This page has only limited features, please log in for full access.
Chansol Hurr completed doctoral training in human integrative cardiovascular physiology in the laboratory at the University of Texas-Austin. He subsequently joined The George Washington University School of Medicine and Health Sciences as a Postdoctoral Fellow in the laboratory where his research efforts were focused on autonomic and central nervous system mechanisms in murine models that contribute to cardiometabolic diseases. He is currently an Assistant Professor in the Department of Physical Education at Jeonbuk National University, South Korea. His current research encompasses the development of innovative strategies for exercise performance in humans.
BACKGROUND: Local cooling, or cryotherapy, has received attention due to its effects on athlete recovery before or after strenuous exercise. This study seeks to verify the effectiveness of 3 min applications of acute local cooling to the lower extremities between sets of a repeated vertical jump exercise. METHODS: Using a randomized crossover design, twelve subjects performed a total of 3 sets of 30 consecutive maximal vertical jumps and were allowed a recovery period of 5 min after each set. In the recovery period, subjects rested with or without a cooling suit worn on their lower legs. Changes in heart rate, blood lactate, and rate of perceived exertion were assessed. RESULTS: Vertical jump performance steadily decreased during 30 consecutive vertical jumps in all 3 sets; however, no differences in jump performance were observed among the groups. Heart rate, blood lactate, and rate of perceived exertion tended to be lower in the cooling recovery group relative to the control group. CONCLUSION: The current study provides evidence that acute local cooling recovery after a vertical jump exercise may not add any performance benefits but may provide a psychological benefit. The effectiveness of acute local cooling in other functional performances should be addressed in further research.
Chansol Hurr. Acute Local Cooling to the Lower Body during Recovery Does Not Improve Repeated Vertical Jump Performance. International Journal of Environmental Research and Public Health 2021, 18, 5026 .
AMA StyleChansol Hurr. Acute Local Cooling to the Lower Body during Recovery Does Not Improve Repeated Vertical Jump Performance. International Journal of Environmental Research and Public Health. 2021; 18 (9):5026.
Chicago/Turabian StyleChansol Hurr. 2021. "Acute Local Cooling to the Lower Body during Recovery Does Not Improve Repeated Vertical Jump Performance." International Journal of Environmental Research and Public Health 18, no. 9: 5026.
Purpose: This study investigated the effects of 12 weeks of moderate intensity elastic band exercise (EBE) on functional fitness and blood pressure parameters in the elderly. Methods: 27 healthy older adults were randomly assigned to an exercise group (n = 15, age: 75.1 ± 1.4 y) and a control group (n = 12, age: 72.3 ± 1.4 y). Participants performed EBE for 60 min, three times a week, over the course of three months. The EBE consisted of incremental resistance and aerobic exercises designed to improve whole body fitness. Functional fitness and resting cardiovascular parameters were assessed before and after the exercise training program. Results: Grip strength, sit and reach, and one-leg stance improved significantly in the exercise group, while no significant improvements were found in chair stand and timed up and go (p < 0.05). Cardiovascular parameters including systolic blood pressure, diastolic blood pressure, mean arterial pressure, and pulse pressure significantly decreased in the exercise group relative to the control group (p < 0.05). Conclusions: Findings of the present study suggest that safe, inexpensive, and easily accessible EBE program with circuit training components play a significant role in improving upper and lower body fitness, as well as cardiovascular fitness, in the elderly.
Hyun-Min Choi; Chansol Hurr; Sukwon Kim. Effects of Elastic Band Exercise on Functional Fitness and Blood Pressure Response in the Healthy Elderly. International Journal of Environmental Research and Public Health 2020, 17, 7144 .
AMA StyleHyun-Min Choi, Chansol Hurr, Sukwon Kim. Effects of Elastic Band Exercise on Functional Fitness and Blood Pressure Response in the Healthy Elderly. International Journal of Environmental Research and Public Health. 2020; 17 (19):7144.
Chicago/Turabian StyleHyun-Min Choi; Chansol Hurr; Sukwon Kim. 2020. "Effects of Elastic Band Exercise on Functional Fitness and Blood Pressure Response in the Healthy Elderly." International Journal of Environmental Research and Public Health 17, no. 19: 7144.
PURPOSE: Some athletes consume alcohol prior to training and sports events, possibly because they believe that alcohol may aid in reducing pain and anxiety, increasing confidence, and promoting aggressiveness. While previous studies have shown that alcohol consumption acutely impairs endurance exercise performance, its effects on anaerobic exercise performance have not been well established. Therefore, this study investigated the effect of a small dose of alcohol on anaerobic exercise performance.METHODS: In a randomized crossover design, nine healthy and recreationally active males (n=6) and females (n=3) participated in the study. Subjects consumed 0.7 g of alcohol per kg of lean body mass or a calorie/volume-matched sucrose beverage. Reaction time tests were performed before and 25 minutes after beverage consumption. Following the second reaction time test, subjects performed the 20-second Wingate anaerobic test (WAnT).RESULTS: Compared to the sucrose drink, alcohol showed no significant effects on peak power (p=.903), average power (p=.970), percentage power drop during WAnT (p=.593), or total energy produced during WAnT (p=.923). Moreover, alcohol did not affect the time course of power output during a 20s WAnT (p=.999 for all time points). In addition, reaction time was not significantly different when comparing alcoholic with sucrose drinks at different timepoint (Before; p=.999, After; p=.364).CONCLUSIONS: Although some athletes consume alcohol prior to engaging in sports events, assuming that it may improve anaerobic exercise performance, the results of the present study show that acute consumption of alcohol does not have effects on anaerobic exercise performance when compared to the control beverage.
Ting-Heng Chou; Chansol Hurr. Effects of Acute Alcohol Consumption on Cycling Anaerobic Exercise Performance: A Randomized Crossover Study. Exercise Science 2020, 29, 264 -271.
AMA StyleTing-Heng Chou, Chansol Hurr. Effects of Acute Alcohol Consumption on Cycling Anaerobic Exercise Performance: A Randomized Crossover Study. Exercise Science. 2020; 29 (3):264-271.
Chicago/Turabian StyleTing-Heng Chou; Chansol Hurr. 2020. "Effects of Acute Alcohol Consumption on Cycling Anaerobic Exercise Performance: A Randomized Crossover Study." Exercise Science 29, no. 3: 264-271.
Suk Won Kim; Chansol Hurr. Effects of acute cooling on cycling anaerobic exercise performance and neuromuscular activity: a randomized crossover study. 2020, 1 .
AMA StyleSuk Won Kim, Chansol Hurr. Effects of acute cooling on cycling anaerobic exercise performance and neuromuscular activity: a randomized crossover study. . 2020; ():1.
Chicago/Turabian StyleSuk Won Kim; Chansol Hurr. 2020. "Effects of acute cooling on cycling anaerobic exercise performance and neuromuscular activity: a randomized crossover study." , no. : 1.
Key points Non‐alcoholic fatty liver disease, characterized in part by elevated liver triglycerides (i.e. hepatic steatosis), is a growing health problem. In this study, we found that hepatic steatosis is associated with robust hepatic sympathetic overactivity. Removal of hepatic sympathetic nerves reduced obesity‐induced hepatic steatosis. Liver sympathetic innervation modulated hepatic lipid acquisition pathways during obesity. Abstract Non‐alcoholic fatty liver disease (NAFLD) affects 1 in 3 Americans and is a significant risk factor for type II diabetes mellitus, insulin resistance and hepatic carcinoma. Characterized in part by excessive hepatic triglyceride accumulation (i.e. hepatic steatosis), the incidence of NAFLD is increasing – in line with the growing obesity epidemic. The role of the autonomic nervous system in NAFLD remains unclear. Here, we show that chronic hepatic sympathetic overactivity mediates hepatic steatosis. Direct multiunit recordings of hepatic sympathetic nerve activity were obtained in high fat diet and normal chow fed male C57BL/6J mice. To reduce hepatic sympathetic nerve activity we utilized two approaches including pharmacological ablation of the sympathetic nerves and phenol‐based hepatic sympathetic nerve denervation. Diet‐induced NAFLD was associated with a nearly doubled firing rate of the hepatic sympathetic nerves, which was largely due to an increase in efferent nerve traffic. Furthermore, established high fat diet‐induced hepatic steatosis was effectively reduced with pharmacological or phenol‐based removal of the hepatic sympathetic nerves, independent of changes in body weight, caloric intake or adiposity. Ablation of liver sympathetic nerves was also associated with improvements in liver triglyceride accumulation pathways including free fatty acid uptake and de novo lipogenesis. These findings highlight an unrecognized pathogenic link between liver sympathetic outflow and hepatic steatosis and suggest that manipulation of the liver sympathetic nerves may represent a novel therapeutic strategy for NAFLD.
Chansol Hurr; Hayk Simonyan; Donald A. Morgan; Kamal Rahmouni; Colin N. Young. Liver sympathetic denervation reverses obesity‐induced hepatic steatosis. The Journal of Physiology 2019, 597, 4565 -4580.
AMA StyleChansol Hurr, Hayk Simonyan, Donald A. Morgan, Kamal Rahmouni, Colin N. Young. Liver sympathetic denervation reverses obesity‐induced hepatic steatosis. The Journal of Physiology. 2019; 597 (17):4565-4580.
Chicago/Turabian StyleChansol Hurr; Hayk Simonyan; Donald A. Morgan; Kamal Rahmouni; Colin N. Young. 2019. "Liver sympathetic denervation reverses obesity‐induced hepatic steatosis." The Journal of Physiology 597, no. 17: 4565-4580.
It has been established that endothelial function in conduit vessels is reduced in young African Americans (AA) relative to Caucasian Americans (CA). However, less is known regarding endothelial function in microvasculature of young AA. We hypothesized that microvascular function in response to local heating of skin is attenuated in young AA relative to age-matched CA due largely to the lack of NO bioavailability, which is in turn improved by intradermal l-arginine supplementation and/or inhibition of arginase. Nine AA and nine CA adults participated in this study. Participants were instrumented with four microdialysis membranes in the cutaneous vasculature of one forearm and were randomly assigned to receive 1) lactated Ringer's solution as a control site; 2) 20 mM NG-nitro-l-arginine (l-NAME) to inhibit NO synthase activity; 3) 10 mM l-arginine to local supplement l-arginine; or 4) a combination of 5.0 mM (S)-(2‑boronoethyl)-l-cysteine-HCL (BEC) and 5.0 mM Nω-hydroxy-nor-l-arginine (nor-NOHA) at a rate of 2.0 μl/min to locally inhibit arginase activity. Cutaneous vascular conductance (CVC) was calculated as red blood cell flux divided by mean arterial pressure. All CVC data were presented as a percentage of maximal CVC (%CVCmax) that was determined by maximal cutaneous vasodilation induced by 44 °C heating plus sodium nitroprusside administration. The response during the 42 °C local heating plateau was blunted in the AA at the control site (CA: 84 ± 12 vs. AA: 62 ± 6 vs. %CVCmax; P < 0.001). This response was improved in AA at the l-arginine site (Control: 62 ± 6 vs. l-arginine: 70 ± 18%CVCmax; P < 0.05) but not in the arginase inhibited site (Control: 62 ± 6 vs. Arginase inhibited: 62 ± 13%CVCmax; P = 0.91). In addition, the AA group had an attenuated NO contribution to the plateau phase during 42 °C local heating relative to the CA group (CA: 56 ± 14 vs. AA: 44 ± 6 Δ %CVCmax; P < 0.001). These findings suggest that 1) cutaneous microvascular function in response to local heating is blunted in young AA when compared to age-matched young CA; 2) this attenuated response is partly related to decrease in NO bioavailability in young AA; and 3) a local infusion of l-arginine, but not arginase inhibition, improves cutaneous microvascular responses to local heating in young AA relative to CA.
Kiyoung Kim; Chansol Hurr; Jordan C. Patik; R. Matthew Brothers. Attenuated cutaneous microvascular function in healthy young African Americans: Role of intradermal l -arginine supplementation. Microvascular Research 2018, 118, 1 -6.
AMA StyleKiyoung Kim, Chansol Hurr, Jordan C. Patik, R. Matthew Brothers. Attenuated cutaneous microvascular function in healthy young African Americans: Role of intradermal l -arginine supplementation. Microvascular Research. 2018; 118 ():1-6.
Chicago/Turabian StyleKiyoung Kim; Chansol Hurr; Jordan C. Patik; R. Matthew Brothers. 2018. "Attenuated cutaneous microvascular function in healthy young African Americans: Role of intradermal l -arginine supplementation." Microvascular Research 118, no. : 1-6.
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.
Chansol Hurr; Jordan Patik; Kiyoung Kim; Kevin M. Christmas; R. Matthew Brothers. Tempol augments the blunted cutaneous microvascular thermal reactivity in healthy young African Americans. Experimental Physiology 2018, 103, 343 -349.
AMA StyleChansol Hurr, Jordan Patik, Kiyoung Kim, Kevin M. Christmas, R. Matthew Brothers. Tempol augments the blunted cutaneous microvascular thermal reactivity in healthy young African Americans. Experimental Physiology. 2018; 103 (3):343-349.
Chicago/Turabian StyleChansol Hurr; Jordan Patik; Kiyoung Kim; Kevin M. Christmas; R. Matthew Brothers. 2018. "Tempol augments the blunted cutaneous microvascular thermal reactivity in healthy young African Americans." Experimental Physiology 103, no. 3: 343-349.
New FindingsWhat is the central question of this study? Is there a difference in the cerebral vascular response to rebreathing-induced hypercapnia between obese and lean individuals? What is the main finding and its importance? The main finding is that obese individuals have an attenuated increase in cerebral vascular conductance during hypercapnia relative to lean individuals. This finding suggests cerebral vascular dysfunction in this population, which might contribute to the greater prevalence of cerebral vascular and neurocognitive disease in this population. Obesity increases the risk of cardiovascular disease by >45%. Furthermore, obesity is a contributory factor to cognitive impairment and Alzheimer's disease. The mechanisms accounting for this increased disease risk have not been clarified. This study tested the hypothesis that the total range of change (a) in cerebral blood velocity (CBV) and cerebral vascular conductance (CVCI) and the maximal (y0) CBV and CVCI achieved during rebreathing-induced hypercapnia would be attenuated in obese individuals. Sixteen lean and 15 obese individuals participated. The magnitude of rebreathing-induced hypercapnia was similar between groups (lean, ∆15 ± 3 mmHg versus obese, ∆15 ± 2 mmHg; P = 0.82). The total range of change in CBV during rebreathing (a; expressed as a percentage) was similar between groups (lean, 91 ± 24% versus obese, 76 ± 19%, P = 0.07), whereas the total range of change in CVCI during rebreathing (a; expressed as a percentage) was attenuated in the obese individuals (lean, 71 ± 20% versus obese, 51 ± 15%, P < 0.01). Likewise, the maximal increase in CBV during rebreathing (y0; expressed as a percentage) was similar between groups (lean, 189 ± 22% versus obese, 179 ± 20%, P = 0.20), whereas the maximal increase in CVCI during rebreathing (y0; expressed as a percentage) was attenuated in the obese individuals (lean, 172 ± 19% versus obese, 155 ± 17 %, P = 0.01). These data indicate that the cerebral vascular response to rebreathing-induced hypercapnia is attenuated in obese individuals. This impairment might be a factor contributing to the elevated cerebral vascular and neurocognitive disease risk in this population.
Chansol Hurr; Jordan Patik; Kiyoung Kim; R. Matthew Brothers. Blunted cerebral vascular responsiveness to hypercapnia in obese individuals. Experimental Physiology 2017, 102, 1300 -1308.
AMA StyleChansol Hurr, Jordan Patik, Kiyoung Kim, R. Matthew Brothers. Blunted cerebral vascular responsiveness to hypercapnia in obese individuals. Experimental Physiology. 2017; 102 (10):1300-1308.
Chicago/Turabian StyleChansol Hurr; Jordan Patik; Kiyoung Kim; R. Matthew Brothers. 2017. "Blunted cerebral vascular responsiveness to hypercapnia in obese individuals." Experimental Physiology 102, no. 10: 1300-1308.
Nonalcoholic fatty liver disease (NAFLD), characterized by an excess accumulation of hepatic triglycerides, is a growing health epidemic. While ER stress in the liver has been implicated in the development of NAFLD, the role of brain ER stress — which is emerging as a key contributor to a number of chronic diseases including obesity — in NAFLD remains unclear. These studies reveal that chemical induction of ER stress in the brain caused hepatomegaly and hepatic steatosis in mice. Conversely, pharmacological reductions in brain ER stress in diet-induced obese mice rescued NAFLD independent of body weight, food intake, and adiposity. Evaluation of brain regions involved revealed robust activation of ER stress biomarkers and ER ultrastructural abnormalities in the circumventricular subfornical organ (SFO), a nucleus situated outside of the blood-brain-barrier, in response to high-fat diet. Targeted reductions in SFO-ER stress in obese mice via SFO-specific supplementation of the ER chaperone 78-kDa glucose–regulated protein ameliorated hepatomegaly and hepatic steatosis without altering body weight, food intake, adiposity, or obesity-induced hypertension. Overall, these findings indicate a novel role for brain ER stress, notably within the SFO, in the pathogenesis of NAFLD.
Julie A. Horwath; Chansol Hurr; Scott D. Butler; Mallikarjun Guruju; Martin D. Cassell; Allyn L. Mark; Robin L. Davisson; Colin N. Young. Obesity-induced hepatic steatosis is mediated by endoplasmic reticulum stress in the subfornical organ of the brain. JCI Insight 2017, 2, 1 .
AMA StyleJulie A. Horwath, Chansol Hurr, Scott D. Butler, Mallikarjun Guruju, Martin D. Cassell, Allyn L. Mark, Robin L. Davisson, Colin N. Young. Obesity-induced hepatic steatosis is mediated by endoplasmic reticulum stress in the subfornical organ of the brain. JCI Insight. 2017; 2 (8):1.
Chicago/Turabian StyleJulie A. Horwath; Chansol Hurr; Scott D. Butler; Mallikarjun Guruju; Martin D. Cassell; Allyn L. Mark; Robin L. Davisson; Colin N. Young. 2017. "Obesity-induced hepatic steatosis is mediated by endoplasmic reticulum stress in the subfornical organ of the brain." JCI Insight 2, no. 8: 1.
A role for oxidative stress in the brain has been suggested in the pathogenesis of diet-induced obesity (DIO), although the underlying neural regions and mechanisms remain incompletely defined. We tested the hypothesis that NADPH oxidase-dependent oxidative stress in the paraventricular nucleus (PVN), a hypothalamic energy homeostasis center, contributes to the development of DIO. Cre/LoxP technology was coupled with selective PVN adenoviral microinjection to ablate p22phox , the obligatory subunit for NADPH oxidase activity, in mice harboring a conditional p22phox allele. Selective deletion of p22phox in the PVN protected mice from high-fat DIO independent of changes in food intake or locomotor activity. This was accompanied by β3-adrenoceptor-dependent increases in energy expenditure, elevations in brown adipose tissue thermogenesis, and browning of white adipose tissue. These data reveal a potentially novel role for brain oxidative stress in the development of DIO by modulating β3-adrenoceptor mechanisms and point to the PVN as an underlying neural site.
Heinrich E. Lob; Jiunn Song; Chansol Hurr; Alvin Chung; Colin N. Young; Allyn L. Mark; Robin L. Davisson. Deletion of p22phox-dependent oxidative stress in the hypothalamus protects against obesity by modulating β3-adrenergic mechanisms. JCI Insight 2017, 2, e87094 .
AMA StyleHeinrich E. Lob, Jiunn Song, Chansol Hurr, Alvin Chung, Colin N. Young, Allyn L. Mark, Robin L. Davisson. Deletion of p22phox-dependent oxidative stress in the hypothalamus protects against obesity by modulating β3-adrenergic mechanisms. JCI Insight. 2017; 2 (2):e87094.
Chicago/Turabian StyleHeinrich E. Lob; Jiunn Song; Chansol Hurr; Alvin Chung; Colin N. Young; Allyn L. Mark; Robin L. Davisson. 2017. "Deletion of p22phox-dependent oxidative stress in the hypothalamus protects against obesity by modulating β3-adrenergic mechanisms." JCI Insight 2, no. 2: e87094.
Bioluminescence imaging is an effective tool for in vivo investigation of molecular processes. We have demonstrated the applicability of bioluminescence imaging to spatiotemporally monitor gene expression in cardioregulatory brain nuclei during the development of cardiovascular disease, via incorporation of firefly luciferase into living animals, combined with exogenous d-luciferin substrate administration. Nevertheless, d-luciferin uptake into the brain tissue is low, which decreases the sensitivity of bioluminescence detection, particularly when considering small changes in gene expression in tiny central areas. Here, we tested the hypothesis that a synthetic luciferin, cyclic alkylaminoluciferin (CycLuc1), would be superior to d-luciferin for in vivo bioluminescence imaging in cardiovascular brain regions. Male C57B1/6 mice underwent targeted delivery of an adenovirus encoding the luciferase gene downstream of the CMV promoter to the subfornical organ (SFO) or paraventricular nucleus of hypothalamus (PVN), two crucial cardioregulatory neural regions. While bioluminescent signals could be obtained following d-luciferin injection (150 mg/kg), CycLuc1 administration resulted in a three- to fourfold greater bioluminescent emission from the SFO and PVN, at 10- to 20-fold lower substrate concentrations (7.5–15 mg/kg). This CycLuc1-mediated enhancement in bioluminescent emission was evident early following substrate administration (i.e., 6–10 min) and persisted for up to 1 h. When the exposure time was reduced from 60 s to 1,500 ms, minimal signal in the PVN was detectable with d-luciferin, whereas bioluminescent images could be reliably captured with CycLuc1. These findings demonstrate that bioluminescent imaging with the synthetic luciferin CycLuc1 provides an improved physiological genomics tool to investigate molecular events in discrete cardioregulatory brain nuclei.
Hayk Simonyan; Chansol Hurr; Colin N. Young. A synthetic luciferin improves in vivo bioluminescence imaging of gene expression in cardiovascular brain regions. Physiological Genomics 2016, 48, 762 -770.
AMA StyleHayk Simonyan, Chansol Hurr, Colin N. Young. A synthetic luciferin improves in vivo bioluminescence imaging of gene expression in cardiovascular brain regions. Physiological Genomics. 2016; 48 (10):762-770.
Chicago/Turabian StyleHayk Simonyan; Chansol Hurr; Colin N. Young. 2016. "A synthetic luciferin improves in vivo bioluminescence imaging of gene expression in cardiovascular brain regions." Physiological Genomics 48, no. 10: 762-770.
Hypertension affects over 25 % of the population with the incidence continuing to rise, due in part to the growing obesity epidemic. Chronic elevations in sympathetic nerve activity (SNA) are a hallmark of the disease and contribute to elevations in blood pressure through influences on the vasculature, kidney, and heart (i.e., neurogenic hypertension). In this regard, a number of central nervous system mechanisms and neural pathways have emerged as crucial in chronically elevating SNA. However, it is important to consider that "sympathetic signatures" are present, with differential increases in SNA to regional organs that are dependent upon the disease progression. Here, we discuss recent findings on the central nervous system mechanisms and autonomic regulatory networks involved in neurogenic hypertension, in both non-obesity- and obesity-associated hypertension, with an emphasis on angiotensin-II, salt, oxidative and endoplasmic reticulum stress, inflammation, and the adipokine leptin.
Chansol Hurr; Colin N. Young. Neural Control of Non-vasomotor Organs in Hypertension. Current Hypertension Reports 2016, 18, 30 -30.
AMA StyleChansol Hurr, Colin N. Young. Neural Control of Non-vasomotor Organs in Hypertension. Current Hypertension Reports. 2016; 18 (4):30-30.
Chicago/Turabian StyleChansol Hurr; Colin N. Young. 2016. "Neural Control of Non-vasomotor Organs in Hypertension." Current Hypertension Reports 18, no. 4: 30-30.
Microvascular dysfunction contributes to the development of cardiovascular and metabolic disease. This study tested the hypothesis that young obese (BMI > 30 kg m− 2), otherwise healthy, adults (N = 15) have impaired microvascular function relative to age and sex matched, lean (BMI < 25 kg m− 2) individuals (N = 14). Participants were instrumented with two microdialysis probes in the cutaneous vasculature of one forearm; one for a wide dose range of infusions of the endothelium-dependent vasodilator methacholine (MCh) and the other for the endothelium-independent vasodilator sodium nitroprusside (SNP). Local temperature at each site was clamped at 33 °C and cutaneous blood flow was indexed by laser Doppler flowmetry (LDF). LDF was recorded while 7 doses of each drug (MCh: 10− 6–1 M; SNP: 5 × 10− 8–5 × 10− 2 M) were infused at a rate of 2 μl/min for 8 min per dose. Both sites finished with heating to 43 °C and 5 × 10− 2 M SNP to achieve site specific maximal vasodilation. Mean arterial blood pressure (MAP) was assessed in the last minute of each dose and was used for subsequent calculation of cutaneous vascular conductance (CVC; LDF/MAP) and responses were normalized to each individual site's maximal response (%CVCmax). Group four-parameter dose response curves were compared with an extra sum of squares F-test. SNP EC50 was greater in obese relative to lean (− 2.931 ± 0.10 vs − 3.746 ± 0.18 Log[SNP] M, P < 0.001); however, there was no difference in MCh EC50 between groups (− 3.796 ± 0.23 vs − 3.852 ± 0.25 Log[MCh] M, P = 0.81). Additionally, baseline and maximal CVC in both sites were similar between groups (all P > 0.05). These results suggest attenuated endothelium-independent response to nitric oxide while endothelium-dependent vasodilation function is maintained.
Jordan Patik; Kevin M. Christmas; Chansol Hurr; R. Matthew Brothers. Impaired endothelium independent vasodilation in the cutaneous microvasculature of young obese adults. Microvascular Research 2016, 104, 63 -68.
AMA StyleJordan Patik, Kevin M. Christmas, Chansol Hurr, R. Matthew Brothers. Impaired endothelium independent vasodilation in the cutaneous microvasculature of young obese adults. Microvascular Research. 2016; 104 ():63-68.
Chicago/Turabian StyleJordan Patik; Kevin M. Christmas; Chansol Hurr; R. Matthew Brothers. 2016. "Impaired endothelium independent vasodilation in the cutaneous microvasculature of young obese adults." Microvascular Research 104, no. : 63-68.
What is the central question of this study? The purpose was to determine whether acute flavanol consumption improves cerebral vasodilatory capacity during rebreathing-induced hypercapnia in African Americans. What is the main finding and its importance? The reduced cerebral vasodilatory response to hypercapnia in young healthy African Americans was improved acutely following consumption of a flavanol-rich beverage. This may have important clinical implications regarding racial differences in cerebrovascular disease risk and possible interventional approaches to offset this risk. African Americans (AAs) have increased risk for cardiovascular and cerebrovascular disease. African Americans have attenuated cerebral vasodilator capacity during hypercapnia relative to Caucasian Americans (CAs). This study tested the hypothesis, using a placebo-controlled crossover design, that acute flavanol consumption improves the range of change in cerebral vascular conductance [CVCI, (a)] and the maximal CVCI (y0) achieved during rebreathing-induced increases in end-tidal carbon dioxide tension. Fourteen college-aged AAs and 14 CAs participated. Both a and y0 were lower in AAs prior to flavanols (for a, AAs, 46 ± 16 versus CAs, 74 ± 18% CVCI, P < 0.001; and for y0, AAs, 151 ± 18 versus CAs, 176 ± 20% CVCI, P = 0.002); however, these variables were increased after flavanols such that there were no differences between groups (for a, AAs, 64 ± 19 versus CAs, 72 ± 22% CVCI, P = 0.35; and for y0, AAs, 166 ± 22 versus CAs, 176 ± 22% CVCI, P = 0.26). Both a and y0 were also lower in AAs prior to placebo (for a, AAs, 52 ± 19 versus CAs, 76 ± 15% CVCI, P = 0.002; and for y0, AAs, 156 ± 20 versus CAs, 177 ± 21% CVCI, P = 0.015), and these differences remained following placebo (for a, AAs, 52 ± 17 versus CAs, 80 ± 20% CVCI, P < 0.001; and for y0, AAs, 152 ± 18 versus CAs, 181 ± 25% CVCI, P = 0.003). These data suggest that acute flavanol consumption improves cerebral vasodilatory capacity during hypercapnia in AAs.
Chansol Hurr; Michelle L. Harrison; R. Matthew Brothers. Acute flavanol consumption improves the cerebral vasodilatory capacity in college-aged African Americans. Experimental Physiology 2015, 100, 1030 -1038.
AMA StyleChansol Hurr, Michelle L. Harrison, R. Matthew Brothers. Acute flavanol consumption improves the cerebral vasodilatory capacity in college-aged African Americans. Experimental Physiology. 2015; 100 (9):1030-1038.
Chicago/Turabian StyleChansol Hurr; Michelle L. Harrison; R. Matthew Brothers. 2015. "Acute flavanol consumption improves the cerebral vasodilatory capacity in college-aged African Americans." Experimental Physiology 100, no. 9: 1030-1038.
Kiyoung Kim; Chansol Hurr; R. Matthew Brothers. Effect of Nitric Oxide Bioavailability on Cutaneous Microvascular Function in Healthy Young African Americans. Medicine and Science in Sports and Exercise 2015, 47, 741 .
AMA StyleKiyoung Kim, Chansol Hurr, R. Matthew Brothers. Effect of Nitric Oxide Bioavailability on Cutaneous Microvascular Function in Healthy Young African Americans. Medicine and Science in Sports and Exercise. 2015; 47 (5S):741.
Chicago/Turabian StyleKiyoung Kim; Chansol Hurr; R. Matthew Brothers. 2015. "Effect of Nitric Oxide Bioavailability on Cutaneous Microvascular Function in Healthy Young African Americans." Medicine and Science in Sports and Exercise 47, no. 5S: 741.
African Americans (AA) have increased risk for cardiovascular, cerebral vascular, and metabolic disease including hypertension, stroke, coronary artery disease, metabolic syndrome, and type II diabetes relative to Caucasian Americans (CA). While it is accepted that endothelial function is impaired in AA; less is known regarding their cerebral vasodilatory capacity to hypercapnia. We hypothesized that AA have a reduction in the total range of change in cerebral blood flow velocity (CBFV) measured in the middle cerebral artery and an index of cerebral vascular conductance (CVCI) in response to changes in partial pressure of end‐tidal carbon dioxide (PETCO2) during rebreathing‐induced hypercapnia when compared with CA. 21 healthy College‐aged AA (10 males) and 21 age and sex matched CA (10 males) subjects participated in this study. A four‐parameter logistic regression was used for curve fitting the responses of CBFV and CVCI relative to changes in PETCO2. The total ranges of change in CBFV (101 ± 18% vs. 69 ± 23%; P < 0.001) and CVCI (83 ± 21% vs. 58 ± 21%; P < 0.001) as well as the maximum increase in CBFV (205 ± 24% vs. 169 ± 24%; P < 0.001) and CVCI (188 ± 30% vs. 154 ± 19%; P < 0.001) were reduced during hypercapnia in AA relative to CA despite a similar increase in PETCO2 (Δ 15 ± 3 mm Hg vs. Δ 15 ± 3 mm Hg, P = 0.65). In conclusion, these data indicate that AA have attenuated cerebral vascular capacity to hypercapnia when compared with CA. This article is protected by copyright. All rights reserved
Chansol Hurr; Kiyoung Kim; Michelle L. Harrison; R. Matthew Brothers. Attenuated cerebral vasodilatory capacity in response to hypercapnia in college‐aged African Americans. Experimental Physiology 2014, 100, 35 -43.
AMA StyleChansol Hurr, Kiyoung Kim, Michelle L. Harrison, R. Matthew Brothers. Attenuated cerebral vasodilatory capacity in response to hypercapnia in college‐aged African Americans. Experimental Physiology. 2014; 100 (1):35-43.
Chicago/Turabian StyleChansol Hurr; Kiyoung Kim; Michelle L. Harrison; R. Matthew Brothers. 2014. "Attenuated cerebral vasodilatory capacity in response to hypercapnia in college‐aged African Americans." Experimental Physiology 100, no. 1: 35-43.
A high degree of interindividual variability exists in the magnitude of heat stress (HS)-induced reductions in orthostatic tolerance relative to normothermia (NT). This variability may be associated with HS-mediated reductions in cerebral perfusion (indexed as middle cerebral artery blood velocity; MCAV(mean)) and altered cerebrovascular regulation.
Joshua F. Lee; Kevin M. Christmas; Michelle L. Harrison; Chansol Hurr; Kiyoung Kim; R. Matthew Brothers. Variability in orthostatic tolerance during heat stress: cerebrovascular reactivity to arterial carbon dioxide. Aviation, Space, and Environmental Medicine 2014, 85, 624 -630.
AMA StyleJoshua F. Lee, Kevin M. Christmas, Michelle L. Harrison, Chansol Hurr, Kiyoung Kim, R. Matthew Brothers. Variability in orthostatic tolerance during heat stress: cerebrovascular reactivity to arterial carbon dioxide. Aviation, Space, and Environmental Medicine. 2014; 85 (6):624-630.
Chicago/Turabian StyleJoshua F. Lee; Kevin M. Christmas; Michelle L. Harrison; Chansol Hurr; Kiyoung Kim; R. Matthew Brothers. 2014. "Variability in orthostatic tolerance during heat stress: cerebrovascular reactivity to arterial carbon dioxide." Aviation, Space, and Environmental Medicine 85, no. 6: 624-630.
Cerebrovascular reactivity represents the capacity of the cerebral circulation to raise blood flow in the face of increased demand, and may be reduced in some clinical and physiological conditions. We tested the hypothesis that the hypercapnia-induced increase in cerebral perfusion is attenuated during heat stress (HS) compared to normothermia (NT), and this response is further reduced during the combined challenges of HS and lower body negative pressure (LBNP). Ten healthy individuals (9 men) undertook rebreathing-induced hypercapnia during NT, HS, and HS + 20 mmHg LBNP (HSLBNP), while cerebral perfusion was indexed from middle cerebral artery blood velocity (MCA V mean). Cerebrovascular responses were calculated from the slope of the change in MCA V mean and cerebral vascular conductance (CVCi) relative to the increase in end tidal carbon dioxide (\( {\text{PET}}_{{{\text{CO}}_{ 2} }} \)) during rebreathing. MCA V mean was similar in HS (55 ± 19 cm s−1) and HSLBNP (52 ± 16 cm s−1), and both values were reduced relative to NT (66 ± 20 cm s−1), yet the rise in MCA V mean per Torr increase in \( {\text{PET}}_{{{\text{CO}}_{ 2} }} \) during rebreathing was similar in each condition (NT: 2.5 ± 0.6 cm s−1 Torr−1; HS: 2.4 ± 0.8 cm s−1 Torr−1; HSLBNP: 2.1 ± 1.1 cm s−1 Torr−1). Likewise, the rate of increase in CVCi was not different between conditions (NT: 2.1 ± 0.65 cm s−1 mmHg−1100 Torr−1; HS: 2.4 ± 0.8 cm s−1 mmHg−1 100 Torr−1; HSLBNP: 2.0 ± 1.0 cm s−1 mmHg−1 100 Torr−1). These data indicate that cerebrovascular reactivity is not compromised during whole-body heat stress alone or when combined with mild orthostatic stress relative to normothermic conditions.
Joshua F. Lee; Kevin M. Christmas; Michelle L. Harrison; Kiyoung Kim; Chansol Hurr; R. Matthew Brothers. Cerebral vasoreactivity: impact of heat stress and lower body negative pressure. Clinical Autonomic Research 2014, 24, 135 -141.
AMA StyleJoshua F. Lee, Kevin M. Christmas, Michelle L. Harrison, Kiyoung Kim, Chansol Hurr, R. Matthew Brothers. Cerebral vasoreactivity: impact of heat stress and lower body negative pressure. Clinical Autonomic Research. 2014; 24 (3):135-141.
Chicago/Turabian StyleJoshua F. Lee; Kevin M. Christmas; Michelle L. Harrison; Kiyoung Kim; Chansol Hurr; R. Matthew Brothers. 2014. "Cerebral vasoreactivity: impact of heat stress and lower body negative pressure." Clinical Autonomic Research 24, no. 3: 135-141.
Obesity is linked with numerous physiological impairments; however, its impact on orthostatic tolerance (OT) remains unknown. This study tested the hypothesis that OT is reduced in obese individuals, and that reduced heart rate (HR) reserve and impaired cerebral autoregulation contribute to impaired OT. Eleven obese (8 females) and 22 non-obese (10 females) individuals were exposed to incremental lower body negative pressure (LBNP) to presyncope while HR, arterial blood pressure, and cerebral perfusion (middle cerebral artery blood velocity; MCA V mean) were measured. OT was quantified with a cumulative stress index (CSI). OT was reduced in obese subjects, and there was an inverse relationship between body mass index (BMI) and OT (R = −0.47). HR was higher at rest and during each level of LBNP completed by all subjects. Similar peak HR (HRpeak) during LBNP between obese and non-obese subjects resulted in obese having a higher %peak HR at rest and at each stage of LBNP compared. Relationships existed for BMI and resting %HRpeak (R = 0.45) and resting %HRpeak and CSI (R = −0.52). Despite lower CSI in obese, MCA V mean and indices of cerebral autoregulation were similar between groups at all time points. These data suggest that OT is reduced in obese and a higher resting HR, but not impaired regulation of cerebral perfusion, may contribute to this reduction.
Joshua F. Lee; Michelle L. Harrison; Kevin M. Christmas; Kiyoung Kim; Chansol Hurr; R. Matthew Brothers. Elevated resting heart rate and reduced orthostatic tolerance in obese humans. Clinical Autonomic Research 2013, 24, 39 -46.
AMA StyleJoshua F. Lee, Michelle L. Harrison, Kevin M. Christmas, Kiyoung Kim, Chansol Hurr, R. Matthew Brothers. Elevated resting heart rate and reduced orthostatic tolerance in obese humans. Clinical Autonomic Research. 2013; 24 (1):39-46.
Chicago/Turabian StyleJoshua F. Lee; Michelle L. Harrison; Kevin M. Christmas; Kiyoung Kim; Chansol Hurr; R. Matthew Brothers. 2013. "Elevated resting heart rate and reduced orthostatic tolerance in obese humans." Clinical Autonomic Research 24, no. 1: 39-46.