The overall aim of the proposed work is to determine whether or not endurance exercise during senescence will reverse the aging-related decline in the cellular properties of the myocardium, thereby leading to an improved myocardial function. Others have suggested that the decreased function of the sarcoplasmic reticulum may be an important factor in the slowing of the isometric contractile duration of cardiac muscle with aging. Moreover, myocardial protein synthesis apparently decreases as the organism ages from maturity to senescence. Therefore, this proposal deals with the examination of the sarcoplasmic reticulum and protein synthesis in greater detail in the hearts of adult and senescent rats followed by the determination of the responsiveness of these two parameters to endurance exercise. The ATP-dependent calcium transport properties of cardiac sarcoplasmic reticulum will be examined using biochemical and morphological techniques to determine (1) calcium flux in relation to the hydrolysis of ATP under a variety of conditions and (2) the density of the calcium transport ATPase, both in situ and in vitro. The rates of myocardial protein synthesis will be estimated for actin, cytochrome c, and ribosomal proteins. The levels of mRNA for both actin and cytochrome c will be measured. Both the sarcoplasmic reticulum and protein synthesis will be examined before and after specified periods of endurance exercise training during senescence. The isometric contractile parameters of isolated papillary muscle will be assessed at each time point of exercise training in order to determine any improvements in myocardial function. These studies will therefore determine the adaptability of cellular factors of the myocardium endurance exercise during senescence in relation to myocardial function. In this manner an insight into those mechanisms involved in the benefitual aspects of exercise during senescence may be gained.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Project (R01)
Project #
1R01AG006221-01
Application #
3117137
Study Section
Experimental Cardiovascular Sciences Study Section (ECS)
Project Start
1986-08-01
Project End
1989-07-31
Budget Start
1986-08-01
Budget End
1987-07-31
Support Year
1
Fiscal Year
1986
Total Cost
Indirect Cost
Name
Baylor College of Medicine
Department
Type
Schools of Medicine
DUNS #
074615394
City
Houston
State
TX
Country
United States
Zip Code
77030
Tate, C A; Helgason, T; Hyek, M F et al. (1996) SERCA2a and mitochondrial cytochrome oxidase expression are increased in hearts of exercise-trained old rats. Am J Physiol 271:H68-72
Taffet, G E; Michael, L A; Tate, C A (1996) Exercise training improves lusitropy by isoproterenol in papillary muscles from aged rats. J Appl Physiol 81:1488-94
Tehrani, M H; Tate, C A; al-Dahan, M I (1995) Age-related levels of GABA/benzodiazepine binding sites in cerebrum of F-344 rats: effects of exercise. Neurobiol Aging 16:199-204
Hamra, M; McNeil, R S (1995) Cardiac adrenergic responses and electrophysiology during ischemia: effect of exercise. Med Sci Sports Exerc 27:993-1002
Hyek, M F; Szilagyi, J E; Tate, C A (1995) A chronically instrumented rat model to assess the altered baroreflex due to exercise. Med Sci Sports Exerc 27:1339-44
Ball, K L; Solaro, R J (1994) Discoordinate regulation of contractile protein gene expression in the senescent rat myocardium. J Mol Cell Cardiol 26:519-25
Tate, C A; Hyek, M F; Taffet, G E (1994) Mechanisms for the responses of cardiac muscle to physical activity in old age. Med Sci Sports Exerc 26:561-7
Tate, C; Hamra, M; Shin, G et al. (1993) Canine cardiac sarcoplasmic reticulum is not altered with endurance exercise training. Med Sci Sports Exerc 25:1246-57
Taffet, G E; Tate, C A (1993) CaATPase content is lower in cardiac sarcoplasmic reticulum isolated from old rats. Am J Physiol 264:H1609-14
McMillin, J B; Taffet, G E; Taegtmeyer, H et al. (1993) Mitochondrial metabolism and substrate competition in the aging Fischer rat heart. Cardiovasc Res 27:2222-8

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