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• W2979411791 abstract "Obesity and a sedentary lifestyle are major contributors to poor metabolic and vascular health. As such, there has been a focus towards understanding the mechanisms underlying improvements in health related to physical activity. However, there remains a need for strategies that encourage patients to perform exercise independently and outside of the laboratory-supervised research setting. Investigations into skeletal muscle microvasculature function can provide insight into the links between cardiovascular and metabolic health. Increased nitric oxide (NO) production via endothelial NO synthase (eNOS) promotes muscle capillary recruitment to increase insulin-stimulated glucose uptake (Vincent et al. 2004). However, the levels of bioavailable NO are reduced in obesity due to quenching by oxidants, such as superoxide. NADPH oxidase (NOX) complexes are predominant sources of superoxide in the endothelium of obese individuals; therefore, the relative activation of eNOS versus NOX may provide an indication of microvascular function. In a recent issue of The Journal of Physiology, Scott et al. (2019) investigated whether home-based exercise can mitigate insulin resistance and vascular dysfunction while eliminating potential barriers of exercise adherence, such as access to facilities. Thirty-two males and females (age 36 ± 10 years) with an elevated risk of developing cardiovascular disease (body mass index 34.3 ± 5 kg/m2; 24.6 5.7 ml/kg/min) performed 12 weeks of exercise training under one of the following conditions: home-based high-intensity interval training (Home-HIT; n = 9), laboratory-based supervised HIT (Lab-HIT; n = 10) or home-based moderate-intensity continuous training (Home-MICT; n = 13). The participants who performed home-based exercise were ‘virtually supervised’ using a heart rate monitor, and instructed to achieve ≥80% or ∼65% of predicted heart rate maximum (HRmax 220 – age) during the intervals or continuous exercise, respectively. The home-based and laboratory-supervised HIT exercise sessions consisted of 1-min bouts of exercise interspersed with 1 min of rest. The Home-MICT group was instructed to perform continuous exercise of either swimming, cycling or walking/running. Participants in each group trained three times per week. To monitor adherence to exercise prescription, HR data obtained from the HR monitors were automatically uploaded to a cloud storage site (www.flow.polar.com) after each session. Endothelial function and aortic stiffness were assessed via flow-mediated dilatation (FMD) and pulse wave velocity (PWV), respectively. Insulin sensitivity was measured using an oral glucose tolerance test (OGTT). Lastly, a resting muscle biopsy was collected to measure markers of metabolic and vascular function via immunofluorescence. The primary finding was that the improvements in endothelium-dependent dilatation, aortic stiffness and insulin sensitivity were comparable between home-based exercise groups and laboratory-supervised exercise. In addition, the improvements in skeletal muscle microvascular function were similar, regardless of the exercise group. Notably, participants in each group also experienced concomitant improvements in . The findings from this study suggest that performing home-based exercise of high or moderate intensity are effective strategies to reduce the risk of developing cardiometabolic disease. Given that the feasibility and practicality of HIT in obese populations have been challenged, Scott et al. (2019) demonstrate that performing HIT at home elicits similar improvements as compared to performing HIT in a laboratory-supervised environment. Endothelial dysfunction and insulin resistance are two pathologies that are detectable early in the progression of cardiometabolic disease. Activation of eNOS is a primary determinant of endothelial function, and Scott et al. (2019) demonstrated similar increases in eNOS protein content among the three exercise groups. Interestingly, the phosphorylation status of eNOS ser1177 was decreased only when normalized to total eNOS content. While eNOS activation can be regulated by various post-translational modifications apart from ser1177 phosphorylation, the functional improvements in brachial FMD indicate that NO bioavailability was improved with training. This contention is supported by reduced protein expression of NOX2 in skeletal muscle terminal arterioles and capillaries. La Favor et al. (2016) have demonstrated that NOX-derived reactive oxygen species (ROS) contributes to endothelial dysfunction in obesity, whereas 8 weeks of interval exercise training restores endothelial function concomitant with reductions in the NOX subunits p22phox and p67phox. Thus, NOX appears to be a significant source of NO quenching and impaired endothelium-dependent dilatation in obese humans. Importantly, the findings of Scott et al. (2019) extend support for interval exercise in reducing the detrimental effects of NOX. Performing home HIT and MICT can increase endothelium-dependent dilatation as well as reduce aortic stiffness in sedentary obese adults. Scott et al. (2019) further demonstrated that Home-HIT, Home-MICT and Lab-HIT resulted in similar improvements in insulin sensitivity. A single exercise session has been reported to increase muscle insulin sensitivity via increases in insulin-stimulated muscle perfusion, Akt substrate of 160 kDa (AS160) phosphorylation and glycogen synthase activity (Sjoberg et al. 2017). The study by Scott et al. (2019) provides support for improvements in whole-body insulin sensitivity, muscle glucose transporter 4 (GLUT4) expression and muscle capillarization with 12 weeks of home-based and laboratory-supervised exercise training. These data suggest that the adaptations in muscle glucose delivery as well as disposal can be conveyed even when exercise is performed with limited supervision at home. In addition, the improvements in substrate utilization may also have extended to improved fat metabolism. Scott et al. (2019) observed a greater number of centrally localized lipid droplets following exercise training and an overall increase in intramuscular triglycerides. The increased availability of lipids was matched with increased mitochondrial density, suggesting enhanced lipid turnover. Physical (e.g. facility access and transportation) and psychological (e.g. self-esteem) barriers should be considered when promoting exercise to increase adherence, and to ultimately maximize the health benefits of exercise. Scott et al. (2019) utilized a strategy that can translate to practical settings for individuals who are naïve to training. Participants were allowed to choose their training group to better reflect the real-world setting and were encouraged to perform bodyweight exercises that did not require equipment. Previous interventions that promote home- or community-based exercise suggest that cardiometabolic disease risk may be reduced with limited supervision; however, patients with type 2 diabetes who performed 6 months of home-based exercise, following an initial supervised programme, did not retain improvements in glycaemic control (Dunstan et al. 2005). Similarly, home-based resistance exercise with equipment and periodic supervision elicited a decrease in fasting insulin levels, but did not improve glycaemic control (Plotnikoff et al. 2010). Thus, improvements in glycaemic control may require more strict supervision following the onset of type 2 diabetes. The study by Scott et al. (2019), conversely, suggests that virtually monitoring HR data of obese non-diabetic participants improves insulin sensitivity and vascular function to the same degree as laboratory-supervised exercise. These findings merit further research to determine whether patients with type 2 diabetes can exhibit similar adaptations with virtually monitored home exercise. Participants were allowed to choose their groups, and those in the Home-MICT group were also able to choose the exercise mode of each session (i.e. swimming, cycling, walking/running). Although the translation to real-world settings holds merit, it is difficult to determine if the same results would have been achieved if the participants were randomly assigned to each group. Randomization can also reveal the effectiveness and feasibility of maintaining desired exercise intensities during the different types of exercise. There were likely to be differences in the relative intensities achieved during different exercise modes based on body position (i.e. prone, sitting, standing). Thus, knowing the number of participants choosing the specific modes of exercise would help to better interpret the findings. Nonetheless, the functional improvements observed with home-based exercise suggest that virtually monitoring home-based exercise may be a suitable strategy to initiate adherence to physical activity in individuals with limited training history or access to facilities. Scott et al. (2019) provide evidence that eliminating external barriers to participating in physical activity, while providing some degree of supervision, is an effective strategy to reduce the risk of developing cardiovascular and metabolic disease. This is important for exercise professionals and clinicians to consider when developing exercise programmes with the goal of improving glucose homeostasis and vascular health in individuals who are sedentary and may be naïve to training. The observations of increased eNOS/NOX concomitant with improved endothelium-dependent dilatation and insulin sensitivity suggests that two early predictors of cardiovascular disease and type 2 diabetes – endothelial dysfunction and insulin resistance – can be delayed or prevented with virtually monitored home-based exercise. Future studies can provide better mechanistic insight into the microvascular adaptations that coincided with Home-HIT, including activation of eNOS and specific NOX isoforms. Although the study was underpowered to detect between-group differences in cardiorespiratory fitness, future larger trials can study Home-HIT and determine the applicability in different populations (e.g. ethnic backgrounds, those with clinical diseases). None. Sole author. C.A.M. is funded by NIH: 2R15HL113854-02. I would like to thank my advisor, Dr Robert C. Hickner, for his valuable feedback and discussions relating to the manuscript." @default.
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• W2979411791 title "Home exercise reduces cardiometabolic disease risk" @default.
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