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Cytochrome P-450 (P-450) content as well as p-nitroanisole (pNA) O-demethylase and UDP-glucuronyltransferase (UDPGT) activities were determined in livers of middle-aged (MA; 12 or 18 months) and aged (24-26 months) rats exercised by either treadmill running or swimming. In addition, aniline hydroxylase activity was measured in MA runners and aged swimmers and compared to respective sham and non-handled controls. Treadmill exercise consisted of running aged and MA rats on a motorized treadmill for 16 and 20 m/min respectively, 60 min/day and 4 times per week, for 8 weeks. Sham rats were placed on the treadmill twice per week for 5 min at 8 m/min. No differences were found in any parameter comparing sham rats to non-handled controls. Running did not affect body weight or hepatic microsomal protein during the 8-week study. A 33-35% decline in microsomal P-450 content in treadmill exercised MA and aged rats was found. PNA O-demethylase activity was decreased 30% in MA and 45% in aged runners and aniline metabolism was inhibited 21% in MA rats. UDPGT activity was not affected by running in MA or aged rats. Swimming exercise was accomplished by placing the rats in a tank of water (32-33 degrees C) filled to a depth of 2 ft. Swim time was 60 min twice daily, 5 times per week. The aged and MA rats were trained for 6 months and 1 year, respectively. Two control groups, non-swimming sedentary (dry control) and 1 min swim/day sham (wet control), were utilized. MA and aged wet controls and swimmers weighted 8% and 15% less respectively, than MA and aged sedentary rats. Microsomal protein was significantly increased in MA swimmers compared to sedentary (20%) and wet control (35%) but no change was found with swimming in the aged rats. The results of the enzymatic studies were variable in the MA rats. Increases in P-450 content were found in wet controls (16%) and swimmers (27%) of the MA group, but only the swimming change was significant. No significant change was determined for pNA metabolism between swimmers and wet (22%) or dry (17%) controls. Aged swimmers and wet controls were more consistent, with no change in any of the parameters except aniline metabolism which was significantly increased in wet controls (25%) and swimmers (28%) as compared to dry controls. No significant change in UDPGT activity was measured in either age group of swimmers.(ABSTRACT TRUNCATED AT 400 WORDS)

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The purpose of this study was to determine whether exercise could prevent the age-related decline in mitogenesis, which has been well documented in rats, mice, and humans. At 1, 6, 12, and 18 mo of age, male Fischer F344 rats were subjected daily to swimming exercise for 6 mo. At the end of the 6-mo training period, spleen lymphocytes were isolated from the exercised rats and from age-matched sedentary controls. The induction of lymphocyte proliferation was measured with the mitogens concanavalin A (ConA) and lipopolysaccharide (LPS). In addition, the ability of the lymphocytes to produce interleukin 2 (IL 2) in response to ConA induction was measured. ConA- and LPS-induced proliferation decreased 41-63% between 7 and 25 mo of age in both exercised and sedentary control rats. ConA-induced IL 2 production decreased 42 and 62% between 7 and 25 mo of age for exercised and sedentary control rats, respectively. Although the age-related decline in mitogen-induced proliferation and IL 2 production was smaller in exercised rats, this was due to a lower level of mitogenesis and IL 2 production in lymphocytes from young exercised rats. Exercise resulted in a significant decrease (23-32%) in mitogen-induced lymphocyte proliferation and IL-2 production in 7-mo-old exercised rats compared with 7-mo-old sedentary rats. However, in the 18- and 24-mo-old rats, mitogen-induced lymphocyte proliferation and IL 2 production was not significantly different between exercised and sedentary control rats.

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The purpose of this paper is to provide insight into the alterations of 6-phosphofructo-1-kinase (PFK) activity and isozyme types of rat skeletal muscle during development and aging. PFK isozymes are tetramers which may be comprised of one or any combination of the three subunit types, L, M, and C. The effects of fusion or terminal differentiation of cultured rat L6 myoblasts leading to formation of myotubles does not have a noticeable effect on total PFK activity. However, the amount of M-type subunit was increased; and the level of the C-type subunit decreased. These subunit changes caused shifts in the isozymic types. The ultimate effects of prenatal development of PFK were characterized in the near-term fetal muscle. This stage of development was accompanied by a significant loss of the C-type subunit and by two-fold increases in the L-type and M-type subunits which accounted for the 40% increase in total PFK activity. After birth, the M-type subunit increased dramatically as did the total PFK activity. Since the L-type and C-type subunits were gradually lost during the subsequent 3 weeks, the homotetramer of the M-type subunit (M4) was the only type which is present in mature muscle. M4 persisted as the only detectable form in skeletal muscle during the remainder of life, but the total PFK activity and amount of M4 decreased after 18 months of age. The decreased total PFK activity in aged skeletal muscle suggested that the expression of PFK genes may have reverted to an immature state when total PFK activity was lower. As shown by both the immunological analysis and direct quantification of subunit types, this clearly did not occur. That is, the loss of PFK activity in aged muscle is a consequence of decreased levels of the M-type subunit and not reappearance of other subunit types such as found in maturing muscle. Further, our examination of aged skeletal muscle indicates that no significant structural changes in M-type subunits had occurred and that inactive or partially active proteins which could crossreact with the M-type subunit were not detectable. It is suggested that the loss of M4 could cause a depression of the glycolytic rate leading to diminished ability of senile muscle to accommodate extreme energy demands.

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Male Fischer rats of four age groups were subjected to a 3-mo exercise training program that consisted of a gradual increase to 1 h/day of forced swimming. Exercise was initiated at 1, 6, 12, or 17-22 mo of age. After the training period there was an increase in the heart weight relative to body weight in all groups, but heart weight was increased only in the two oldest groups. The specific activities of both actomyosin ATPase and creatine kinase isolated from cardiac muscle decreased with age. In animals that started exercise training at 6 mo of age the activities of both enzymes were higher than that of the age-matched sedentary controls, but the oldest animals (17-22 mo) responded negatively (i.e., a decreased enzymatic activity compared with sedentary individuals of the same age). These results suggest that, after a certain age, the initiation of endurance exercise may not result in the same adaptive response as occurs in younger animals. In the case of actomyosin ATPase this may be a consequence of a different distribution of myosin isozymes.

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Male Fischer 344 rats were subjected to regular forced exercise beginning at weaning and continued until sacrificed at ages ranging from 2 to 18 months. Littermates served as sedentary controls. At all ages examined, the exercised animals had greater heart and lower body weights. Actomyosin was isolated from the myocardium and the ATPase activity of the contractile protein preparation was measured. Only the sedentary animals exhibited an age-related loss in enzyme activity. The physically trained animals had substantially higher ATPase specific activity than the controls at all ages. This difference in ATPase specific activity may be the result of the synthesis of different isozymic forms of myosin or changes in the regulatory proteins of actomyosin (tropomyosin and troponin). It is suggested that lifelong regular exercise may alter the known biochemical changes in the heart muscle that relate to declining cardiac function.

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In adult caged house flies, maintained on a complete diet of powdered whole milk, cane sugar and water, the median longevity, maximal longevity, and percentage that exhibit complete wing retention at death are increased as the number of individuals per cage is correspondingly decreased from 240 to 10 flies per cage. These effects are more marked for the shorter-lived males than for the females. Female longevities at all population densities are more significantly reduced by a restricted diet of sugar and water only. Under conditions of individual confinement, the life expectancy of the female house fly is no greater than that of the male. These results are in agreement with earlier suggestions that increased physical activity including interaction among individuals in a restricted population decreases longevity.

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Male Fischer 344 rats from a long inbred colony (by brother-sister mating) were subjected to moderate (forced swimming) physical activity on a regular basis, beginning at 3 weeks following weaning. Normally caged, sedentary littermates were employed as controls at each age level. Exercised animals showed a greater total ventricular mass and correspondingly lower body weight, and the heart to body weight ratio for experimental animals about 25% higher at all ages, beginning at 3 months following onset of exercise. Finally, the specific activity of myocardial creatine phosphokinase was consistently higher for the exercised animals, beginning at 3 months of age and through 16 months of such exercise. These data support previous findings from this laboratory, as well as by others, that long-term moderate exercise begun early in life has a continuing, beneficial effect on the mammalian heart, both at the gross functional and intracellular biochemical levels.

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Myocardial creatine phosphokinase (CPK) was extracted from crushed tissue in 0.01 M Tris buffer at pH 9.0 and purified by successive ammonium chloride and ethanol precipitations. The CPK activity was estimated by measuring the rate of phosphocreatine formation by the transphosphorylation of creatine by ATP. There was a slight rise in CPK activity from 1 to 2 months of age. Thereafter, there was a progressive fall in the CPK activity of 14% by 7-9 months of age, 20% by about one year of age, and 25% by 16-24 months of age. These data indicate that, with advancing age, there is an inability to rapidly restore adequate cellular levels of the high-energy substrate ATP during muscular contraction. Since the loss with age of myocardial CPK parallels a strong biochemical correlate for known declining cardiac function in aging mammals, including man.

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Although myocardial actomyosin ATPase specific activity determined at Ca2+ levels of 1 x 10(-3) to 1 x 10(-2) M is consistently higher in two-month old male Fischer rats than in twelve-month old individuals, this difference can be eliminated if the enzyme is assayed at lower calcium concentrations. This suggests that the previously reported, declining actomyosin ATPase activity in the rat myocardium with advancing age may represent an age-related diminished ability of calcium to reverse the known inhibition upon actomyosin ATPase by the regulatory proteins.

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Actomyosin was extracted from myocardial homogenates from male rats of different ages of a long-inbred Fischer rat colony maintained under controlled conditions of temperature, humidity, and light. ATPase specific activity rose to a maximum at 2 months of age; this was followed by a progressive decline by about 25% at 16 months of age. However, the extractable actomyosin remained constant during this period. This loss in actomyosin ATPase specific activity is in good agreement with previously reported decrements in both stroke index and myocardial calcium content and an increase in myocardial contraction duration in aged rats.

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Survival data are reported for 572 male non-breeding Fischer rats, representing offspring from brother-sister matings, maintained at a constant temperature and humidity, exposed to twelve hours of artificial lighting and to twelve hours of darkness per day, and fed a standard laboratory diet ad libitum. The mean longevity for these male rats was 642 days and the median longevity was 659 days; the longest-lived individual survived to 1192 days. Animals surviving beyond the median life span for this colony were found to lose a greater percentage of body weight during the last few weeks before death than did shorter-lived animals. Offspring born of parents one year of age showed no significant difference in longevity from those of three-month old parents. Moreover, the longer any animal lived, the greater the maximan weight which he obtained.

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