Effects of Physical Fitness on Stress Resilience in Older Adults
During the aging process there is a progressive decline in the ability of the organism to resist stress and repair damage. Stress is defined here as a threat, real or interpreted, to the physiological or psychological integrity (i.e. homeostasis) of an individual, that results in physiological and/or behavioral responses.
The rate of aging varies among individuals of the same species and in humans is affected by gender, genetic factors, socioeconomic status, and lifestyle choices such as smoking and diet. Another important factor in the process of aging is physical function and fitness.
Exercise training can ameliorate or counteract many of the physiological decrements of aging and is associated with a decreased risk for many of the diseases linked to chronic elevation of cortisol and/or oxidative stress. Exercise training leads to physiological adaptations that in general result in a blunted stress response to acute exercise at the same absolute intensity, as well as increased tolerance for exercise.
The effects of aging on various physiological functions are often not observed until the system is challenged.
Thus, resting or basal levels of stress markers may not be measurably different between apparently healthy young and older adults, but often differ markedly during the response to a perturbation, indicating that aging leads to a reduction in stress resilience (i.e. the capacity of the organism to upregulate defensive and repair responses that allow ready recovery from an acute challenge.)
If the primary effect of exercise training is to maintain this resilience, then the effect of exercise training would be most readily detected in populations that exhibit markedly decreased stress resilience, such as the aged or those with chronic disease.
Older adults commonly experience a decreased ability to recover from stressors such as illness, injury or exertion, when compared to younger adults However, the responses in older individuals are highly heterogeneous, suggesting that age alone is not a good predictor of outcome.
One factor that inversely correlates with morbidity and mortality in older adults is aerobic capacity measured as maximal oxygen consumption (VO2 max). Because mortality in the modern age is rarely related to the ability to outrun predators, greater aerobic fitness (or the physical activity required to maintain aerobic fitness) must endow protection against dangers relevant to the modern world, such as the aforementioned acute stressors.
Exercise training may be an effective tool in preventing the age-associated decline in stress resilience through maintaining antioxidant defenses and improved neuroendocrine autoregulation, thereby delaying the onset of chronic age-related disease. In fact, physically active adults have both lower levels and later occurring onset of disability ('compressed morbidity'), when compared to nonexercisers.
The paradox of exercise is that acutely, it is a 'stressor' that results in increased formation of reactive oxygen species (ROS) and activation of the neuroendocrine response. However, regular exercise training results in systemic adaptations that include a blunted neuroendocrine response to a given absolute workload, and decreased oxidative damage through enhanced endogenous antioxidant activity and/or decreased production of ROS.
While exercise training is widely recognized as being beneficial in reducing the risk for chronic diseases, the mechanisms that underlie this protection are not well understood.
By understanding the mechanism(s), it may be possible not only to optimize the type of exercise training used, but to design pharmacological interventions to enhance the effects of exercise training. Investigating stress resilience responses to two stressors not directly related to exercise stress, ischemia/reperfusion and psychosocial stress, will enable us to dissect the mechanisms that are most relevant to the beneficial effects of exercise training on morbidity and mortality.
By using acute trials to challenge the system and examining the response, we expect to amplify the differences between physically fit and unfit older adults, giving us greater sensitivity when examining the contributions of specific mechanisms.
The aims of this study are:
- To determine effects of physical fitness on oxidative stress resilience
- To determine the effects of physical fitness on acute oxidative stress response, comparing fit and unfit older men and women. Acute oxidative stress will be assessed by measuring local changes in plasma F2-isoprostanes in response to a forearm ischemia-reperfusion protocol.
- To determine the effects of physical fitness on resting oxidative stress levels, comparing fit and unfit older men and women. Resting oxidative stress will be assessed by measuring urinary excretion products of oxidative damage to lipids, proteins, and nucleic acids adducts. These markers will be measured in first morning urines on 5 separate days.
- To determine the effects of physical fitness on total serum antioxidant capacity, at rest and after acute oxidative stress comparing fit and unfit older men and women.
- To determine the effects of physical fitness on neuroendocrine stress reactivity, as assessed by measurements of the pituitary-adrenal axis response (plasma ACTH, plasma cortisol, salivary cortisol) to a validated psychosocial laboratory stressor, comparing fit and unfit older men and women
- To investigate relationships and correlations between intra-individual responses to a defined oxidative stressor (forearm ischemia-reperfusion) and a controlled psychosocial stress stimulus.
Procedure: This study requires 5 visits (2 screening visits and 3 study visits). Study volunteers will give informed consent and be pre-screened by medical history, physical exam including a resting EKG, routine laboratory screening, and their fitness levels will be measured. Maximal oxygen consumption (VO2 max) and leg power will be used to classify an individual's fitness level. The participant will undergo a psychosocial laboratory stressor, and oxidative stress challenge.
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