Recreational physical activity and risk of Parkinson's disease

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA. <>
Movement Disorders (Impact Factor: 5.68). 01/2008; 23(1):69-74. DOI: 10.1002/mds.21772
Source: PubMed


The purpose of this study was to investigate associations between recreational physical activity and Parkinson's disease (PD) risk. We prospectively followed 143,325 participants in the Cancer Prevention Study II Nutrition Cohort from 1992 to 2001 (mean age at baseline = 63). Recreational physical activity was estimated at baseline from the reported number of hours per week on average spent performing light intensity activities (walking, dancing) and moderate to vigorous intensity activities (jogging/running, lap swimming, tennis/racquetball, bicycling/stationary bike, aerobics/calisthenics). Incident cases of PD (n = 413) were confirmed by treating physicians and medical record review. Relative risks (RR) were estimated using proportional hazards models, adjusting for age, gender, smoking, and other risk factors. Risk of PD declined in the highest categories of baseline recreational activity. The RR comparing the highest category of total recreational activity (men > or = 23 metabolic equivalent task-hours/week [MET-h/wk], women > or = 18.5 MET-h/wk) to no activity was 0.8 (95% CI: 0.6, 1.2; P trend = 0.07). When light activity and moderate to vigorous activity were examined separately, only the latter was found to be associated with PD risk. The RR comparing the highest category of moderate to vigorous activity (men > or = 16 MET-h/wk, women > or = 11.5 MET-h/wk) to the lowest (0 MET-h/wk) was 0.6 (95% CI: 0.4, 1.0; P trend = 0.02). These results did not differ significantly by gender. The results were similar when we excluded cases with symptom onset in the first 4 years of follow-up. Our results may be explained either by a reduction in PD risk through moderate to vigorous activity, or by decreased baseline recreational activity due to preclinical PD.

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    • "Physical activity has been demonstrated to lead to tremendous health benefits in individuals of all ages and in both healthy and disease states. It is only in the last two decades that epidemiological studies have suggested that a lifetime of physical activity may provide protection from a wide range of neurological disorders, including PD [19], Alzheimer's disease (AD) [20], and cognitive impairment associated with aging [21]. For example, a study by Chen and colleagues demonstrated that maintaining strenuous levels of physical activity in young adulthood was associated with a reduced risk of acquiring PD in later life [22]. "
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    ABSTRACT: Animal studies have been instrumental in providing evidence for exercise-induced neuroplasticity of corticostriatal circuits that are profoundly affected in Parkinson’s disease. Exercise has been implicated in modulating dopamine and glutamate neurotransmission, altering synaptogenesis, and increasing cerebral blood flow. In addition, recent evidence supports that the type of exercise may have regional effects on brain circuitry, with skilled exercise differentially affecting frontal-striatal related circuits to a greater degree than pure aerobic exercise. Neuroplasticity in models of dopamine depletion will be reviewed with a focus on the influence of exercise on the dorsal lateral striatum and prefrontal related circuitry underlying motor and cognitive impairment in PD. Although clearly more research is needed to address major gaps in our knowledge, we hypothesize that the potential effects of exercise on inducing neuroplasticity in a circuit specific manner may occur through synergistic mechanisms that include the coupling of an increasing neuronal metabolic demand and increased blood flow. Elucidation of these mechanisms may provide important new targets for facilitating brain repair and modifying the course of disease in PD.
    10/2015; 1(1):25-35. DOI:10.3233/BPL-150021
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    • "Taken together, these studies suggest that physical activity prior to neurotoxic 6-OHDA insult may provide neuroprotective benefit in terms of behavioral performance. This mirrors the results seen in human epidemiological studies, which have shown that increased physical activity decreases the risk for PD (Chen et al., 2005; Sasco et al., 1992; Thacker et al., 2008). Forced exercise has also been shown to decrease the behavioral and neurochemical deficits when implemented after a 6-OHDA lesion. "
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    ABSTRACT: Studies on exercise before and after toxin-induced hemiparkinsonism have reported promising findings in terms of amelioration of motor asymmetry in adult, 6-hydroxydopamine (6-OHDA) rats. However, recent studies have had more mixed results. Therefore, the purpose of this study was to further explore the notion of exercise, in particular forced exercise, as a potential neuroprotective therapy when implemented before and after 6-OHDA hemiparkinsonism. To explore this, two experiments were conducted: Experiment 1 - exercise before a 6-OHDA lesion; and, Experiment 2 - exercise after a 6-OHDA lesion. In Experiment 1, rats were randomly assigned into one of two 4-week experimental conditions, a forced exercise condition and a non-exercise control condition. Then, after the experimental conditions rats were injected with 6-OHDA into the right medial forebrain bundle. In Experiment 2, rats were first injected with 6-OHDA and were then randomly assigned into one of two 4-week experimental groups, a forced exercise group and a non-exercise control group. Outcomes in both experiments did not show any differences in terms of motor behavioral tests (i.e., apomorphine rotations, forelimb placement asymmetry, exploratory rearing) between the forced exercise and sedentary control groups. Based on our results and in light of the body of literature, it is possible that the stress of shock-motivated forced running utilized in this study may have cancelled beneficial behavioral effects. Additionally, it is possible that the one-week delay in the forced exercise protocol implementation in Experiment 2 may have prevented behavioral rescue.
    Brain research 11/2013; 1543. DOI:10.1016/j.brainres.2013.10.054 · 2.84 Impact Factor
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    • "In comparison to the number of studies of cognitive function in AD, there have been much fewer examinations of the potential disease modifying effects of physical activity on the development of cognitive impairment in Parkinson's disease (PD). The clinical evidence supporting a benefit of engaging physical activity associated with reduced risk of developing PD remains inconclusive (Thacker et al., 2008; Sasco, 1992) although a community-based randomised study examining Tango dancing reported improvements of Unified Parkinson's disease Rating scores of offmedication patients (Duncan and Earhart, 2012). By comparison, the findings of a randomised controlled trial of training on a rotating treadmill based on the hypothesis that this would limit turning movement-related falls revealed limited short-term benefits (McNeely and Earhart, 2012) which was largely consistent with the findings of a meta-analysis that reported no significant effect of motor training on the risk ratio of falling incidence (Allen et al., 2011). "
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    ABSTRACT: This review will provide an overview of the non-drug based approaches that have been demonstrated to enhance cognitive function of the compromised brain, primarily focussed on the two most widely adopted paradigms of environmental enrichment and enhanced physical exercise. Environmental enrichment involves the generation of novelty and complexity in animal housing conditions which facilitates enhanced sensory and cognitive stimulation as well as physical activity. In a wide variety of animal models of brain disorders, environmental enrichment and exercise have been found to have beneficial effects, including cognitive enhancement, delayed disease onset, enhanced cellular plasticity and associated molecular processes. Potential cellular and molecular mechanisms will also be discussed, which have relevance for the future development of 'enviromimetics', drugs which could mimic or enhance the beneficial effects of environmental stimulation. This article is part of a Special Issue entitled 'Cognitive Enhancers'.
    Neuropharmacology 07/2012; 64(1):515-28. DOI:10.1016/j.neuropharm.2012.06.029 · 5.11 Impact Factor
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