To date, the only ‘potential’ known mechanism documented was based on studies performed on mice (Mus musculus).
Like humans, mice possess a similar mode of lipid metabolism and respond to exercise in a similar fashion; that is, the greater the exercise’s intensity, the greater the response [8].
Mice also possess identical lipoprotein receptors found in their liver and adipose sites [8].
In a study performed by Garelnabi et al. (2005), mice exercised for two weeks showed a dramatic increase in scavenger receptor B1 (SR-B1), CD36, and LDLR [8].
SR-B1 and CD36 are multifunctional proteins known for their ability to recognize oxidized LDL and facilitate their removal via direct uptake in the liver. Likewise, LDLR mediates the cellular uptake and degradation of plasma LDL [8].
– This possibly suggests that LDL receptor mediated clearance of LDL could be important in the antiatherogenic benefits of exercise [8].
– There was a 2 to 3 fold increase in SR-BI expression in the exercising animals and a 4 fold induction of CD36 gene expression, suggesting that reverse cholesterol transport could play an important role in exercise-induced benefits [8].
