Lower vascular conductance responses to handgrip exercise are improved following acute antioxidant supplementation in young individuals with post-traumatic stress disorder.

Young 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.

Exaggerated pressor responses, but unaltered blood flow regulation and functional sympatholysis during lower limb exercise in young, non-Hispanic black males.

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.

Impact of acute antioxidant supplementation on vascular function and autonomic nervous system modulation in young adults with PTSD.

Posttraumatic stress disorder (PTSD) has been associated with an increase in risk of cardiovascular disease (CVD). The goal of this study was to determine if peripheral vascular dysfunction, a precursor to CVD, was present in young adults with PTSD, and if an acute antioxidant (AO) supplementation could modify this potential PTSD-induced vascular dysfunction. Thirteen individuals with PTSD were recruited for this investigation and were compared with 35 age- and sex-matched controls (CTRL). The PTSD group participated in two visits, consuming either a placebo (PTSD-PL) or antioxidants (PTSD-AO; vitamins C and E; α-lipoic acid) before their visits, whereas the CTRL subjects only participated in one visit. Upper and lower limb vascular functions were assessed via flow-mediated dilation and passive leg movement technique. Heart rate variability was utilized to assess autonomic nervous system modulation. The PTSD-PL condition, when compared with the CTRL group, reported lower arm and leg microvascular function as well as sympathetic nervous system (SNS) predominance. After acute AO supplementation, arm, but not leg, microvascular function was improved and SNS predominance was lowered to which the prior difference between PTSD group and CTRL was no longer significant. Young individuals with PTSD demonstrated lower arm and leg microvascular function as well as greater SNS predominance when compared with age- and sex-matched controls. Furthermore, this lower vascular/autonomic function was augmented by an acute AO supplementation to the level of the healthy controls, potentially implicating oxidative stress as a contributor to this blunted vascular/autonomic function.

Examining sex differences in sitting-induced microvascular dysfunction: Insight from acute vitamin C supplementation.

PURPOSE: Lower limb microvascular dysfunction resulting from prolonged sitting (PS) bouts has been revealed to occur independent of sex. Although acute antioxidant supplementation has been reported to blunt conduit artery dysfunction following PS in young males, it is unknown if this protective effect extends to the microvasculature or is relevant in young females, who possess intrinsic vascular protective mechanisms specific to antioxidant defense. Therefore, this study employed an acute antioxidant supplementation to further examine sex differences during PS with a specific focus on microvascular function. METHODS: On two separate visits, 14 females (23 ± 3 years) and 12 males (25 ± 4 years) had leg microvascular function (LMVF) assessed (via the passive leg movement technique) before and after 1.5 h of sitting. Prior to each visit, one gram of vitamin C (VC) or placebo (PL) was consumed. RESULTS: PS significantly reduced LMVF [PL: (M: -34 ± 20; F: -23 ± 18%; p < 0.01) independent of sex (p = 0.7)], but the VC condition only blunted this reduction in males (VC: -3 ± 20%; p < 0.01), but not females (VC: -18 ± 25%; p = 0.5). CONCLUSION: Young males and females reported similar reductions LMVF following PS, but only the young males reported a preservation of LMVF following the VC supplementation. This finding in young females was highlighted by substantial variability in LMVF measures in response to the VC condition that was unrelated to changes in the potential contributors to sitting-induced reductions in LMVF (e.g. lower limb venous pooling, reduced arterial shear rate). NEW AND NOTEWORTHY: In this study, we employed an acute Vitamin C (VC) supplementation to examine sex differences in leg microvascular function (LMVF) following a bout of prolonged sitting. This study revealed that prolonged sitting reduced LMVF independent of sex, but only young males reported an attenuation to this lowered LMVF following VC supplementation. The young females revealed substantial variability in sitting-induced changes to LMVF that could not be explained by the potential contributors to sitting-induced reductions in LMVF (e.g. lower limb venous pooling, reduced arterial shear rate).

Vascular Responses to Passive and Active Movement in Premenopausal Females: Comparisons across Sex and Menstrual Cycle Phase.

PURPOSE: Adequate, robust vascular responses to passive and active movement represent two distinct components linked to normal, healthy cardiovascular function. Currently, limited research exists determining if these vascular responses are altered in premenopausal females (PMF) when compared across sex or menstrual cycle phase. METHODS: Vascular responses to passive leg movement (PLM) and handgrip (HG) exercise were assessed in PMF ( n = 21) and age-matched men ( n = 21). A subset of PMF subjects ( n = 11) completed both assessments during the early and late follicular phase of their menstrual cycle. Microvascular function was assessed during PLM via changes in leg blood flow, and during HG exercise, via steady-state arm vascular conductance. Macrovascular (brachial artery [BA]) function was assessed during HG exercise via BA dilation responses as well as BA shear rate-dilation slopes. RESULTS: Leg microvascular function, determined by PLM, was not different between sexes or across menstrual cycle phase. However, arm microvascular function, demonstrated by arm vascular conductance, was lower in PMF compared with men at rest and during HG exercise. Macrovascular function was not different between sexes or across menstrual cycle phase. CONCLUSIONS: This study identified similar vascular function across sex and menstrual cycle phase seen in microvasculature of the leg and macrovascular (BA) of the arm. Although arm microvascular function was unaltered by menstrual cycle phase in PMF, it was revealed to be significantly lower when compared with age-matched men highlighting a sex difference in vascular/blood flow regulation during small muscle mass exercise.

High sodium intake differentially impacts brachial artery dilation when evaluated with reactive versus active hyperemia in salt resistant individuals.

This study sought to determine if high sodium (HS) intake in salt resistant (SR) individuals attenuates upper limb arterial dilation in response to reactive (occlusion) and active (exercise) hyperemia, two stimuli with varying vasodilatory mechanisms, and the role of oxidative stress in this response. Ten young, SR participants (9 males, 1 female) consumed a 7-day HS (6,900 mg/day) and a 7-day recommended sodium intake (RI: 2,300 mg/day) diet in a randomized order. On the last day of each diet, brachial artery (BA) function was evaluated via reactive (RH-FMD: 5 min of cuff occlusion) and active [handgrip (HG) exercise] hyperemia after consumption of both placebo (PL) and antioxidants (AO). The HS diet significantly elevated sodium excretion (P < 0.05), but mean arterial blood pressure was unchanged. During the PL condition, the HS diet significantly reduced RH-FMD when compared with RI diet (P = 0.01), but this reduction was significantly restored (P = 0.01) when supplemented with AO (HS + PL: 5.9 ± 3.4; HS + AO: 8.2 ± 2.7; RI + PL: 8.9 ± 4.7; RI + AO: 7.0 ± 2.1%). BA shear-to-dilation slopes, evaluated across all HG exercise workloads, were not significantly different across sodium intervention or AO supplementation. In SR individuals, HS intake impaired BA function when assessed via RH-FMD, but was restored with acute AO consumption suggesting oxidative stress as a contributor to this dysfunction. However, exercise-induced BA dilation was unaltered, potentially implicating an inability of HS intake to influence the mechanisms responsible for effectively maintaining skeletal muscle perfusion during exercise.NEW & NOTEWORTHY 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.