Rodent models for resolving extremes of exercise and health

Garton, Fleur C., North, Kathryn N., Koch, Lauren G., Britton, Steven L., Nogales-Gadea, Gisela and Lucia, Alejandro (2016) Rodent models for resolving extremes of exercise and health. Physiological Genomics, 48 2: 82-92. doi:10.1152/physiolgenomics.00077.2015

Author Garton, Fleur C.
North, Kathryn N.
Koch, Lauren G.
Britton, Steven L.
Nogales-Gadea, Gisela
Lucia, Alejandro
Title Rodent models for resolving extremes of exercise and health
Journal name Physiological Genomics   Check publisher's open access policy
ISSN 1531-2267
Publication date 2016-02-01
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1152/physiolgenomics.00077.2015
Open Access Status Not yet assessed
Volume 48
Issue 2
Start page 82
End page 92
Total pages 11
Place of publication Bethesda, MD, United States
Publisher American Physiological Society
Language eng
Subject 1314 Physiology
1311 Genetics
Abstract The extremes of exercise capacity and health are considered a complex interplay between genes and the environment. In general, the study of animal models has proven critical for deep mechanistic exploration that provides guidance for focused and hypothesisdriven discovery in humans. Hypotheses underlying molecular mechanisms of disease and gene/tissue function can be tested in rodents to generate sufficient evidence to resolve and progress our understanding of human biology. Here we provide examples of three alternative uses of rodent models that have been applied successfully to advance knowledge that bridges our understanding of the connection between exercise capacity and health status. First we review the strong association between exercise capacity and all-cause morbidity and mortality in humans through artificial selection on low and high exercise performance in the rat and the consequent generation of the “energy transfer hypothesis.” Second we review specific transgenic and knockout mouse models that replicate the human disease condition and performance. This includes human glycogen storage diseases (McArdle and Pompe) and α-actinin-3 deficiency. Together these rodent models provide an overview of the advancements of molecular knowledge required for clinical translation. Continued study of these models in conjunction with human association studies will be critical to resolving the complex gene-environment interplay linking exercise capacity, health, and disease.
Keyword Disease
Genetic loci
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: HERDC Pre-Audit
Institute for Molecular Bioscience - Publications
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Created: Fri, 03 Nov 2017, 16:49:59 EST