Document Detail

Exercise assessment of transgenic models of human cardiovascular disease.
MedLine Citation:
PMID:  12746466     Owner:  NLM     Status:  MEDLINE    
Exercise provides one of the most severe, yet physiological, stresses to the intact cardiovascular system and is a major determinant of the utilization of metabolic substrates. The adaptations to exercise are the result of a coordinated response of multiple organ systems, including cardiovascular, pulmonary, endocrine-metabolic, immunologic, and skeletal muscle. With the proliferation of genetically altered murine models of cardiovascular disease, the importance of developing methods of accurate physiological phenotyping is critical. There are numerous examples of transgenic models in which the baseline cardiovascular phenotype is unchanged or minimally changed from the wild type, only to become manifest during the stress of exercise testing. In this review, we cover the basics of the murine cardiovascular response to exercise and the importance of attending to strain differences, compare different exercise methodologies (constant workload treadmill, incremental workload treadmill, swimming) and hemodynamic monitoring systems, and examine the murine response to exercise conditioning. Several examples where exercise studies have contributed to the elucidation of cardiovascular phenotypes are reviewed: the beta-adrenergic receptor knockouts, phospholamban knockout, dystrophin knockout (mdx), and the mutant alpha-myosin heavy chain (R403Q) transgenic.
Daniel Bernstein
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Publication Detail:
Type:  Journal Article; Review     Date:  2003-05-13
Journal Detail:
Title:  Physiological genomics     Volume:  13     ISSN:  1531-2267     ISO Abbreviation:  Physiol. Genomics     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-05-14     Completed Date:  2003-06-06     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  9815683     Medline TA:  Physiol Genomics     Country:  United States    
Other Details:
Languages:  eng     Pagination:  217-26     Citation Subset:  IM; S    
Division of Pediatric Cardiology, Stanford University, Palo Alto, California 94304, USA.
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MeSH Terms
Cardiovascular Diseases / physiopathology*
Disease Models, Animal*
Mice, Transgenic / physiology*
Physical Conditioning, Animal / physiology*

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