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BACKGROUND: Social networks can influence physical activity, but little is known about how best to engineer online and in-person social networks to increase activity. PURPOSE: The purpose of this study was to conduct a randomized trial based on the Social Networks for Activity Promotion model to assess the incremental contributions of different procedures for building social networks on objectively measured outcomes. METHODS: Physically inactive adults (n = 308, age, 50.3 (SD = 8.3) years, 38.3 % male, 83.4 % overweight/obese) were randomized to one of three groups. The Promotion group evaluated the effects of weekly emailed tips emphasizing social network interactions for walking (e.g., encouragement, informational support); the Activity group evaluated the incremental effect of adding an evidence-based online fitness walking intervention to the weekly tips; and the Social Networks group evaluated the additional incremental effect of providing access to an online networking site for walking as well as prompting walking/activity across diverse settings. The primary outcome was mean change in accelerometer-measured moderate-to-vigorous physical activity (MVPA), assessed at 3 and 9 months from baseline. RESULTS: Participants increased their MVPA by 21.0 min/week, 95 % CI [5.9, 36.1], p = .005, at 3 months, and this change was sustained at 9 months, with no between-group differences. CONCLUSIONS: Although the structure of procedures for targeting social networks varied across intervention groups, the functional effect of these procedures on physical activity was similar. Future research should evaluate if more powerful reinforcers improve the effects of social network interventions. TRIAL REGISTRATION NUMBER: The trial was registered with the ClinicalTrials.gov (NCT01142804).

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Physiological adaptations to exercise training are well recognized and contribute importantly to health and fitness. Cardiovascular diseases, such as hypertension and heart failure, are often associated with elevated activity of the sympathetic nervous system. This review aims to provide comprehensive overview on the role of exercise training on muscle sympathetic nerve activity (MSNA) regulation in humans, with a focus on recent advances in at-risk populations. Collectively, these studies converge to demonstrate that aerobic exercise training reduces resting MSNA in populations at heightened cardiovascular risk, but do not appear to alter resting MSNA in healthy adults. We provide directions for future research which might address gaps in our knowledge regarding sympathoneural adaptations to exercise training.

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OBJECTIVES: This study aimed to evaluate the feasibility of using a compact elliptical device to increase energy expenditure during sedentary activities. A secondary aim was to evaluate if two accelerometers attached to the elliptical device could provide reliable and valid assessments of participants' frequency and duration of elliptical device use. DESIGN: Physically inactive adults (n=32, age range=25-65) were recruited through local advertisements and selected using stratified random sampling based on sex, body mass index (BMI), and age. METHODS: Indirect calorimetry was used to assess participants' energy expenditure while seated and while using the elliptical device at a self-selected intensity level. Participants also self-reported their interest in using the elliptical device during sedentary activities. Two Actigraph GT3X accelerometers were attached to the elliptical device to record time-use patterns. RESULTS: Participants expended a median of 179.1 kilocalories per hour while using the elliptical device (range=108.2-269.0), or a median of 87.9 more kilocalories (range=19.7-178.6) than they would expend per hour of sedentary sitting. Participants reported high interest in using the elliptical device during TV watching and computer work, but relatively low interest in using the device during office meetings. Women reported greater interest in using the elliptical device than men. The two accelerometers recorded identical time-use patterns on the elliptical device and demonstrated concurrent validity with time-stamped computer records. CONCLUSIONS: Compact elliptical devices could increase energy expenditure during sedentary activities, and may provide proximal environmental cues for increasing energy expenditure across multiple life domains.

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Hyperthyroidism induces marked changes in hemodynamics. Although considerable research has been done to study the effect of hyperthyroidism on the cardiovascular system, few studies have isolated the short-term, nongenomic effects of thyroid hormone on cardiovascular responses to exercise. We used near-infrared spectroscopy to measure muscle oxygenation, Doppler ultrasound to measure skeletal muscle blood flow, and microneurography to measure muscle sympathetic nerve activity (MSNA) during fatiguing dynamic handgrip in twelve healthy males (26 ± 1 years). Subjects were measured separately in both the euthyroid state, and acute hyperthyroid state (approximately ten times the normal levels of T3), induced by oral dosage of 300 µg of triiodothyronine (T3). Forearm blood flow was increased as a function of exercise time in the euthyroid and hyperthyroid state (Δ161.8 ± 45.0 mL/min and Δ140.7 ± 16.3 mL/min, respectively) but there was no significant difference between trials. Forearm vascular conductance (FVC) also increased as a function of exercise time with no significant difference between treatments at submaximal exercise but was significantly less with T3 treatment. MSNA was not different at rest or during submaximal exercise; however, MSNA was significantly greater at fatigue during the hyperthyroid state. Muscle oxyhemoglobin concentration was decreased during exercise in both euthyroid and hyperthyroid states (Δ19.7 ± 10.8% and Δ14.8 ± 9.6%, respectively); whereas deoxyhemoglobin concentration was increased (Δ50.0 ± 4.1% and Δ50.0 ± 6.2%, respectively). These results indicate that T3 had no direct effect on skeletal muscle oxygenation or blood flow during dynamic exercise, but elicited greater MSNA and lower FVC during fatiguing exercise.

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Melatonin attenuates muscle sympathetic nerve responses to sympathoexcitatory stimuli, but it is unknown whether melatonin similarly attenuates reflex changes in skin sympathetic nerve activity (SSNA). In this double-blind, placebo-controlled, crossover study, we tested the hypothesis that melatonin (3 mg) would attenuate the SSNA response to mental stress (mental arithmetic). Twelve healthy subjects underwent experimental testing on two separate days. Three minutes of mental stress occurred before and 45 min after ingestion of melatonin (3 mg) or placebo. Skin temperature was maintained at 34°C. Reflex increases in SSNA (peroneal nerve), mean arterial pressure, and heart rate (HR) to mental stress before and after melatonin were determined. Melatonin lowered HR (pre, 66 ± 3 beats/min; and post, 62 ± 3 beats/min, P = 0.046) and SSNA (pre, 14,282 ± 3,706 arbitrary units; and post, 9,571 ± 2,609 arbitrary units, P = 0.034) at rest. In response to mental stress, SSNA increases were significantly attenuated following melatonin ingestion (second minute, 114 ± 30 vs. 74 ± 14%; and third minute, 111 ± 29 vs. 54 ± 12%, both P < 0.05). The mean arterial pressure increase to mental stress was blunted in the third minute (20 ± 2 vs. 17 ± 2 mmHg, P = 0.032), and the HR increase was blunted in the first minute (33 ± 3 vs. 29 ± 3 beats/min, P = 0.034) after melatonin. In summary, exogenous melatonin attenuates the SSNA response to mental stress.

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Incidences of adverse cardiac events and orthostatic hypotension are associated with diurnal variations. The primary purpose of the present study was to determine if the vestibulosympathetic reflex (VSR) follows a diurnal variation in humans. We hypothesized that the VSR would be attenuated at night based on the relation between melatonin and the VSR. Arterial blood pressure, heart rate, calf blood flow, and muscle sympathetic nerve activity (MSNA) were measured in nine healthy subjects (28 ± 1 yr, 5 men and 4 women) at rest and during head-down rotation. Each subject was tested during the day at 11:34 ± 13 and again at night 22:10 ± 5. MSNA was significantly decreased at night compared with day (8 ± 1 vs. 11 ± 2 bursts/min, respectively, P < 0.02). Heart rate and arterial blood pressure at rest were significantly increased at night compared with day (heart rate: 70 ± 4 vs. 66 ± 4 beats/min and mean arterial blood pressure: 91 ± 2 vs. 87 ± 1 mmHg, respectively). MSNA and hemodynamic responses to head-down rotation were not significantly altered at night compared with day (changes of 3 ± 1 bursts/min and 25 ± 6% for MSNA and calf blood flow, respectively). The data indicate that MSNA at rest decreases during the late evening hours and exhibits a diurnal variation, whereas the VSR does not. In summary, diurnal variation of orthostatic hypotension in humans does not appear to be associated with changes in the VSR and MSNA at rest.

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BACKGROUND: High rates of physical inactivity compromise the health status of populations globally. Social networks have been shown to influence physical activity (PA), but little is known about how best to engineer social networks to sustain PA. To improve procedures for building networks that shape PA as a normative behavior, there is a need for more specific hypotheses about how social variables influence PA. There is also a need to integrate concepts from network science with ecological concepts that often guide the design of in-person and electronically-mediated interventions. Therefore, this paper: (1) proposes a conceptual model that integrates principles from network science and ecology across in-person and electronically-mediated intervention modes; and (2) illustrates the application of this model to the design and evaluation of a social network intervention for PA. METHODS/DESIGN: A conceptual model for engineering social networks was developed based on a scoping literature review of modifiable social influences on PA. The model guided the design of a cluster randomized controlled trial in which 308 sedentary adults were randomly assigned to three groups: WalkLink+: prompted and provided feedback on participants' online and in-person social-network interactions to expand networks for PA, plus provided evidence-based online walking program and weekly walking tips; WalkLink: evidence-based online walking program and weekly tips only; Minimal Treatment Control: weekly tips only. The effects of these treatment conditions were assessed at baseline, post-program, and 6-month follow-up. The primary outcome was accelerometer-measured PA. Secondary outcomes included objectively-measured aerobic fitness, body mass index, waist circumference, blood pressure, and neighborhood walkability; and self-reported measures of the physical environment, social network environment, and social network interactions. The differential effects of the three treatment conditions on primary and secondary outcomes will be analyzed using general linear modeling (GLM), or generalized linear modeling if the assumptions for GLM cannot be met. DISCUSSION: Results will contribute to greater understanding of how to conceptualize and implement social networks to support long-term PA. Establishing social networks for PA across multiple life settings could contribute to cultural norms that sustain active living. TRIAL REGISTRATION: ClinicalTrials.gov NCT01142804.

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The study examined whether cardiorespiratory fitness modifies cardiovascular responses by normotensive men and women during the Stroop color-word interference test. Independent of age and an estimate of body fatness, fitness level was positively related (R² = .39 and .51) to increases in limb blood flow and vascular conductance, coherent with cardiac-vagal withdrawal and a decrease in heart period, among women but not men. Fitness was unrelated to changes in systolic and diastolic blood pressures and muscle sympathetic nerve activity. The augmented hemodynamic responses among fitter women were not consistent with passive vasodilation via withdrawal of sympathetic neural tone. The results encourage further gender comparisons testing whether fitness augments limb blood flow during mental stress by neurohumoral and flow-mediated vasodilatory mechanisms or by increased cardiac output.

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Mental stress (MS) is a known trigger of myocardial infarction and sudden death. By activating the sympathetic nervous system, MS may have deleterious effect on the cardiovascular system but this process is not completely understood. The primary aim of this study was to quantify the effect of MS on skin sympathetic nerve activity (SSNA). The secondary aim was to determine the reproducibility of SSNA to MS within a given day and ~1 week later. Ten subjects (26±1 yr.) performed two bouts of mental arithmetic lasting 3 min. The bouts were separated by 45 min. One week later the subjects returned to repeat MS. All experiments were conducted in the supine posture during the morning hours. To maintain neutral skin temperature, each subject wore a custom suit (34-35°C). Skin blood flow and sweat rate were measured on the dorsal foot. MS elicited a marked increase in SSNA within the first 10 s (184±42%; P<0.01) in all subjects, which was less during the remaining period of MS but remained elevated (87±20; P<0.01). The pattern of responses to MS was unchanged during the second bout (10 s, 247±55%; 3 min avg., 133±29%) and during the retest 1 week later (10 s, 196±55%; 3 min avg., 117±36%). MS did not significantly affect cutaneous vascular conductance or sweat rate during any trial. In summary, MS elicits robust and reproducible increases in SSNA in humans which may be followed over time to observe alterations in the regulation of the autonomic nervous system.

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The mechanism(s) for post-bed rest (BR) orthostatic intolerance is equivocal. The vestibulosympathetic reflex contributes to postural blood pressure regulation. It was hypothesized that muscle sympathetic nerve responses to otolith stimulation would be attenuated by prolonged head-down BR. Arterial blood pressure, heart rate, muscle sympathetic nerve activity (MSNA), and peripheral vascular conductance were measured during head-down rotation (HDR; otolith organ stimulation) in the prone posture before and after short-duration (24 h; n = 22) and prolonged (36 ± 1 day; n = 8) BR. Head-up tilt at 80° was performed to assess orthostatic tolerance. After short-duration BR, MSNA responses to HDR were preserved (Δ5 ± 1 bursts/min, Δ53 ± 13% burst frequency, Δ65 ± 13% total activity; P < 0.001). After prolonged BR, MSNA responses to HDR were attenuated ∼50%. MSNA increased by Δ8 ± 2 vs. Δ3 ± 2 bursts/min and Δ83 ± 12 vs. Δ34 ± 22% total activity during HDR before and after prolonged BR, respectively. Moreover, these results were observed in three subjects tested again after 75 ± 1 days of BR. This reduction in MSNA responses to otolith organ stimulation at 5 wk occurred with reductions in head-up tilt duration. These results indicate that prolonged BR (∼5 wk) unlike short-term BR (24 h) attenuates the vestibulosympathetic reflex and possibly contributes to orthostatic intolerance following BR in humans. These results suggest a novel mechanism in the development of orthostatic intolerance in humans.

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1. Cyclo-oxygenase-2 (COX-2)-derived prostaglandins are important in controlling sodium excretion and renin release. In the present study, we tested the hypothesis that a clinical dose of celecoxib would impair urinary sodium excretion and elevate blood pressure (BP) during dietary salt loading. 2. Twelve normotensive individuals (mean (± SEM) age 35 ± 2 years) completed two separate 17 day dietary perturbations, one taking 200 mg/day celecoxib (CX2) and the other taking placebo (PL), randomized with a 1 month wash out. The controlled 17 day diet consisted of a 3 day run-in diet, 7 days of a low-salt (LS, 20 mmol sodium/day) diet and 7 days of a high-salt diet (HS, 350 mmol sodium/day) diet. The order in which the diets were applied was randomized. Data were collected on the last day of the LS and HS diets. 3. Plasma and urinary prostaglandins were modestly lower during celecoxib (P < 0.05). Urinary sodium excretion was greater (P < 0.01) during the HS diet (253 ± 10 vs 281 ± 27 mmol/24 h for PL vs CX2, respectively) compared with the LS diet (14 ± 3 vs 17 ± 7 mmol/24 h for PL vs CX2, respectively; P(drug) = 0.26). Celecoxib did not alter creatinine clearance (P > 0.50). Twenty-four hour mean arterial BP was similar during PL (87 ± 2 vs 87 ± 2 mmHg for LS and HS, respectively) and CX2 (88 ± 2 vs 87 ± 2 mmHg for LS and HS, respectively; P = 0.85), with no effect of dietary salt (P > 0.80). Plasma renin activity, angiotensin II and aldosterone were all suppressed with dietary salt loading (P < 0.05), with no effect of drug (P > 0.35). 4. In conclusion, blood pressure and renal function were not adversely affected by celecoxib, even during dietary salt loading. These findings support current guidelines suggesting minimal cardiovascular risks associated with short-term, low-dose use of celecoxib in young to middle-aged adults.

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The glycerol dehydration test (GDT) has been used to test for the presence of Ménière's disease and elicits acute alterations in vestibular reflexes in both normal and pathological states. Activation of the vestibulosympathetic reflex (VSR) increases muscle sympathetic nerve activity (MSNA) and peripheral vascular resistance. We hypothesized that the GDT would attenuate the VSR through fluid shifts of the inner ear. Sixteen male subjects (26 ± 1 yr) were randomly assigned to be administered either glycerol mixed with cranberry juice (97 ± 3 ml glycerol + equal portion of cranberry juice; n = 9) or a placebo control [water + cranberry juice (100 ml each); n = 7]. Subjects in both groups performed head-down rotation (HDR), which engages the VSR, before and after administration of either the glycerol or placebo. MSNA (microneurography), arterial blood pressure, and leg blood flow (venous occlusion plethysmography) were measured during HDR. Before glycerol administration, HDR significantly increased MSNA burst frequency (Δ8 ± 1 bursts/min; P < 0.01) and total activity (Δ77 ± 18%; P < 0.01) and decreased calf vascular conductance (-Δ20 ± 3%; P < 0.01). However, HDR performed postadministration of glycerol resulted in an attenuated MSNA increase (Δ3 ± 1 bursts/min, Δ22 ± 3% total activity) and decrease in calf vascular conductance (-Δ7 ± 4%). HDR significantly increased MSNA burst frequency (Δ5 ± 1 and Δ5 ± 2 bursts/min) and total activity (Δ58 ± 13% and Δ52 ± 18%) in the placebo group before and after placebo, respectively (P < 0.01). Likewise, decreases in calf vascular conductance during HDR before and after placebo were not different (-Δ13 ± 4% and -Δ14 ± 2%, respectively; P < 0.01). These results suggest that fluid shifts of the inner ear via glycerol dehydration attenuate the VSR. These data provide support that inner ear fluid dynamics can have a significant impact on blood pressure regulation via the VSR in humans.

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Melatonin is synthesized and released into the circulation by the pineal gland in a circadian rhythm. Melatonin has been demonstrated to differentially alter blood flow to assorted vascular beds by the activation of different melatonin receptors in animal models. The purpose of the present study was to determine the effect of melatonin on blood flow to various vascular beds in humans. Renal (Doppler ultrasound), forearm (venous occlusion plethysmography), and cerebral blood flow (transcranial Doppler), arterial blood pressure, and heart rate were measured in 10 healthy subjects (29±1 yr; 5 men and 5 women) in the supine position for 3 min. The protocol began 45 min after the ingestion of either melatonin (3 mg) or placebo (sucrose). Subjects returned at least 2 days later at the same time of day to repeat the trial after ingesting the other substance. Melatonin did not alter heart rate and mean arterial pressure. Renal blood flow velocity (RBFV) and renal vascular conductance (RVC) were lower during the melatonin trial compared with placebo (RBFV, 40.5±2.9 vs. 45.4±1.5 cm/s; and RVC, 0.47±0.02 vs. 0.54±0.01 cm·s(-1)·mmHg(-1), respectively). In contrast, forearm blood flow (FBF) and forearm vascular conductance (FVC) were greater with melatonin compared with placebo (FBF, 2.4±0.2 vs. 1.9±0.1 ml·100 ml(-1)·min(-1); and FVC, 0.029±0.003 vs. 0.023±0.002 arbitrary units, respectively). Melatonin did not alter cerebral blood flow measurements compared with placebo. Additionally, phentolamine (5-mg bolus) after melatonin reversed the decrease in RVC, suggesting that melatonin increases sympathetic outflow to the kidney to mediate renal vasoconstriction. In summary, exogenous melatonin differentially alters vascular blood flow in humans. These data suggest the complex nature of melatonin on the vasculature in humans.

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Melatonin has been reported to decrease nerve activity of medial vestibular nuclei in the rat and is associated with attenuated muscle sympathetic nerve activity (MSNA) responses to baroreceptor unloading in humans. The purpose of this study was to determine if melatonin alters the vestibulosympathetic reflex (VSR) and vestibulocollic reflex (VCR) in humans. In study 1, MSNA, arterial blood pressure, and heart rate were measured in 12 healthy subjects (28 ± 1 yr; 6 men, 6 women) during head-down rotation (HDR) before and 45 min after ingestion of either melatonin (3 mg) or placebo (sucrose). Subjects returned at least 2 days later at the same time of day to repeat the trial after ingesting the opposite treatment (melatonin or placebo). Melatonin significantly attenuated MSNA responses during HDR compared with placebo (burst frequency Δ 4 ± 1 vs. Δ 7 ± 1 bursts/min, and total MSNA Δ 51 ± 20 and Δ 96 ± 15%, respectively; P < 0.02). In study 2, vestibular evoked myogenic potentials (VEMP) were measured in 10 healthy subjects (26 ± 1 yr; 4 men and 6 women) before and after ingestion of 3 mg melatonin. Melatonin did not alter the timing of the p13 and n23 peaks (pre-melatonin 13.2 ± 0.4 and 21.3 ± 0.6 ms vs. post-melatonin 13.5 ± 0.4 and 21.4 ± 0.7 ms, respectively) or the p13-n23 interpeak amplitudes [pre-melatonin 22.5 ± 4.6 arbitrary units (au) and post-melatonin 22.7 ± 4.6 au]. In summary, melatonin attenuates the VSR and supports the concept that melatonin negatively affects orthostatic tolerance. However, melatonin does not alter the VCR in humans suggesting melatonin's effect on the VSR appears to be mediated by the utricles.

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Animal models have shown that peripheral chemoreceptors alter their firing patterns in response to changes in plasma osmolality, which, in turn, may modulate sympathetic outflow. The purpose of this study was to test the hypothesis that increases in plasma osmolality augment muscle sympathetic nerve activity (MSNA) responses to chemoreceptor activation. MSNA was recorded from the peroneal nerve (microneurography) during a 23-min intravenous hypertonic saline infusion (3% NaCl; HSI). Chemoreceptor activation was elicited by voluntary end-expiratory apnea. MSNA responses to end-expiratory apnea were calculated as the absolute increase from the preceding baseline period. Plasma osmolality significantly increased from pre- to post-HSI (284 ± 1 to 290 ± 1 mOsm/kg H(2)O; P < 0.01). There was a significant overall effect of osmolality on sympathetic activity (P < 0.01). Duration of the voluntary end-expiratory apnea was not different after HSI (pre = 40 ± 5 s; post = 41 ± 4 s). MSNA responses to end-expiratory apnea were not different after HSI, expressed as an absolute change in burst frequency (n = 11; pre = 8 ± 2; post = 11 ± 1 burst/min) and as a percent increase in total activity (pre = 51 ± 4% AU; post = 53 ± 4% AU). A second group of subjects (n = 8) participated in 23-min volume/time-control intravenous isotonic saline infusions (0.9% NaCl). Isotonic saline volume-control infusions yielded no change in plasma osmolality or MSNA at rest. Furthermore, MSNA responses to apnea following isotonic saline infusion were not different. In summary, elevated plasma osmolality increased MSNA at rest and during apnea, but contrary to the hypothesis, MSNA responsiveness to apnea was not augmented. Therefore, this study does not support a neural interaction between plasma osmolality and chemoreceptor stimulation.

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Endurance training has been associated with increased orthostatic intolerance. The purpose of the present study was to test the hypothesis that endurance training reduces renal vasoconstriction to orthostatic stress. Blood pressure, heart rate, and renal blood flow velocity were measured during a 25-min 60 degrees head-up tilt (HUT) test before and after 8 wk of endurance training in eight healthy sedentary subjects (26 +/- 1 yrs). Training elicited a 21 +/- 3% increase in peak oxygen uptake (V(O(2)peak)) and a reduction in heart rate at rest of 8 +/- 2 beats/min. During HUT, heart rate progressively increased (approximately 20 beats/min) over the 25-min HUT trial both before and after training. Systolic arterial blood pressure during HUT was unchanged with training, whereas diastolic arterial blood pressure was lower at the end of HUT after training. Before training renal blood flow velocity (Delta14 +/- 5 cm/s) and renal vascular conductance (Delta22 +/- 7%) decreased during HUT, whereas after training renal blood flow velocity (Delta2 +/- 5 cm/s) and renal vascular conductance (Delta1 +/- 12%) did not change significantly during HUT. Renal blood flow velocity and vascular conductance responses to HUT did not change in control subjects during the 8-wk period. These results demonstrate that endurance training reduces renal vasoconstriction during an orthostatic challenge and may contribute to training-induced orthostatic intolerance.

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The effects of aerobic exercise training (ET) on muscle sympathetic nerve activity (MSNA) and renal vascular responses to mental stress (MS) have not been determined in humans. We hypothesized that aerobic ET would reduce MSNA and renal vasoconstriction during MS. MSNA, mean arterial pressure (MAP), heart rate, renal blood flow velocity (RBFV), and peak oxygen uptake (V(O2peak)) were recorded in 23 healthy adults. Fourteen subjects participated in 8 wk of aerobic ET, while nine subjects served as sedentary controls (Con). ET significantly increased V(O2peak) (Delta18 +/- 1%; P < 0.001) and decreased RBFV at rest (60 +/- 4 to 48 +/- 3 cm/s; P < 0.01), whereas Con did not alter V(O2peak) or RBFV. ET did not alter resting MSNA (11 +/- 1 to 9 +/- 1 bursts/min) or MAP (84 +/- 2 to 83 +/- 2 mmHg), and these findings were similar in the Con group. MS elicited similar increases in MSNA (approximately Delta2 bursts/min; P < 0.05), MAP (approximately Delta15 mmHg; P < 0.001), and heart rate (approximately Delta20 beats/min; P < 0.001) before and after ET, and the responses were not different between ET and Con. Likewise, MS elicited similar decreases in RBFV and renal vascular conductance before and after ET, and the responses were not different between ET and Con. Perceived stress levels during MS were similar before and after the 8-wk study in both ET and Con. In conclusion, ET does not alter MSNA and renal vascular responses to MS in healthy humans.

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Cardiovascular-related mortality peaks during cold winter months, particularly in older adults. Acute physiological responses, such as increases in blood pressure, in response to cold exposure may contribute to these associations. To determine whether the blood pressure-raising effect (pressor response) of non-internal body temperature-reducing cold stress is greater with age, we measured physiological responses to 20 min of superficial skin cooling, via water-perfused suit, in 12 younger [25 +/- 1 (SE) yr old] and 12 older (65 +/- 2 yr old) adults. We found that superficial skin cooling elicited an increase in blood pressure from resting levels (pressor response; P < 0.05) in younger and older adults. However, the magnitude of this pressor response (systolic and mean blood pressure) was more than twofold higher in older adults (P < 0.05 vs. younger adults). The magnitude of the pressor response was similar at peripheral (brachial) and central (estimated in the aorta) measurement sites. Regression analysis revealed that aortic pulse wave velocity, a measure of central arterial stiffness obtained before cooling, was the best predictor of the increased pressor response to superficial skin cooling in older adults, explaining approximately 63% of its variability. These results indicate that there is a greater pressor response to non-internal body temperature-reducing cold stress with age in humans that may be mediated by increased levels of central arterial stiffness.

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