The Contribution of Former Work-Related Activity Levels to Predict Physical Activity and Sedentary Time during Early Retirement: Moderating Role of Educational Level and Physical Functioning

Background

The transition to retirement introduces a decline in total physical activity and an increase in TV viewing time. Nonetheless, as more time becomes available, early retirement is an ideal stage to implement health interventions. Therefore, knowledge on specific determinants of physical activity and sedentary time is needed. Former work-related physical activity has been proposed as a potential determinant, but concrete evidence is lacking. The aim of this study was to examine if former work-related sitting, standing, walking or vigorous activities predict physical activity and sedentary time during early retirement. Additionally, moderating effects of educational level and physical functioning were examined.

Methods

In total, 392 recently retired Belgian adults (>6 months, <5 years) completed the International Physical Activity Questionnaire, the SF-36 Health Survey and a questionnaire on sociodemographics and former work-related activities. Generalized linear regression analyses were conducted in R. Moderating effects were examined by adding cross-products to the models.

Results

More former work-related sitting was predictive of more screen time during retirement. Lower levels of former work-related vigorous activities and higher levels of former work-related walking were associated with respectively more cycling for transport and more walking for transport during retirement. None of the predictors significantly explained passive transportation, cycling and walking for recreation, and leisure-time moderate-to-vigorous physical activity during retirement. Several moderating effects were found, but the direction of the interactions was not univocal.

Conclusions

Former-work related behaviors are of limited importance to explain physical activity during early retirement, so future studies should focus on other individual, social and environmental determinants. Nonetheless, adults who previously had a sedentary job had higher levels of screen time during retirement, so this is an important subgroup to focus on during interventions. Because of the inconsistent moderating effects of educational level and physical functioning, no clear recommendations can be formulated.     

Towards a resource‐based habitat approach for spatial modelling of vector‐borne disease risks

Given the veterinary and public health impact of vector‐borne diseases, there is a clear need to assess the suitability of landscapes for the emergence and spread of these diseases. Current approaches for predicting disease risks neglect key features of the landscape as components of the functional habitat of vectors or hosts, and hence of the pathogen. Empirical–statistical methods do not explicitly incorporate biological mechanisms, whereas current mechanistic models are rarely spatially explicit; both methods ignore the way animals use the landscape (i.e. movement ecology). We argue that applying a functional concept for habitat, i.e. the resource‐based habitat concept (RBHC), can solve these issues. The RBHC offers a framework to identify systematically the different ecological resources that are necessary for the completion of the transmission cycle and to relate these resources to (combinations of) landscape features and other environmental factors. The potential of the RBHC as a framework for identifying suitable habitats for vector‐borne pathogens is explored and illustrated with the case of bluetongue virus, a midge‐transmitted virus affecting ruminants. The concept facilitates the study of functional habitats of the interacting species (vectors as well as hosts) and provides new insight into spatial and temporal variation in transmission opportunities and exposure that ultimately determine disease risks. It may help to identify knowledge gaps and control options arising from changes in the spatial configuration of key resources across the landscape. The RBHC framework may act as a bridge between existing mechanistic and statistical modelling approaches.     

High-fat diet overrules the effects of training on fiber-specific intramyocellular lipid utilization during exercise

In this study, we compared the effects of endurance training in the fasted state (F) vs. the fed state [ample carbohydrate intake (CHO)] on exercise-induced intramyocellular lipid (IMCL) and glycogen utilization during a 6-wk period of a hypercaloric (～+30% kcal/day) fat-rich diet (HFD; 50% of kcal). Healthy male volunteers (18-25 yrs) received a HFD in conjunction with endurance training (four times, 60-90 min/wk) either in F (n = 10) or with CHO before and during exercise sessions (n = 10). The control group (n = 7) received a HFD without training and increased body weight by ～3 kg (P < 0.001). Before and after a HFD, the subjects performed a 2-h constant-load bicycle exercise test in F at ～70% maximal oxygen uptake rate. A HFD, both in the absence (F) or presence (CHO) of training, elevated basal IMCL content by ～50% in type I and by ～75% in type IIa fibers (P < 0.05). Independent of training in F or CHO, a HFD, as such, stimulated exercise-induced net IMCL breakdown by approximately twofold in type I and by approximately fourfold in type IIa fibers. Furthermore, exercise-induced net muscle glycogen breakdown was not significantly affected by a HFD. It is concluded that a HFD stimulates net IMCL degradation by increasing basal IMCL content during exercise in type I and especially IIa fibers. Furthermore, a hypercaloric HFD provides adequate amounts of carbohydrates to maintain high muscle glycogen content during training and does not impair exercise-induced muscle glycogen breakdown.     

Alterations in protein and gene expression within the barrel cortices of ZnT3 knockout mice: experience-independent and dependent changes

Much evidence exists for the involvement of vesicular zinc in neurotransmission and cortical plasticity. Recent studies have reported that mice deficient in zinc transporter-3 protein (ZnT3) and thus, vesicular zinc, have significant behavioural and biochemical deficits. Here, we examined whether phenotypic differences existed in the barrel cortices of ZnT3 KO mice using functional proteomics and quantitative PCR. Additionally, by manipulating whisker input, we also investigated experience-dependent changes in protein and gene expression, thereby assaying how cortical plasticity is different in the absence of vesicular zinc. The GABA metabolizing protein ABAT was observed in lower abundances consistently in KO mice. Several presynaptic proteins were identified that were abundant in differing amounts between the WT and KO groups in an experience-dependent manner. At baseline, we observed a decrease in the relative expression of Dlg4, Grin2a, Mt3, and Ntrkb genes in KO mice. The reduced expression of Nrtkb persisted with whisker plucking. These data demonstrate that fundamental changes in the expression of proteins and genes important in neurotransmission occur in the absence of vesicular zinc. Furthermore, the complement of experience-dependent changes were different between WT and KO mice, indicating that the lack of vesicular zinc affects the process of cortical plasticity.     

Proteinase-activated receptor-2 exerts protective and pathogenic cell type-specific effects in Alzheimer's disease

The proteinase-activated receptors (PARs) are a novel family of G protein-coupled receptors, and their effects in neurodegenerative diseases remain uncertain. Alzheimer's disease (AD) is a neurodegenerative disorder defined by misfolded protein accumulation with concurrent neuroinflammation and neuronal death. We report suppression of proteinase-activated receptor-2 (PAR2) expression in neurons of brains from AD patients, whereas PAR2 expression was increased in proximate glial cells, together with up-regulation of proinflammatory cytokines and chemokines and reduced IL-4 expression (p < 0.05). Glial PAR2 activation increased expression of formyl peptide receptor-2 (p < 0.01), a cognate receptor for a fibrillar 42-aa form of beta-amyloid (Abeta(1-42)), enhanced microglia-mediated proinflammatory responses, and suppressed astrocytic IL-4 expression, resulting in neuronal death (p < 0.05). Conversely, neuronal PAR2 activation protected human neurons against the toxic effects of Abeta(1-42) (p < 0.05), a key component of AD neuropathogenesis. Amyloid precursor protein-transgenic mice, displayed glial fibrillary acidic protein and IL-4 induction (p < 0.05) in the absence of proinflammatory gene up-regulation and neuronal injury, whereas PAR2 was up-regulated at this early stage of disease progression. PAR2-deficient mice, after hippocampal Abeta(1-42) implantation, exhibited enhanced IL-4 induction and less neuroinflammation (p < 0.05), together with improved neurobehavioral outcomes (p < 0.05). Thus, PAR2 exerted protective properties in neurons, but its activation in glia was pathogenic with secretion of neurotoxic factors and suppression of astrocytic anti-inflammatory mechanisms contributing to Abeta(1-42)-mediated neurodegeneration.     

Metformin and exercise reduce muscle FAT/CD36 and lipid accumulation and blunt the progression of high-fat diet-induced hyperglycemia

Derangements in skeletal muscle fatty acid (FA) metabolism associated with insulin resistance in obesity appear to involve decreased FA oxidation and increased accumulation of lipids such as ceramides and diacylglycerol (DAG). We investigated potential lipid-related mechanisms of metformin (Met) and/or exercise for blunting the progression of hyperglycemia/hyperinsulinemia and skeletal muscle insulin resistance in female Zucker diabetic fatty rats (ZDF), a high-fat (HF) diet-induced model of diabetes. Lean and ZDF rats consumed control or HF diet (48 kcal %fat) alone or with Met (500 mg/kg), with treadmill exercise, or with both exercise and Met interventions for 8 wk. HF-fed ZDF rats developed hyperglycemia (mean: 24.4 +/- 2.1 mM), impairments in muscle insulin-stimulated glucose transport, increases in the FA transporter FAT/CD36, and increases in total ceramide and DAG content. The development of hyperglycemia was significantly attenuated with all interventions, as was skeletal muscle FAT/CD36 abundance and ceramide and DAG content. Interestingly, improvements in insulin-stimulated glucose transport and increased GLUT4 transporter expression in isolated muscle were seen only in conditions that included exercise training. Reduced FA oxidation and increased triacylglycerol synthesis in isolated muscle were observed with all ZDF rats compared with lean rats (P < 0.01) and were unaltered by therapeutic intervention. However, exercise did induce modest increases in peroxisome proliferator-activated receptor-gamma coactivator-1alpha, citrate synthase, and beta-hydroxyacyl-CoA dehydrogenase activity. Thus reduction of skeletal muscle FAT/CD36 and content of ceramide and DAG may be important mechanisms by which exercise training blunts the progression of diet-induced insulin resistance in skeletal muscle.     

The use of ancestral haplotypes in the molecular diagnosis of familial breast cancer

Mutations in BRCA1 and BRCA2 account for about 40% of families with an inherited susceptibility to breast and/or ovarian cancer. Mutational analysis of these two genes has become the standard of care for families with a strong suggestion of inherited susceptibility. Methodologies for screening vary, but one of the more popular techniques is dHPLC, due to its combination of high sensitivity and low cost. The presence of a large number of polymorphisms in the two BRCA genes complicates dHPLC analysis, often leading to complex elution profiles. There are concerns that a pattern produced by a sample heterozygous for a polymorphism may be very similar to that produced by a sample heterozygous for a unique mutation within the same amplicon. Further molecular analysis is often required to resolve whether any given shift is due to a polymorphism or a disease-causing mutation. The use of ancestral haplotypes was explored as a means to minimize the need for further analysis. Groups of 86 patients were genotyped for 12 BRCA1 polymorphisms or 20 BRCA2 polymorphisms. For BRCA1, eight distinct haplotypes were identified, which are largely derivatives of two main lineages. For BRCA2, 17 distinct haplotypes were identified, leading to a much more complex polymorphic pattern. With this knowledge, we have defined a system to determine which patients, if any, require further investigations. This method could be used to supplement any comprehensive screening methodology for other large genes that lie within strong regions of linkage disequilibrium such as NF1, CFTR, MLH1, or MSH2.