New research has demonstrated the effects of exercise on cognitive competency, especially in aging individuals. An accumulation of research may demonstrate how aging of an individual may be reduced by exercise and raising general activity levels.
Observations of cognitive aging suggest changes in the organisation and structure of the aging central nervous system may contribute to its development and increase the propensity to develop neurodegeneration. The factors which lead to aging and the changes within the brain are a current focus of research and this may lead to therapies designed to alleviate cognitive reductions and related neurodegenerative conditions.
The evidence suggests alterations in the functioning of neurons in the hippocampus and prefrontal cortex in particular results in cognitive impairment during aging. Concurrent inflammation in the cells of the immune system might also occur and this may lead to the pathology within these cells. Mononuclear phagocytes a type of immune cell may protect, defend and trigger immune responses although this may also lead to deleterious auto-immune responses. Alterations to the neurovascular unit which comprises endothelial cells (part of the blood brain barrier), neurons and immune cells may be a key source of neural dysfunction. The blood brain barrier is crucial to prevent toxic substances crossing from the vascular system to the central nervous system. Studies in mice also demonstrate vascular alterations pre-exist the presentation of neuronal dysfunction. Taken together these findings demonstrate how neural degeneration underlies cognitive deterioration.
Exercise may have encouraging effects on the integrity and function of the neuronal system. It may stimulate the growth of new neurons, reduce inflammation, increase the growth of new blood vessels and increase cerebral blood flow. A study by Soto and colleagues additionally lends support to this idea, experiments on aged mice indicate exercise may be protective of further neural and cognitive decline. The mice exhibit improved cognitive ability, reduced immune response and reversal of many of the signs of neural and vascular degeneration.
Long term exercise may protect individuals in regard to age-related alterations in the expression of genes in the heart, which indirectly affect the brain. Genes alterations significantly affected by age were reduced in mice exercising throughout life in comparison to those with a sedentary life and fewer fold changes in gene expression were observed. This reflects a prevailing direction of research and may show how exercise, diet and toxins effect or protect the genetic material in cells. Genetic mutations may correlate with aging, the higher the number of mutations a cell has been through the elderly age a cell is and these may follow DNA interference from environmental factors. A cell which may have been mutated genetically in both DNA strands, avoids recognition by enzymes and therefore repair is unfeasible leaving the cell and DNA vulnerable. Reducing the aging of the cells may well be due to protective responses activated by exercise and good nutrients, although many substances may accelerate the aging process by interfering with genetic material. Studies on alzheimers medications strongly indicate the drugs slow the progression of the condition by slowing the aging process and reducing the likelihood of leakage from blood vessels in the brain.
Exercise may be known to protect from and reverse aging and cognitive reduction. Individuals who are aging or those experiencing cognitive impairment might endeavour to exercise and profit from the benefits to physical and cognitive health. The understanding of neurodegenerative conditions may be advancing and the prospect they may be averted in the future to an extent seems to be a possibility. If the younger and elderly generations aim to make the changes to their lifestyle, diet and outlook, it may be plausible to curtail cognitive aging and its causes.
How does exercise influence wellbeing in a productive manner?