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Studies of bone mineral content (MC) of the limbs in normal populations have shown there is an increase of MC during adolescence, a maximum MC for both sexes between 30 and 40 years of age and a subsequent decrease which is at least twice as great in females than in males. There are different findings in the literature on the course of these MC changes with aging. The present cross-sectional study of 180 subjects over age 70 showed a slight increase in the annual decrease of radius MC in females and a distinct acceleration of the MC decrease in males after about 80 years. This occurred for both a pure cortical measuring site of the radius (1/3-site) and for a mixed cancellous/compact site of the distal radius (1/10-site). These findings differ from those in other populations.

In human striated muscle obtained in surgery, an age-dependent decrease in aldolase and creatine kinase specific activities and an increase in DNA content per wet weight was found. In the group of the elderly (64–84 years), the enzymes decreased by 40–60% when compared with a group between 24 and 47 years old, while DNA content rose by a factor of 1.53 indicating loss of tissue water. Titration of aldolase and creatine kinase molecules by specific antibodies against aldolase A and creatine kinase MM isozymes, respectively, revealed very little accumulation of aldolase cross-reacting material in the old age group (1.13 fold), and no accumulation of inactive creatine kinase molecules. Similar conclusions can be drawn from thermostability analyses of these two enzymes. The data do not support the view that accumulation of modified proteins due to ranom errors or to post-translational alterations is a general or causative phenomenon of aging in human muscle tissue.

Histomorphometric analysis of age-related structural changes in the brain was performed in CW1 female mice, 3, 9, 24 and 32 months of age. Cholinergic regions, such as the hippocampus, NBM and the medial habenula (MH) were investigated in more detail focusing on morphological parameters. The thickness of the frontoparietal cortex (FPC), and the surface area of the dorsal hippocampus and the MH were found to decrease significantly from 9 to 24 months of age. Except for the unique appearance of pseudo-cysts within the FPC, the structural changes culminated by 24 months. Cells' degeneration, in the CA3 hippocampal subfield, was noted already by 9 months of age whereas in other regions the cells' surface area decreased only between 9 and 24 months. Lipofuscin accumulation was most pronounced in the large neurons of the cortex, hippocampus and NBM at 24 months of age.

The effect of wheel running on the levels of fructose 1,6-bisphosphate aldolase A (EC 4.1.2.13) in striated muscles of young and old mice was compared. Short-term (6–10 weeks) and long-term (over 12 months) regimens were included in the study. The studies were conducted on the CW-1 outbred strain and on the C57/BL inbred strain of mice. It was shown that, in the short-term regimens, old animals of both strains showed either no increase (C57/BL) or a reduction (CW-1) in aldolase activity in hind leg muscles. On the other hand, young animals of both strains showed increases in aldolase activity of 10–20%. In the long-term regimen young and intermediate age animals showed 30–100% increases in aldolase activity in hind leg muscles over control sedentary animals. This adaptive capacity to exercise was not observed in old animals. However, long-term exercise regimen prevented the age-associated decline in aldolase activity found in sedentary animals.

CWI mice at the age of 6, 22 and 27 months were subjected to a controlled physical training program for 5 weeks. Changes in specific activity of the enzymes aldolase, superoxide dismutase and catalase of the total hind-leg muscle tissues were followed. During the training period, specific activities of these muscle enzymes exhibited an adaptive increase in the 6 and 22 months groups. In senile (27 months) mice, however, enzyme activities decreased as a consequence of the physical challenge. Total body weight was not altered under these conditions. Immunotitration of extracts with anti-aldolase and anti-creatine kinase antibodies showed no significant differences, indicating that there was no accumulation or disappearance of faulty proteins during aging and physical exercise.

Three age groups (6, 22 and 27 months) of CWI mice (female, outbred strain) were subjected to a physical training program for up to 5 weeks. During the training period the body weight remained constant in all groups. Hind leg muscle mass increased in response to the exercise in 6 and 22 month old mice but decreased in the senescent (27 months) animals. Physical exercise also increased the key enzyme creatine kinase in the 6 months group and to a lesser degree in the 22 months group. By contrast, senile animals showed a progressive loss of the enzyme throughout the training period. Similar changes — though less-pronounced — were seen with regard to soluble protein and to total DNA. The data indicate that old animals (22 months) are still able to adapt adequately to physical training while senile mice (27 months) respond paradoxically by a negative adaptation to a physical challenge.