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Symposium Reports |
1 Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK
Abstract
Below the lactate threshold (
L), ventilation
responds in close proportion to CO2 output
to regulate arterial partial pressure of CO2
. While ventilatory control models have traditionally included proportional feedback (central and carotid chemosensory) and feedforward (central and peripheral neurogenic) elements, the mechanisms involved remain unclear. Regardless, putative control schemes have to accommodate the close dynamic coupling between
and
. Above
L,
is driven down to constrain the fall of arterial pH by a compensatory hyperventilation, probably of carotid body origin. When
requirements are high (as in highly fit endurance athletes),
can attain limiting proportions. Not only does this impair gas exchange at these work rates, but there may be an associated high metabolic cost for generation of respiratory muscle power, which may be sufficient to divert a fraction of the cardiac output away from the muscles of locomotion to the respiratory muscles, further compromising exercise tolerance.
(Received 18 December 2006;
accepted after revision 15 January 2007; first published online 18 January 2007)
Corresponding author S. A. Ward: Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK. Email: s.a.ward{at}leeds.ac.uk
This article has been cited by other articles:
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S. A. Ward Muscle-energetic and cardio-pulmonary determinants of exercise tolerance in humans: Muscle-energetic and cardio-pulmonary determinants of exercise tolerance in humans Exp Physiol, March 1, 2007; 92(2): 321 - 322. [Full Text] [PDF] |
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