects of humoral factors on ventilation kinetics during recovery after impulse-like exercise. Acta. Physiol. Hung. 2012; 99, 185-193.
[19] Smith CA, Rodman JR, Chenuel JA, Henderson KS, Dempsey JA. Response time and sensitivity of the ventilatory response to CO in unanesthetized intact dogs: central vs. peripheral chemoreceptors. J. Appl. Physiol. 2006; 100, 13-19.
[20] Medbø JI, Noddeland H, Hanem S. Acid-base status of arterial and femoral-venous blood during and after intense cycle exercise. Acta. Kinesiol. Univ. Tartu. 2009; 14, 66-94.
[21] Haouzi P, Chenuel B, Chalon B. Effects of body position on the ventilatory response following an impulse exercise in
humans. J. Appl. Physiol. 2002; 92: 1423-1433.
[22] Zavorsky GS, Cao J, Mayo NE, Gabbay R, Murias JM. Arterial versus capillary blood gases: a meta-analysis. Respir. Physiol. Neurobiol. 2007; 155: 268-279.
[23] Jones NL, Robertson DG, Kane JW. Difference between end-tidal and arterial PCO2 in exercise. J. Appl. Physiol. 1979; 47: 954-960.
[24] Bruce R.M. The control of ventilation during exercise: a lesson in critical thinking. Adv. Physiol. Educ. 2017; 41: 539 -547.
[25] Chowdhuri S, and Badr MS. Control of Ventilation in Health and Disease. Chest. 2017; 151(4):917-929
[26] Hladky S.B and Barrand A.M. Fluid and ion transfer across the blood– brain and blood–cerebrospinal fluid barriers;a comparative account of mechanisms and roles. Hladky and Barrand Fluids Barriers CNS 2016; 13:19
[27] Clement ID, Pandit JJ, Bascom DA, Robbins PA. Ventilatory chemoreflexes at rest following a brief period of heavy exercise in man. J. Physiol. 1996; 495: 875 884.
[28] Blain GM, Mangum TS, Sidhu SK, Weavil JC, Hureau TJ, Jessop JE, Bledsoe AD, Richardson RS and Amann M. Group III/IV muscle afferents limit the intramuscular metabolic perturbation during whole body exercise in humans. J Physiol. 2016; 594(18): 5303-5315
[29] Haouzi P, Chenuel B, Chalon B, Huszczuk A. 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. 2001; 499: 349-356.
[30] Fukuba Y, Kitano A, Hayashi N, Yoshida T, Ueoka H, Endo MY, Miura A. Effects of femoral vascular occlusion on ventilatory responses during recovery from exercise in human. Respir. Physiol & Neurobiol. 2007; 155: 29-34.