Document Detail


Modulation of cardiac contractility by muscle metaboreflex following efforts of different intensities in humans.
MedLine Citation:
PMID:  16782848     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Accumulation of metabolic end products within skeletal muscle stimulates sensory nerves, thus evoking a pressor response termed "metaboreflex." The aim of this study was to evaluate changes in hemodynamics occurring during metaboreflex activation obtained by postexercise muscle ischemia (PEMI) after two different exercise intensities. In twelve healthy subjects, the metaboreflex was studied with the PEMI method at the start of recovery from one leg-dynamic knee extension performed at intensities of 30% (PEMI 30%) and 70% (PEMI 70%) of the maximum workload achieved in a preliminary test. Control exercise recovery tests at the same intensities were also conducted. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were that 1) during metaboreflex, exercise conducted against the higher workload caused a more pronounced blood pressure increase than the strain conducted against the lower workload; and 2) during PEMI 70%, this blood pressure response was mainly achieved through enhancement of myocardial contractility that increased stroke volume and, in turn, cardiac output, whereas during PEMI 30%, the blood pressure response was reached predominantly by means of vasoconstriction. Thus a substantial enhancement of myocardial contractility was reached only in the PEMI 70% test. These results suggest that hemodynamic regulation during metaboreflex engagement caused by PEMI in humans is dependent on the intensity of the previous effort. Moreover, the cardiovascular response during metaboreflex is not merely achieved by vasoconstriction alone, but it appears that there is a complex interplay between peripheral vasoconstriction and heart contractility recruitment.
Authors:
Antonio Crisafulli; Enrico Salis; Gianluigi Pittau; Luigi Lorrai; Filippo Tocco; Franco Melis; Pasquale Pagliaro; Alberto Concu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-06-16
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  291     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-11-08     Completed Date:  2007-01-16     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H3035-42     Citation Subset:  IM    
Affiliation:
Dept. of Science Applied to Biological Systems, University of Cagliari, 09124 Cagliari, Italy. crisafulli@tiscali.it
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MeSH Terms
Descriptor/Qualifier:
Adult
Blood Pressure / physiology
Cardiac Output / physiology
Cardiography, Impedance
Exercise / physiology*
Humans
Male
Muscle, Skeletal / innervation*,  metabolism*
Myocardial Contraction / physiology*
Neurons, Afferent / physiology*
Physical Exertion / physiology
Stroke Volume / physiology
Vascular Resistance / physiology
Vasoconstriction / physiology

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


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