Linked Life Data

3128524

Source:http://linkedlifedata.com/resource/pubmed/id/3128524

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1988-5-13
pubmed:abstractText
We studied the role of central command mediation of exercise hyperpnea by comparing the ventilatory and arterial CO2 partial pressure (PaCO2) responses to voluntary (ExV) and electrically induced (ExE) muscle contractions in normal, awake human subjects. We hypothesized that if central command signals are critical to a normal ventilatory response, then ExE should cause a slower ventilatory response resulting in hypercapnia at the onset of exercise. ExE was induced through surface electrodes placed over the quadriceps and hamstring muscles. ExE and ExV produced leg extension (40/min) against a spring load that increased CO2 production (VCO2) 100-1,000 ml/min above resting level. PaCO2 and arterial pH during work transitions and in the steady state did not differ significantly from rest (P greater than 0.05) or between ExE and ExV. The temporal pattern of ventilation, tidal volume, breathing frequency, and inspired and expired times, and the ventilation-VCO2 relationship were similar between ExE and ExV. We conclude that since central command was reduced and/or eliminated by ExE, central command is not requisite for the precise matching of alveolar ventilation to increases in VCO2 during low-intensity muscle contractions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
218-25
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Ventilatory and PaCO2 responses to voluntary and electrically induced leg exercise.
pubmed:affiliation
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.