Objective: The current randomized controlled trial tested the hypothesis that both aerobic training and dynamic resistance training will improve inflammation, endothelial function and 24-h ambulatory blood pressure (ABP) in middle-aged adults with hypertension, but aerobic training would be more effective. Methods: Forty-two hypertensive patients on at least one antihypertensive medication (19 men/23 women; 30–59 years of age) were randomly assigned to 12 weeks of supervised aerobic training (n = 15), resistance training (n = 15) or a nonexercise control (n = 12) group. Inflammation, endothelial function, 24-h ABP and related measures were evaluated at pre and postintervention. Results: We found that aerobic training and resistance training were well tolerated. Both aerobic training and resistance training reduced daytime systolic ABP (−7.2 ± 7.9 and −4.4 ± 5.8 mmHg; P < 0.05) and 24-h systolic ABP (−5.6 ± 6.2 and −3.2 ± 6.4 mmHg; P < 0.05). aerobic training and resistance training both improved brachial artery flow-mediated dilation by 1.7 ± 2.8 and 1.4 ± 2.6%, respectively (7.59 ± 3.36 vs. 9.26 ± 2.93 and 7.24 ± 3.18 vs. 8.58 ± 2.37; pre vs. post P < 0.05). However, only aerobic training decreased markers of inflammation (C-reactive protein, monocyte chemoattractant protein-1, vascular cell adhesion molecule-1 and lectin-like oxidized LDL receptor-1) and endothelin-1 and increased nitrite and nitrate levels (P < 0.05). Conclusion: Healthcare providers should continue to emphasize aerobic training for hypertension management given the established role of nitric oxide, endothelin-1 and chronic low-level inflammation in the pathogenesis of cardiovascular disease. However, our study demonstrates that resistance training should also be encouraged for middle-aged hypertensive patients. Our results also suggest that even if patients are on antihypertensive medications, regular aerobic training and resistance training are beneficial for blood pressure control and cardiovascular disease risk reduction.

This exploratory study investigated the effects of early vs. delayed time-restricted eating (TRE) plus caloric restriction (CR) on body weight, body composition, and cardiometabolic parameters in adults with overweight and obesity. Adults (20 to 40 years) were randomized to 1 of 3 groups for 8 weeks: early TRE (eTRE; 8:00-16:00) plus CR, delayed TRE (dTRE; 12:00-20:00) plus CR, or only CR (CR; 8:00-20:00). All groups were prescribed a 25% energy deficit relative to daily energy requirements. Thirteen participants completed the study in the eTRE and CR groups, and eleven in the dTRE group (n=37). After the interventions, there was no significant difference between the three groups for any of the outcomes. Compared to baseline, significant decreases were observed in body weight (eTRE group: -4.2 kg; 95% CI, -5.6 to -2.7; dTRE group: -4.8 Kg; 95% CI, -5.9 to -3.7; CR: -4.0 kg; 95% CI, -5.9 to -2.1), fat mass (eTRE group: -2.9 kg; 95% CI, -3.9 to -1.9; dTRE group: -3.6 Kg; 95% CI, -4.6 to -2.5; CR: -3.1 kg; 95% CI, -4.3 to -1.8), and fasting glucose levels (eTRE group: -4 mg/dL; 95% CI, -8 to -1; dTRE group: -2 mg/dL; 95% CI, -8 to 3; CR: -3 mg/dL; 95% CI, -8 to 2). In a free-living setting, TRE with a caloric deficit, regardless of the time of day, promotes similar benefits in weight loss, body composition and cardiometabolic parameters. However, given the exploratory nature of our study, further investigation is needed to confirm these findings.

Purinergic signalling is a mechanism of extracellular communication that modulates events related to exercise, such as inflammation and coagulation. Herein, we evaluated the effects of acute moderate-intensity exercise on the activities of purinergic enzymes and plasma levels of adenine nucleotides in individuals with distinct metabolic characteristics. We analysed the relationship between purinergic parameters, inflammatory responses and cardiometabolic markers. Twenty-four healthy males were assigned to three groups: normal weight sedentary (n = 8), overweight sedentary (n = 8) and normal weight physically active (n = 8). The volunteers performed an acute session of moderate-intensity aerobic exercise on a treadmill at 70% ofV O 2 peak ; blood samples were drawn at baseline, immediately post-exercise and at 1 h post-exercise. Immediately post-exercise, all subjects showed increases in ATP, ADP, AMP and p-nitrophenyl thymidine 5′-monophosphate hydrolysis, while AMP hydrolysis remained increased at 1 h after exercise. High-performance liquid chromatography analysis demonstrated lower levels of ATP and ADP at post-and 1 h post-exercise in all groups. Conversely, adenosine and inosine levels increased at postexercise, but only adenosine remained augmented at 1 h after exercise in all groups. With regard to inflammatory responses, the exercise protocol increased tumour necrosis factor α (TNF-α) and interleukin 8 (IL-8) concentrations in all subjects, but only TNF-α remained elevated at 1 h after exercise. Significant correlations were found between the activity of 5′-nucleotidase, adenosine levels,V O 2 peak , triglyceride, TNF-α and IL-8 levels. Our findings suggest a purinergic signalling pathway that participates, at least partially, in the inflammatory responses triggered by acute moderate-intensity

Background: Reduced glutathione (GSH) is one of the main thiols involved in antioxidant defense. Changes in circulatory levels of GSH during exercise are associated with hyperthermia and dehydration. The mechanisms by which these alterations occur are not entirely known. We hypothesize that erythrocytes could be an important source of circulatory GSH during heat stress conditions. We performed two separate experiments to address this hypothesis. Methods: In the first experiment, we sought to investigate the impact of exercise in the heat and dehydration on erythrocyte levels of GSH. A total of 10 men performed 60 min of cycling at 60% VO2peak in the heat (38.0 ± 0.9 °C) or in a control temperate environment (23.0 ± 1.0 °C), both with and without dehydration. Relative humidity ranged from 50 to 70%. Blood samples were taken before and after exercise to measure GSH and oxidized (GSSG) glutathione. In the second experiment, erythrocytes were isolated from blood samples taken at rest and heated in vitro to determine the impact of heat on erythrocyte glutathione content. Tubes with erythrocytes were exposed to water baths at different temperatures; one tube was exposed to a water bath at 35 °C and the other tube to a water bath at 41 °C for a period of 30 min. After exposure to heat, plasma and erythrocytes were extracted for GSH and GSSG analyses. Results: Dehydration decreased circulatory GSH, regardless of ambient temperature (temperate and heat decreased 15.35% and 30.31%, respectively), resulting in an altered redox balance. Heat increased GSH levels in vitro. Conclusion: Our data suggest that dehydration decreases circulatory GSH levels regardless of environmental temperature. In addition, in vitro data suggests that erythrocytes may contribute to the release of GSH during exposure to heat stress.

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