The reflex bradycardia produced by a transient phenylephrine-induced rise of arterial pressure was investigated in man during rest and supine exercise, before and after autonomic blockade of the heart. Reflex bradycardia diminished proportionally to the tachycardia of exercise. Propranolol slowed the heart at rest and during exercise, but increased the reflex response only at rest, having no effect during exercise. Atropine, or atropine with propranolol, blocked the reflex during rest and exercise. The tachycardia following hypotension induced by amyl nitrite was similarly affected by the two drugs. Tachycardia induced by standing up and by isoprenaline also diminished the reflex bradycardia. It is concluded that reflex heart rate changes following sudden changes of arterial pressure are predominantly parasympathetic, and diminish during exercise in parallel with the decrease of parasympathetic tone. The reflex response is determined partly by the interaction of parasympathetic and sympathetic impulses at the sinoatrial node, shown by the effects of peripheral sympathetic stimulation and blockade at rest. During exercise central depression of the reflex may also occur. KEY WORDSphenylephrine atropine propranolol amyl nitrite posture parasympathetic nerves sympathetic nerves

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The effects of beta-adrenergic blockade induced by intravenous propranolol hydrochloride (0.2 mg/kg) on ventilatory and gas exchange responses to exercise were studied during tests in which the work rate was either increased progressively or maintained at a constant load in six healthy young male subjects. Heart rate during exercise decreased by about 20% and cardiac output, as estimated by a modification of the method of Kim et al. (J. Appl. Physiol. 21: 1338-1344, 1966), by about 15%. The relation between work rate and O2 uptake (VO2) was unaffected by propranolol, whereas maximal O2 uptake (VO2max) decreased by 5% and the anaerobic threshold, estimated noninvasively, was lowered by 23%. The relations between CO2 output (VCO2) and end-tidal CO2 partial pressure (PCO2) and between VCO2 and minute ventilation (VE) were both unaffected. The time constants for changes of VO2, VCO2, and VE during on-transients from unloaded pedaling to either a moderate (ca. 50% VO2max) or a heavy (ca. 67% VO2max) work rate in the control studies were in agreement with previously reported values, i.e., 42, 60, and 69 s, respectively. beta-Blockade was associated with a significantly increased time constant for VO2 of 61 s but with less consistent and insignificant changes for VCO2 and VE. There was a small but significant increase of the time constant for heart rate from 40 to 45 s. It is concluded that propranolol exerts its primary influence during exercise on the cardiovascular system without any discernible effect on ventilatory control.

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SUMMARY1. The breathing pattern, that is the relation between tidal volume (VT) and the inspiratory (T1) and expiratory (TE) durations, has been studied for individual breaths (forty in each steady state).2. Five healthy subjects were studied in steady-state exercise on a bicycle ergometer breathing air; three of them were also studied in hypercapnia, at rest and during exercise, and two of them also during exercise on a treadmill.3. Tidal volume and respiratory frequency both increased with work load. The increase in frequency was largely due to a progressive decrease in TE; T, also decreased. 5. A simple model of the respiratory cycle which fits both the observed mean and breath-by-breath patterns and which involves no new assumptions is presented.

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The ventilatory response to hypoxia (PAO2 55 and 45 Torr) at each of four levels of PACO2 was studied in five healthy subjects before and after a rise in rectal temperature of 1.4 degrees C had been induced by means of a heated flying suit. At a given level of chemical drive both ventilation and mean inspiratory flow increased after heating, frequency relatively more than tidal volume. In isoventilation comparisons mean inspiratory flow was identical in normo- and hyperthermia, whereas the durations of inspiration (TI) and expiration (TE) were proportionately shortened. It is suggested that a rise in temperature shortens TI by affecting a central "clock" and that TE changes are secondary to changes in end-inspiratory volume. The euoxic CO2 response in hyperthermia was suggestive of multiplication between CO2 and temperature. Hypoxic sensitivity was significantly increased, indicating a temperature effect on the arterial chemoreceptors. The breathing pattern was in either temperature condition identical in euoxia and in hypoxia.

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