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 N-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.

Consumption of a representative fast‐food meal (FFMeal) acutely impairs peripheral conduit artery vascular function; however, the effect on cerebral vascular function remains unknown. This study tested the hypothesis that a FFMeal would impair cerebral vascular function as indexed by an attenuated increase in cerebral vascular conductance (CVCI) in the middle cerebral artery (MCA) during a hypercapnic challenge. Ten healthy men (age: 24 ± 3 years, BMI: 24.3 ± 3.8 kg/m2) were studied under two conditions; a standardized FFMeal (990 kcals, 50% fat, 36% carbohydrate, 14% protein, and 2120 mg sodium) and a fasting control condition. Basal hemodynamics, cerebral vasomotor reactivity (CVMR), and brachial artery flow‐mediated dilation (BA FMD) were completed after an overnight fast (Pre) and again 2 h and 4 h later both days. To assess CVMR, subjects rebreathed from a 5‐L bag while MCA velocity (MCAV mean) was measured using transcranial Doppler (TCD) ultrasound and converted into CVCI (MCAV mean/mean arterial pressure). Peripheral artery endothelial function was assessed via BA FMD following a standard 5‐min occlusion protocol. As expected, BA FMD was reduced at 2 h (Pre: 6.6 ± 1.7% vs. 5.2 ± 1.8%, P = 0.01). However, despite significant impairment in BA FMD, neither peak CVCI %baseline nor CVMR was affected by the FFMeal (Control–Pre: 1.9 ± 1.1, 2 h: 2.1 ± 1.1, 4 h: 1.7 ± 1.1 ∆CVCI%·∆PETCO 2 −1 vs. FFMeal–Pre: 2.1 ± 1.1, 2 h: 2.2 ± 0.7, 4 h: 1.9 ± 0.9 ∆CVCI%·∆PETCO 2 −1, time × condition P = 0.88). These results suggest that cerebral vascular reactivity to hypercapnia in healthy young men is not altered by an acute FFMeal.

Age is the greatest risk factor for chronic disease and is associated with a marked decline in functional capacity and quality of life. A key factor contributing to loss of function in older adults is the decline in skeletal muscle function. While the exact mechanism(s) remains incompletely understood, age‐related mitochondrial dysfunction is thought to play a major role. To explore this question further, we studied 15 independently living seniors (age: 72 ± 5 years; m/f: 4/11; BMI: 27.6 ± 5.9) and 17 young volunteers (age: 25 ± 4 years; m/f: 8/9; BMI: 24.0 ± 3.3). Skeletal muscle oxidative function was measured in forearm muscle from the recovery kinetics of muscle oxygen consumption using near‐infrared spectroscopy (NIRS). Muscle oxygen consumption was calculated as the slope of change in hemoglobin saturation during a series of rapid, supra‐systolic arterial cuff occlusions following a brief bout of exercise. Aging was associated with a significant prolongation of the time constant of oxidative recovery following exercise (51.8 ± 5.4 sec vs. 37.1 ± 2.1 sec, P = 0.04, old vs. young, respectively). This finding suggests an overall reduction in mitochondrial function with age in nonlocomotor skeletal muscle. That these data were obtained using NIRS holds great promise in gerontology for quantitative assessment of skeletal muscle oxidative function at the bed side or clinic.

Long-term burn survivors have reduced aerobic capacity, placing them at increased risk for cardiovascular disease, morbidity, and mortality. However, the exact mechanism contributing to a reduced aerobic capacity remains incompletely understood, but may be related to adverse cardiovascular remodeling. Therefore, it was hypothesized that well-healed burn survivors would exhibit adverse left ventricular (LV) remodeling and impaired LV function. To test this hypothesis, 22 well-healed moderately burned individuals (age: 41 ± 14 years; BMI: 27.7 ± 5.4 kg/m 2 ; male/female: 12/10; extent of burn: 37 ± 12 %BSA), 11 well-healed severely burned individuals (age: 43 ± 12 years; BMI: 29.5 ± 5.8 kg/m 2 ; male/female: 8/3; extent of burn: 73 ± 11 %BSA), and 12 healthy, age-matched controls (age: 34 ± 9 years; BMI: 28.6 ± 5.2 kg/m 2 ; male/female: 5/7) were enrolled in the study. All subjects were sedentary, performing less than 30 minutes of aerobic exercise per day, 3 days per week. LV morphology and function were assessed via cardiac magnetic resonance imaging. In contrast to the hypothesis, neither the presence nor severity of burn injury adversely affected LV morphology or function, when compared with equally sedentary nonburned controls. However, of note, LV mass of all three groups was in the lowest 5th percentile compared with normative values. Finally, group differences in LV morphology were largely explained by differences in aerobic capacity. Taken together, these data suggest a prior burn injury itself does not result in pathological remodeling of the LV and support a role for aerobic exercise training to improve cardiac function.

Microvascular dysfunction contributes to the development of hypertension and insulin resistance. The black population is at an elevated risk of both conditions relative to other racial groups. Previous studies indicate that college-aged black men, compared to their white counterparts, have impaired microvascular function as assessed by post-occlusion reactive hyperemia (RH). It is unknown whether this racial disparity is present in healthy, young adult black (BW) and white women (WW). Furthermore, whether nitric oxide-mediated cutaneous microvascular hyperemia during local heating (LH) is different in these populations has not been determined. Purpose: The purpose of this study was to test the hypothesis that college-aged BW exhibit blunted RH and attenuated LH induced cutaneous hyperemia compared to agematched WW. Methods: College-aged BW (n=7) and WW (n=7) were studied during the early follicular phase of the menstrual cycle. For RH, brachial artery diameter and blood velocity were measured via Doppler ultrasound before and after 5 min of forearm occlusion. For LH, a microdialysis membrane was inserted in the dermis of the forearm and perfused with Ringer's solution. Red blood cell flux was assessed with laser Doppler after ~40 min of continuous 39ºC LH. Maximal flux was established with 28 mM sodium nitroprusside infusion and 43ºC LH. Brachial BP was measured throughout and cutaneous vascular conductance (CVC) was calculated as flux / MAP and reported as % of max CVC. Results: WW and BW were matched for age (21 ± 3 vs 20 ± 1 y, P = 0.58) and BMI (23 ± 2 vs 23 ± 3 kg/m 2 , P = 0.94). There were no differences between WW and BW in baseline blood velocity (23.1 ± 5.7 vs 24.4 ± 11.6 cm/s, P = 0.79) or blood flow (98.9 ± 38.3 vs 114.5 ± 80.7 ml/min, P = 0.65). WW and BW also had similar peak blood velocity (109.2 ± 13.8 vs 109.7 ± 28 cm/s, P = 0.97), peak blood flow (453.7 ± 164.7 vs 482.5 ± 187.7 ml/min, P = 0.77), and total blood flow AUC during the 120 s after cuff release (487.4 ± 178.5 vs 486.8 ± 190.1 ml, P = 0.99). However, compared to WW, BW had a significantly blunted CVC during 39ºC LH (66 ± 17 vs 45 ± 10 %max, P = 0.02). Conclusions: BW had blunted blood flow responses to LH compared to WW despite similar blood velocity and flow responses during RH. This suggests that LH is more sensitive than RH to early impairments in microvascular function.