Browsing by Author "Johnson, Blair D."

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    Arterial stiffness is not acutely modified by consumption of a caffeinated soft drink sweetened with high‐fructose corn syrup in young healthy adults
    (Wiley, 2021) Freemas, Jessica A.; Greenshields, Joel T.; Baker, Tyler; Carter, Stephen J.; Johnson, Blair D.; Schlader, Zachary J.; Medicine, School of Medicine
    We tested the hypothesis that ingestion of a caffeinated soft drink sweetened with high-fructose corn syrup acutely increases arterial stiffness. In a randomized counterbalanced, crossover design, fourteen healthy adults (25 ± 3 years, 6 women) reported to the laboratory for two experimental visits where 500 ml of tap water (H2 O) or 500 ml of Mountain Dew® (a caffeinated soft drink sweetened with high-fructose corn syrup (HFCS)) were consumed. Arterial stiffness (carotid-to-femoral pulse wave velocity (cfPWV)), peripheral and central blood pressures were measured pre-consumption, 30 min post-consumption, and 120 min post-consumption. Prior to each measurement period, beat-to-beat hemodynamic measures were collected. Changes in heart rate, blood pressure, and cardiac output from pre-consumption did not differ between trials at any timepoint (p ≥ 0.06). Moreover, changes in peripheral or central blood pressures from pre-consumption did not differ between trials (p ≥ 0.84). Likewise, changes in cfPWV from pre-consumption to 30 min post-consumption (HFCS: 0.2 ± 0.3 m/s, H2 O: 0.0 ± 0.3 m/s, p = 0.34) and 120 min post-consumption (HFCS: 0.3 ± 0.4 m/s, H2 O: 0.2 ± 0.3 m/s, p = 0.77) did not differ. Changes in aortic augmentation pressure, augmentation index, augmentation index corrected to a heart rate of 75 bpm, and reflection magnitude did not differ between conditions at 30 min post- (p ≥ 0.55) or 120 min post- (p ≥ 0.18) consumption. In healthy young adults, ingesting 500 ml of a commercially available caffeinated soft drink sweetened with high-fructose corn syrup does not acutely change indices of arterial stiffness and wave reflection.
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    Cutaneous microvascular vasodilatory consequences of acute consumption of a caffeinated soft drink sweetened with high‐fructose corn syrup
    (Wiley, 2021) Greenshields, Joel T.; Keeler, Jason M.; Freemas, Jessica A.; Baker, Tyler B.; Johnson, Blair D.; Carter, Stephen J.; Schlader, Zachary J.; Medicine, School of Medicine
    This study tested the hypotheses that compared to drinking water, consumption of a caffeinated soft drink sweetened with high-fructose corn syrup (HFCS) attenuates the cutaneous vasodilatory response to local skin heating without (Protocol 1) and following ischemia-reperfusion injury (Protocol 2). In a randomized, counterbalanced crossover design, 14 healthy adults (25 ± 3 year, 6 women) consumed 500 ml of water (water) or a caffeinated soft drink sweetened with HFCS (Mtn. Dew, DEW). Thirty minutes following beverage consumption local skin heating commenced on the right forearm (Protocol 1), while on the left forearm ischemia-reperfusion commenced with 20 min of ischemia followed by 20 min of reperfusion and then local skin heating (Protocol 2). Local skin heating involved 40 min of heating to 39℃ followed by 20 min of heating to 44℃. Skin blood flow (SkBf, laser Doppler) data were normalized to mean arterial pressure and are presented as a cutaneous vascular conductance (CVC) and as percentage of the CVC response during heating to 44℃ (%CVCmax ). Protocol 1: During local heating at 39℃, no differences were observed in CVC (water: 2.0 ± 0.6 PU/mmHg; DEW: 2.0 ± 0.8 PU/mmHg, p = 0.83) or %CVCmax (water: 59 ± 14%; DEW 60 ± 15%, p = 0.84) between trials. Protocol 2: During local skin heating at 39℃, no differences were observed in CVC (water: 1.7 ± 0.5 PU/mmHg; DEW: 1.5 ± 0.5 PU/mmHg, p = 0.33) or %CVCmax (water: 64 ± 15%; DEW 61 ± 15% p = 0.62) between trials. The cutaneous microvascular vasodilator response to local heating with or without prior ischemia-reperfusion injury is not affected by acute consumption of a caffeinated soft drink sweetened with HFCS.
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    Kidney injury risk during prolonged exposure to current and projected wet bulb temperatures occurring during extreme heat events in healthy young men
    (American Physiological Society, 2022) Hess, Hayden W.; Stooks, Jocelyn J.; Baker, Tyler B.; Chapman, Christopher L.; Johnson, Blair D.; Pryor, Riana R.; Basile, David P.; Monroe, Jacob C.; Hostler, David; Schlader, Zachary J.; Cellular and Integrative Physiology, School of Medicine
    Wet bulb temperatures (Twet) during extreme heat events are commonly 31°C. Recent predictions indicate that Twet will approach or exceed 34°C. Epidemiological data indicate that exposure to extreme heat events increases kidney injury risk. We tested the hypothesis that kidney injury risk is elevated to a greater extent during prolonged exposure to Twet = 34°C compared with Twet = 31°C. Fifteen healthy men rested for 8 h in Twet = 31 (0)°C and Twet = 34 (0)°C. Insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP-2), and thioredoxin 1 (TRX-1) were measured from urine samples. The primary outcome was the product of IGFBP7 and TIMP-2 ([IGFBP7·TIMP-2]), which provided an index of kidney injury risk. Plasma interleukin-17a (IL-17a) was also measured. Data are presented at preexposure and after 8 h of exposure and as mean (SD) change from preexposure. The increase in [IGFBP7·TIMP-2] was markedly greater at 8 h in the 34°C [+26.9 (27.1) (ng/mL)2/1,000) compared with the 31°C [+6.2 (6.5) (ng/mL)2/1,000] trial (P < 0.01). Urine TRX-1, a marker of renal oxidative stress, was higher at 8 h in the 34°C [+77.6 (47.5) ng/min] compared with the 31°C [+16.2 (25.1) ng/min] trial (P < 0.01). Plasma IL-17a, an inflammatory marker, was elevated at 8 h in the 34°C [+199.3 (90.0) fg/dL; P < 0.01] compared with the 31°C [+9.0 (95.7) fg/dL] trial. Kidney injury risk is exacerbated during prolonged resting exposures to Twet experienced during future extreme heat events (34°C) compared with that experienced currently (31°C), likely because of oxidative stress and inflammatory processes. NEW AND NOTEWORTHY: We have demonstrated that kidney injury risk is increased when men are exposed over an 8-h period to a wet bulb temperature of 31°C and exacerbated at a wet bulb temperature of 34°C. Importantly, these heat stress conditions parallel those that are encountered during current (31°C) and future (34°C) extreme heat events. The kidney injury biomarker analyses indicate both the proximal and distal tubules as the locations of potential renal injury and that the injury is likely due to oxidative stress and inflammatio
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    Normalization of flow-mediated dilation to shear stress area under the curve eliminates the impact of variable hyperemic stimulus
    (BioMed Central, 2008-09-04) Padilla, Jaume; Johnson, Blair D.; Newcomer, Sean C.; Wilhite, Daniel P.; Mickleborough, Timothy D.; Fly, Alyce D.; Mather, Kieren J.; Wallace, Janet P.; Medicine, School of Medicine
    Background Normalization of brachial artery flow-mediated dilation (FMD) to individual shear stress area under the curve (peak FMD:SSAUC ratio) has recently been proposed as an approach to control for the large inter-subject variability in reactive hyperemia-induced shear stress; however, the adoption of this approach among researchers has been slow. The present study was designed to further examine the efficacy of FMD normalization to shear stress in reducing measurement variability. Methods Five different magnitudes of reactive hyperemia-induced shear stress were applied to 20 healthy, physically active young adults (25.3 ± 0. 6 yrs; 10 men, 10 women) by manipulating forearm cuff occlusion duration: 1, 2, 3, 4, and 5 min, in a randomized order. A venous blood draw was performed for determination of baseline whole blood viscosity and hematocrit. The magnitude of occlusion-induced forearm ischemia was quantified by dual-wavelength near-infrared spectrometry (NIRS). Brachial artery diameters and velocities were obtained via high-resolution ultrasound. The SSAUC was individually calculated for the duration of time-to-peak dilation. Results One-way repeated measures ANOVA demonstrated distinct magnitudes of occlusion-induced ischemia (volume and peak), hyperemic shear stress, and peak FMD responses (all p < 0.0001) across forearm occlusion durations. Differences in peak FMD were abolished when normalizing FMD to SSAUC (p = 0.785). Conclusion Our data confirm that normalization of FMD to SSAUC eliminates the influences of variable shear stress and solidifies the utility of FMD:SSAUC ratio as an index of endothelial function.