Effects of beta‐adrenergic blockade on the ventilatory responses to hypoxic and hyperoxic exercise in man.

Abstract

SUMMARY1. The ventilatory responses to step changes from rest to 100 W cycling exercise were studied in five healthy human subjects. Exercise was performed in hypoxia (end-tidal 02 pressure, PET,02' 50-55 mmHg), a condition characterized by a marked enhancement of arterial chemoreceptor activity, and in hyperoxia (PETo°2 > 250 mmHg), a condition in which arterial chemoreceptor activity is largely suppressed. The subjects were studied at each 02 level after placebo and after an oral dose of 120 mg propranolol.2. The magnitude of phase 1, the immediate, rapid ventilatory response at the onset of work, was unaffected by hypoxia and at both oxygen levels it was also unaffected by propranolol.3. Phase 2, analysed from 20 to 120 s after the onset of exercise, was significantly affected by both 02 level and fl-blockade. The kinetics of the ventilatory changes in this phase were well described in all four conditions by a simple exponential function. The overall mean time constants after placebo were shorter in hypoxia (31-0 s) than in hyperoxia (40-2 s), and at each 02 level longer after propranolol, in hypoxia 61-3 s and in hyperoxia 106-0 s 4. Continuous analysis of gas sampled at the mouth with a mass spectrometer showed constancy of end-tidal Pco2 throughout the step change in hypoxia both with and without f-blockade. In contrast, in both hyperoxic conditions PETCo2 rose, mainly in phase 2, to a value 5-6 mmHg higher than the starting value. 5. The steady-state ventilation was higher in hypoxia than in hyperoxia, and endtidal CO2 pressure, PETC02, correspondingly lower. Neither ventilation nor Pco2were, however, affected by propranolol in either condition. 6. It is concluded that the arterial chemoreceptors are important for both the rate of adaptation of ventilation to a new rate of metabolism during a step change of work rate, and for the matching of ventilation to C02 flow which normally ensures isocapnia. The further slowing of the dynamics of the ventilatory response in hyperoxia as well as the preserved isocapnia in hypoxia after fl-blockade argue against any major role of f8-adrenergic mechanisms for these functions of the arterial chemoreceptors. The observed effects are considered to be secondary to the reduced cardiac output and an increased CO2 storage initially during exercise following fiadrenergic blockade.

Carvedilol reduces exercise‐induced hyperventilation: A benefit in normoxia and a problem with hypoxia

“…Finally, we did not investigate whether the reduced ventilatory response with hypoxia in patients treated with beta‐blockers is peculiar to heart failure patients or whether it is also present in normal subjects. Indeed, in normal subjects who live at high altitude, the chemoreflex response to hypoxia seems to be unaffected by beta‐blockers [38].…”

Respiratory Compensation Point during Incremental Exercise as Related to Hypoxic Ventilatory Chemosensitivity and Lactate Increase in Man.

“…They are marked increases in K ϩ and catecholamine concentrations, pH/PCO 2 oscillation of the arterial blood and the O 2 -labile component estimated by Dejours' O 2 test, which likely result in increased activities of the carotid bodies during exercise [3][4][5][6]. Increased plasma concentrations of K ϩ [14,32] and catecholamines [33] have also been considered to contribute to increases in HVR during exercise. In the present study, the resting estimate of HVR was used as an index of the exercise estimate of HVR based on previous studies [11,12,14] showing that individuals with higher HVR at rest tended to have higher HVR during exercise, although this tendency (correlation between both) was lower for women, as mentioned above.…”

Cardio‐Selective Beta‐Blocker: Pharmacological Evidence and Their Influence on Exercise Capacity

“…Studies by Beloka et al suggest that decreased aerobic exercise capacity under beta‐adrenergic blockade goes along with decreased ventilation regardless of the present metabolic rate [72]. Moreover, beta‐blockade was shown to reduce the sensitivity of arterial chemoceptors to potassium stimulation during exercise, thereby modulating the regulation of exercise ventilation [79], although effects could be secondary to reduced cardiac output [80]. Duration of beta‐blocker treatment prior to exercise testing seems not to significantly alter exercise responses [81].…”