Journal of Applied Physiology
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J Appl Physiol (June 25, 2004). doi:10.1152/japplphysiol.00365.2004
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Submitted on April 5, 2004
Accepted on June 18, 2004

IMPROVEMENT OF ALVEOLAR-CAPILLARY MEMBRANE DIFFUSING CAPACITY WITH EXERCISE TRAINING IN CHRONIC HEART FAILURE

Marco Guazzi1*, Giuseppe Reina2, Gabriele Tumminello1, and Maurizio Guazzi3

1 Cardiology Division, San Paolo Hospital, Cardiopulmonary Laboratory, University of Milano, Milano, Italy
2 Institute of Statistics and Biometry, University of Milano, Milano, Italy
3 Institute of Cardiology, University of Milano, Milano, Italy

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

Chronic heart failure (CHF) may impair pulmonary gas diffusing capacity, an effect that contributes to exercise limitation. We sought to investigate whether improvement of diffusing ability is one of the mechanisms whereby physical training increases aerobic efficiency in this disease. 16 CHF patients were trained (40-min stationary braked cycling, 4 times/week) for 8 weeks; 15 sedentary similar patients were followed-up as controls. Training increased lung diffusion (DLco+25%) alveolar-capillary conductance (DM+15%), pulmonary capillary blood volume (VC+10%), peak exercise O2 uptake (peak VO2+13%), VO2 at anaerobic threshold (VO2 AT+20%), and decreased the slope of exercise ventilation to CO2 output (VE/VCO2-14%). Training also improved the flow-mediated brachial artery dilation (BAD: from 4.8±0.4 to 8.2±0.4%). All these changes were significant compared with baseline and controls. Hemodynamics were obtained in the last 10 patients enrolled in each group. Training did not affect hemodynamics at rest, and enhanced the increase of cardiac output (+226% vs +187%) and stroke volume (+59% vs +49%) and the decrease of pulmonary arteriolar resistance (-28% vs -13%), at peak exercise. Hemodynamics were unchanged in controls after 8 weeks. Variations with training in DLco and DM correlated with those in peak VO2 (r=0.64, p =0.007 and r= 0.51, p=0.04, respectively) and with those in BAD (r=0.78, p<0.001 and r=0.50, p=0.04, respectively). After detraining (8 weeks), DLco, DM, VC, peak VO2, VO2 AT, VE/VCO2 slope, cardiac output, stroke volume, pulmonary arteriolar resistance at peak exercise and BAD reverted to levels similar to baseline and to those in controls. Our results document, for the first time, that exercise training improves the alveolar-capillary membrane diffusing capacity in CHF, and support the possibility that this effect may contribute to the enhancement of exercise performance.




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