<qa>  What is the primary purpose of the study?Both statin drugs and exercise training are known to exert anti-inflammatory effects. We found that both high levels of physical activity and an exercise training program reduced markers of inflammation and lowered monocyte Toll-like receptor 4 TLR4 expression. It has not been determined whether statins exert their anti-inflammatory effects through the toll-like receptors or whether combined statinexercise treatment will exert synergistic anti-inflammatory effects. Thus, the primary purposes of this study are two-fold: 1 Determine whether rosuvastatin treatment downregulates LPS-induced inflammatory responses, serum hsCRP, and monocyte TLR4 expression in hypercholesterolemic patients; and 2 Determine whether adding exercise training to rosuvastatin treatment induces an anti-inflammatory synergy and further lowers LPS-induced inflammatory response, hsCRP, and TLR4 expression. Thirty two hypercholesterolemic total cholesterol 200 mgdL, LDL 130 mgdL will be randomly divided into two groups: statin ST and statin and exercise STE. Sixteen physically active, no-statin subjects will also be recruited as a control groupCON. After baseline blood sampling, ST and STE groups will begin a 10-week course of rosuvastatin calcium treatment 10 mgd after which a second blood sample will be obtained. The STE group will then begin a 10 week three days per week combined endurance 20 min at 70 of heart rate reserve and resistive training 2 sets of 10 upper- and lower-body exercises program. The ST group will not exercise and both STE and ST groups will continue taking their medication, as prescribed. A final blood sample will be taken at the end of this 10-week segment. Blood samples will also be taken from the CON group at 0, 10 and 20 weeks. Monocyte expression of TLR4, CD14 LPS receptor and CD16 monocyte maturation marker will be assessed using flow cytometry. LPS-stimulated inflammatory cytokine production and serum levels of hsCRP, TNF-a, oxLDL, LDL, HDL, endotoxin, LPS binding protein, and sCD14 will also be measured at each time point baseline, 10 weeks, 20 weeks. These experiments will allow us to determine whether rosuvastatin downregulates TLR4, an important mediator of inflammation, and whether exercise, known to lower TLR4 expression, can augment the rosuvastatin effects. Regular exercise and statin treatment are known to reduce disease risk, but the benefits of these treatments is infrequently attributed to their anti-inflammatory effects. It is important to document mechanisms of anti-inflammatory action for exercise training and statin treatment and to determining whether these treatments have combined beneficial effects. 