Dynamics of cardiac, respiratory, and metabolic function in men in response to step work load

Abstract

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.

Heart rate recovery after exercise: relations to heart rate variability and complexity

“…Heart rate rapidly decreases during the first 1-2 min after the cessation of exercise, and gradually thereafter. During recovery from moderate and heavy exercise heart rate remains elevated above the pre-exercise level for a relatively long period of time (up to 60 min) (2,18,(26)(27)(28). Because of the presumed parasympathetic origin of both HRV and the rate of heart rate decrease after exercise we hypothesized that the HRV indices before and after exercise could be associated with the rate of heart rate recovery.…”

“…We did not attempt to control breathing pattern in order to avoid subject's discomfort and metabolic and blood gas changes due to unwanted hypo-or hyperventilation. It was shown that minute ventilation, tidal volume and respiratory frequency gradually decrease during post-exercise recovery (27). The tidal volume drop could reduce the HF increase during recovery; on the other hand, the HF increase could be to some extent caused by the post-exercise respiratory frequency decrease.…”

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.…”

“…C02 flow from venous blood to the lung, i.e., the product of cardiac output (Q) and mixed venous C02 content (Cv~o2) causes an increase in ventilation during excercise by means of some unidentified mechanisms. More recently, MIYAMOTO et al (1981MIYAMOTO et al ( , 1982 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 ventilation during the unsteady-state of step exercise. However, the mechanism linking C02 flow to ventilation has remained unsettled.…”