The skeletal muscles of animals and humans with type 2 diabetes have decreased oxidative capacity. Aerobic exercise can improve muscle oxidative capacity, but no data are available on the amount of exercise required. We investigated the effects of voluntary running exercise and running distance on the skeletal muscle properties of nonobese rats with type 2 diabetes. Six-week-old male diabetic Goto-Kakizaki rats were divided into nonexercised (GK) and exercised (GK-Ex) groups. The rats in the GK-Ex group were permitted voluntary running exercise on wheels for 6 weeks. Age-matched male Wistar rats (WR) were used as nondiabetic controls. Fasting blood glucose and HbA1c levels were higher in the GK and GK-Ex groups than in the WR group and lower in the GK-Ex group than in the GK group. Succinate dehydrogenase (SDH) activity and peroxisome proliferator-activated receptor γ coactivator-1α (Pgc-1α) mRNA levels in the soleus and plantaris muscles were higher in the WR and GK-Ex groups than in the GK group. HbA1c and total cholesterol levels were negatively correlated with running distance and SDH activity and Pgc-1α mRNA levels in the soleus muscle were positively correlated with running distance. The onset and progression of diabetes in nonobese diabetic rats were effectively inhibited by running longer distances.
Myostatin (MSTN), an important negative regulator of skeletal muscle, plays an important role in skeletal muscle health. In previous study, we found that the expression of MSTN was different during skeletal muscle injury repair. Therefore, we explored the expression changes of MSTN at different time points during skeletal muscle injury repair after eccentric exercise. In addition, MSTN is regulated by follistatin (FST) and decorin (DCN) in vivo, so our study examined the time-specific changes of FST, DCN and MSTN in the circulation and skeletal muscle during skeletal muscle injury repair after eccentric exercise, and to explore the reasons for the changes of MSTN in the process of exercise-induced muscle injury repair, to provide a basis for promoting muscle injury repair. The rats performed one-time eccentric exercise. Blood and skeletal muscle were collected at the corresponding time points, respectively immediate after exercise (D0), one day (D1), two days (D2), three days (D3), seven days (W1) and fourteen days (W2) after exercise (n=8). The levels of MSTN, FST, DCN in serum and mRNA and protein expression in muscle were detected. MSTN changes in the blood and changes in DCN and FST showed the opposite trend, except immediately after exercise. The change trends of mRNA and protein of gastrocnemius DCN and MSTN are inconsistent, there is post-transcriptional regulation of MSTN and DCN in gastrocnemius. Acute eccentric exercise might stimulate the secretion of DCN and FST into the circulation and inhibit MSTN. MSTN may be regulated by FST and DCN after acute eccentric exercise.
Rheumatoid arthritis (RA) and its animal model adjuvant arthritis (AA) are inflammatory diseases characterized by chronic inflammation, systemic oxidative stress and disturbed mitochondrial bioenergetics of skeletal muscle. The present study aimed to evaluate the effects of coenzyme Q10 - CoQ10 (100 mg/kg b.w.), omega-3-polyunsaturated fatty acids - ω-3-PUFA (400 mg/kg b.w.) and their combined treatment in AA on impaired skeletal muscle mitochondrial bioenergetics, inflammation and changes in levels CoQ9 and CoQ10 in plasma. Markers of inflammation (C-reactive protein, monocytechemotactic protein-1), antioxidant capacity of plasma, respiratory chain parameters of skeletal muscle mitochondria and concentrations of CoQ9 and CoQ10 in plasma and in muscle tissue were estimated. Treatment of the arthritic rats with CoQ10, ω-3-PUFA alone and in combination partially reduced markers of inflammation and increased antioxidant capacity of plasma, significantly increased concentrations of coenzyme Q in mitochondria and improved mitochondrial function in the skeletal muscle. Combined treatment has similar effect on the mitochondrial function as monotherapies; however, it has affected inflammation and antioxidant status more intensively than monotherapies. Long-term supplementary administration of coenzyme Q10 and ω-3-PUFA and especially their combination is able to restore the impaired mitochondrial bioenergetics and antioxidant status in AA., Jarmila Kucharská, Silvester Poništ, Oľga Vančová, Anna Gvozdjáková, Oľga Uličná, Lukáš Slovák, Mohsen Taghdisiesfejir, Katarína Bauerová., and Obsahuje bibliografii