Physical inactivity is associated with increased cardiovascular disease, obesity, type II diabetes and some types of cancers. Studies have shown that genetics play a significant role in the regulation of voluntary physical activity. However, these studies involve ad libitum access to wheel running, which may cause confounded results due to a training effect, especially in inherently high active animals. This study investigated the levels of gene expression of four potential candidate genes that have been noted to be expressed differentially between high and low active animals: Myostatin (Mstn), Calsequestrin 1 (Casq1), Glucose Transporter member 4 (Slc2a4), and Leptin Receptor (Lepr). These genes where evaluated in previously used high active (C57L/J, n=6) and low active (C3H/HeJ, n=6) inbred mice that were housed with a locked running wheel. The locked wheel eliminated potential training effects on gene expression. Total RNA was isolated from soleus and nucleus accumbens tissue and quantitative real-time PCR was performed. Mstn, Casq1, and Slc2a4 were evaluated in soleus tissue while Lepr was assessed in the nucleus accumbens of the brain. Gene expression was calculated as a ratio of the cross point of the target gene to the control gene, RN18S. None of the potential candidate genes were found to be significantly different between high and low active animals [Mstn (p=.93), Casq1 (p=.63), and Slc2a4 (p=.27), Lepr (p=.09)]. These results suggest that if these four genes are involved in regulation of physical activity, their primary action is not exerted through differential gene expression. In conclusion, potential training effects of exposure to running wheels must be considered in future investigations of the mechanisms of physical activity.



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