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Emerging evidence suggests contrasting health effects for leisure-time and occupational physical activity. In this systematic review, we synthesized and described the epidemiological evidence regarding the association between occupational physical activity and cardiovascular disease (CVD) mortality. A literature search was performed in PubMed, Embase, CINAHL, PsycINFO and Evidence-Based Medicine Reviews, from database inception to 17 April 2020. Articles were included if they described original observational prospective research, assessing the association between occupational physical activity and CVD mortality among adult workers. Reviews were included if they controlled for age and gender and at least one other relevant variable. We performed meta-analyses on the associations between occupational physical activity and CVD mortality. We screened 3345 unique articles, and 31 articles (from 23 studies) were described in this review. In the meta-analysis, occupational physical activity showed no significant association with overall CVD mortality for both males [hazard ratio (HR) 1.00, 95% confidence interval (CI) 0.87-1.15] and females (HR 0.95, 95% CI 0.82-1.09). Additional analysis showed that higher levels of occupational physical activity were non-significantly associated with a 15% increase in studies reporting on the outcome ischemic heart disease mortality (HR 1.15, 95% CI 0.88-1.49). While the beneficial association between leisure-time physical activity and CVD mortality has been widely documented, occupational physical activity was not found to have a beneficial association with CVD mortality. This observation may have implications for our appreciation of the association between physical activity and health for workers in physically demanding jobs, as occupational physical activity may not be health enhancing.

Objectives Recent meta-analyses suggest a physical activity health paradox: high levels of occupational physical activity (OPA) increase cardiovascular disease (CVD) risk, while leisure-time physical activity (LTPA) decreases risk. However, studies of women and cerebrovascular disease are limited. This report examines physical activity effects on stroke and transient ischemic attack (TIA) among working women in the United States. Methods OPA history, health status, and lifestyle were assessed by baseline interviews of 31 270 employed Sister Study participants aged 35-74 years. OPA was assessed at six intensity levels (lowest: \"mostly sitting\"); the highest three were combined as \"high intensity work.\" Independent OPA and LTPA effects on 6-year cerebrovascular disease incidence were estimated in adjusted Cox proportional hazard models. Results Stroke (N=441) and TIA (N=274) risk increased with more standing and higher intensity work at current and longest held job. Compared with mostly sitting, high intensity work at the current job increased TIA risk by 57% [hazard ratio (HR) 1.57, 95% confidence interval (CI) 1.04-2.38]. High intensity OPA at the longest held job increased risk for stroke by 44% (HR 1.44; 95% CI 1.08-1.93). Among women with CVD, sitting and standing equally, especially at the current job, increased risks up to two-fold (TIA HR 1.98, 95% CI 1.10-3.55) compared with mostly sitting at work. LTPA showed inverse associations. Conclusions Higher intensity levels of OPA increased stroke and TIA risks, while LTPA decreased risks; results corroborate the physical activity health paradox for women and cerebrovascular disease. More standing at work increased cerebrovascular disease risks, especially for women with CVD.

Objectives This study aimed to assess the effects of physically demanding work – measured as energy expenditure (EE) during occupational physical activities (OPA)– on risk of acute myocardial infarction (AMI) among men with and without preexisting ischemic heart disease (IHD). Methods The 20-year prospective study examined 1891 middle-aged working men using absolute (kcal/day) and relative (relative aerobic strain and percent oxygen uptake reserve) measures of EE. Linear and quadratic hazard models were explored in Cox regression analyses adjusting for 19 potential confounders and considering interactions with baseline IHD. Results Relative EE measures were positively associated with 20-year incidence of AMI in linear and quadratic hazard models and interacted with IHD. Each 10% increase of relative aerobic strain increased AMI risk by 18% among men without IHD [hazard ratio (HR) 1.18, 95% confidence interval (95% CI) 1.08–1.28, P=0.001] and by 8% among men with IHD (HR 1.08, 95% CI 0.98–1.20, P=0.129) in fully adjusted linear models. Results for quadratic models and percent oxygen uptake reserve were similar. Absolute EE did not predict AMI. Age, baseline IHD, systolic blood pressure, anti-hypertensive medication, body mass index, blood glucose, low-density lipoprotein cholesterol, cholesterol-lowering medication, mental stress, and smoking were independently associated with AMI, but not income, social support, alcohol, or conditioning leisure-time physical activity. Conclusions In contrast to absolute EE, relative workload measures that take individual fitness into account were positively associated with AMI incidence among men without IHD. For men with IHD, associations were also positive but weaker possibly due to healthy worker selection effects. These findings provide evidence for a positive association between OPA and AMI among men.

ObjectivesIt remains unclear whether different types of shift work impose similar risks for cardiovascular events in middle-aged workers, especially those with pre-existing ischaemic heart disease (IHD). This study investigated the relations between different shift types and incident acute myocardial infarction (AMI) among men with and without pre-existing IHD, respectively.MethodsWe analysed data on 1891 men, aged 42–60 years at baseline, in the prospective Kuopio Ischemic Heart Disease Risk Factor Study cohort, using Cox proportional hazard models with adjustment for demographic, biological, behavioural and psychosocial job factors. We evaluated the associations of baseline shift work with 20-year incidence of AMI, and their modification by pre-existing IHD, using both stratified analysis and models with product terms between shift work and IHD.ResultsTravelling work (at least 3 nights per week away from home) was strongly positively associated with AMI among men with IHD (HR=2.45, 95% CI 1. 08 to 5.59) but not among men without (HR=0.93, 95% CI 0.43 to 2.00). No clear associations were found between other types of shift work and AMI for both men with and without IHD. On both additive and multiplicative scales, baseline IHD status positively modified the association of travelling work with AMI (relative excess risk for interaction=3.23, 95% CI −0.50 to 6.97, p for multiplicative interaction=0.044).ConclusionsWe found mixed results for the associations between different types of shift work and AMI among those with and without pre-existing IHD. Future research should investigate these associations and effect modification for a broad spectrum of work schedules.

Objective It is unknown if aerobic exercise overloads or improves the cardiovascular system among workers with high occupational physical activity. This was investigated in a worksite randomized controlled trial (RCT) of aerobic exercise among cleaners. Methods We randomized 116 cleaners between 18–65 years. The aerobic exercise group (N=57) performed worksite aerobic exercise (30 minutes twice a week) and the reference group (N=59) received lectures. Cardiorespiratory fitness, blood pressure (BP) and diurnal heart rate (HR) for measuring aerobic workload [%HR reserve (%HRR)] were collected at baseline and after four months. A repeated measure 2×2 multi-adjusted mixed-model design was applied to compare the between-group differences in an intention-to-treat analysis. Results Between-group differences (P<0.01) were found: cardiorespiratory fitness 2.2 [standard error (SE) 0.8] ml O2× min−1 × kg−1 [95% confidence interval (95% CI) 0.6–3.8], aerobic workload −3.5 (SE 1.2) %HRR (95% CI −5.9–−1.0), resting HR −3.8 (SE 1.2) bpm (95% CI −6.1–−1.4), sleeping HR −3.8 (SE 1.1) bpm (95% CI −5.9–−1.7), and systolic BP 3.6 (SE 1.3) mmHg (95% CI 1.1–6.0). Conclusions Worksite aerobic exercise seems to improve cardiorespiratory fitness, aerobic workload, and resting and sleeping HR, but increase systolic BP among cleaners. Beneficial physiological cardiovascular effects are seen from aerobic exercise, but also a harmful effect is evident. Therefore, recommendations should take into consideration the potential cardiovascular overload from additional aerobic exercise on workers with high levels of occupational physical activity.

Objectives This study aimed to disentangle the interplay between occupational physical activity (OPA) and leisure-time physical activity (LTPA) in affecting cardiovascular health by examining: (i) interactions betweenOPA and LTPA and their combined effect on 20-year incidence of acute myocardial infarction (AMI) and (ii) the effect of OPA on AMI that is mediated through LTPA. Methods We analyzed data on 1891 men, aged 42-60 years at baseline, from the prospective Kuopio Ischemie Heart Disease Risk Factor Study. OPA was measured as relative aerobic strain (RAS), accounting for workers' cardiorespiratory fitness. Averaged 12-month LTPA and potential confounders were assessed by questionnaires. Analyses were stratified by the presence of ischemie heart disease (IHD) at baseline. Results We found potential multiplicative, but not additive, interactions between OPA and LTPA among men with IHD. The multivariable Cox model, adjusted for age, education, smoking, alcohol consumption, psychosocial job factors, and participation in an unrelated drug trial, showed that high OPA positively predicted AMI at low LTPA levels for both men with and without IHD: hazard ratio (HR) 1.27 [95% confidence interval (95% CI) 0.96-1.68] and HR 1.59 (95% CI 0.99-1.68), respectively. The combination of high OPA and low LTPA constituted the group associated with the highest risk for AMI, irrespective of IHD status. LTPA was not independently predictive of AMI and did not mediate the impact of OPA on AMI. Conclusions LTPA interacted with OPA on the multiplicative scale only. LTPA did not mediate the effect of OPA on AMI.

Excessive sitting and standing are proposed risk factors for cardiovascular diseases (CVDs), possibly due to autonomic imbalance. This study examines the association of objectively measured sitting and standing with nocturnal autonomic cardiac modulation. The cross-sectional study examined 490 blue-collar workers in three Danish occupational sectors. Sitting and standing during work and leisure were assessed during 1–5 days using accelerometers. Heart rate (HR) and heart rate variability (HRV) were obtained during nocturnal sleep as markers of resting autonomic modulation. The associations of sitting and standing still (h/day) with HR and HRV were assessed with linear regression models, adjusted for age, gender, body mass index, smoking, and physical activity. More sitting time during leisure was associated with elevated HR (p = 0.02), and showed a trend towards reduced HRV. More standing time at work was associated with lower HR (p = 0.02), and with increased parasympathetic indices of HRV (root mean squared successive differences of R-R intervals p = 0.05; high-frequency power p = 0.07). These findings, while cross-sectional and restricted to blue-collar workers, suggest that sitting at leisure is detrimental to autonomic cardiac modulation, but standing at work is beneficial. However, the small effect size is likely insufficient to mitigate the previously shown detrimental effects of prolonged standing on CVD.

BET1 is required, together with its SNARE complex partners GOSR2, SEC22b, and Syntaxin‐5 for fusion of endoplasmic reticulum‐derived vesicles with the ER‐Golgi intermediate compartment (ERGIC) and the cis ‐Golgi. Here, we report three individuals, from two families, with severe congenital muscular dystrophy (CMD) and biallelic variants in BET1 (P1 p.(Asp68His)/p.(Ala45Valfs*2); P2 and P3 homozygous p.(Ile51Ser)). Due to aberrant splicing and frameshifting, the variants in P1 result in low BET1 protein levels and impaired ER‐to‐Golgi transport. Since in silico modeling suggested that p.(Ile51Ser) interferes with binding to interaction partners other than SNARE complex subunits, we set off and identified novel BET1 interaction partners with low affinity for p.(Ile51Ser) BET1 protein compared to wild‐type, among them ERGIC‐53. The BET1/ERGIC‐53 interaction was validated by endogenous co‐immunoprecipitation with both proteins colocalizing to the ERGIC compartment. Mislocalization of ERGIC‐53 was observed in P1 and P2’s derived fibroblasts; while in the p.(Ile51Ser) P2 fibroblasts specifically, mutant BET1 was also mislocalized along with ERGIC‐53. Thus, we establish BET1 as a novel CMD/epilepsy gene and confirm the emerging role of ER/Golgi SNAREs in CMD. SYNOPSIS This study describes three individuals with a progressive early‐onset congenital muscular dystrophy, and additional epilepsy in one, caused by biallelic variants in the BET1 gene. BET1, along with its SNARE complex partners, is essential for ER‐to‐Golgi trafficking. In Family 1, compound heterozygous variants p.(Asp68His)/p.(Ala45Valfs*2) cause aberrant splicing and frameshifting, resulting in very low BET1 protein levels. Variants in Family 2 (homozygous p.(Ile51Ser)) do not impact BET1 protein levels, interactions with ER‐to‐Golgi SNARE complex members, or SNARE function in yeast. Mutant Ile51Ser BET1 shows massively reduced binding of the novel Bet1 interaction partner ERGIC‐53, which is also mislocalized in patient fibroblasts. There is a significant slowing of Golgi‐reconstitution in patient fibroblasts and impaired ER‐to‐Golgi trafficking in HeLa cells. This study adds to the emerging role of ER/Golgi SNARE dysfunction in the causation of muscular dystrophy. Graphical Abstract This study describes three individuals with a progressive early‐onset congenital muscular dystrophy, and additional epilepsy in one, caused by biallelic variants in the BET1 gene. BET1, along with its SNARE complex partners, is essential for ER‐to‐Golgi trafficking.