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J Appl Physiol (November 23, 2001). doi:10.1152/japplphysiol.00724.2001
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Articles in PresS, published online ahead of print November 23, 2001
J Appl Physiol, 10.1152/jap.00724.2001
Submitted on July 11, 2001
Accepted on November 17, 2001

EXERCISE HYPERPNEA IN CHRONIC HEART FAILURE: RELATIONSHIPS TO LUNG STIFFNESS AND EXPIRATORY FLOW LIMITATION

PierGiuseppe Agostoni1, Riccardo Pellegrino2, Cristina Conca1, Joseph R Rodarte3, and Vito Brusasco4*

1 Istituto di Cardiologia, Universita di Milano, Milano, Italy
2 Fisiopatologia Respiratoria e Cardiologia, Azienda S. Croce e Carle, Cuneo, Italy
3 Pulmonary Section, Baylor College of Medicine, Houston, Texas, USA
4 Dipartimento di Scienze Motorie e Riabilitative, Universita di Genova, Genova, Italy

* To whom correspondence should be addressed. E-mail: brusasco{at}dism.unige.it, oftedahl.lynette@mayo.edu.

The changes in breathing pattern and lung mechanics in response to incremental exercise were compared in 14 subjects with chronic heart failure and 15 normal subjects. In chronic heart failure subjects, exercise hyperpnea was achieved by increasing breathing frequency more than tidal volume. The rate of increase in breathing frequency with carbon dioxide output was inversely correlated (r = -0.61, p<0.05) with dynamic lung compliance measured at rest, but not with static lung compliance either at rest or at maximum exercise. Although decrease in expiratory flow reserve near functional residual capacity in chronic heart failure occurred earlier with exercise than in the normal subjects (p <0.01), it was not correlated with changes in breathing pattern or occurrence of tachypnea. Tachypnea was achieved in chronic heart failure subjects with an increase in duty cycle, due to a greater than normal decrease in expiratory time with exercise. We conclude that in chronic heart failure pre-existing increase in lung stiffness plays a significant role in causing tachypnea during exercise. The results of the present study do not support the hypothesis that dynamic compression of the airways downstream from the flow limiting segment occurring during exercise contributes to hyperpnea.




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