별지 2. 2016 IMPACT 심포지엄 초록접수양식

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Effects of Aging and Exercise Training on Mitochondrial Function and Insulin Resistance

in Rat Skeletal Muscle

Mi Hyun No1, Han Sam Jo2, Mal Soon Shin2, Chang Ju Kim2, Hyo Bum Kwak1,*

1Department of Kinesiology, Inha University, Incheon 402-751, Korea; 2Department of Physiology, KyungHee University, Seoul 130-701, Korea

Aging is characterized by a progressive loss of muscle mass and muscle strength called ‘sarcopenia’. Age-related muscle atrophy is due to loss of muscle fibers associated with mitochondrial dysfunction. Accumulating evidence shows that impairment in skeletal muscle mitochondria with aging is thought to play a primary role in insulin resistance. The development of insulin resistance, particularly in skeletal muscle (organ of insulin-mediated glucose disposal), is closely associated with type II diabetes. The purpose of this study was to identify the role of exercise in aging-induced sarcopenia,mitochondrial dysfunction, and insulin resistance in rat skeletal muscles. Four and 20 month old Fischer 344 rats were randomly assigned to young sedentary (YS), young exercise (YE), old sedentary (OS), or old exercise (OE) groups. Exercise training groups ran on a treadmill at 15 m/min (young) or 10 m/min (old), 45 min/day, 5 day/week for 8 weeks. The skeletal muscles such as soleus (SOL, Type I) and white gastrocnemius (WG, Type IIb) were permeabilized by sarponin for determination of mitochondrial respiratory capacity, Ca2+ retention capacity, and mitochondrial H2O2 emission. Exercise training attenuated age-induced decrease in only gastrocnemius (Type II) mass. Insulin resistance by oral glucose tolerance test was elevated in OS rats. However, exercise training preserved whole body insulin sensitivity in OE rats. The mitochondrial respiratory capacity and Ca2+ retention capacity were decreased by aging and protected by exercise training in both SOL and WG. In addition, exercise attenuated age-induced mitochondrial H2O2 emitting potential in both SOL and WG. These data demonstrate that regular exercise training prevents the impairment of mitochondrial function in skeletal muscles as well as sarcopeniainduced by aging, supporting the concept that the exercise regulation of mitochondrial dysfunction with aging is a primary factor protecting against aging-induced sarcopenia and insulin resistance in skeletal muscle.

Key words: aging, exercise, mitochondrial function, insulin resistance, skeletal muscle