Skeletal muscle is adapting to the needs of the body by changes of various gene expression that control mitochondrial biogenesis, angiogenesis, and the composition of muscle fiber types. Recently, it was revealed that PGC-1α, which is an auxiliary transcription factor, plays a key role in the aforementioned adaptation phenomena. It means that various signal transduction systems within muscle directly affect the expression and activation of PGC-1α and also PGC-1s activates various programs for muscle adaptation. Therefore, this review assessed PGC-1α to understand the reaction and adaptation phenomena of muscle against the biological stimulus such as exercise and came to the conclusion that PGC-1α and PGC-1β significantly affect skeletal muscle in various ways, and also have an affect on the increase of exercise capacity, inducing of angiogenesis and the prevention of muscle atrophy and degeneration.

Decreases in high-density lipoprotein cholesterol (HDL-C) levels are associated with an increased risk of coronary artery disease (CAD), whereas increased HDL-C levels are related to a decreased risk of CAD and myocardial infarction. Although HDL prevents the oxidation of low-density lipoprotein under normal conditions, it triggers a structural change, inhibiting antiarteriosclerotic and anti-inflammatory functions, under pathological conditions such as oxidative stress, inflammation, and diabetes. HDL can transform into various structures based on the quantitative reduction and deformation of apolipoprotein A1 and is the primary cause of increased levels of dysfunctional HDL, which can lead to an increased risk of CAD. Therefore, analyzing the structure and components of HDL rather than HDL-C after the application of an exercise training program may be useful for understanding the effects of HDL.

The objective of this study was to analyze the effects of aerobic and resistance exercise on myokines expression in the skeletal muscle of middle-aged rats with high fat diet-induced obesity, to investigate the feasibility of using exercise training to reduce inflammation. Male 50-week-old Sprague Dawley rats were divided into normal diet, normal diet + exercise, high fat diet, and high fat diet + exercise groups. After six weeks on a high fat diet to induce obesity, a 12-week exercise program was implemented, which combined aerobic exercise (treadmill running) and resistance exercise (ladder climbing) three times a week for 75 min per session. We analyzed the protein levels of interleukins (IL) 6, 7, and 8, C-X-C motif chemokine receptor 2, and vascular endothelial growth factor in skeletal muscles by western blotting. Body weight decreased significantly during the 12-week exercise program in the exercise groups compared to the non-exercise groups (p < 0.05). The levels of all myokines analyzed were significantly lower in the skeletal muscle of the high fat diet group compared to the normal diet group (p < 0.05). After completing the 12-week exercise program, IL-7, IL-8, C-X-C motif chemokine receptor 2, and vascular endothelial growth factor expressions were significantly higher in the high fat diet + exercise group compared to the high fat diet group (p < 0.05). However, while IL-6 expression was significantly lower in the high fat diet and high fat diet + exercise groups compared to the normal diet group (p < 0.05), it was not significantly affected by exercise. In conclusion, high fat diet-induced obesity resulted in decreased myokines in the skeletal muscles, but combined exercise training of aerobic and resistance exercise increased myokines secretion in the skeletal muscle of obese rats, and is thought to help reduce inflammation.

We investigated the change in myokine expression related to hypertrophy (IL-4, IL-6, IL-10) and atrophy (TNF-α, NFκB, IL-1β) in middle-aged rats after resistance exercise with ladder climbing. 50- and 10-week-old male Wistar rats were randomly assigned to two groups: the sedentary and exercise groups. The exercise groups underwent a ladder-climbing exercise for 8 weeks. While the tibialis anterior muscle mass in the young group significantly increased after the ladder-climbing exercise, the middle-aged group did not show any changes after undergoing the same exercise. To understand the molecular mechanism causing this difference, we analyzed the change in hypertrophy- and atrophy-related myokine levels from the tibialis anterior muscle. After 8 weeks of ladder-climbing exercise, the IL-4 and IL-10 protein levels did not change. However, the IL-6 level significantly increased after exercise training, but the amount of increase in the young training group was higher than in the middle-aged training group. IL-1β and TNF-α as well as NFκB protein levels were significantly higher in the middle-aged group than in the young group. Except for TNF-α, exercise training did not affect IL-1β and NFκB protein levels. The TNF-α level significantly decreased in the middle-aged exercise training group. AMPK and PGC-1α levels also significantly increased after exercise training, but there was no difference between age-related groups. Therefore, 8-week high-intensity exercise training using ladder climbing downregulates the skeletal muscle production of myokine involved in atrophy and upregulates hypertrophic myokine. However, the extent of these responses was lower in the middle-aged than young group.