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Am J Physiol Heart Circ Physiol (July 29, 2004). doi:10.1152/ajpheart.00455.2004
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Submitted on May 14, 2004
Accepted on July 21, 2004

EXERCISE HYPERVENTILATION, DYSPNEA SENSATION AND ERGOREFLEX ACTIVATION IN LONE ATRIAL FIBRILLATION

Marco Guazzi1*, Sebastiano Belletti1, Gabriele Tumminello1, Cesare Fiorentini1, and Maurizio D Guazzi2

1 Cardiology Division, San Paolo Hospital, Cardiopulmonary Laboratory, University of Milano, Milano, Italy
2 University of Milano, Institue of Cardiology, Milano, Italy

* To whom correspondence should be addressed. E-mail: Marco.Guazzi{at}unimi.it.

Lone atrial fibrillation may be associated with daily-life disability and exercise limitation. The extracardiac pathophysiology of these effects is poorly explored. In 35 subjects with lone atrial fibrillation (mean age 67±7 years) we investigated pulmonary function, symptom-limited cardiopulmonary exercise performance, muscle ergoreflex (handgrip exercise) contribution to ventilation and brachial artery flow-mediated dilation (as a measure of endothelial function) before and after (average interval 20±5 days) restoring sinus rhythm with external cardioversion. Respiratory volumes and lung diffusing capacity at rest were within normal limits during both atrial fibrillation and after restoring sinus rhythm. Cardioversion was associated with the following changes: a decrease of the slope of exercise ventilation vs carbon dioxide (CO2) production (from 35±5 to 29±3; p<0.01) and of dyspnea sensation (Borg scale from 4 to 2) and an increase of peak oxygen uptake (VO2) (from 16±4 to 20±5 ml.min-1.kg-1; p<0.01), VO2 at anaerobic threshold (from 11±2 to 13±2 ml.min-1.kg-1; p<0.05) and O2 pulse (from 8±3 to 11±3 ml.beat-1; p<0.01). After cardioversion, the observed improvement in ventilatory efficiency was accompanied by a significant peak end-tidal CO2 increase (from 33±2 to 37±2 mmHg; p<0.01) and no changes in dead space to tidal volume ratio (from 0.23±0.03 to 0.23±0.02; p=ns). In addition, the ergoreflex contribution to ventilation was remarkably attenuated, and the brachial artery flow-mediated dilatation significantly augmented (from 0.32±0.07 to 0.42±0.08 mm; p<0.01). Ten patients had atrial fibrillation relapse, and, compared to values after restoration of regular sinus rhythm, invariably showed worsening of endothelial function, exercise ventilatory efficiency and muscle ergoreflex contribution to ventilation. In subjects with lone atrial fibrillation, an impairment in ventilatory efficiency appears to be involved in the pathophysiology of exercise limitation, and to be primarily related with a demodulated peripheral control of ventilation.




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