Abstract
According to the cardiodynamic hypothesis proposed by Wasserman et al.,1,2 CO2 flow from venous blood to the lung (QCO2), i.e., the product of cardiac output (Q) and mixed venous CO2 content (CVCO2), causes an increase in ventilation during exercise by means of some unidentified mechanisms. Close correlation between CO2 output (VCO2) and ventilation (VE) has repeatedly been observed during the steady- and unsteady-state of exercise.3,4,5 More recently, Miyamoto et al.6 have determined the kinetics of Q by adopting an ensemble-averaging technique to impedance cardiography, evidently showing that the change in Q precedes that in VE during the unsteady- state, of step, impulse and sinusoidal exercise.5 However, the mechanism which links CO2 flow to hyperpnea remains uncertain.
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© 1989 Plenum Press, New York
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Miyamoto, Y., Niizeki, K., Sugawara, T., Nakazono, Y., Kawahara, K., Mussell, M. (1989). The Validity of the Cardiodynamic Hypothesis for Exercise Hyperpnea in Man. In: Swanson, G.D., Grodins, F.S., Hughson, R.L. (eds) Respiratory Control. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0529-3_5
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DOI: https://doi.org/10.1007/978-1-4613-0529-3_5
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