A biobehavioral observational study to understand the multilevel determinants of cardiovascular health in Black women: the BLOOM Study protocol.

BACKGROUND: The racial/ethnic and gender disparities in cardiovascular disease (CVD) morbidity and mortality in the United States are evident. Across nearly every metric, non-Hispanic Black women have poorer overall cardiovascular health. Emerging evidence shows a disproportionately high burden of increased CVD risk factors in Black women of childbearing age, which has a far-reaching impact on both maternal and child outcomes, resulting in premature onset of CVD and further widens the racial disparities in CVD. There is growing recognition that the fundamental driver of persistent racial/ethnic disparities in CVD, as well as disparities in behavioral risk factors such as physical activity and sleep, is structural racism. Further, the lived personal experience of racial discrimination not only has a negative impact on health behaviors, but also links to various physiological pathways to CVD risks, such as internalized stress resulting in a pro-inflammatory state. Limited research, however, has examined the interaction between daily experience and health behaviors, which are influenced by upstream social determinants of health, and the downstream effect on biological/physiological indicators of cardiovascular health in non-pregnant Black women of childbearing age. METHODS/DESIGN: The BLOOM Study is an observational study that combines real-time ambulatory assessments over a 10-day monitoring period with in-depth cross-sectional lab-based physiological and biological assessments. We will use a wrist-worn actigraphy device to capture 24-h movement behaviors and electronic ecological momentary assessment to capture perceived discrimination, microaggression, and stress. Blood pressure will be captured continuously through a wristband. Saliva samples will be self-collected to assess cortisol level as a biomarker of psychological stress. Lab assessments include a fasting venous blood sample, and assessment of various indices of peripheral and cerebral vascular function/health. Participants' address or primary residence will be used to obtain neighborhood-level built environmental and social environmental characteristics. We plan to enroll 80 healthy Black women who are between 18 and 49 years old for this study. DISCUSSION: Results from this study will inform the development of multilevel (i.e., individual, interpersonal, and social-environmental levels) lifestyle interventions tailored to Black women based on their lived experiences with the goal of reducing CVD risk. GOV IDENTIFIER: NCT06150989.

Epinephrine iontophoresis attenuates changes in skin blood flow and abolishes cutaneous contamination of near-infrared diffuse correlation spectroscopy estimations of muscle perfusion.

Near-infrared diffuse correlation spectroscopy (NIR-DCS) is an optical imaging technique for measuring relative changes in skeletal muscle microvascular perfusion (i.e., fold change above baseline) during reactive hyperemia testing and exercise and is reported as a blood flow index (BFI). Although it is generally accepted that changes in BFI are primarily driven by changes in muscle perfusion, it is well known that large, hyperthermia-induced changes in cutaneous blood flow can uncouple this relationship. What remains unknown, is how much of an impact that changes in cutaneous perfusion have on NIR-DCS BFI and estimates of skeletal muscle perfusion under thermoneutral conditions, where changes in cutaneous blood flow are assumed to be relatively low. We therefore used epinephrine iontophoresis to pharmacologically block changes in cutaneous perfusion throughout a battery of experimental procedures. The data show that 1) epinephrine iontophoresis attenuates changes in cutaneous perfusion for up to 4-h posttreatment, even in the face of significant neural and local stimuli, 2) under thermoneutral conditions, cutaneous perfusion does not significantly impact NIR-DCS BFI during reactive hyperemia testing or moderate-intensity exercise, and 3) during passive whole body heat stress, when cutaneous vasodilation is pronounced, epinephrine iontophoresis preserves NIR-DCS measures of skeletal muscle BFI during moderate-intensity exercise. Collectively, these data suggest that cutaneous perfusion is unlikely to have a major impact on NIR-DCS estimates of skeletal muscle BFI under thermoneutral conditions, but that epinephrine iontophoresis can be used to abolish cutaneous contamination of the NIR-DCS BFI signal during studies where skin blood flow may be elevated but skeletal muscle perfusion is of specific interest.

Sympathetic transduction at rest and during cold pressor test in young healthy non-Hispanic Black and White women.

Non-Hispanic Black (BL) individuals have the highest prevalence of hypertension and cardiovascular disease (CVD) compared with all other racial/ethnic groups. Previous work focused on racial disparities in sympathetic control and blood pressure (BP) regulation between young BL and White (WH) adults, have mainly included men. Herein, we hypothesized that BL women would exhibit augmented resting sympathetic vascular transduction and greater sympathetic and BP reactivity to cold pressor test (CPT) compared with WH women. Twenty-eight young healthy women (BL: n = 14, 22 [Formula: see text] 4 yr; WH: n = 14, 22 [Formula: see text] 4 yr) participated. Beat-to-beat BP (Finometer), common femoral artery blood flow (duplex Doppler ultrasound), and muscle sympathetic nerve activity (MSNA; microneurography) were continuously recorded. In a subset (BL n = 10, WH n = 11), MSNA and BP were recorded at rest and during a 2-min CPT. Resting sympathetic vascular transduction was quantified as changes in leg vascular conductance (LVC) and mean arterial pressure (MAP) following spontaneous bursts of MSNA using signal averaging. Sympathetic and BP reactivity were quantified as changes in MSNA and MAP during the last minute of CPT. There were no differences in nadir LVC following resting MSNA bursts between BL (-8.70 ± 3.43%) and WH women (-7.30 ± 3.74%; P = 0.394). Likewise, peak increases in MAP following MSNA bursts were not different between groups (BL: +2.80 ± 1.42 mmHg; vs. WH: +2.99 ± 1.15 mmHg; P = 0.683). During CPT, increases in MSNA and MAP were also not different between BL and WH women, with similar transduction estimates between groups (ΔMAP/ΔMSNA; P = 0.182). These findings indicate that young, healthy BL women do not exhibit exaggerated sympathetic transduction or augmented sympathetic and BP reactivity during CPT.NEW & NOTEWORTHY This study was the first to comprehensively investigate sympathetic vascular transduction and sympathetic and BP reactivity during a cold pressor test in young, healthy BL women. We demonstrated that young BL women do not exhibit exaggerated resting sympathetic vascular transduction and do not have augmented sympathetic or BP reactivity during cold stress compared with their WH counterparts. Collectively, these findings suggest that alterations in sympathetic transduction and reactivity are not apparent in young, healthy BL women.

The acute effect of whole-body heat therapy on peripheral and cerebral vascular reactivity in Black and White females.

Among females in the U.S., Black females suffer the most from cardiovascular disease and stroke. While the reasons for this disparity are multifactorial, vascular dysfunction likely contributes. Chronic whole-body heat therapy (WBHT) improves vascular function, but few studies have examined its acute effect on peripheral or cerebral vascular function, which may help elucidate chronic adaptative mechanisms. Furthermore, no studies have investigated this effect in Black females. We hypothesized that Black females would have lower peripheral and cerebral vascular function relative to White females and that one session of WBHT would mitigate these differences. Eighteen young, healthy Black (n = 9; 21 ± 3 yr; BMI: 24.7 ± 4.5 kg/m2) and White (n = 9; 27 ± 3 yr; BMI: 24.8 ± 4.1 kg/m2) females underwent one 60 min session of WBHT (49 °C water via a tube-lined suit). Pre- and 45 min post-testing measures included post-occlusive forearm reactive hyperemia (peripheral microvascular function, RH), brachial artery flow-mediated dilation (peripheral macrovascular function, FMD), and cerebrovascular reactivity (CVR) to hypercapnia. Prior to WBHT, there were no differences in RH, FMD, or CVR (p > 0.05 for all). WBHT improved peak RH in both groups (main effect of WBHT: 79.6 ± 20.1 cm/s to 95.9 ± 30.0 cm/s; p = 0.004, g = 0.787) but not Δ blood velocity (p > 0.05 for both groups). WBHT improved FMD in both groups (6.2 ± 3.4 % to 8.8 ± 3.7 %; p = 0.016, g = 0.618) but had no effect on CVR in either group (p = 0.077). These data indicate that one session of WBHT acutely improves peripheral micro- and macrovascular but not cerebral vascular function in Black and White females.

Application of blood flow restriction in hypoxic environment augments muscle deoxygenation without compromising repeated sprint exercise performance.

NEW FINDINGS: What is the central question of this study? Does applying blood flow restriction during the rest periods of repeated sprint exercise in a hypoxic environment lead to greater local hypoxia within exercising muscles without compromising training workload? What is the main finding and its importance? Repeated sprint exercise with blood flow restriction administered during rest periods under systemic hypoxia led to severe local hypoxia within the exercised muscles without a reduction in power output. The maintained power output might be due to elevated neuromuscular activation. Accordingly, the proposed repeated sprint exercise in the current study may be an effective training modality. ABSTRACT: Repeated sprint exercise (RSE) is a popular training modality for a wide variety of athletic activities. The purpose of this study was to assess the combined effects of systemic hypoxia and blood flow restriction (BFR) on muscle deoxygenation and RSE performance. Twelve healthy young men performed a standard RSE training modality (five sets of 10 s maximal sprint with a 60 s rest) under four different conditions: (1) normoxic control (NC), normoxia (N, 20.9%) + control BFR (C, 0 mmHg); (2) normoxic BFR (NB), normoxia (N, 20.9%) + BFR (B, 140 mmHg); (3) hypoxic control (HC), hypoxia (H, 13.7%) + control BFR (C, 0 mmHg); and (4) hypoxic BFR (HB): hypoxia (H, 13.7%) + BFR (B, 140 mmHg). BFR was only administered during the rest period of the respective RSE trials. In the local exercising muscles, muscle oxygen saturation ( Sm O 2 $\textit{Sm}{O}_{2}$ ) and neuromuscular activity were measured using near-infrared spectroscopy and surface electromyography, respectively. SmO2 was lower in systemic hypoxia conditions relative to normoxia conditions (P < 0.05). A rther decrease in SmO2 was observed in HB relative to HC (Set 1: HC 70.0 ± 17.5 vs. HB 57.4 ± 11.3%, P = 0.001; Set 4: HC 67.5 ± 14.6 vs. HB 57.0 ± 12.0%, P = 0.013; Set 5: HC 61.0 ± 15.3 vs. HB 47.7 ± 11.9%, P < 0.001). No differences in RSE performance were observed between any of the conditions (P > 0.05). Interestingly, an elevated neuromuscular activity was seen in response to the BFR, particularly during conditions of systemic hypoxia (P < 0.05). Thus, RSE with BFR administered during rest periods under systemic hypoxia led to severe local hypoxia without compromising training workload.

Contributions of endothelin-1 and l-arginine to blunted cutaneous microvascular function in young, black women.

Non-Hispanic black (BL) individuals have the greatest prevalence of cardiovascular disease (CVD), relative to other racial/ethnic groups (e.g., non-Hispanic white population; WH), which may be secondary to blunted vascular function. Although women typically present with reduced CVD relative to men of the same racial/ethnic group, the prevalence is similar between BL women and men though the mechanisms differ. This study hypothesized that reduced microvascular function in young, BL women is associated with endothelin-1 (ET-1) overactivity or insufficient l-arginine bioavailability. Nine BL and nine WH women participated (age: 20 ± 2 vs. 22 ± 2 yr). Cutaneous microvascular function was assessed during 39°C local heating, whereas lactated Ringer's (control), BQ-123 (ET-1 receptor type A antagonist), BQ-788 (ET-1 receptor type B antagonist), or l-arginine were infused via intradermal microdialysis to modify cutaneous vascular conductance (CVC). Subsequent infusion of Nω-nitro-l-arginine methyl ester allowed for quantification of the nitric oxide (NO) contribution to vasodilation, whereas combined sodium nitroprusside and 43°C heating allowed for normalization to maximal CVC (%CVCmax). BL women had blunted %CVCmax and NO contribution to dilation during the 39°C plateau (P < 0.027 for both). BQ-123 improved this response through augmented NO-mediated dilation (P < 0.048 for both). BQ-788 and l-arginine did not alter the CVC responses (P > 0.835 for both) or the NO contribution (P > 0.371 for both). Cutaneous microvascular function is reduced in BL women, and ET-1 receptor type A may contribute to this reduced function. Further research is needed to better characterize these mechanisms in young, BL women.NEW & NOTEWORTHY Cardiovascular disease remains a burden in the United States non-Hispanic black (BL) population, although its manifestation through blunted vasodilation in this population is different between men and women. Accordingly, this study determined that reduced microvascular function in young, BL women may be partially controlled by endothelin-1 (ET-1) type A receptors, although neither type B receptors nor insufficient l-arginine bioavailability seems to contribute to this response. Accordingly, further research is needed to better characterize these ET-1 related mechanisms and illuminate other pathways that may contribute to this disparate vascular function in young, BL women.

On the use and misuse of cerebral hemodynamics terminology using transcranial Doppler ultrasound: a call for standardization.

Cerebral hemodynamics, e.g., cerebral blood flow, can be measured and quantified using many different methods, with transcranial Doppler ultrasound (TCD) being one of the most commonly used approaches. In human physiology, the terminology used to describe metrics of cerebral hemodynamics are inconsistent and in some instances technically inaccurate; this is especially true when evaluating, reporting, and interpreting measures from TCD. Therefore, this perspective article presents recommended terminology when reporting cerebral hemodynamic data. We discuss the current use and misuse of the terminology in the context of using TCD to measure and quantify cerebral hemodynamics and present our rationale and consensus on the terminology that we recommend moving forward. For example, one recommendation is to discontinue the use of the term "cerebral blood flow velocity" in favor of "cerebral blood velocity" with precise indication of the vessel of interest. We also recommend clarity when differentiating between discrete cerebrovascular regulatory mechanisms, namely, cerebral autoregulation, neurovascular coupling, and cerebrovascular reactivity. This will be a useful guide for investigators in the field of cerebral hemodynamics research.

Young, non-Hispanic Black men and women exhibit divergent peripheral and cerebral vascular reactivity.

NEW FINDINGS: What is the central question of the study? Do peripheral and cerebral vascular function differ between young non-Hispanic Black men and women? What is the main finding and its importance? The non-Hispanic Black women in this study presented greater peripheral conduit artery and cerebrovascular reactivity, yet similar peripheral microvascular function relative to the non-Hispanic Black men. These preliminary findings suggest that young Black women and men possess divergent vascular function, possibly contributing to the unique non-Hispanic Black sex differences in cardiovascular and cerebrovascular diseases. ABSTRACT: In the USA, cardiovascular and cerebrovascular diseases remain more prominent in the non-Hispanic Black (BL) population relative to other racial/ethnic groups. Typically, sex differences emerge in the manifestation of these diseases, though these differences may not fully materialize in the BL population. While numerous mechanisms are implicated, differences in vascular function likely contribute. Research has demonstrated blunted vasodilatation in several vascular regions in BL versus non-Hispanic White individuals, though much of this work did not assess sex differences. Therefore, this study aimed to ascertain if indices of vascular function are different between young BL women (BW) and men (BM). Eleven BW and 15 BM (22 (4) vs. 23 (3) years) participated in this study. Each participant underwent testing for brachial artery flow-mediated dilatation (FMD), post-occlusive reactive hyperaemia and cerebral vasomotor reactivity during rebreathing-induced hypercapnia. BW exhibited greater adjusted FMD than BM (P < 0.05 for all), but similar or lower reactive hyperaemia when assessed as blood velocity (P > 0.39 for all) or blood flow reactivity (P < 0.05 for all), respectively. Across a range of hypercapnia, BW had greater middle cerebral artery blood velocity and cerebrovascular conductance index than BM (P < 0.001 for both). These preliminary data suggest that young BW have greater vascular function relative to young BM, though this was inconsistent across different indices. These findings provide insight into the divergent epidemiological findings between BM and BW. Further research is needed to elucidate possible mechanisms and relate these physiological responses to epidemiological observations.

Validity of transcranial Doppler ultrasonography-determined dynamic cerebral autoregulation estimated using transfer function analysis.

Transcranial Doppler ultrasonography (TCD) is used widely to evaluate dynamic cerebral autoregulation (dCA). However, the validity of TCD-determined dCA remains unknown because TCD is only capable of measuring blood velocity and thus only provides an index as opposed to true blood flow. To test the validity of TCD-determined dCA, in nine healthy subjects, dCA was evaluated by transfer function analysis (TFA) using cerebral blood flow (CBF) or TCD-measured cerebral blood velocity during a perturbation that induces reductions in TCD-determined dCA, lower body negative pressure (LBNP) at two different stages: LBNP - 15 mmHg and - 50 mmHg. Internal carotid artery blood flow (ICA Q) was assessed as an index of CBF using duplex Doppler ultrasound. The TFA low frequency (LF) normalized gain (ngain) calculated using ICA Q increased during LBNP at - 50 mmHg (LBNP50) from rest (P = 0.005) and LBNP at - 15 mmHg (LBNP15) (P = 0.015), indicating an impaired dCA. These responses were the same as those obtained using TCD-measured cerebral blood velocity (from rest and LBNP15; P = 0.001 and P = 0.015). In addition, the ICA Q-determined TFA LF ngain from rest to LBNP50 was significantly correlated with TCD-determined TFA LF ngain (r = 0.460, P = 0.016) despite a low intraclass correlation coefficient. Moreover, in the Bland-Altman analysis, the difference in the TFA LF ngains determined by blood flow and velocity was within the margin of error, indicating that the two measurement methods can be interpreted as equivalent. These findings suggest that TCD-determined dCA can be representative of actual dCA evaluated with CBF.

Influence of sex on heightened vasoconstrictor mechanisms in the non-Hispanic black population.

Cardiovascular disease (CVD) affects individuals of all races and ethnicities; however, its prevalence is highest in non-Hispanic black individuals (BL) relative to other populations. While previous research has provided valuable insight into elevated CVD risk in the BL population, this work has been almost exclusively conducted in men. This is alarming given that BL women suffer from CVD at an equivalent rate to BL men and each has a greater prevalence when compared to all other ethnicities, regardless of sex. The importance of investigating sex differences in mechanisms of cardiovascular function is highlighted by the National Institute of Health requiring sex to be considered as a biological variable in research studies to better our "understanding of key sex influences on health processes and outcomes." The mechanism(s) responsible for the elevated CVD risk in BL women remains unclear and is likely multifactorial. Limited studies in BL women suggest that, while impaired vasodilator capacity is involved, heightened vasoconstrictor tone and/or responsiveness may also contribute. Within this mini-review, we will discuss potential mechanisms of elevated rates of hypertension and other CVDs in BL individuals with a particular focus on young, otherwise healthy, college-aged women. To stimulate academic thought and future research, we will also discuss potential mechanisms for impaired vascular function in BL women, as well as possible divergent mechanisms between BL men and women based on either preliminary data or plausible speculation extending from findings in the existing literature. Last, we will conclude with potential future research directions aimed at better understanding the elevated risk for hypertension and CVD in BL women.

Acute consumption of flavanol-rich cocoa beverage improves attenuated cutaneous microvascular function in healthy young African Americans.

Flavanols have beneficial effects on vascular health and we have recently demonstrated that cerebral vasodilatory capacity in healthy young African Americans (AA) is improved with acute flavanol intake relative to aged-matched Caucasian Americans (CA). However, whether the positive benefits of acute flavanol consumption would also be present in the cutaneous microvascular circulation of AA remains unknown. Thus, we hypothesized that acute consumption of flavanol-rich cocoa (FC) would improve the previously reported reduced cutaneous microvascular responses to local heating in young AA. Seven AA and seven CA participated in this double-blind crossover study. Data were collected on two different days, separated by a minimum of one week. Two intradermal microdialysis membranes were inserted in the forearm and each site was randomly assigned to receive lactated Ringer's solution or NO synthase (NOS) inhibitor. Participants were randomly assigned to consume either a non-flavanol containing (NF) beverage or FC beverage. Cutaneous vascular conductance (CVC) was calculated as cutaneous blood flux/mean arterial pressure and normalized as % maximal CVC (%CVCmax). The difference in %CVCmax between the Ringer's site and NOS inhibited site was calculated to assess NO contribution (Δ %CVCmax). In the Ringer's site, acute consumption of FC beverage improved %CVCmax during 39 °C heating when compared to NF beverage in AA (NF: 36 ±â€¯6 vs. FC: 47 ±â€¯5%CVCmax; P < .01) while there was similar %CVCmax during 39 °C heating between beverages in CA (NF: 55 ±â€¯4 vs. FC: 59 ±â€¯5%CVCmax; P = .40). During 39 °C heating, NO contribution was significantly higher with FC beverage than NF beverage in AA (NF: 27 ±â€¯5 vs. FC: 35 ±â€¯4 Δ %CVCmax; P = .03) while there was similar NO contribution between beverages in CA (NF: 42 ±â€¯4 vs. FC: 45 ±â€¯4 Δ %CVCmax; P = .36). This data suggests that acute consumption of FC could be a therapeutic solution to improve an attenuated microvascular function in young AA.

Racial disparities in cardiovascular disease risk: mechanisms of vascular dysfunction.

Cardiovascular disease (CVD) accounts for a third of all deaths in the United States making it the leading cause of morbidity and mortality. Although CVD affects individuals of all races/ethnicities, the prevalence of CVD is highest in non-Hispanic black (BL) individuals relative to other populations. The mechanism(s) responsible for elevated CVD risk in the BL population remains incompletely understood. However, impaired vascular vasodilator capacity and exaggerated vascular vasoconstrictor responsiveness are likely contributing factors, both of which are present even in young, otherwise healthy BL individuals. Within this review, we highlight some historical and recent data, collected from our laboratories, of impaired vascular function, in terms of reduced vasodilator capacity and heightened vasoconstrictor responsiveness, in the peripheral and cerebral circulations in BL individuals. We provide data that such impairments may be related to elevated oxidative stress and subsequent reduction in nitric oxide bioavailability. In addition, divergent mechanisms of impaired vasodilatory capacity between BL men and women are discussed. Finally, we propose several directions where future research is needed to fill in knowledge gaps, which will allow for better understanding of the mechanisms contributing to impaired vascular function in this population. Ultimately, this information will allow for better lifestyle and therapeutic approaches to be implemented in an effort to minimize the increased CVD burden in the BL population.

Sex differences in the mechanisms mediating blunted cutaneous microvascular function in young black men and women.

The black population exhibits attenuated vasodilatory function across their lifespan, yet little is known regarding the mechanisms of this impairment. Recent evidence suggests a potential role for oxidative stress. Therefore, we tested the hypothesis that NADPH oxidase (NOX) and/or xanthine oxidase (XO) contribute to blunted nitric oxide (NO)-mediated cutaneous microvascular function in young black adults. In 30 white and black subjects (8 men and 7 women in each group), local heating was performed while NOX and XO were inhibited by apocynin and allopurinol, respectively, via intradermal microdialysis. The plateau in cutaneous vascular conductance (red blood cell flux/mean arterial pressure) during 39°C local heating at each site was compared with a control site perfused with lactated Ringer solution. Subsequent inhibition of NO synthase via Nω-nitro-l-arginine methyl ester allowed for quantification of the NO contribution to vasodilation during heating. Black individuals, relative to white individuals, had a blunted cutaneous vascular conductance plateau at the control site (45 ± 9 vs. 68 ± 13%max, P < 0.001) that was increased by both apocynin (61 ± 15%max, P < 0.001) and allopurinol (58 ± 17%max, P = 0.005). Black men and black women had similar responses to heating at the control site ( P = 0.99), yet apocynin and allopurinol increased this response only in black men (both P < 0.001 vs. control). The NO contribution was also increased via apocynin and allopurinol exclusively in black men. These findings suggest that cutaneous microvascular function is reduced because of NOX and XO activity in black men but not black women, identifying a novel sex difference in the mechanisms that contribute to blunted vascular responses in the black population. NEW & NOTEWORTHY We demonstrate that cutaneous microvascular responses to local heating are consistently reduced in otherwise healthy young black men and women relative to their white counterparts. Inhibition of NADPH oxidase and xanthine oxidase via apocynin and allopurinol, respectively, augments microvascular function in black men but not black women. These data reveal clear sex differences in the mechanisms underlying the racial disparity in cutaneous microvascular function.

Attenuated forearm vascular conductance responses to rhythmic handgrip in young African-American compared with Caucasian-American men.

Previous studies have demonstrated that African-American (AA) individuals have heightened vasoconstrictor and reduced vasodilator responses under resting conditions compared with Caucasian-American (CA) individuals. However, potential differences in vascular responses to exercise remain unclear. Therefore, we tested the hypothesis that, compared with CA subjects, AA subjects would present an attenuated increase in forearm vascular conductance (FVC) during rhythmic handgrip exercise. Forearm blood flow (FBF; duplex Doppler ultrasound) and mean arterial pressure (MAP; finger photoplethysmography) were measured in healthy young CA ( n = 10) and AA ( n = 10) men during six trials of rhythmic handgrip performed at workloads of 4, 8, 12, 16, 20, and 24 kg. FVC (calculated as FBF/MAP), FBF, and MAP were similar between groups at rest (FVC: 63 ± 7 ml·min-1·100 mmHg-1 in CA subjects vs. 62 ± 7 ml·min-1·100 mmHg-1 in AA subjects, P = 0.862). There was an intensity-dependent increase in FVC during exercise in both groups; however, AA subjects presented lower FVC (interaction P < 0.001) at 8-, 12-, 16-, 20-, and 24-kg workloads (e.g., 24 kg: 324 ± 20 ml·min-1·100 mmHg-1 in CA subjects vs. 241 ± 21 ml·min-1·100 mmHg-1 in AA subjects, P < 0.001). FBF responses to exercise were also lower in AA subjects (interaction P < 0.001), whereas MAP responses did not differ between groups (e.g., ∆MAP at 24 kg: +19 ± 2 mmHg in CA subjects vs. +19 ± 2 mmHg in AA subjects, interaction P = 0.950). These findings indicate lower hyperemic responses to rhythmic handgrip exercise in AA men compared with CA men. NEW & NOTEWORTHY It is known that African-American individuals have heightened vasoconstriction and reduced vasodilation under resting conditions compared with Caucasian-American individuals. Here, we identified that the hyperemic response to moderate and high-intensity rhythmic handgrip exercise was lower in healthy young African-American men.

Pronounced and sustained cutaneous vasoconstriction during and following cyrotherapy treatment: Role of neurotransmitters released from sympathetic nerves.

Cryotherapy is a therapeutic technique using ice or cold water applied to the skin to manage soft tissue trauma and injury. While beneficial, there are some potentially detrimental side effects, such as pronounced vasoconstriction and tissue ischemia that are sustained for hours post-treatment. This study tested the hypothesis that this vasoconstriction is mediated by 1) activation of post-synaptic α-adrenergic receptors and/or 2) activation of post-synaptic neuropeptide Y1 (NPY Y1) receptors. 8 subjects were fitted with a commercially available cryotherapy unit with a water perfused bladder on the lateral portion of the right calf. Participants were instrumented with four intradermal microdialysis probes beneath the bladder. The following conditions were applied at the four treatment sites: 1) control (Ringer solution), 2) combined post-synaptic ß-adrenergic receptors and neuropeptide (NPY) Y1 receptors blockade (P+B site), 3) combined post-synaptic α-adrenergic receptor, ß-adrenergic receptor, and NPY Y1 receptor blockade (Y+P+B site), and 4) blockade of pre-synaptic release of all neurotransmitters from the sympathetic nerves (BT site). Following thermoneutral baseline data collection, 1°C water was perfused through the bladder for 30min, followed by passive rewarming for 60min. Skin temperature (Tskin) fell from ~34°C to ~18.5°C during active cooling across all sites and there was no difference between sites (P>0.05 vs. control for each site). During passive rewarming Tskin rose to a similar degree in all sites (P>0.05 relative to the end of cooling). In the first 20min of cooling %CVC was reduced at all sites however, this response was blunted in the BT and the Y+P+B sites (P>0.05 for all comparisons). By the end of cooling the degree of vasoconstriction was similar between sites with the exception that the reduction in %CVC in the Y+B+P site was less relative to the reduction in the control site. %CVC was unchanged in any of the sites during passive rewarming such that each remained similar to values obtained at the end of active cooling. These findings indicate that the initial vasoconstriction (i.e. within the 1st 20min) that occurs during cryotherapy induced local cooling is achieved via activation of post-synaptic α-adrenergic receptors; whereas nonadrenergic mechanisms predominate as the duration of cooling continues. The sustained vasoconstriction that occurs following cessation of the cooling stimulus does not appear to be related to activation of post-synaptic α-adrenergic receptors or NPY Y1 receptor.

Tempol augments the blunted cutaneous microvascular thermal reactivity in healthy young African Americans.

NEW FINDINGS: What is the central question of this study? The purpose was to determine whether there is a difference between African Americans and Caucasians in cutaneous microvascular function and whether this difference is attributable to elevated oxidative stress. What is the main finding and its importance? The main finding is that African Americans have an attenuated cutaneous vasodilatation during local heating relative to Caucasians that is restored with local infusion of the superoxide dismutase mimetic, tempol. This suggests that superoxide mediates microvascular dysfunction and might contribute to the greater prevalence of cardiovascular disease in this population. ABSTRACT: African Americans (AA) have elevated risk for cardiovascular disease relative to other populations. We hypothesized that the cutaneous hyperaemic response to local heating is reduced in young AA relative to Caucasian Americans (CA) and that this is attributable to elevated oxidative stress. As such, ascorbic acid (a global antioxidant) and tempol (a superoxide dismutase mimetic) would improve this response in AA. Microdialysis fibres received lactated Ringer solution (control), 10 mm ascorbic acid or 10 µm 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (tempol) at a rate of 2.0 µl min-1 . Cutaneous vascular conductance (CVC) was calculated as the red blood cell flux divided by mean arterial pressure. Data were presented as a percentage of maximal CVC (%CVCmax ) induced by 44°C heating plus sodium nitroprusside. Twenty-four (12 AA, 12 CA) young (23 ± 4 years old) subjects participated. During 39°C heating, the %CVCmax was lower in AA at the control (CA, 65 ± 20% versus AA, 47 ± 15%; P < 0.05) and ascorbic acid sites (CA, 73 ± 14% versus AA: 49 ± 17%; P < 0.01). At the tempol site, there were no differences between groups. This was followed by infusion of 10 mm l-NAME at all sites to assess the contribution of nitric oxide to vasodilatation during local heating. The contribution of nitric oxide was lower in AA relative to CA at 39°C; however, this was restored with tempol. These data suggest that: (i) cutaneous vasodilatation in response to local heating is blunted in AA relative to CA; and (ii) elevated superoxide generation attenuates nitric oxide-mediated cutaneous vasodilatation in AA.

Tolerance to a haemorrhagic challenge during heat stress is improved with inspiratory resistance breathing.

NEW FINDINGS: What is the central question of this study? Does inspiratory resistance breathing improve tolerance to simulated haemorrhage in individuals with elevated internal temperatures? What is the main finding and its importance? The main finding of this study is that inspiratory resistance breathing modestly improves tolerance to a simulated progressive haemorrhagic challenge during heat stress. These findings demonstrate a scenario in which exploitation of the respiratory pump can ameliorate serious conditions related to systemic hypotension. ABSTRACT: Heat exposure impairs human blood pressure control and markedly reduces tolerance to a simulated haemorrhagic challenge. Inspiratory resistance breathing enhances blood pressure control and improves tolerance during simulated haemorrhage in normothermic individuals. However, it is unknown whether similar improvements occur with this manoeuvre in heat stress conditions. In this study, we tested the hypothesis that inspiratory resistance breathing improves tolerance to simulated haemorrhage in individuals with elevated internal temperatures. On two separate days, eight subjects performed a simulated haemorrhage challenge [lower-body negative pressure (LBNP)] to presyncope after an increase in internal temperature of 1.3 ± 0.1°C. During one trial, subjects breathed through an inspiratory impedance device set at 0 cmH2 O of resistance (Sham), whereas on a subsequent day the device was set at -7 cmH2 O of resistance (ITD). Tolerance was quantified as the cumulative stress index. Subjects were more tolerant to the LBNP challenge during the ITD protocol, as indicated by a > 30% larger cumulative stress index (Sham, 520 ± 306 mmHg min; ITD, 682 ± 324 mmHg min; P < 0.01). These data indicate that inspiratory resistance breathing modestly improves tolerance to a simulated progressive haemorrhagic challenge during heat stress.

Association between aerobic fitness and cerebrovascular function with neurocognitive functions in healthy, young adults.

Studies of the effects of physical activity on cognition suggest that aerobic fitness can improve cognitive abilities. However, the physiological mechanisms for the cognitive benefit of aerobic fitness are less well understood. We examined the association between aerobic fitness and cerebrovascular function with neurocognitive functions in healthy, young adults. Participants aged 18-29 years underwent measurements of cerebral vasomotor reactivity (CVMR) in response to rebreathing-induced hypercapnia, maximal oxygen uptake (VO2max) during cycle ergometry to voluntary exhaustion, and simple- and complex-neurocognitive assessments at rest. Ten subjects were identified as having low-aerobic fitness (LF < 15th fitness percentile), and twelve subjects were identified as having high-aerobic fitness (HF > 80th fitness percentile). There were no LF versus HF group differences in cerebrovascular hemodynamics during the baseline condition. Changes in middle cerebral artery blood velocity and CVMR during hypercapnia were elevated more in the HF than the LF group. Compared to the LF, the HF performed better on a complex-cognitive task assessing fluid reasoning, but not on simple attentional abilities. Statistical modeling showed that measures of VO2max, CVMR, and fluid reasoning were positively inter-correlated. The relationship between VO2max and fluid reasoning, however, did not appear to be reliably mediated by CVMR. In conclusion, a high capacity for maximal oxygen uptake among healthy, young adults was associated with greater CVMR and better fluid reasoning, implying that high-aerobic fitness may promote cerebrovascular and cognitive functioning abilities.

Can assessment of afferent thermal sensitivity shed light onto multiple sclerosis diagnosis and disease progression?

Podcast available at: http://www.yada-yada.co.uk/wiley/ExperimentalPhysiology/audio/Ep1_july17.mp3.