The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

Patients:6 healthy subjects mean age 25.5 years were studied.TypeofStudy:This study determined the effects of selective beta-adrenergic blockade with Lopresor on the oxygen flow in arterial blood (Q̇aO2) and oxygen flow in mixed venous blood (oxygen return, Q̇v̄O2) in humans exercising in normoxia and in acute normobaric hypoxia.DosageDuration:Initially 7.5 mg iv bolus; additional doses up to 30-40 mg until a quasi-complete receptor blockade was achieved.Results:Without Lopresor, PaO2 and PaCO2 were lower in hypoxia than in normoxia. In both hypoxia and normoxia conditions, Lopresor did not induce significant differences in PaO2 and PaCO2 with respect to control condition. Arterialized blood pH was higher in hypoxia than in normoxia and was unaffected by Lopresor. [La]b was higher in hypoxia than in normoxia and was unaffected by Lopresor. The highest [La]b values were observed at 150 W in hypoxia. Without Lopresor the fH, SV, Q̇ and Q̇aO2 increased significantly at exercise in both normoxia and in hypoxia. fH was systematically and significantly higher in hypoxia than in normoxia at each workload. SaO2 and CaO2 were lower in hypoxia than in normoxia. In hypoxia, they also decreased with increasing workload. As a result of this, and despite the lower arterial-venous O2 differences in hypoxia, the O2 extraction coefficient was greater in hypoxia than in normoxia. In normoxia the difference between Q̇aO2 and V̇02 (=Q̇V̄O2) did not change with increasing workload. In hypoxia, Q̇V̄O2 decreased as a function of workload. The resting Q̇v̄O2 value in normoxia was significantly lower than the corresponding invariant values at exercise. In hypoxia the resting Q̇V̄O2 value did not differ significantly from the corresponding value in normoxia. However, the Q̇V̄O2 values at 100 and 150 power (W) in C were significantly lower than the corresponding values in normoxia. With Lopresor, the fH, SV, Q̇, and Q̇aO2 increased significantly during exercised in both normoxia and hypoxia conditions. At rest and at each workload, Lopresor systematically and significantly decreased fH, both in normoxia and in hypoxia. The lower fH at any given V̇O2 implied a significant increase in the oxygen pulse with Lopresor. Q̇ values were found significantly higher at each fH level under Lopresor in hypoxia than in normoxia as a consequence of increased SV. SV values were significantly higher under Lopresor than in control condition in both normoxia and hypoxia. In normoxia, Q̇ was significantly decreased by Lopresor at 100 power (W) exercise and above, and in hypoxia at rest and at 50 W. As in control condition, SaO2 and CaO2 were lower in hypoxia than in normoxia. In hypoxia they also decreased with increasing workload. In both conditions the values observed under Lopresor were not significantly different from those found in control condition. The Q̇v̄O2 decrease as a function of workload in hypoxia paralleled an analogous decrease in SaO2.AdverseEffects:No adverse events were mentionedAuthorsConclusions:The results of the present study are in agreement with the tested hypothesis, as this study showed that selective blockade of beta1-adrenergic receptors decreased Q̇aO2 and Q̇v̄O2 significantly during exercise in normoxia as well as during rest and light exercise in hypoxia.FreeText:Experiments were performed in normoxia and in acute normobaric hypoxia. In both conditions the subjects performed two incremental exercise tests, one without Lopresor and one after having induced quasi-complete beta-adrenergic blockade with Lopresor. Tests: oxygen consumption (V̇O2), carbon dioxide output (V̇CO2), expired ventilation (V̇E), heart rate (fH, electrocardiography), SaO2 (oximetry), hemoglobin (Hb), blood lactate concentration ([La]b), cardiac output (Q̇), stroke volume (SV), arterialized blood carbon dioxide partial pressure (PaCO2), and arterialized blood oxygen partial pressure (PaO2).