الفهرس 
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Abstract
The present investigation aimed to study the effect of exogenous CoQ10 supplementation on SIM in experimentally induced hypercholesterolemia in rats. To achieve this aim, fifty male albino rats were used. Rats were divided into five experimental groups; normal, hypercholesterolemic non-treated, hypercholesterolemic CoQ10-treated, hypercholesterolemic atorvastatin-treated and hypercholesterolemic combined CoQ10&atorvastatin-treated groups. By the end of the experimental period, rats were subjected to exercise endurance test. Then blood samples were collected, from the retro-orbital venous plexus, for estimation of lipid profile, CPK, L/P ratio, MDA and TAC. Rats were then sacrificed and hemi-diaphragm was dissected free and mounted in organ bath for recording the strength of muscle contraction at the start and after 30 min activity. Glucose uptake by hemi-diaphragm was estimated in samples from the bathing solution after 30 min activity and 30 min recovery. After that, samples from gastrocnemius muscles were dissected free and fixed in formalin 10% solution for histopathology by using both H&E stain and caspase 3 immune marker.
Hypercholesterolemic non-treated group showed that exercise endurance capacity was significantly lower when compared to the corresponding value in normal group. This was explained by the significantly higher plasma lipids, L/P ratio and MDA and significantly lower TAC in hypercholesterolemic non-treated group in when compared to the corresponding values in normal group. Surprisingly, it was found that the in vitro strength of contraction of diaphragm at the start and after 30 min activity and glucose uptake by diaphragm after 30 min activity and 30 min recovery were insignificantly changed when compared to the
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corresponding values in normal group. this was directly attributed to insignificant change in plasma CPK level and the insignificant change in muscle structure or apoptosis when compared to normal group
Hypercholesterolemic CoQ10-treated group showed insignificant change in all the previously mentioned parameters except for MDA, which was significantly lower and TAC, which was significantly higher when compared to the corresponding values in hypercholesterolemic-non treated group. Also, there was non-significant changes in muscle structure and apoptosis by histopathology
Hypercholesterolemic atorvastatin-treated group showed that blood lipid, exercise endurance capacity, strength of contraction of diaphragm after 30 min activity and glucose uptake by diaphragm after 30 min activity and 30 min recovery were significantly lower. These results were explained by the significantly higher L/P ratio, MDA and CPK in hypercholesterolemic atorvastatin-treated group when compared to the corresponding values in hypercholesterolemic non-treated group. examination of hypercholesterolemic atorvastatin-treated group by H&E stain showed no prominent striation of muscle fibers, inflammatory infiltration and fibrosis. By caspase 3 marker showed sever apoptosis in most of muscle fibers.
Hypercholesterolemic combined CoQ10&atorvastatin-treated group showed that plasma lipids were significantly lower, while the exercise endurance capacity, strength of contraction of diaphragm after 30 min activity and glucose uptake by diaphragm after 30 min activity and 30 min recovery were significantly higher when compared to the corresponding
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values in hypercholesterolemic atorvastatin-treated group. These results were explained by the significantly lower CPK, L/P ratio & MDA, and significantly higher TAC when compared to the corresponding values in hypercholesterolemic atorvastatin-treated group. All the previously mentioned parameters were insignificantly changed when compared to the corresponding values in hypercholesterolemic non-treated, hypercholesterolemic CoQ10-treated groups.
The results of the present investigation cleared that CoQ10 alone had no detected beneficial effects on skeletal muscle performance in hypercholesterolemic rats; probably because its endogenous production is already sufficient in case of hypercholesterolemia.
Atorvastatin treatment has deleterious effects on skeletal muscle performance and provoke the incidence SIM. Many studies reported that SIM was related to reduction in the endogenous production of CoQ10, which led to mitochondrial dysfunction and oxidative stress imbalance.
Combining CoQ10 with atorvastatin during treatment of hypercholesterolemia was effective in preventing SIM by improving the mitochondrial function and reducing oxidative stress.