Relationship Between Activity Levels and Cognitive Impairment in Older Adults
September 30, 2011 4 minutes read
Relationship Between Activity Levels and Cognitive Impairment in Older Adults
Abstract & Commentary
By Harold L. Karpman, MD, FACC, FACP, Clinical Professor of Medicine, UCLA School of Medicine. Dr. Karpman serves on the speakers bureau for Forest Laboratories.
Synopsis: Greater daily activity energy expenditure appears to reduce the incidence of cognitive impairment in a dose-response manner.
Source: Middleton LE, et al. Activity energy expenditure and incident cognitive impairment in older adults. Arch Intern Med 2011;171:1251-1257.
Multiple published studies have clearly demonstrated that people who are more physically active in midlife and in late life have lower rates of dementia and cognitive impairment as they reach late life; in other words, physical activity appears to be one of the best preventive strategies against cognitive impairment in the elderly population.1-5 These studies have all been dependent on self-reporting of physical activity which, of course, may be inaccurate, especially in people with cognitive dysfunction. Self-reported physical activity correlates only moderately with objective measurements6 and often excludes activity not readily quantifiable by frequency and duration.
Middleton and her colleagues investigated the relationship between activity energy expenditure (AEE), which is an objective measure of total activity, and the incidence of cognitive impairment.7 Total energy expenditure between two clinic visits approximately 15 days apart was measured by using the doubly labeled water (DLW) method.8-10 Activity energy expenditure was calculated as 90% of total energy expenditure minus the resting metabolic rate, which was carefully measured. After adjustment for baseline Modified Mini-Mental State Examination scores, self-reported health, and the presence or absence of diabetes mellitus, older adults in the highest sex-specific tertile of AEE were found to have lower odds of having incident cognitive impairment than those individuals in the lowest tertile. There was also a significant dose response between AEE and the incidence of cognitive impairment.
Commentary
Many published studies have reported that people who are more physically active have lower risk of developing cognitive impairment in older age.2-5 The currrent study7 confirms this conclusion by providing new evidence that objectively measured total daily activity is associated with a significantly reduced incidence of cognitive impairment. Although it is still not clear whether the physical activity has to be moderate or vigorous, or whether even low-intensity physical activity will produce the same degree of cognitive impairment reduction, there appears to be a strong dose-response relationship between the amount of energy expenditure and the resulting cognitive impairment. The mechanism by which the lack of adequate physical activities is related to impairment in late-life cognition is uncertain; however, results of some research studies have suggested that physical activity may improve neuroplasticity by modifying levels of brain-derived neurotrophic factor.11-13 In addition, increased physical activity appears to be associated with a reduced accumulation of beta-amyloid plaque, which has been demonstrated to be present in individuals with Alzheimer's disease.14 Finally, regular physical activity is associated with reduced rates and severity of vascular risk factors including hypertension, obesity, and type II diabetes mellitus, each of which is associated with an increased risk of cognitive impairment.
Multiple studies, including the Middleton study,7 have strongly suggested that increased levels of AEE on a daily basis are associated with a reduced incidence of cognitive impairment in older adults. Hopefully, it will be demonstrated that even low-intensity activities of daily living (which can be performed by virtually all older adults) provide sufficient excercise intensity to prevent progressive cognitive impairment. In summary, physicians should encourage couch potatoes no matter what their age to get up and get moving in a motivated and meaningful manner to reduce their chances of developing cognitive impairment.
References
1. Middleton LE, et al. Promising strategies for the prevention of dementia. Arch Neurol 2009;66:1210-1215.
2. Russian EB, et al. Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older. Ann Inter Med 2006;144:73-81.
3. Laurin D, et al. Physical activity and risk of cognitive impairment and dementia in elderly persons. Arch Neurol 2001;58:498-504.
4. Rockwood K, et al. Physical activity and the maintenance of cognitive function. Alzheimers Dement 2007; 3(2 Suppl):S38-S44.
5. Rovio S, et al. Leisure time physical activity at midlife and the risk of dementia and Alzheimer's disease. Lancet Neurol 2005;4:705-711.
6. Westerterp KR. Assessment of physical activity: A critical appraisal. Eur J App Physiol 2009;105:823-828.
7. Middleton LE, et al. Activity energy expenditure and incident cognitive impairment in older adults. Arch Intern Med 2011;171:1251-1257.
8. Blanc S, et al. Influence of the late isotopic equilibration in urine on the accuracy of the H2O method in the elderly. J Appl Physiol 2002;92:1036-1004.
9. Weir JB. New methods for calculating metabolic rate with special reference to protein metabolism. J Physiol 1949;109:1-9.
10. Elia M, et al. Total energy expenditure in the elderly. Eur J Clin Nutr 2000;54(suppl 3):S93-S103.
11. Cotman CW, et al. Exercise to build brain health: Key roles of growth factor cascades and inflammation. Trends Neurosci 2007;30:464-472.
12. Gomez-Pinilla F, et al. Brain derived neurotrophic factor functions as a metabotrophin to mediate the effects of exercise on cognition. Eur J Neurosci 2008; 28:2278-2287.
13. Vaynman S, et al. Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition. Eur J Neurosci 2004;20:2580-2590.
14. Adlard PA, et al. Voluntary exercise decreases amyloid load in a transgenic model of Alzheimer's disease. J Neurosci 2005;25:4217-4221.
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