Regular aerobic exercise has numerous benefits on human physiology, arguably by serving as a hormetic stressor resulting in positive adaptations over time. It has long been known that aerobic exercise at a variety of intensities and durations induces intestinal permeability, which is a feature of many pathologies of the gastrointestinal tract and metabolic diseases. Given the health benefits of exercise, it seems unlikely that intestinal permeability induced by exercise outweighs the positive adaptations. In fact, a growing body of evidence suggests adoption of exercise regimens lasting weeks to months improves indicators of intestinal permeability. In this brief review, we summarize factors contributing to acute exercise-induced intestinal permeability and what is known about chronic exercise and the gut barrier. Additionally, we outline known and theoretical adaptations of the gut to chronic exercise that may explain emerging reports that exercise improves markers of gut integrity.
Fasting triacylglycerols have long been associated with cardiovascular disease (CVD) and other cardiometabolic conditions. Evidence suggests that non-fasting triglycerides (i.e. measured within 8 h of eating) better predict CVD than fasting triglycerides, which has led several organisations to recommend non-fasting lipid panels as the new clinical standard. However, unstandardised assessment protocols associated with non-fasting triglyceride measurement may lead to misclassification, with at-risk individuals being overlooked. A third type of triglyceride assessment, postprandial testing, is more controlled, yet historically has been difficult to implement due to the time and effort required to execute it. Here, we review differences in assessment, the underlying physiology and the pathophysiological relevance of elevated fasting, non-fasting and postprandial triglycerides. We also present data suggesting that there may be a distinct advantage of postprandial triglycerides, even over non-fasting triglycerides, for early detection of CVD risk and offer suggestions to make postprandial protocols more clinically feasible.
Adverse childhood experiences (ACEs) are psychosocial stressors that occur during sensitive developmental windows and are associated with increased lifetime cardiovascular disease (CVD) risk in a dose-dependent manner. Vascular endothelial dysfunction is a pathophysiological mechanism that promotes hypertension and CVD, and may be a mechanism by which ACEs contribute to lifetime CVD risk. We examined whether exposure to ACEs is associated with reduced vascular endothelial function (VEF) in otherwise healthy, young adult women (20.7 ± 3 years) with (ACE+) versus without (ACE-) ACEs, explored whether differences in circulating SIRT1 or systemic oxidative stress could explain ACEs-related differences in VEF, and examined the ability of a pilot, 8-week exercise intervention to augment VEF and SIRT1, or reduce oxidized LDL cholesterol (oxLDL) in ACE+ young adult women. Forty-two otherwise healthy young adults completed this study. Prior to the intervention, VEF (P = 0.002) and SIRT1 (P = 0.004) were lower in the ACE+ than ACE- group, but oxLDL concentrations were not different (P = 0.77). There were also significant associations (P ≤ 0.04) among FMD, SIRT1, and oxLDL in the ACE+, but not ACE- group. Adjusting for circulating SIRT1 and oxLDL reduced the differences in FMD observed between groups (P = 0.10), but only SIRT1 was a significant adjuster of the means (P < 0.05). The exercise intervention employed was unable to enhance VEF or SIRT1 in the ACE+ exercise group. Our data suggest that ACEs likely increase susceptibility to hypertension and CVD via reduced vascular function, perhaps through a SIRT1 pathway-related mechanism.
Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver disease that includes non-alcoholic steatohepatitis (non-alcoholic steatohepatitis [NASH]) and has been recognized as the most prevalent chronic liver disease worldwide. 1 The prevalence of NAFLD is growing in concert with sedentary lifestyles, poor dietary habits and obesity rates, which are as high as 40% in adults and 19% in children. 2 Unfortunately, roughly 95% of obese adults have NAFLD and half the US population is expected to be obese by 2030, 3 making NAFLD a major public health concern.Components of the metabolic syndrome including insulin resistance, excess visceral and total adiposity, and dyslipidemia, are
Background: A large post-meal triglyceride (TG) response is an independent risk factor for cardiovascular disease, but postprandial lipemia assessments are not clinically practical in their current form. Therefore, we assessed the validity of an abbreviated, clinically feasible protocol in measuring postprandial lipemia. Method: Eighteen healthy adults (8 male and 10 female) completed 3 high-fat meal trials in random order: (1) a Standard in Lab (SL) protocol wherein blood draws (to determine TG) were made from a catheter at baseline and hourly for 6 h; (2) an Abbreviated in Lab (AL) protocol in which participants remained in the laboratory but blood draws were only made at baseline and 4 h post-meal; and (3) an Abbreviated with Freedom (AF) protocol in which participants vacated the laboratory between the meal and the 4-h blood draw. Results: TG increase from baseline was very similar (p = 0.93) across the 3 trials (SL: 68.5 ± 62.7 mg/dL; AL: 71.1 ± 58.0 mg/dL; AF: 66.7 ± 46.4 mg/dL), as were 4-h TG levels (SL: 144.6 ± 84.2 mg/dL; AL: 171.4 ± 88.2 mg/dL; AF: 157.7 ± 76.7 mg/dL; p = 0.49). Similarly, total and incremental area under the curve (AUC) were not significantly different across the trials (p = 0.12 and 0.91, respectively). Conclusion: The TG results of the clinically feasible, abbreviated protocol were similar to those of the more exhaustive standard protocol. The AF protocol could be a valid and feasible clinical tool for measurement of postprandial lipemia and assessment of cardiovascular risk, although studies in larger and more diverse cohorts are needed.
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