Cardiorespiratory dynamics during sinusoidal and impulse exercise in man.

Abstract

Dynamic characteristics of ventilation, cardiac output, and gas exchange during sinusoidally varying work rates for the periods from 1 to 12 min and impulse work rate with a duration of 10 sec were studied on five healthy men in an upright position. Changes in work rate were given by controlling externally the electromagnetic braking system of a bicycle ergometer. Stroke volume, heart rate, and cardiac output during exercise were determined continuously by using an automated impedance cardiograph. Breath by breath determination in minute ventilation, respiratory frequency, tidal volume, oxygen consumption, carbon dioxide output, end-tidal pressures of oxygen and carbon dioxide, and gas exchange ratio were conducted. From these and steady-state response data amplitude and phase relations between each variable and the input work loads were obtained utilizing the frequency analysis techniques. The response characteristics to sinusoidal stimuli were well represented by first-order models with time constants for VE, Vcoz, V o ,, and Q averaging 75, 67, 52, and 36 sec, respectively. The kinetics of HR closely resembled that of Q. There was a close link between both the dynamics of VE and Vco 2. On the other hand, the responses to impulse stimuli were better described by second-order models in which fast and slow response components were connected in parallel. However, the contribution of the fast component to total response was small. Although this response may support in its form the neurohumoral concept to explain exercise hyperpnea, a tight linkage was observed between VE and VCO2 responses to impulse stimuli. Thus, hyperpnea during the unsteady-state of exercise may be explained by the cardiodynamic hypothesis.

Neural and humoral factors affecting ventilatory response during exercise.

“…Summarizing the previous data, it appears that the time constant for J" is about 50-60 s, which is very close to, but slightly less than, the time constant for VE [35,39,40,63], while the time constant for J" is about 40s. A shorter time constant of 20-25 s has been determined for Q [39,40,43] (see Fig.…”

“…the product of cardiac output (Q) and mixed venous C02 content (Cvc02), is a prime determinant of hyperpnea during exercise. More recently, MIYAMOTO et al [39,40,43] determined the kinetics of Q by adopting an ensemble-averaging technique to impedance cardiography, evidently showing that the change in Q precedes that in ventilation during most of the unsteady-state period of exercise except for phase I. The impedance technique has recently been proved to be valid as an appropriate method for estimating stroke volume during exercise in comparison with dilution [45] and C02 rebreathing methods [19].…”

“…Since transfer functions relating exercise stimuli to cardiorespiratory responses are known to be represented roughly by a first order system with a minimum time delay [ 35,39,40,63], the kinetics thereof can be determined by unique time constants. So far, studies to determine the time constants for these variables have been carried out adopting various types of exercise forcings such as step [35,39,63], impulse [4,40], sinusoidal [4,12,40], and pseudo-random forcings [8,24]. The time constants obtained by these techniques were generally in good agreement in spite of the difference in the types of forcing, suggesting a rather linear property of the regulatory system within a subanaerobic range of exercise load.…”

Cardiodynamic factors affecting hyperpnea during steady-state exercise in man.

“…Although the correlation coefficient between Q and VE was high in the steady-states of exercise ( Fig. 1 and Table 3), the kinetics of Q is reported to be much faster (about 25s in time constant) than that of VE (about 60 s) when observed in the unsteady-state of exercise (MIYAMOTO et al, 1982(MIYAMOTO et al, , 1983. The correlation between VE and QCO2 was also significant ( Fig.…”

“…Since the significant difference in the kinetics exists between VE and Q (and Qco2), it would be unlikely that Q (or Qco2) plays a major role in exercise hyperpnea, even if venous chemoreceptors are assumed. Significant correlations between VE and Vco2 have been repeatedly observed during the steady-state as well as the unsteady-state of exercise (WASSERMAN et al, 1967;LINNARSSON, 1974;CASABURI et al, 1977;DIAMOND et al, 1977;MIYAMOTO et al, 1982MIYAMOTO et al, , 1983. Although the kinetics of both variables have been observed to be very similar to one another, emphasis has been laid on the fact that changes in Vco2 always precedes those in VE.…”