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Control of Breathing During Exercise

  1. Hubert V. Forster1,
  2. Philippe Haouzi2,
  3. Jerome A. Dempsey3

Published Online: 1 JAN 2012

DOI: 10.1002/cphy.c100045

Comprehensive Physiology

Comprehensive Physiology

How to Cite

Forster, H. V., Haouzi, P. and Dempsey, J. A. 2012. Control of Breathing During Exercise. Comprehensive Physiology. 2:743–777.

Author Information

  1. 1

    Medical College of Wisconsin, Department of Physiology, Milwaukee, Wisconsin

  2. 2

    Pennsylvania State University, College of Medicine and Department of Pulmonary Medicine and Heart and Vascular Institute, Penn State Milton Hershey Medical Center, Hershey, Pennsylvania

  3. 3

    The John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin

Publication History

  1. Published Online: 1 JAN 2012


During exercise by healthy mammals, alveolar ventilation and alveolar-capillary diffusion increase in proportion to the increase in metabolic rate to prevent PaCO2 from increasing and Pao2 from decreasing. There is no known mechanism capable of directly sensing the rate of gas exchange in the muscles or the lungs; thus, for over a century there has been intense interest in elucidating how respiratory neurons adjust their output to variables which can not be directly monitored. Several hypotheses have been tested and supportive data were obtained, but for each hypothesis, there are contradictory data or reasons to question the validity of each hypothesis. Herein, we report a critique of the major hypotheses which has led to the following conclusions. First, a single stimulus or combination of stimuli that convincingly and entirely explains the hyperpnea has not been identified. Second, the coupling of the hyperpnea to metabolic rate is not causal but is due to of these variables each resulting from a common factor which link the circulatory and ventilatory responses to exercise. Third, stimuli postulated to act at pulmonary or cardiac receptors or carotid and intracranial chemoreceptors are not primary mediators of the hyperpnea. Fourth, stimuli originating in exercising limbs and conveyed to the brain by spinal afferents contribute to the exercise hyperpnea. Fifth, the hyperventilation during heavy exercise is not primarily due to lactacidosis stimulation of carotid chemoreceptors. Finally, since volitional exercise requires activation of the CNS, neural feed-forward (central command) mediation of the exercise hyperpnea seems intuitive and is supported by data from several studies. However, there is no compelling evidence to accept this concept as an indisputable fact. © 2012 American Physiological Society. Compr Physiol 2:743-777, 2012.