Vascular dysfunction and exercise intolerance contribute to chronic kidney disease (CKD)-related cardiovascular disease. Passive heat exposure provides a physiological stimulus for beneficial vascular adaptations and improvements in exercise capacity but has not yet been investigated in CKD. The purpose of this pilot study was to examine the physiological response to an acute bout of passive heat exposure in patients with CKD. In this randomized, crossover trial, 10 participants with Stage G2-G4 CKD were enrolled (means ± SE; age, 41 ± 4 yr; 6 females; estimated glomerular filtration rate, 55 ± 7 mL/min/1.73 m2). After completing a baseline visit, participants completed two experimental visits: passive heat exposure via far-infrared sauna (HT; 25 min, 60°C) and thermoneutral control (CON; 25 min, 22°C). Macrovascular function, assessed by flow-mediated dilation (FMD), and microvascular function, assessed by the blood flow response to passive limb movement, were measured after a 60-min recovery period following exposure on each experimental visit. Exercise capacity was assessed with the 6-min walk test. Urinary markers of kidney function and injury were collected immediately and over 24 h following visits. FMD (3.84 ± 0.61 vs. 6.68 ± 0.76%, P < 0.01) and leg blood flow response to passive limb movement (area under the curve, 179 ± 29 vs. 243 ± 23 arbitrary units, P = 0.01) were greater following HT compared with CON. There was a clinically meaningful difference in 6-min walk distance between CON (632 ± 29 yards) and HT (670 ± 30 yards, P < 0.01). There were no significant changes in kidney function or biomarkers of acute kidney injury following HT. In this pilot study, a single bout of passive heat exposure acutely improved vascular function and exercise capacity in patients with CKD.NEW & NOTEWORTHY This is the first known study to examine the acute vascular, renal, and exercise response to a single bout of passive heat exposure in chronic kidney disease (CKD). Macrovascular function, microvascular function, and exercise capacity were acutely greater after a single session of passive heating, without any effect on kidney function or markers of kidney injury. These preliminary pilot findings could inform future clinical trials of chronic heat therapy for cardiovascular health in CKD.

Chronic anxiety, evidenced by a clinical diagnosis of generalized anxiety disorder (GAD) or symptoms consistent with GAD, has been linked to irregular sleep patterns that, when present, are accompanied by impaired vascular function and reduced acute blood pressure control, contributing to elevated cardiovascular disease risk. We performed a retrospective analysis to determine whether resistance exercise training (RET) improves outcomes in individuals with chronic anxiety previously identified as having elevated sleep irregularity and concomitant physiological impairments. Twenty young adults (25 ± 4 yr) with chronic anxiety completed 10 wk of RET. Based on prior characterization, participants were stratified into high (≥67.67 min) and low (<67.67 min) total sleep time irregularity (TSTI) groups, representing those with impaired versus relatively preserved vascular and autonomic function, respectively. Primary outcomes included macrovascular function (exercise-induced flow-mediated dilation; FMD) and cardiovagal baroreflex sensitivity (cBRS). Significant group × RET interactions were observed for all primary outcomes (P < 0.05). Post hoc analyses showed that the high TSTI group improved FMD (P < 0.01) and cBRS (P = 0.04), whereas the low TSTI group showed no significant changes (P > 0.05). In this retrospective analysis, individuals with chronic anxiety characterized by elevated sleep irregularity and baseline impairments exhibited significant improvements in vascular and autonomic function following RET. These findings suggest that RET may be particularly effective in targeting cardiovascular dysfunction in higher-risk anxiety phenotypes.NEW & NOTEWORTHY This retrospective analysis suggests that resistance exercise training (RET) preferentially improves cardiovascular function in individuals with chronic anxiety characterized by elevated sleep irregularity and baseline vascular and autonomic impairments. Only this higher-risk subgroup exhibited significant gains in vascular function and acute blood pressure control (cardiovagal baroreflex sensitivity), highlighting the potential preferential responsiveness of RET in this higher-risk anxiety phenotype.

Chronic anxiety is a highly prevalent condition in young adults that is often associated with irregular sleep patterns, potentially augmenting cardiovascular disease (CVD) risk. Sleep irregularity is significantly associated with elevated oxidative stress and lower vascular function and blood pressure control in individuals with chronic anxiety. This study examined whether these impairments in vascular function and blood pressure control are driven by elevations in oxidative stress. Twenty-five young adults (24 ± 4 yr) with generalized anxiety disorder (GAD) or elevated GAD symptoms were assessed for total sleep time irregularity (TSTI) via wrist-worn accelerometry and separated into high TSTI and low TSTI groups via median split. Precursors to CVD development including oxidative stress (whole blood superoxide levels), vascular function (exercise-induced flow-mediated dilation), and blood pressure control (cardiovagal baroreflex sensitivity) were evaluated in both groups following both acute antioxidant (alpha-lipoic acid, vitamin C, and vitamin E) or placebo (microcrystalline cellulose) supplementation. The high TSTI group displayed significantly greater oxidative stress, significantly lower vascular function, and significantly lower blood pressure control. Following antioxidant supplementation, oxidative stress and blood pressure control were significantly improved in the high TSTI group, whereas vascular function was significantly improved independent of group. Antioxidant supplementation reduced oxidative stress and normalized blood pressure control differences between groups, implicating oxidative stress as a key mechanism linking sleep irregularity and CVD risk in young adults with chronic anxiety.NEW & NOTEWORTHY This study is the first to identify oxidative stress as a mediator of early cardiovascular disease (CVD) risk associated with total sleep time irregularity (TSTI) in young adults with chronic anxiety. Antioxidant supplementation reduced oxidative stress and improved blood pressure regulation in the high TSTI group. These findings suggest that oxidative stress plays a central role in linking chronic anxiety, sleep irregularity, and elevated CVD risk.

Post-traumatic stress disorder (PTSD) is associated with elevated cardiovascular disease (CVD) risk, yet the underlying physiological characterization in young adults remain unclear. This study examines whether autonomic and/or vascular dysfunction predominates as an early precursor to CVD development in young adults with PTSD and explores the potential contribution of oxidative stress (OXS). Forty-four young adults (22 PTSD, 22 controls; 19F/3M per group) free from cardiometabolic disease were evaluated for OXS, autonomic regulation and vascular function. OXS was quantified via electron paramagnetic resonance analysis of whole blood superoxide concentration. Autonomic function was assessed using an isometric handgrip exercise (exercise pressor reflex) and a Valsalva manoeuvre to determine cardiovagal baroreflex sensitivity (cBRS). Local vascular control was evaluated through rapid onset vasodilation (ROV) in response to a brief forearm contraction. Compared with controls, the PTSD group exhibited significantly higher resting systolic (P < 0.01) and mean arterial pressure (P = 0.04) and elevated superoxide levels (P < 0.01). cBRS was markedly reduced in PTSD during Phase IV of the Valsalva manoeuvre (P < 0.01), indicating impaired autonomic regulation. In contrast, vascular conductance and blood flow responses to the ROV and exercise pressor tests were preserved. These findings suggest that OXS and baroreflex dysfunction, rather than local vascular impairment, represent early detectable maladaptations potentially contributing to heightened CVD risk in young adults with PTSD. Early identification and mitigation of oxidative and autonomic imbalances may help prevent premature cardiovascular decline in this population.

Chronic anxiety is commonly associated with poor sleep patterns, which may contribute to an increased risk of cardiovascular disease (CVD) through mechanisms like oxidative stress, vascular dysfunction, and poor blood pressure control. As sleep disturbances, particularly poor sleep quality and/or regularity, have been independently linked to CVD development, this study explored whether sleep quality/regularity in young adults with chronic anxiety is associated with early indicators of CVD risk, specifically oxidative stress, vascular function, and blood pressure control. Twenty-eight young (24 ± 4 yr) participants with a prior clinical diagnosis of generalized anxiety disorder (GAD) or elevated GAD symptoms (GAD-7 > 10) had their sleep quality [total sleep time (TST) and sleep efficiency (SE)] and regularity [via TST/SE standard deviations (SD)] assessed for seven consecutive days. Various precursors to CVD development such as oxidative stress, brachial artery function, microvascular function, and blood pressure control [exercise pressor responses and cardiovagal baroreflex sensitivity (cBRS)] were also evaluated. Pearson's correlations were used to determine potential relationships between sleep quality/regularity and CVD precursors. Both sleep irregularity variables [SE-SD (r = 0.61; P < 0.01) and TST-SD (r = 0.39; P = 0.04)], but neither of the sleep quality variables, were positively correlated with oxidative stress. TST-SD alone was significantly associated with lower brachial artery function (r = -0.44; P = 0.02) and cBRS (r = 0.43; P = 0.02), with TST-SD median splits further highlighting these differences. The study found that irregular TST in individuals with chronic anxiety was significantly associated with higher oxidative stress, lower brachial artery function, and blunted blood pressure control (lower cBRS), key precursors of CVD.NEW & NOTEWORTHY This study examined the relationship between sleep irregularity and early cardiovascular disease (CVD) precursors in young adults with chronic anxiety. Key findings revealed that irregular total sleep time, rather than overall sleep quality, was significantly associated with greater oxidative stress, lower brachial artery function, and diminished blood pressure control. These results suggest that sleep irregularity in individuals with chronic anxiety may play a critical role in the development of CVD in this population.

Heightened muscle sympathetic nerve activity (MSNA) contributes to impaired vasodilatory capacity and vascular dysfunction associated with aging and cardiovascular disease. The contribution of elevated MSNA to the vasodilatory response during passive leg movement (PLM) has not been adequately addressed. This study sought to test the hypothesis that elevated MSNA diminishes the vasodilatory response to PLM in healthy young males (n = 11, 25 ± 2 year). Post exercise circulatory occlusion (PECO) following 2 min of isometric handgrip (HG) exercise performed at 25% (ExPECO 25%) and 40% (ExPECO 40%) of maximum voluntary contraction was used to incrementally engage the metaboreceptors and augment MSNA. Control trials were performed without PECO (ExCON 25% and ExCON 40%) to account for changes due to HG exercise. PLM was performed 2 min after the cessation of exercise and central and peripheral hemodynamics were assessed. MSNA was directly recorded by microneurography in the peroneal nerve (n = 8). Measures of MSNA (i.e., burst incidences) increased during ExPECO 25% (+ 15 ± 5 burst/100 bpm) and ExPECO 40% (+ 22 ± 4 burst/100 bpm) and returned to pre-HG levels during ExCON trials. Vasodilation, assessed by the change in leg vascular conductance during PLM, was reduced by 16% and 44% during ExPECO 25% and ExPECO 40%, respectively. These findings indicate that elevated MSNA attenuates the vasodilatory response to PLM and that the magnitude of reduction in vasodilation during PLM is graded in relation to the degree of sympathoexcitation.

Regular physical activity and endurance exercise training prevent age-related vascular endothelial dysfunction in the arm in men. However, the effects of physical activity and/or endurance exercise training in the legs, which have a greater predisposition for vascular disease, have not been completely elucidated. This study sought to examine the impact of aging, physical activity, and endurance exercise training on leg vascular function in men. Flow-mediated dilation (FMD) of the superficial femoral and popliteal arteries (SFA and PA, respectively) was assessed in a total of 39 men, comprised of 10 young sedentary (Y; 23 ± 2 yr), 8 older sedentary (OS; 76 ± 8 yr), 9 older physically active (OA; 71 ± 8 yr), and 12 older endurance exercise trained (OT) subjects with exceptional aerobic exercise capacity (V̇o2max) for their age (70 ± 3 yr, V̇o2max = 53 ± 6 mL·kg-1·min-1). FMD was lower in the OS group compared with the Y in the SFA (Y: 4.3 ± 2.1%, OS: 1.7 ± 1.0%, P = 0.005) and PA (Y: 5.8 ± 2.4%, OS: 1.9 ± 1.1%, P < 0.05). SFA and PA FMD were not different from OS in the OA group (SFA: 2.8 ± 1.5%; PA: 1.6 ± 1.0%) but were higher than OS in the OT group (SFA: 3.4 ± 2.3%, P = 0.043; PA: 4.2 ± 3.0%, P = 0.025) and not different from Y. There was evidence of a moderate-strong correlation between SFA (r = 0.32, P = 0.052) and PA (0.36, P = 0.037) FMD and V̇o2max but not physical activity levels. These findings suggest that habitual physical activity in general, and endurance exercise training in particular, diminishes the detrimental effect of aging on lower limb vascular function in men, and this may be linked to an augmented V̇o2max.NEW & NOTEWORTHY In the current study, we provide evidence of a relation between high levels of physical activity associated with lifelong endurance exercise training and protection from age-related declines in vascular endothelial function in the lower limb in men. Moreover, our findings suggest that aerobic fitness, in particular, may confer the benefits of endurance exercise training in maintaining lower limb endothelial function with advancing age.

PURPOSE: Mental health disorders like anxiety, depression, and PTSD affect many in the U.S., often co-occurring and increasing cardiovascular disease (CVD) risk, especially in women. Resistance exercise training (RET) shows promise in improving mental health, muscle strength, and metabolic health while potentially mitigating cardiovascular dysfunction. This study examines whether RET enhances blood pressure control—a key CVD risk factor—in young women with anxiety, mood, or trauma-related disorders. We hypothesized that RET would improve blood pressure control, with the most pronounced benefits observed in individuals with the poorest initial blood pressure regulation. METHODS: Twenty-four young women with anxiety, mood, or trauma-related mental health disorders completed 10 weeks of RET. Symptoms (anxiety and depression), resting blood pressure (BP), and BP control were evaluated pre- and post-RET. BP control was assessed via exercise pressor responses (2-minute isometric exercise at 30% maximal voluntary contraction) and cardiovagal baroreflex sensitivity (cBRS: 15-second breath hold). Participants were divided into “high” and “low” function sub-groups via median splits to assess RET effectiveness based on pre-RET values, with group x RET interactions analyzed. RESULTS: When all participants were examined together, psychological symptoms (p < 0.01 for all) and resting BP (MAP (Pre-RET: 88 ± 7; Post-RET: 84 ± 9 mmHg); p < 0.01) were significantly improved following RET, but no significant improvements in any BP control variables were observed. Following median-splits of all variables, it was revealed the RET was highly effective at improving certain aspects of BP control during exercise in those with the “lowest” BP control. This was evident by reduced DBP responses to isometric exercise (group x RET interaction effect: p = 0.04) [“low” group (∆DBP: Pre-RET: 12.9 ± 2.3; Post-RET: 6.5 ± 7.8 mmHg; p < 0.01); “high” group (∆DBP: Pre-RET: 5.4 ± 2.7; Post-RET: 7.5 ± 5.1 mmHg; p = 0.32), and improved cBRS (group x RET interaction effect: p = 0.04), specific to improved heart rate responses to rapid elevations in systolic blood pressure [“low” group (cBRS Phase IV: Pre-RET: 5.5 ± 2.5; Post-RET: 10.2 ± 4.8 mmHg.ms -1 ; p = 0.03); “high” group (cBRS Phase IV: Pre-RET: 14.0 ± 5.4; Post-RET: 12.0 ± 6.1 mmHg.ms -1 ; p < 0.34)]. CONCLUSION: This study demonstrated that RET is a powerful intervention for significantly reducing negative psychological symptoms and lowering resting BP in young women with anxiety, mood, and/or trauma-related mental health disorders. Regarding BP control, RET had the greatest impact on participants with the most impaired regulation, characterized by heightened DBP responses during exercise and reduced cBRS following rapid blood pressure elevations. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

AbstractYoung individuals with post‐traumatic stress disorder (PTSD) display peripheral vascular and autonomic nervous system dysfunction, two factors potentially stemming from a redox imbalance. It is currently unclear if these aforementioned factors, observed at rest, alter peripheral haemodynamic responses to exercise in this population. This study examined haemodynamic responses to handgrip exercise in young individuals with PTSD following acute antioxidant (AO) supplementation. Thirteen young individuals with PTSD (age 23 ± 3 years), and 13 age‐ and sex‐matched controls (CTRL) participated in the study. Exercise‐induced changes to arm blood flow (BF), mean arterial pressure (MAP) and vascular conductance (VC) were evaluated across two workloads of rhythmic handgrip exercise (3 and 6 kg). The PTSD group participated in two visits, consuming either a placebo (PL) or AO prior to their visits. The PTSD group demonstrated significantly lower VC (P = 0.04) across all exercise workloads (vs. CTRL), which was significantly improved following AO supplementation. In the PTSD group, AO supplementation improved VC in participants possessing the lowest VC responses to handgrip exercise, with AO supplementation significantly improving VC responses (3 and 6 kg: P < 0.01) by blunting elevated exercise‐induced MAP responses (3 kg: P = 0.01; 6 kg: P < 0.01). Lower VC responses during handgrip exercise were improved following AO supplementation in young individuals with PTSD. AO supplementation was associated with a blunting of exercise‐induced MAP responses in individuals with PTSD displaying elevated MAP responses. This study revealed that young individuals with PTSD exhibit abnormal, peripherally mediated exercise responses that may be linked to a redox imbalance.

Background Electronic (e-) cigarettes are increasingly popular tobacco products on the US market. Traditional tobacco products are known to cause vascular dysfunction, one of the earliest indicators of cardiovascular disease (CVD) development. However, little is known about the effect of regular e-cigarette use on vascular function. The purpose of this study was to investigate the impact of regular e-cigarette use on vascular function and cardiovascular health in young, healthy adults. Methods Twenty-one regular users of e-cigarettes (ECU) and twenty-one demographically matched non-users (NU) completed this study. Vascular health was assessed in the cutaneous microcirculation through different reactivity tests to evaluate overall functionality, endothelium-dependent vasodilation (EDD), and endothelium-independent vasodilation (EID). Macrovascular function was assessed using flow-mediated dilation (FMD). Results Our results suggest that regular users of e-cigarettes present with premature microvascular impairment when compared to non-users. Specifically, they exhibit lower hyperemic ( p = 0.003), thermal ( p = 0.010), and EDD ( p = 0.004) responses. No differences in EID between the groups were identified. We also identified that individuals who use e-cigarettes for longer than 3 years also present with systemic manifestations, as observed by significantly reduced macrovascular ( p = 0.002) and microvascular ( p ≤ 0.044) function. Conclusions Our novel data suggests that young, apparently healthy, regular users of e-cigarettes present with premature vascular dysfunction in the microcirculation when compared to non-users. We have also identified systemic vascular dysfunction affecting both the micro and macrovasculature in those young individuals who used e-cigarettes for longer than 3 years. Taken together, these findings associate regular e-cigarette use with premature vascular dysfunctions and adverse cardiovascular outcomes.

Electronic nicotine delivery systems, often referred to as e-cigarettes, are popular tobacco products frequently advertised as safer alternatives to traditional cigarettes despite preliminary data suggesting a potential negative cardiovascular impact. Cardiorespiratory fitness is a critical cardiovascular health marker that is diminished in individuals who consume traditional tobacco products. Whether the use of e-cigarettes impacts cardiorespiratory fitness is currently unknown. Thus, the purpose of this study was to investigate the impact of regular e-cigarette use on cardiorespiratory fitness in young healthy adults. Twenty-six users of e-cigarettes (ECU, 13 males, and 13 females; age: 24 ± 3 yr; e-cigarette usage 4 ± 2 yr) and 16 demographically matched nonusers (NU, 6 males, and 10 females; age: 23 ± 3 yr) participated in this study. Cardiorespiratory fitness was measured by peak oxygen consumption (V̇o2peak) during a cardiopulmonary exercise test. Measurements of chronotropic response, hemodynamic, oxygen extraction, and utilization were also evaluated. Our results suggest that regular users of e-cigarettes exhibited significantly lower peak oxygen consumption when compared with nonusers, even when controlled by fat-free mass and lean body mass. Hemodynamic changes were not different between both groups during exercise, whereas lower chronotropic responses and skeletal muscle oxygen utilization were observed in users of e-cigarettes. Results from the present study demonstrate that young, apparently healthy, regular users of e-cigarettes exhibit significantly reduced cardiorespiratory fitness, lower chronotropic response, and impaired skeletal muscle oxygen utilization during exercise. Overall, our findings contribute to the growing body of evidence that supports adverse effects of regular e-cigarette use on cardiovascular health.NEW & NOTEWORTHY E-cigarettes are tobacco products frequently used by youth and young adults. Little is known about the long-term health effects of their prolonged use. Results from the present study demonstrate that young, apparently healthy, regular users of e-cigarettes exhibit significantly reduced cardiorespiratory fitness, a marker of cardiovascular health and a predictor of all-cause mortality. We also identified that the young users of e-cigarettes present with lower chronotropic response and impaired skeletal muscle oxygen utilization during exercise.

Purpose: Young non-Hispanic black (BL) males have displayed lower blood flow (BF) and vascular conductance (VC), but intact functional sympatholysis, during upper limb exercise when compared to non-Hispanic white (WH) males. This study sought to explore if similar differences were also present in the lower limbs.Methods: Thirteen young BL males and thirteen WH males completed one visit comprised of rhythmic lower limb (plantar flexion) exercise as well as upper limb (handgrip) exercise for a limb-specific comparison. Limb BF, mean arterial pressure (MAP), and VC were evaluated at three submaximal workloads (8, 16, and 24 kg). To determine potential limb differences in functional sympatholysis, the impact of sympathetic nervous system activation (via cold-pressor test (CPT)) was evaluated at rest and during steady state exercise (30 % of maximal voluntary contraction) on a subsequent visit.Results: MAP responses to lower and upper limb exercise were elevated in young BL males (vs WH males), resulting in significantly lower VC responses in the upper limb, but not the lower limb. Further, BL males, when compared to WH males, revealed no differences in functional sympatholysis, evident by similar responses in both the exercising leg and arm VC during CPT.Conclusion: The findings of the current study indicate that although elevated MAP responses were observed during both lower and upper limb exercise in young BL males, vascular conductance was only hindered in the upper limbs. This may potentially highlight enhanced compensatory mechanisms in the lower limb (vs upper limb) to maintain perfusion in young BL males.

BACKGROUND: Electronic cigarettes (e-cigs) are popular tobacco products that are currently advertised as a safer alternative to traditional cigarettes. Preliminary data, primarily from animal studies, suggests that e-cigs are associated with an increased cardiovascular disease (CVD) risk. Cardiorespiratory fitness is a marker of cardiovascular (CV) health and a predictor of CV mortality, which is diminished in traditional tobacco users. However, the effect of chronic e-cigs usage on cardiorespiratory fitness and associated CVD risk in otherwise healthy individuals without established CVD or CVD risk factor, is currently unknown. PURPOSE: The purpose of this study was to investigate the impact of chronic e-cig use on cardiorespiratory fitness and CVD risk in healthy young adults. METHODS: Ten chronic e-cig users (ECU, 4 males and 6 females; age: 24±3 yr; e-cigs usage 3±1.5 yr.) and ten demographical matched, never users (NU, 4 males and 6 females; age: 22.7±2 yr.) participated in this study. Cardiorespiratory fitness was measured by peak oxygen consumption (VO2peak) via a respiratory gas exchange analyzer during a cardiopulmonary exercise test. CVD risk was calculated using Framingham’s 30-year CVD risk score accounting for 8 risk factors (age, sex, systolic blood pressure, total cholesterol, high-density lipoprotein, presence of diabetes mellitus, hypertension treatment, and smoking status). RESULTS: Chronic e-cig users exhibited significantly lower VO2peak (ECU vs. NU; 30.9±4.9 vs. 37.8±6.4 ml/kg/min; p=0.015) and percent predicted (ECU vs. NU; 85.9±16 vs. 105.4±14 % predicted; p=0.001) when compared to never users. Framingham’s 30-year CVD risk score was significantly higher in ECU than in NU (7.7± 4.8, vs. 2.7±0.8 %; p=0.017). Furthermore, an inverse association was identified between VO2peak and 30-year CVD risk ( r=-0.720; p= 0.030). CONCLUSIONS: For the first time, we have identified significantly reduced cardiorespiratory fitness, a marker of CV health and mortality risk, in chronic e-cig users when compared to never users. In addition, chronic e-cig users exhibit higher CVD risk scores. Results from our study imply a negative effect of chronic e-cig use on CV health in otherwise young, apparently healthy adults. Future studies are warranted to investigate the long-term effects of e-cig use on CV health. Supported in part by a Rapid Response Project NIDA/FDA (PRM). Supported in part by a Rapid Response Project NIDA/FDA (PRM). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Mental health disorders (MHD), such as generalized anxiety disorder (GAD) and posttraumatic stress disorder (PTSD), are debilitating psychiatric conditions that are associated with a greater risk of developing cardiovascular disease (CVD). This elevated CVD risk may be linked to peripheral vascular dysfunction and augmented blood pressure (BP) reactivity, two factors that can disrupt blood flow/nutrients delivery to active tissues and impede defense against vascular insults leading to the development of atherosclerosis and hypertension. Resistance training (RT) has been previously implemented to improve psychological symptoms in individuals with MHD, but the extent is unknown to which RT can potentially reduce CVD risk, specifically by improving vascular function and reducing BP reactivity in individuals with MHD. PURPOSE: The study sought to determine the impact of 10 weeks of RT on vascular function and BP reactivity in individuals with MHD. METHODS: Twelve young individuals with a previously diagnosed MHD (GAD: n = 9; PTSD: n = 3; 10 females/2 males) completed 10 weeks of RT (3 days/week; exercise sessions = 3 sets of bench press, squat, bent-over row, and Romanian deadlift @ 80% one repetition maximum). Microvascular function (MF) was assessed pre- and post-training via blood flow (BF) responses to a two-second isometric handgrip contraction (30% pre-training maximal voluntary contraction (MVC)). BP reactivity was evaluated pre- and post-training via changes to systolic (SBP) and diastolic (DBP) blood pressure during a two-minute isometric handgrip contraction (30% MVC). RESULTS: Following the 10 weeks of RT, individuals with MHD reported significantly greater MF [∆ BF (PRE: 108 ± 77; POST: 139 ± 97 milliliters.minute-1; p = 0.04); BF area-under-the-curve (PRE: 18 ± 13; POST: 25 ± 19 milliliters; p = 0.04)] and lower BP reactivity [∆ SBP @ 2 minutes (PRE: 23 ± 19; POST: 15 ± 10 mmHg; p = 0.02); ∆ DBP @ 2 minutes (PRE: 13 ± 8; POST: 8 ± 9 mmHg; p = 0.03)] when compared to pre-training values. CONCLUSION: This study revealed that 10 weeks of RT significantly increased MF and reduced BP reactivity in individuals with MHD. Therefore, RT may act as an effective intervention to improve both psychological and physiological symptoms of mental health disorders, thereby reducing the risk of CVD in individuals with MHD.

BACKGROUND: Microvascular dysfunction is a marker of endothelial vascular damage and is considered one of the earliest indicators of cardiovascular disease (CVD) development. Frequent cannabis use has been previously linked to increased CVD risk. However, whether microvascular health is impacted by cannabis use in otherwise healthy young adults has not been explored yet. PURPOSE: The purpose of this study was to investigate the impact of frequent cannabis usage on microvascular health in young healthy adults. METHODS: Thirteen frequent cannabis users (CU, 5 males and 8 females; age:23±3 yo; used cannabis 2.5±2 days/week) and thirteen demographical matched never users (NU, 5 males and 8 females; age:22±1 yo) completed a comprehensive assessment of microvascular function. Microvascular health was assessed using Laser Doppler Imaging coupled with Post Occlusive Reactive Hyperemia (PORH), to evaluate overall microvascular function, and Local Thermal Hyperemia (LTH) to evaluate neurogenic and endothelial mechanisms of vascular function. Blood flow was calculated as cutaneous vascular conductance, considering red blood cell flux and mean arterial blood pressure. RESULTS: Cannabis users exhibited significantly ( p=0.01) lower microvascular function when compared to never users (PORH, CU: 0.68±0.18 vs. NU: 0.85±0.14 mmHg/PU). Of note, microvascular function was significantly ( p=0.03) reduced in those that use cannabis more than 2.5 days/week (n=5; 0.55±0.10) when compared to those who used it less frequently (n=8; 0.76±0.18 mmHg/PU). In addition, neurogenic mechanisms (CU:1.31±0.57 vs. NU: 1.89±0.48 mmHg/PU; p=0.009) and endothelial mechanisms (CU: 1.61±0.44 vs. NU: 1.96±0.35 mmHg/PU; p=0.03) were significantly lower in cannabis users when compared to never users. CONCLUSIONS: Our results suggest that frequent cannabis users exhibit reduced microvascular health in comparison to never users, suggesting worse long-term CVD outcomes. Specifically, those that use cannabis more than 2 times per week exhibit lower microvascular function. In addition, cannabis use negatively impact neurogenic and endothelial microvascular mechanisms that warrant further investigation. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Objectives: Cardiorespiratory fitness (CRF) is influenced by body composition quantity and quality in heart failure with preserved ejection fraction (HFpEF) and obesity. Bioelectrical impedance analysis (BIA) provides a noninvasive quantitative and qualitative body composition assessment. The aim of this study was to determine the role of phase angle (PhA), a BIA-measure of skeletal muscle quality and body cell mass, on CRF in patients with obesity and HFpEF. Methods: Fifty-nine consecutive outpatients with HFpEF underwent cardiopulmonary exercise testing to measure CRF. Single -frequency segmental BIA was used to measure PhA and body composition quantity. Resting Doppler echocardiography and biomarkers were measured to assess cardiac function and systemic inflammation. Results: Compared with patients with lower PhA, patients with higher PhA (above mean 5.8) presented a greater absolute peak oxygen consumption (V0(2); 1.83 [1.3-2.1] versus 1.39 [1.1-1.6] L/min, P= 0.003), VO2 peak adjusted for body weight (17.5 [12.3-18.1] versus 13.3 [12.7-15.2] mL/kg/min, P = 0.040), and a lower edema index (48.7 [2.9] versus 51.4% [2.7], P < 0.001) and N-terminal pro-B-type natriuretic peptide (NTproBNP; 64 [50-121] versus 183 [68-343.5] pg/dL, P < 0.001). In the overall sample, PhA was correlated with absolute VO2 peak (r = 0.468, P < 0.001), V02 peak adjusted for body weight (r = 0.368, P = 0.004), V02 peak adjusted for fat-free mass (r = 0.315, P = 0.015), edema index (r = 0.508, P < 0.001), and NT-proBNP (r = 0.579, P < 0.001). PhA remained a significant predictor for CRF even after adjustment for potential confounders and HFpEF severity. Conclusion: In patients with obesity and HFpEF, a greater PhA is an independent predictor for favorable CRF. (c) 2023 Elsevier Inc. All rights reserved.

This study examined if high sodium (HS) intake in salt resistant (SR) individuals attenuates brachial artery (BA) flow-mediated dilation in response to reactive (occlusion) and active (exercise) hyperemia. In SR individuals, HS intake impaired reactive hyperemia-induced BA dilation, but not exercise-induced BA dilation. This finding suggests that although brachial artery nitric oxide bioavailability may be reduced following HS intake, the redundant mechanisms associated with adequate upper limb blood flow regulation during exercise are maintained.