Abstract Insulin resistance (IR) is a key pathophysiological link between metabolic syndrome and type 2 diabetes. Among people living with HIV (PLWH), both antiretroviral therapy (ART) and chronic immune activation may potentiate IR. This study aimed to identify clinical and cardiometabolic correlates of IR. We conducted a cross‐sectional study among 233 adults (142 PLWH and 91 people without HIV) attending routine medical checkups at Livingstone University Teaching Hospital, Zambia. Fasting glucose and insulin were used to calculate HOMA2‐IR, with values >1.9 defining IR. Anthropometry, blood pressure, lipid parameters, hs‐CRP, renal function, and echocardiographic measures were assessed. Multivariable logistic regression estimated adjusted odds ratios (aORs) and 95% confidence intervals, with HIV status retained a priori. Model selection emphasized parsimony, while multicollinearity was assessed using Spearman correlations and variance inflation factors (VIFs). Highly correlated predictors were not entered simultaneously. Model discrimination and calibration were assessed using the AUC and Hosmer‐Lemeshow goodness‐of‐fit test, respectively. IR was present in 37 of 233 participants (15.9%). Compared with participants without IR, those with IR had higher BMI (28.4 vs. 24.45 kg/m 2 , p = 0.0002), waist circumference (99.7 vs. 82.5 cm, p < 0.0001), total cholesterol (4.87 vs. 4.31 mmol/L, p = 0.046), triglycerides (0.950 vs. 0.755 mmol/L, p = 0.0068), and VLDL cholesterol (0.400 vs. 0.300 mmol/L, p = 0.005), as well as higher hs‐CRP concentrations ( p = 0.0008). IVSD and LVPWD were also greater among participants with IR ( p = 0.002 and p = 0.016, respectively). In the parsimonious multivariable model, waist circumference was independently associated with higher odds of IR (aOR 1.045 per cm; 95% CI: 1.012–1.080; p = 0.008), while HIV status, hypertension, triglycerides, and IVSD were not independently associated with IR. The model demonstrated moderate discrimination (AUC = 0.767; 95% CI: 0.676–0.858) with no evidence of significant lack of calibration (Hosmer–Lemeshow p = 0.164). IR was present in approximately one in six adults in this high HIV‐burden setting and was characterized by greater adiposity, dyslipidemia, inflammation, and cardiac structural differences. After adjustment, WC was the only independent correlate of IR, while HIV status was not independently associated. These findings underscore the importance of incorporating adiposity and broader cardiometabolic assessment into routine care, including HIV care, and support prospective studies to clarify the temporal and mechanistic relationships between these factors.
Abstract Variable stress (VS) is associated with increased cardiovascular risk, and its effects may be intensified during pregnancy. However, the cardiovascular impacts of VS during pregnancy on maternal health are not yet understood. Thus, the aim of this study was to evaluate the impact of VS during gestation on the endothelial function of Wistar rats in the postpartum period. Pregnant rats were divided into Control (C) and VS groups. Stress protocol was applied during the third week of gestation and lasted 8 days. After the lactation period, thoracic aorta and blood were collected for vascular reactivity assessment and platelet aggregation evaluation. Protein abundance was evaluated by western blot. Mothers who experienced VS had higher levels of corticosterone ( p = 0.04), confirming the effectiveness of the model. VS animals showed greater sensitivity ( p = 0.05) to phenylephrine and reduced relaxation by acetylcholine ( p = 0.048), as well as a lower expression of eNOSp ser1177 ( p = 0.007) and increased platelet aggregation ( p = 0.02). Variable stress at the end of gestation seems to cause alterations in both the vasoconstrictor response and endothelium‐dependent vasodilation and may be related to reduced eNOS activation that persists even after lactation.
Abstract Heart rate variability (HRV) is a popular, non‐invasive measure of cardiovagal tone. Some research has found that HRV increases from the follicular to the luteal phase of the menstrual cycle, however limited studies investigate the oral contraceptive pill (OCP) cycle. Therefore, the purpose of this study was to determine the influence of second‐generation OCP (OCP2) phase on HRV in the laboratory using electrocardiogram, and in a free‐living situation using the OURA® smart ring. 19 females using an OCP2 underwent measurements of HRV in the morning during the placebo and active phase of their OCP2 cycle and wore an OURA® smart ring. All HRV parameters, including those in the time and frequency domain, were lower in the active phase (all p 0.05) however, these differences did not persist after covarying for resting HR (all p > 0.05), except for ECG‐derived root mean square of successive differences and the standard deviation of successive differences. Diastolic and mean arterial blood pressure were lower in the active phase compared to the placebo phase ( p < 0.05). Therefore, we conclude that HRV is lower in the active phase compared to the placebo phase of the OCP2 cycle, reflecting the integrative regulation of cardiovascular homeostasis.
Abstract Maximal oxygen uptake (VO 2 max) strongly predicts all‐cause mortality, yet the step limiting it shifts along the oxygen transport cascade, and women remain underrepresented in the literature underpinning exercise guidelines. This narrative review integrates the mechanistic determinants of VO 2 max, examines how the rate‐limiting step shifts with training status, modality, environment, and biological sex, and—as its principal contribution—systematically grades the evidence for sex‐specific adaptation as established, emerging, or speculative. Convective oxygen delivery predominates in untrained individuals, whereas a substantial proportion of elite athletes develop exercise‐induced arterial hypoxemia (EIAH) reflecting pulmonary diffusion limitation. Women's lower absolute VO 2 max is largely explained by blood volume and oxygen‐carrying capacity. Sex differences in the magnitude of central cardiac remodeling are meta‐analytically supported, but the proposed time‐course difference rests on a single small cohort ( n = 12), and peripheral‐dominant adaptation derives from limited samples. Recent direct comparisons of EIAH between sexes conflict, and menstrual‐cycle phase has at most a small effect on aerobic performance. Where evidence is strongest, sex‐stratified interpretation is defensible; where weakest, individualized approaches remain a research direction. Adequately powered, sex‐stratified, methodologically standardized studies are the field's most pressing need.
Abstract To compare the acute effects of a single serving of Arabica and chicory coffee with a no‐coffee reference condition on exercise performance, cardiometabolic responses, and post‐exercise biomarkers in healthy young male adults. Twenty‐two moderately active young male adults aged 18–25 years completed a single‐blind controlled crossover study. The no‐coffee reference session was completed first; the Arabica and chicory coffee order was randomized with a 3‐day washout. Beverages (180 mL) were consumed 45 min before a 20‐m shuttle‐run test. Performance, cardiometabolic variables, and post‐exercise LPL, TNF‐α, adiponectin, and IL‐6 were assessed. Shuttle‐run performance, perceived exertion, and estimated VO 2 max did not differ among conditions (all p > 0.05). No significant condition × time interactions were observed for cardiometabolic variables. Post‐exercise LPL protein concentrations differed significantly among conditions ( p = 0.038) and were numerically highest after chicory coffee (27.72 ng/mL). IL‐6 showed a non‐significant trend toward lower concentrations after chicory coffee (38.03 pg/mL; p = 0.094); TNF‐α and adiponectin did not differ significantly. Neither beverage improved acute exercise performance. Arabica and chicory coffee nevertheless showed different post‐exercise biomarker patterns that warrant confirmation in larger crossover studies.
