Document Detail


New perspectives concerning feedback influences on cardiorespiratory control during rhythmic exercise and on exercise performance.
MedLine Citation:
PMID:  22826128     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The cardioaccelerator and ventilatory responses to rhythmic exercise in the human are commonly viewed as being mediated predominantly via feedforward 'central command' mechanisms, with contributions from locomotor muscle afferents to the sympathetically mediated pressor response. We have assessed the relative contributions of three types of feedback afferents on the cardiorespiratory response to voluntary, rhythmic exercise by inhibiting their normal 'tonic' activity in healthy animals and humans and in chronic heart failure. Transient inhibition of the carotid chemoreceptors during moderate intensity exercise reduced muscle sympathetic nerve activity (MSNA) and increased limb vascular conductance and blood flow; and reducing the normal level of respiratory muscle work during heavier intensity exercise increased limb vascular conductance and blood flow. These cardiorespiratory effects were prevented via ganglionic blockade and were enhanced in chronic heart failure and in hypoxia. Blockade of μ opioid sensitive locomotor muscle afferents, with preservation of central motor output via intrathecal fentanyl: (a) reduced the mean arterial blood pressure (MAP), heart rate and ventilatory responses to all steady state exercise intensities; and (b) during sustained high intensity exercise, reduced O(2) transport, increased central motor output and end-exercise muscle fatigue and reduced endurance performance. We propose that these three afferent reflexes - probably acting in concert with feedforward central command - contribute significantly to preserving O(2) transport to locomotor and to respiratory muscles during exercise. Locomotor muscle afferents also appear to provide feedback concerning the metabolic state of the muscle to influence central motor output, thereby limiting peripheral fatigue development.
Authors:
Jerome A Dempsey
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Publication Detail:
Type:  Lectures; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-07-23
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-10     Completed Date:  2013-02-11     Revised Date:  2013-09-03    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  4129-44     Citation Subset:  IM    
Affiliation:
John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin - Madison, 1300 University Ave, Room 4245 MSC, Madison, WI 53706-1532, USA. jdempsey@wisc.edu
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MeSH Terms
Descriptor/Qualifier:
Afferent Pathways / physiology
Animals
Awards and Prizes
Cardiovascular Physiological Phenomena
Carotid Body / physiology
Chemoreceptor Cells / physiology
Exercise / physiology*
Feedback, Physiological / physiology
Humans
Muscle, Skeletal / innervation,  physiology
Physical Endurance / physiology
Physical Exertion / physiology*
Physiology
Respiratory Muscles / innervation,  physiology
Respiratory Physiological Phenomena
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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