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1Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, and University of Texas Southwestern Medical Center-Dallas, Dallas, Texas; and 2Department of Comparative Bioscience, University of Wisconsin-Madison, Madison, Wisconsin
Submitted 21 July 2007 ; accepted in final form 6 November 2007
Arterial isocapnia is a hallmark of moderate exercise in humans and is maintained even when resting arterial PCO2 (PaCO2) is raised or lowered from its normal level, e.g., with chronic acid-base changes or acute increases in respiratory dead space. When resting ventilation and/or PaCO2 are altered, maintenance of isocapnia requires active adjustments of the exercise ventilatory response [slope of the ventilation (
E)-CO2 production (
CO2) relationship, 
E/
CO2]. On the basis of animal studies, it has been proposed that a central neural mechanism links the exercise ventilatory response to the resting ventilatory drive without need for changes in chemoreceptor feedback from rest to exercise, a mechanism referred to as short-term modulation (STM). We tested the hypothesis that STM is elicited by increased resting ventilatory drive associated with added external dead space (DS) in humans. Twelve young men were studied in control conditions and with added DS (200, 400, and 600 ml; randomized) at rest and during mild-to-moderate cycle exercise. 
E/
CO2 increased progressively as DS volume increased (P < 0.0001). While resting end-tidal PCO2 (PETCO2) increased with DS, the change in PETCO2 from rest to exercise was not increased, indicating that increased chemoreceptor feedback from rest to exercise cannot account for the greater exercise ventilatory response. We conclude that STM of the exercise ventilatory response is induced in young men when resting ventilatory drive is increased with external DS, confirming the existence of STM in humans.
exercise hyperpnea; respiratory control; hypercapnia
This article has been cited by other articles:
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C.-S. Poon The classic potentiation of exercise ventilatory response by increased dead space in humans is more than short-term modulation J Appl Physiol, July 1, 2008; 105(1): 390 - 390. [Full Text] [PDF] |
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H. E. Wood, G. S. Mitchell, and T. G. Babb Reply to Dr. Poon J Appl Physiol, July 1, 2008; 105(1): 391 - 391. [Full Text] [PDF] |
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