The Disposable Soma Theory of Biological Aging
This theory was put forward by Thomas Kirkwood, and it posits that the limited amount of energy found in all organisms is divided between the reproductive functions and maintenance of non-reproductive (soma) activities. Additionally, the theory notes that aging entails various degrading processes, which give rise to the accumulation of damages.
However, the organism compensates for these damages at the expense of reproductive functions. Moreover, since older animals experience minimal evolution effects as a result of the accumulation of damage, Kirkwood (1979, p. 531) notes that there is no need for animals to waste energy resources for maintenance functions while neglecting the reproductive functions to live far beyond the reproductive age.
As a result, the disposable soma theory links reproduction to lifespan processes by stating that the evolutionary significance of life declines as the organisms advance to reproductive maturity (Kirkwood, 1979, p. 538). Furthermore, the linkage between lifespan and reproduction is so rigid that the evolutional value of life cannot be achieved without encountering some adverse effects such as aging (Kirkwood, 1979, p. 546).
The Free-radical Theory of Aging and its Implications for Healthy Aging
Free radicals are those atoms containing unpaired electrons. The free radical theory has it that the radicals produced by body cells can also destroy them, and as a result, the aging of cells occurs (Nelson, n.d., par. 1). Here, the mitochondrion forms the primary target of the free radical-induced damage to cells because the free radicals are produced by the same cells, which produce chemical energy in an organism.
Conversely, studies conducted on laboratory animals show that the eradication of the free radicals from the body can increase the maximum lifespan (Nelson, n.d., par. 2-6). As a result, there is evidence to link the effect of free radicals on cells to some aspects of aging. However, additional studies show that dietary antioxidants, which are known to eliminate free radicals, cannot increase the maximum lifespan because they are unable to penetrate the mitochondrial cells producing radicals.
Accordingly, the free radical theory of aging implies that healthy aging can be achieved through dietary restrictions and the consumption of some dietary supplements. Here, the proponents of the theory argue that despite the dietary antioxidants failing to increase the maximum lifespan, there is evidence to show that some supplements such as vitamin E and C are very beneficial in terms of increasing the survival rate of organisms until they reach maximum lifespan (Nelson, n.d., par. 10).
The effect of aging changes on the resting and exercising heart
At rest, the heart rate of an elderly person is less than that of a young healthy person. Here, it is worth noting that the signaling mechanism of the sympathetic nervous system declines with age, and thus, the ability to signal the pacemaker is reduced. Moreover, some pathways of the sympathetic nervous system lose some functions due to fat deposition and the development of fibrous tissues. Furthermore, the heart’s pacemaker (the SA node) loses some cells, and thus, its functions are compromised (Potts, 2008, p. 1 of 6).
Conversely, the body’s ability to endure physical activity declines with age. This inability is attributable to the aging heart because, during physical activity, the heart rate in an aging heart cannot rise to the maximum. Moreover, the diminished heart rate occurs due to a lack of or reduced communication between the heart and the brain of an elderly person. Additionally, the force of contraction in aging hearts does not increase to the maximum during exercising (Potts, 2008, p. 1 of 6).
Aging Changes and the Reserve Capacity of the Heart
In young people, striated muscles including the cardiac muscles grow by acquiring additional contractile cells and through postnatal enlargement, a phenomenon referred to as hypertrophy (Goldspink, 2005, p. 1334). However, in elderly individuals, there is a loss of contractile cells, which cannot be replaced despite the cell renewal mechanisms being intact. As a result, the reserve capacity of the heart including the skeletal muscles diminishes with age.
The normal aging changes in the Respiratory System and their Significance to Respiratory Diseases
Normally, the age-related changes in the respiratory system involve the reduction of the strength and activity of the muscles, stiffened lungs, and a rigid chest compartment. Moreover, there is an increase in the residual volume and a decrease in vital capacity despite that the volume of the lungs is constant (Reeds et al., 1998, p. 1463).
Furthermore, the total surface area of the alveoli is decreased by 20% and it seems to collapse after expiration. In addition, the ability of an elderly person to control breathing diminishes with age (Reeds et al., 1998, p. 1465). Accordingly, these aging changes make the respiratory system vulnerable to various environmental factors, which are very important in the development of different respiratory diseases.
Age-related Changes in T-lymphocytes and their Impact in the development of Infections and Cancer
A prominent feature of aging in humans involves increased mortality and morbidity rates as a result of increased infections. On the other hand, aging is a major risk factor in the development of cancer (Conn, 2006, p. 33). These factors are associated with diminished immune functions whereby the T-lymphocytes fail to detect infected or cancer cells in the body.
Studies involving cultured T-lymphocytes show that at old age, the T-cells are unable to divide, and in some cases, their ability to express the CD28 signaling molecules is lost (Conn, 2006, p. 33). Additionally, the T-cells exhibit altered cytokine patterns, shortened telomeres, low cytolytic activity, and resistance to apoptosis. Overall, in the presence of these changes, elderly persons experience poor vaccine response, diminished immunity, osteoporotic fractures, and increased disease infections.
Reference list
Conn, M.P., 2006. Handbook of models for human aging. London, UK: Elsevier Inc.
Goldspink, D.F., 2005. Aging and activity: their effects on the functional reserve capacities of the heart and vascular smooth and skeletal muscles. Ergonomics, 14(48), pp. 1334-1351.
Kirkwood, T.B. & Holliday, F.R., 1979. The evolution of aging and longevity. Proceedings of the Royal Society of London, 205, pp. 531-546.
Nelson, N.C., n.d. The free radical theory of aging. Columbus, OH: Ohio State University, Department of Physics.
Potts, W.J., 2008. The aging heart. USA: US National Institute of Health.
Reed, D. Forey, D. et al., 1998. Predictors of healthy aging in men with high life expectancies. American Journal of Public Health, 88, pp. 1463-1468.