Purpose: Exercise-induced dyspnea in patients with cardiopulmonary diseases may be related to sympathetic nervous system activation, with increased metabo- and/or chemosensitivities. Whether this mechanism plays a role in exercising normal subjects remains unclear.
Methods: Muscle sympathetic nerve activity (MSNA), HR, ventilation (V˙E), O2 saturation (SpO2), and end-tidal PCO2 (PetCO2) were measured in 14 healthy young adults after 1 wk of β1-receptor blockade with bisoprolol 5 mg·d−1 versus placebo after a double-blind, placebo-controlled, randomized crossover design. The MSNA and the ventilatory responses to hyperoxic hypercapnia (7% CO2 in O2), ΔV˙E/ΔPetCO2, and isocapnic hypoxia (10% O2 in N2), ΔV˙E/ΔSpO2, and to an isometric muscle contraction followed by a local circulatory arrest (metaboreflex) were determined at rest followed by an incremental cardiopulmonary exercise test.
Results: Bisoprolol did not change the V˙E and MSNA responses to hypercapnia, hyperoxia, or isometric muscle contraction or ischemia. Bisoprolol decreased maximum O2 uptake (P < 0.05), workload (P < 0.05), and HR (P < 0.0001) andboth V˙E/V˙O2 and V˙E/V˙CO2 slopes (P < 0.05).
Conclusions: These results suggest that decreased aerobic exercise capacity after intake of β-blockers is accompanied by decreased ventilation at any metabolic rate. However, this occurs without detectable change in the sympathetic nervous system tone or in metabo- or chemosensitivity and is therefore probably of hemodynamic origin.