OBJECTIVES:Lack of physical activity (PA) and prolonged sitting time (ST) are associated with increased risk of mortality and chronic illnesses, including depression. While there have been claims that the two risks are 'independent', their joint and stratified effects are unclear. The aim of this study was to explore the combined effects of physical activity and sitting time on the 12year risk of depressive symptoms (DS) in young women.

DESIGN:Cohort-9061 young participants in the Australian Longitudinal Study on Women's Health completed triennial surveys from 2000 (age 22-27), to 2012.

METHODS:Generalised Estimating Equation models were used to calculate the joint effects of PA and ST on DS, with<4h/day of ST and the highest PA quartile as the reference categories. Relationships between PA and DS, and between ST and DS, were also examined after stratification by ST and PA respectively.

RESULTS:In the adjusted joint effects model, compared with the reference category (low sitting, high PA), odds for DS were significantly higher in women who sat for>4, 6 and 8h/day and reported doing no PA. In every physical activity category, women who sat for≥10h/day were at highest risk of DS (OR for lowest physical activity quartile, 1.72 [95% CI=1.38-2.14]; OR for highest physical activity quartile, 1.49 [95% CI=1.16-1.91]). After stratification by ST, odds of DS were reduced in women who reported any physical activity (compared with none), exceptwhen ST was>10h/day. After stratification by physical activity, the increased risk of sitting 8-10h/day was attenuated by any physical activity, but there was no reduction in risk of depressive symptoms with increasing PA levels in women who sat for≥10h per day.

CONCLUSIONS:These data suggest that there are both joint and stratified effects of too little activity and too much sitting on the risk of depressive symptoms in young women. High levels of PA are protective against the hazards of high ST at this life stage, except in women with very high levels of sitting.

BACKGROUND:Apply a more novel approach to systematically examine (1) associations of clustered cardio-metabolic risk and cardio-metabolic risk factors, and (2) theoretical substitution of sedentary time with either sleep, light physical activity (LPA) or moderate-and-vigorous physical activity (MVPA) and substituting LPA with MVPA.

METHODS:Physical activity and sleep were objectively measured in 410 Flemish adults (55.5[±9.6] years, 64% men) with a SenseWear Pro 3 Armband. Cardio-metabolic risk factors (obesity, hyperglycemia, dyslipidemia, and hypertension,), cardiorespiratory fitness were objectively measured. Isotemporal substitution analyses were performed to assess the associations between substituting time from a potentially negative behavior into another, potentially positive, behavior.

RESULTS:Theoretical substitution of sedentary time with MVPA was associated with decreased clustered cardio-metabolic risk (b = -0.06 [-0.08;-0.04]) and substituting LPA with MVPA was associated with a decrease in clustered cardio-metabolic risk (b = -0.08 [-0.11;-0.04]). Substituting sedentary time with LPA or sleep improved HDL-cholesterol, systolic and diastolic blood pressures, and waist circumference.

CONCLUSION:Theoretical replacement of sedentary time with either sleep, LPA or MVPA was positively associated with improved cardio-metabolic risk factor status. Interventions for increasing cardio-metabolic health can focus on replacing sedentary time with either sleep, LPA or MVPA depending on the risk parameters that need to be targeted.

Non-pharmacological therapies, such as physical activity interventions, are an appealing alternative or add-on to current pharmacological treatment of cognitive symptoms in patients with dementia. In this meta-analysis, we investigated the effect of physical activity interventions on cognitive function in dementia patients, by synthesizing data from 802 patients included in 18 randomized control trials that applied a physical activity intervention with cognitive function as an outcome measure. Post-intervention standardized mean difference (SMD) scores were computed for each study, and combined into pooled effect sizes using random effects meta-analysis. The primary analysis yielded a positive overall effect of physical activity interventions on cognitive function (SMD[95% confidence interval]=0.42[0.23;0.62], p<.01). Secondary analyses revealed that physical activity interventions were equally beneficial in patients with Alzheimer's disease (AD, SMD=0.38[0.09;0.66], p<.01) and in patients with AD or a non-AD dementia diagnosis (SMD=0.47[0.14;0.80], p<.01). Combined (i.e. aerobic and non-aerobic) exercise interventions (SMD=0.59[0.32;0.86], p<.01) and aerobic-only exercise interventions (SMD=0.41[0.05;0.76], p<.05) had a positive effect on cognition, while this association was absent for non-aerobic exercise interventions (SMD=-0.10[-0.38;0.19], p=.51). Finally, we found that interventions offered at both high frequency (SMD=0.33[0.03;0.63], p<.05) and at low frequency (SMD=0.64[0.39;0.89], p<.01) had a positive effect on cognitive function. This meta-analysis suggests that physical activity interventions positively influence cognitive function in patients with dementia. This beneficial effect was independent of the clinical diagnosis and the frequency of the intervention, and was driven by interventions that included aerobic exercise.

A higher level of physical activity (PA) is associated with decreased risk of mortality, dementia, and depression, yet the mechanisms involved are not well understood, and little evidence exists for Mexican Americans. With data from the Sacramento Area Latino Study on Aging (1998-2007), we used Cox proportional hazards regression to separately evaluate associations of baseline PA level with mortality, dementia/cognitive impairment without dementia (CIND), and depressive symptoms, and we estimated the mediating effects of inflammatory markers in additive hazard models. A low level of PA (<35 metabolic equivalent of task-hours/week) was associated with increased mortality (hazard ratio (HR) = 1.50, 95% confidence interval (CI): 1.20, 1.88), dementia/CIND (HR = 1.37, 95% CI: 0.96, 1.96), and depressive symptoms (HR = 1.23, 95% CI: 1.00, 1.52). A low PA level added 512 (95% CI: -34, 1,058) cases of dementia/CIND per 100,000 person-years at risk (direct effect), while, through a mediating path, interleukin 6 (IL-6) added another 49 (95% CI: 5, 94) cases, or 9% of the total effect. For mortality, 8%-10% of the PA total effect was mediated through IL-6, tumor necrosis factorα (TNF-α), or TNF-α receptors. None of the inflammatory markers mediated the association between PA and depressive symptoms. Our results suggest that antiinflammation (especially as assessed by IL-6 and TNF-α levels) may partly explain how PA protects against dementia/CIND and mortality.

The early indications of vitamin C deficiency are unremarkable (fatigue, malaise, depression) and may manifest as a reduced desire to be physically active; moreover, hypovitaminosis C may be associated with increased cold duration and severity. This study examined the impact of vitamin C on physical activity and respiratory tract infections during the peak of the cold season. Healthy non-smoking adult men (18-35 years; BMI<34 kg/m2; plasma vitamin C<45µmol/L) received either 1000 mg of vitamin C daily (n = 15) or placebo (n = 13) in a randomized, double-blind, eight-week trial. All participants completed the Wisconsin Upper Respiratory Symptom Survey-21 daily and the Godin Leisure-Time Exercise Questionnaire weekly. In the final two weeks of thetrial, the physical activity score rose modestly for the vitamin C group vs. placebo after adjusting for baseline values: +39.6% (95% CI [-4.5,83.7]; p = 0.10). The number of participants reporting cold episodes was 7 and 11 for the vitamin C and placebo groups respectively during the eight-week trial (RR = 0.55; 95% CI [0.33,0.94]; p = 0.04) and cold duration was reduced 59% in the vitamin C versus placebo groups (-3.2 days; 95% CI [-7.0,0.6]; p = 0.06). These data suggest measurable health advantages associated with vitamin C supplementation in a population with adequate-to-low vitamin C status.

Analyses in nutritional epidemiology usually assume a uniform effect of a nutrient. Previously, four subgroups of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of Finnish male smokers aged 50-69 years were identified in which vitamin E supplementation either significantly increased or decreased the risk of pneumonia. The purpose of this present study was to quantify the level of true heterogeneity in the effect of vitamin E on pneumonia incidence using the I 2 statistic. The I 2 value estimates the percentage of total variation across studies that is explained by true differences in the treatment effect rather than by chance, with a range from 0 to 100 %. The I 2 statistic for the effect of vitamin E supplementation on pneumonia risk for five subgroups of the ATBC population was 89 % (95 % CI 78, 95 %), indicating that essentially all heterogeneity was true variation in vitamin E effect instead of chance variation. The I 2 statistic for heterogeneity in vitamin E effects on pneumonia risk was 92 % (95 % CI 80, 97 %) for three other ATBC subgroups defined by smoking level and leisure-time exercise level. Vitamin E decreased pneumonia risk by 69 % among participants who had the least exposure to smoking and exercised during leisure time (7·6 % of the ATBC participants), and vitamin E increased pneumonia risk by 68 % among those who had the highest exposure to smoking and did not exercise (22 % of the ATBC participants). These findings refute there being a uniform effect of vitamin E supplementation on the risk of pneumonia.

Aim:This study was aimed at investigating the effects and molecular mechanisms of physical activity intervention on Parkinson's disease (PD) and providing theoretical guidance for the prevention and treatment of PD.

Methods:Four electronic databases up to December 2019 were searched (PubMed, Springer, Elsevier, and Wiley database), 176 articles were selected. Literature data were analyzed by the logic analysis method.

Results:(1) Risk factors of PD include dairy products, pesticides, traumatic brain injury, and obesity. Protective factors include alcohol, tobacco, coffee, black tea, and physical activity. (2) Physical activity can reduce the risk and improve symptoms of PD and the beneficial forms of physical activity, including running, dancing, traditional Chinese martial arts, yoga, and weight training. (3) Different forms of physical activity alleviate the symptoms of PD through different mechanisms, including reducing the accumulation of-syn protein, inflammation, and oxidative stress, while enhancing BDNF activity, nerve regeneration, and mitochondrial function.

Conclusion:Physical activity has a positive impact on the prevention and treatment of PD. Illustrating the molecular mechanism of physical activity-induced protective effect on PD is an urgent need for improving the efficacy of PD therapy regimens in the future.