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β-Adrenergic Blockade and Metabo-Chemoreflex Contributions to ExerciseCapacity

BELOKA, SOFIA1; GUJIC, MARKO1; DEBOECK, GAEL1; NISET, GEORGES1; CIARKA, AGNIESZKA1; ARGACHA, JEAN-FRANÇOIS1; ADAMOPOULOS, DIONYSIOS1; VAN DE BORNE, PHILIPPE1; NAEIJE, ROBERT2

Medicine & Science in Sports & Exercise: November 2008 - Volume 40 - Issue 11 - pp 1932-1938
doi: 10.1249/MSS.0b013e31817fbe11
BASIC SCIENCES: Original Investigations

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.

1Department of Cardiology, Erasme Hospital, and 2Department of Physiology, Université Libre de Bruxelles, Brussels, BELGIUM

Address for correspondence: Robert Naeije, M.D., Department of Physiology, Erasme Campus, CP 604, 808, Lennik Road, 1070 Brussels, Belgium; E-mail: rnaeije@ulb.ac.be.

Submitted for publication February 2008.

Accepted for publication May 2008.

©2008The American College of Sports Medicine