Stroke volume, heart rate, cardiac output, tidal volume, respiratory frequency, minute ventilation, end-tidal tensions of O2 and CO2, O2 uptake, CO2 output, and respiratory exchange ratio were measured simultaneously in healthy male volunteers before, during, and after upright bicycle exercise from 0 to 360 and 720 kpm/min. The circulatory variables were determined continuously once per 20 cardiac cycles and the respiratory variables breath by breath using separate computer-based systems in which an impedance pneumograph and an impedance cardiograph were incorporated. Stroke volume, heart rate, and cardiac output started to increase without measurable delay at the onset of exercise. Stroke volume increased by 20% from resting control value in response to the mildest exercise and essentially leveled off with a further increase in work load. Time constant for cardiac output increased with the increasing work load. Time constant for minute ventilation was much longer than that for cardiac output and independent of work intensity. A good synchronization between the ventilation and cardiac output responses at an initial period of transitions from rest to exercise and from exercise to rest seems to support the concept of cardiodynamic hyperpnea.

Transient and steady-state responses of stroke volume (SV), heart rate (HR), cardiac output (Q), left ventricular ejection time (LVET), preejection period (PEP), and the ratio of LVET to PEP during bicycle exercises of 50 and 100 W were studied in four healthy male subjects in supine and upright postures. A computer-based system in which impedance cardiography was incorporated served to determine the above parameters on a 10-s interval basis. SV remained almost unchanged in response to exercises in a supine posture, whereas it increased significantly in an upright posture, although the individual differences among subjects were found to be large. The half-response times of variables to a step work load were determined. An approximate accordance was observed among the response times for HR, Q, and LVET/PEP. There was an inverse relationship between LVET and HR, the slope of which was found to be steeper in the supine posture than in the upright posture, reflecting the difference between the SV responses in both postures. LVET fell shortly after the cessation of exercise despite the decreasing HR. Inasmuch as the paradoxical reduction of LVET was also found in the case where SV remained unchanged in response to exercise, no changes in SV can be the cause thereof. Thus, a transient increase in ejection rate, which is due to either the increased myocardial contractility or decreased peripheral vascular resistance, may be responsible for the phenomenon.

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Transitional changes in stroke volume, heart rate, and cardiac

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.