β-Blockade reduces tidal volume during heavy exercise in trained and untrained men

M. J. Joyner, S. M. Jilka, J. A. Taylor, J. K. Kalis, J. Nittolo, R. W. Hicks, T. G. Lohman, J. H. Wilmore

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

The effects of β-blockade on tidal volume (VT), breath cycle timing, and respiratory drive were evaluated in 14 endurance-trained [maximum O2 uptake (V̇O2(max)) ~65 ml·kg-1·min-1] and 14 untrained (V̇O2(max) ~50 ml·kg-1·min-1) male subjects at 45, 60, and 75% of unblocked V̇O2(max) and at V̇O2(max). Propranolol (PROP, 80 mg twice daily), atenolol (ATEN, 100 mg once a day) and placebo (PLAC) were administered in a randomized double-blind design. In both subject groups both drugs attenuated the increases in VT associated with increasing work rate. CO2 production (V̇CO2) was not changed by either drug during submaximal exercise but was reduced in both subject groups by both drugs during maximal exercise. The relationship between minute ventilation (V̇E) and V̇CO2 was unaltered by either drug in both subject groups due to increases in breathing frequency. In trained subjects VT was reduced during maximal exercise from 2.58 l/breath on PLAC to 2.21 l/breath on PROP and to 2.44 l/breath on ATEN. In untrained subjects VT at maximal exercise was reduced from 2.30 l/breath on PLAC to 1.99 on PROP and 2.12 on ATEN. These observations indicate that 1) since V̇E vs. V̇CO2 was not altered by β-adrenergic blockade, the changes in VT and f did not result from a general blunting of the ventilatory response to exercise during β-adrenergic blockade; and 2) blockade of β1- and β2-receptors with PROP caused larger reductions in VT compared with blockade of β1-receptors only (ATEN), suggesting that β2-mediated bronchodilation plays a role in the VT response to heavy exercise.

Original languageEnglish (US)
Pages (from-to)1819-1825
Number of pages7
JournalJournal of applied physiology
Volume62
Issue number5
DOIs
StatePublished - 1987

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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