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BACKGROUND: hysical activity exerts a variety of long-term health benefits in older adults. In particular, it is assumed to be a protective factor against cognitive decline and dementia.
METHODS/DESIGN: Randomised controlled assessor blinded 2-armed trial (n = 60) to explore the exercise- induced neuroprotective and metabolic effects on the brain in cognitively healthy older adults. Participants (age ≥ 65), recruited within the setting of assisted living facilities and newspaper advertisements are allocated to a 12-week individualised aerobic exercise programme intervention or a 12-week waiting control group. Total follow-up is 24 weeks. The main outcome is the change in cerebral metabolism as assessed with Magnetic Resonance Spectroscopic Imaging reflecting changes of cerebral N-acetyl-aspartate and of markers of neuronal energy reserve. Imaging also measures changes in cortical grey matter volume. Secondary outcomes include a broad range of psychometric (cognition) and movement-related parameters such as nutrition, history of physical activity, history of pain and functional diagnostics. Participants are allocated to either the intervention or control group using a computer-generated randomisation sequence. The exercise physiologist in charge of training opens sealed and opaque envelopes and informs participants about group allocation. For organisational reasons, he schedules the participants for upcoming assessments and exercise in groups of five. All assessors and study personal other than exercise physiologists are blinded.
DISCUSSION: Magnetic Resonance Spectroscopic Imaging gives a deeper insight into mechanisms of exercise-induced changes in brain metabolism. As follow-up lasts for 6 months, this study is able to explore the mid-term cerebral metabolic effects of physical activity assuming that an individually tailored aerobic ergometer training has the potential to counteract brain ageing.
NCT02343029 (clinicaltrials.gov; 12 January 2015).
There is mounting evidence that aerobic exercise has a positive effect on cognitive functions in older adults. To date, little is known about the neurometabolic and molecular mechanisms underlying this positive effect. The present study used magnetic resonance spectroscopy and quantitative MRI to systematically explore the effects of physical activity on human brain metabolism and grey matter (GM) volume in healthy aging. This is a randomised controlled assessor-blinded two-armed trial (n=53) to explore exercise-induced neuroprotective and metabolic effects on the brain in cognitively healthy older adults. Participants (age >65) were allocated to a 12-week individualised aerobic exercise programme intervention (n=29) or a 12-week waiting control group (n=24). The main outcomes were the change in cerebral metabolism and its association to brain-derived neurotrophic factor (BDNF) levels as well as changes in GM volume. We found that cerebral choline concentrations remained stable after 12 weeks of aerobic exercise in the intervention group, whereas they increased in the waiting control group. No effect of training was seen on cerebral N-acetyl-aspartate concentrations, nor on markers of neuronal energy reserve or BDNF levels. Further, we observed no change in cortical GM volume in response to aerobic exercise. The finding of stable choline concentrations in the intervention group over the 3 month period might indicate a neuroprotective effect of aerobic exercise. Choline might constitute a valid marker for an effect of aerobic exercise on cerebral metabolism in healthy aging.
Background: Associations between age, concerns or history of falling, and various gait parameters are evident. Limited research, however, exists on how such variables moderate the age-related decline in gait characteristics. The purpose of the present study was to investigate the moderating effects of concerns of falling (formerly referred to as fear of falling), history of falls & diseases, and sociodemographic characteristics on changes in gait characteristics with increasing age in the elderly. Methods: In this individual participant level data re-analysis, data from 198 participants (n = 125 females) from 60 to 94 years of age were analysed (mean 73.9, standard deviation 7.7 years). Dependent variables were major spatiotemporal gait characteristics, assessed using a capacitive force measurement platform (zebris FDM-T). Age (independent variable) and the moderating variables concerns of falling (FES-I), gender/sex, history of falls and fall-related medical records, number of drugs daily taken, and body mass index were used in the statistical analysis. Hierarchical linear mixed moderation models (multilevel analysis) with stepwise (forward) modelling were performed. Results: Decreases of gait speed (estimate = −.03, equals a decrease of 0.03 m/s per year of ageing), absolute (− 1.4) and gait speed-normalized (−.52) stride length, step width (−.08), as well as increases in speed normalized cadence (.65) and gait speed variability (.15) are all age-related (each p < .05). Overall and specific situation-related concerns of falling (estimates: −.0012 to −.07) were significant moderators. History of potentially gait- and/or falls-affecting diseases accelerated the age-related decline in gait speed (−.002) and its variability (.03). History of falls was, although non-significant, a relevant moderator (in view of increasing the model fit) for cadence (.058) and gait speed (−.0027). Sociodemographics and anthropometrics showed further moderating effects (sex moderated the ageing effect on stride length, .08; height moderated the effect on the normalised stride length, .26; BMI moderated the effects on step width, .003). Conclusion: Age-related decline in spatiotemporal gait characteristics is moderated by concerns of falling, (non-significantly) by history of falls, significantly by history of diseases, and sociodemographic characteristics in 60–94 years old adults. Knowing the interactive contributions to gait impairments could be helpful for tailoring interventions for the prevention of falls. Trial registration: Re-analysis of [21–24].