Considerations and Future Perspectives

As with all human studies, interpreting results with caution is required. The majority of cited literature assesses immune responses in healthy individuals and thus their immune system may be working optimally in preventing infection and disease.

Therefore, although at times no effects for exercise are observed this should be expected. Subsequently, when exercise studies are applied to individuals with chronic diseases such as cancer or CVD the results are often positive [9, 112, 113]. Because these individuals are immunocompromised by their disease, exercise often promotes enhancements in function.

We have specifically avoided discussing the interactions of exercise and immune function in those infected with latent viral infections for the following reasons. Immunesenescence is associated with repeated antigenic exposure over time and an exhaustion of immune function [114]. Latent infections with herpes viruses such as CMV and EBV are known to promote clonal expansion of viral specific T-cells. These cells occupy a relatively large immune space compared to uninfected hosts and may contribute to a reduced capacity to deal with novel pathogens. Indeed, in the IRP the presence of CMV and EBV is associated with mortality in the elderly [115]. These viral infections are characterized by an altered phenotype of T-and NK-cells and acute bouts of exercise are known to mobilize cell phenotypes differently in infected versus uninfected [116]. However, the role of CMV and EBV in the pathogenesis of ageing is not clear and its relationship with inflammation and physical function with age is questionable [117, 118]. Thus, the suggested need to remove these viral specific cells via exercise may not be the mechanism by which exercise improves measures of senescence. In fact removal of these cells may increase re-activation of CMV, EBV or their cousin herpes virus varicella-zoster, responsible for shingles in the elderly. Furthermore, CMV specific T-cells have reduced expression of the programmed death-1 receptor (PD-1) [119]. Malignant tumors often express the PD-1 ligand which inhibits T-cell tumor cytotoxicity; therefore removal of CMV specific T-cells may increase the risk of cancer.

As the immune system of the older adult is dominated by the actions of the myeloid compared to the lymphoid lineage, much more work is needed to determine the role of exercise in modifying viral specific T-cells. Clearly, there will be a number of such cells which are senescent and contribute to poor immunity; however this remains to be determined.

A major limitation of the role exercise and energy balance plays on immune function in the old is the lack of standardized testing protocols, participant populations and low participant numbers. A number of studies have compared interventions of various exercise intensities, modes and durations on health measures such as glucose tolerance, cardiovascular function and physical function [99,120]. With the recent development of the National Institute of Health common fund designed to understand the molecular transducers of exercise perhaps we will have a clearer understanding of how exercise can modify the immune system.

In summary, exercise training and regular physical activity likely promotes an anti-inflammatory and anti-immunesenescence effect. A repeated acute bout of activity increases heart rate and works multiple muscle groups stimulating a mobilization of immune cells into the peripheral blood. Where these cells go and what happens after exercise remains unknown, but this repetitive exercise over time can modify aspects of immunesenescence. Whether these effects are rejuvenating or delay the impact of inflammation and senescence remains to be seen. What is clear is that physical activity and energy balance influence the immune and inflammatory responses reducing the risk of age-associated disease and infection.

 
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