Our first major objective is to determine whether or not rats that exercise regularly live longer than freely eating sedentary controls, or than paired weight sedentary controls that are food restricted to maintain their body weights the same as those of the exercisers. Our second major objective is to determine whether exercise slows, or compensates for, certain of the deleterious changes in structure and function that occur with aging. We propose to evaluate the effects of exercise on changes with age in: 1. the respiratory capacity of heart and skeletal muscle; 2. the size, number and structure of skeletal muscle fibers; 3. the O2 uptake capacity, fatigue resistance, and high energy phosphage stores of skeletal muscle; 4. the contractile properties of fast-twitch and slow-twitch skeletal muscles; 5. the prolongation of the time to peak tension and the half relaxation time of the myocardium; 6. the rate of protein synthesis in the cerebral cortex; 7. thyroid hormone turnover; 8. whole body minimal O2 composition; 9. obesity, lean body mass, and bone; 10. glucose tolerance and insulin sensitivity; and 11. the sensitivity of the pancreas (beta-cells) to stimulation of insulin release by glucose and arginine, and on the maximum capacity to secrete insulin. Our third objective is to further test the validity of the """"""""rate of living"""""""" theory of aging by determining the effect on longevity of elevation of metabolic rate in rats by means of cold exposure.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Project (R01)
Project #
5R01AG000425-21
Application #
3114069
Study Section
Respiratory and Applied Physiology Study Section (RAP)
Project Start
1978-07-01
Project End
1987-06-30
Budget Start
1985-07-01
Budget End
1986-06-30
Support Year
21
Fiscal Year
1985
Total Cost
Indirect Cost
Name
Washington University
Department
Type
Schools of Medicine
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
Koh, Jin-Ho; Hancock, Chad R; Terada, Shin et al. (2017) PPAR? Is Essential for Maintaining Normal Levels of PGC-1? and Mitochondria and for the Increase in Muscle Mitochondria Induced by Exercise. Cell Metab 25:1176-1185.e5
Leong, Josiah K; Pestilli, Franco; Wu, Charlene C et al. (2016) White-Matter Tract Connecting Anterior Insula to Nucleus Accumbens Correlates with Reduced Preference for Positively Skewed Gambles. Neuron 89:63-9
Kim, Sang Hyun; Koh, Jin Ho; Higashida, Kazuhiko et al. (2015) PGC-1? mediates a rapid, exercise-induced downregulation of glycogenolysis in rat skeletal muscle. J Physiol 593:635-43
Kim, Sang Hyun; Asaka, Meiko; Higashida, Kazuhiko et al. (2013) ?-Adrenergic stimulation does not activate p38 MAP kinase or induce PGC-1? in skeletal muscle. Am J Physiol Endocrinol Metab 304:E844-52
Higashida, Kazuhiko; Kim, Sang Hyun; Jung, Su Ryun et al. (2013) Effects of resveratrol and SIRT1 on PGC-1? activity and mitochondrial biogenesis: a reevaluation. PLoS Biol 11:e1001603
Holloszy, John O (2013) ""Deficiency"" of mitochondria in muscle does not cause insulin resistance. Diabetes 62:1036-40
Han, Dong-Ho; Kim, Sang Hyun; Higashida, Kazuhiko et al. (2012) Ginsenoside Re rapidly reverses insulin resistance in muscles of high-fat diet fed rats. Metabolism 61:1615-21
Han, Dong-Ho; Hancock, Chad R; Jung, Su Ryun et al. (2011) Deficiency of the mitochondrial electron transport chain in muscle does not cause insulin resistance. PLoS One 6:e19739
Higashida, Kazuhiko; Kim, Sang Hyun; Higuchi, Mitsuru et al. (2011) Normal adaptations to exercise despite protection against oxidative stress. Am J Physiol Endocrinol Metab 301:E779-84
Hancock, Chad R; Han, Dong-Ho; Higashida, Kazuhiko et al. (2011) Does calorie restriction induce mitochondrial biogenesis? A reevaluation. FASEB J 25:785-91

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