Aging is associated with a progressive decline in skeletal muscle mass and strength. The decline, known as sarcopenia, could lead to physical disability, poor quality of life, and death. In addition, the older population usually experiences age-related muscle changes that affect muscle mass and functional abilities. Skeletal muscle is a highly dynamic organ that is responsible for generating movement required for the activities of daily living, peak physical performance, and metabolic health. Indeed, progressive decline in skeletal muscle function with age is associated with metabolic dysfunction, chronic disease susceptibility, loss of mobility, and an overall increase in mortality rate. Thus sarcopenia are highly prevalent and important risk factors for disability and increased mortality in individuals as they age. Normal muscle mass and function maintenance is thought to be dependent on the dynamic balance between positive and negative regulators of muscle growth. Emerging evidence suggests that bone morphogenetic proteins (BMPs), brain-derived neurotrophic factor (BDNF), follistatin (FST), and irisin could function as positive muscle growth regulators, whereas activins A and B, myostatin, growth and differentiation factor-15 (GDF-15), and transforming growth factor-beta (TGF-beta) negatively regulate muscle growth. Ample of studies have suggested that resistance exercise training and long-term, high intensity endurance exercise training may ameliorate sarcopenia and induce skeletal muscle hypertrophy and age-dependent adaptations in myofiber function. However, the effect of moderate-intensity endurance exercise training on prevent/delay age-related skeletal muscle sarcopenia is in controversy. Our previous study has demonstrated that light moderate endurance training may stimulate satellite cell activation, and might contribute to the growth in myocytes. Recently, an intensive study demonstrated that long-term leisure-time physical activity might reduce age-related muscle wasting. In recent years, many studies have confirmed that zebrafish exhibit a decline in whole-organism performance and trainability with age. These findings closely resemble the senescence-related declines in physical ability experienced by humans and mammalian aging models and therefore support the use of zebrafish as a model for human exercise and aging. Based on the above-mentioned points, we hypothesize that long-term moderate-intensity endurance exercise training may ameliorate sarcopenia and change in muscle morphology and activity in aging populations using a zebrafish model. The specific aims of this 2-year project are as follows: (1) to assess sprint and endurance swimming abilities, and ability to perform routine behaviors after long-term moderate-intensity endurance exercise training, (2) to determine if the exercise training can diminish the deleterious effects of aging through activation of myofiber hypertrophy, (3) to investigate levels of the positive regulators (BMPs, BDNF, FST, and irisin) and the negative regulators (activins A and B, myostatin, GDF-15, and TGF-beta) of muscle mass using Western blotting analysis after long-term moderate-intensity endurance exercise training.
|Effective start/end date||8/1/18 → 7/1/20|
- endurance exercise
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