Inverse Association between Exercising Blood Pressure Response and Left Ventricular Chamber Size and Mass in Women Who Habitually Resistance Train.

Exercise is a major modifiable lifestyle factor that leads to temporarily increased systolic blood pressure (SBP), which is thought to influence left ventricular mass normalized to body surface area (LVM/BSA). This relationship has never been studied in women who habitually perform resistance exercise. PURPOSE: To determine if a direct correlation exists between the SBP response to resistance exercise (change from rest; eSBP) and LVM/BSA in young healthy women who habitually resistance train. METHODS: Leg extension resistance exercise was performed while continuously monitoring blood pressure using finger plethysmography. LVM was estimated using echocardiography. Data are shown as mean ± SD. RESULTS: Thirty-one women participated (age 23 ± 3 years, height 164 ± 7 cm, body mass 63.7 ± 10.3 kg). Resting SBP (110 ± 8 mmHg, r = 0.355, p = 0.049) was shown to be directly correlated to LVM/BSA (72.0 ± 28.4 g/m2). Conversely, eSBP (30.8 ± 14.6 ∆mmHg, r = -0.437, p = 0.014) was inversely related to LVM/BSA. eSBP was not correlated to interventricular septum width (0.88 ± 0.12 cm, r = -0.137, p = 0.463) or posterior wall thickness (0.91 ± 0.15 cm, r = -0.084, p = 0.654). eSBP was inversely related to left ventricle internal diameter during diastole (LVIDd) (4.25 ± 0.33 cm, r = -0.411, p = 0.021). CONCLUSION: Counter to the hypothesis, these data suggest an inverse association between eSBP during resistance exercise and LVM/BSA in healthy young women who resistance train. This relationship is due to a smaller LVIDd with greater eSBP.

Impact of a family history of hypertension and physical activity on left ventricular mass.

BACKGROUND: A positive family history of hypertension (FHH) (+FHH) is associated with elevated left ventricular mass (LVM). Regular physical activity (PA) may eliminate differences in LVM between +FHH and negative family history of hypertension (-FHH) adults. The aim of this study was to determine if a +FHH is associated with a greater LVM compared to a -FHH group within a sample of young, mostly active healthy adults with and without statistically controlling for PA. METHODS: Healthy young (18-32 y) participants self-reported FHH status and habitual moderate and vigorous PA frequency. Participants then underwent an echocardiogram. RESULTS: Of the 61 participants, 32 (M=11, W=21; non-active=8) reported -FHH and the remaining 29 (M=13, W=16; non-active=2) reported a +FHH. Mann-Whitney tests found the +FHH group had greater LVM (-FHH 129.5±41.8, +FHH 155.2±42.6 g, P=0.015) and LVM/body surface area (BSA) (-FHH 73.5±17.4, +FHH 88.4±17.3 g/m2, P=0.004). Separate ANCOVA models accounting for moderate and vigorous PA found that FHH status independently predicted LVM/BSA and PA frequencies were significant modifiers (ANCOVA controlling moderate PA: FHH status P=0.004, partial η2=0.133; moderate PA P=0.020, partial η2=0.089), (ANCOVA controlling vigorous PA: FHH status P=0.004, partial η2=0.132; vigorous PA P=0.007, partial η2=0.117). CONCLUSIONS: This analysis suggests that physically active young adults with a +FHH have elevated LVM compared to their -FHH counterparts. This finding is independent of their habitual moderate and vigorous physical activity frequencies.

Oxygen Consumption and Blood Pressure Are Not Influenced by Use of a Backpack Hip Strap.

INTRODUCTION: Several studies have explored the effect of backpack carriage on physiologic responses while walking, but few have focused specifically on the influence of the use of a hip strap on these responses. The aim of this study was to investigate the effect of a backpack hip strap on physiologic responses when walking at a moderate intensity while carrying a backpack with a standardized relative load of 30% of the wearer's body mass. METHODS: Twenty-three healthy, active participants carrying backpacks walked on a treadmill at a speed and grade that elicited 40-50% of their heart rate reserve. Participants completed 2 counterbalanced 30-min trials, one with the hip strap in the strapped condition and one with the hip strap unfastened. Metabolic, heart rate, blood pressure, and muscle oxygen saturation (SmO2) responses were recorded during both trials. For each variable, 5-min intervals were averaged at baseline, 5, 10, 15, 20, 25, and 30 min. A repeated measures ANOVA test was used to evaluate the differences between the conditions at each time point. Data reported are the values from the final 5-min interval (30 min) and are reported as mean±SD. RESULTS: No differences were found between strapped and unstrapped trials for oxygen consumption (strapped 21.9±4.2 mL·kg-1·min-1; unstrapped 22.0±4.4 mL·kg-1·min-1, P=0.842), Δmean arterial pressure (strapped +5±17 Δmm Hg; unstrapped +12±14 Δmm Hg, P=0.128) or muscle oxygen saturation of the quadriceps (strapped 86±15%; unstrapped 90±12%, P=0.359) and calf (strapped 73±19%; unstrapped 81±12%, P=0.888). CONCLUSIONS: These results suggest that wearing a hip strap does not influence physiologic responses up to 30 min of moderate intensity walking while carrying 30% of the wearer's mass.

The effects of a respiratory training mask on steady-state oxygen consumption at rest and during exercise.

No studies have directly measured ventilatory and metabolic responses while wearing a respiratory training mask (RTM) at rest and during exercise. Eleven aerobically fit adults (age: 21 ± 1 years) completed a randomized cross-over study while wearing an RTM or control mask during cycling at 50% Wmax. An RTM was retrofitted with a gas collection tube and set to the manufacturer's "altitude resistance" setting of 6,000 ft (1,800 m). Metabolic gas analysis, ratings of perceived exertion, and oxygen saturation (SpO2) were measured during rest and cycling exercise. The RTM did not affect metabolic, ventilation, and SpO2 at rest compared to the control mask (all, effect of condition: P > 0.05). During exercise, the RTM blunted respiratory rate and minute ventilation (effect of condition: P < 0.05) compared to control. Similar increases in VO2 and VCO2 were observed in both conditions (both, effect of condition: P > 0.05). However, the RTM led to decreased fractional expired O2 and increased fractional expired CO2 (effect of condition: P < 0.05) compared to the control mask. In addition, the RTM decreased SpO2 and increased RPE (both, effect of condition: P < 0.05) during exercise. Despite limited influence on ventilation and metabolism at rest, the RTM reduces ventilation and disrupts gas concentrations during exercise leading to modest hypoxemia.

Naltrexone alters cardiovascular function following acute forced swimming in mice.

Purpose: Naltrexone (NTX) is an opioid antagonist that can reverse the physiological effects of opioid receptors when bound. Opioid receptors have been found to play a role in cardiovascular (CV) function, and thus, binding of NTX may alter CV activity at rest and in response to acute and chronic exercise (EX). We hypothesized that opioid receptor blockade will alter the typical CV responses following acute EX. Methods: We assessed the effects of opioid receptor blockade on CV function via echocardiography in mice following an acute bout of forced swimming (FSw), a model of rodent EX. We administered opioid receptor antagonist, NTX, or saline in mice before FSw and in the absence of an FSw perturbation. Furthermore, we assessed how NTX can influence maximal EX capacity on a rodent treadmill. Results: Our data shows that NTX administration does not decrease maximal EX capacity in mice (P > 0.05). However, NTX attenuated cardiac output following FSw (FSw = 52.5 ± 2.5 ml/min vs. FSw + NTX = 32.7 ± 5.2 ml/min; P < 0.05) when compared with saline control (33.5 ± 3.8 ml/min). Further, the administration of NTX in the non-EX condition significantly (P < 0.05) reduced ejection fraction. Conclusion: These data suggest that normal opioid receptor activation is necessary for typical CV function following FSw.

Influence of Age and Estradiol on Sympathetic Nerve Activity Responses to Exercise in Women.

INTRODUCTION: Postmenopausal women (PMW) display exaggerated increases in blood pressure (BP) during exercise, yet the mechanism(s) involved remain unclear. Moreover, research on the impact of menopausal changes in estradiol on cardiovascular control during exercise are limited. Herein, we tested the hypothesis that sympathetic responses during exercise are augmented in PMWcompared with young women (YW), and estradiol administration attenuates these responses. METHODS: Muscle sympathetic nerve activity (MSNA) and mean arterial pressure (MAP) were measured in 13 PMW (58 ± 1 yr) and 17 YW (22 ± 1 yr) during 2 min of isometric handgrip. Separately, MSNA and BP responses were measured during isometric handgrip in six PMW (53 ± 1 yr) before and after 1 month of transdermal estradiol (100 µg·d-1). A period of postexercise ischemia (PEI) to isolate muscle metaboreflex activation followed all handgrip bouts. RESULTS: Resting MAP was similar between PMW and YW, whereas MSNA was greater in PMW (23 ± 3 vs 8 ± 1 bursts per minute; P < 0.05). During handgrip, the increases in MSNA (PMW Δ16 ± 2 vs YW Δ6 ± 1 bursts per minute; P < 0.05) and MAP (PMW Δ18 ± 2 vs YW Δ12 ± 2 mm Hg; P < 0.05) were greater in PMW and remained augmented during PEI. Estradiol administration decreased resting MAP but not MSNA in PMW. Moreover, MSNA (PMW (-E2) Δ27 ± 8 bursts per minute versus PMW (+E2) Δ12 ± 5 bursts per minute; P < 0.05) and MAP (Δ31 ± 8 mm Hg vs Δ20 ± 6 mm Hg; P < 0.05) responses during handgrip were attenuated in PMW after estradiol administration. Likewise, MAP responses during PEI were lower after estradiol. CONCLUSIONS: These data suggest that PMW exhibit an exaggerated MSNA and BP response to isometric exercise, due in part to heightened metaboreflex activation. Furthermore, estradiol administration attenuated BP and MSNA responses to exercise in PMW.

Young healthy adults with a family history of hypertension have increased microvascular reactivity but decreased macrovascular function.

OBJECTIVE: To determine whether, like hypertensives, normotensive adults with a family history of hypertension (+FHH) display lower microvascular reactivity and conduit artery function than normotensive adults without a family history of hypertension (-FHH). METHODS: A forearm vascular occlusion test was performed on healthy normotensive adults while resting in the supine position. A near-infrared spectroscopy sensor placed on the forearm measured skeletal muscle oxygen saturation kinetics to determine microvascular reactivity. Simultaneously, an ultrasound probe placed on the brachial artery above the occlusion cuff was used to assess flow-mediated dilation; a test of macrovascular function. RESULTS: Twenty-two participants were included in this investigation (-FHH n = 13, +FHH n = 9). Following cuff release, the resaturation slope (1st 10 s median ± SD, -FHH 2.76 ± 2.10, +FHH 5.59 ± 2.47%/s; p = .036) was greater in +FHH when accounting for the magnitude and rate of the decrease in skeletal muscle oxygen saturation during occlusion. Conversely, flow-mediated dilation (median ± SD, -FHH 5.96 ± 5.22, +FHH 4.10 ± 3.17%∆; p = .031) was lower in +FHH when accounting for baseline artery diameter and shear rate. CONCLUSIONS: Young +FHH adults have altered microvascular and macrovascular reactivity compared with young -FHH adults.

Mild dehydration following voluntary water intake reduction does not affect anaerobic power performance.

BACKGROUND: Dehydration is common among athletes. The negative impact of dehydration on aerobic performance is well characterized. However, little is known about the effect of dehydration on anaerobic performance particularly when dehydration results from insufficient water intake, not water loss due to body temperature regulation. The purpose of this study was to examine the effect of dehydration on anaerobic performance following voluntary water intake reduction. METHODS: Fifteen healthy adults completed two exercise sessions, euhydrated (EUD) and dehydrated (DEH). Sessions consisted of baseline anthropometric and blood lactate measurement followed by a 30-second Wingate test and three vertical jump trials to measure anaerobic performance. Additional blood lactate measurements were taken immediately and at 5, 10, and 15 minutes after taking the Wingate test. RESULTS: The dehydration protocol resulted in a reduction in body mass (EUD 69.1±17.2 kg, DEH 68.1±16.6 kg, P=0.039). The 30-s Wingate peak power (EUD 971±302 W, DEH 960±316 W, P=0.578) was not different between conditions, nor was the vertical jump height (EUH 26.4±4.5 cm, DEH 26.6±3.6 cm, P=0.778). Blood lactate (P<0.001) was elevated immediately following the 30-s Wingate test which remained throughout the trial. There were no differences in blood lactate between conditions. CONCLUSIONS: Acute anaerobic power and exercise performance is not negatively affected by voluntary dehydration.

Cardiorespiratory fitness and the relationship between body fat and resting testosterone in men.

Objective: To examine the effect of cardiovascular fitness, i.e. VO2max, on the relationship between weight status and resting testosterone level (RTL) in males.Materials and methods: A subset of male participants from the 2003-2004 National Health and Nutrition Examination Survey were analyzed by weight status, i.e. normal, overweight, obese, and all participants. Bivariate correlation coefficients were computed for RTL, percent body fat (BF%), and VO2max. Partial correlation coefficients were computed between RTL and BF% controlling for VO2max and between RTL and VO2max controlling for BF%.Results: Bivariate correlations between RTL and BF%, and RTL and VO2max were significant in all groups. The partial correlation coefficients between RTL and BF% controlling for VO2max were significant in the normal and all participants group. When RTL and VO2max were analyzed controlling for BF% only the all participants group remained significant.Conclusion: Cardiovascular fitness or weight status may independently influence RTL in males.

Apocynin and Tempol ameliorate dietary sodium-induced declines in cutaneous microvascular function in salt-resistant humans.

It has previously been shown that high dietary salt impairs vascular function independent of changes in blood pressure. Rodent studies suggest that NADPH-derived reactive oxygen species mediate the deleterious effect of high salt on the vasculature, and here we translate these findings to humans. Twenty-nine healthy adults (34 ± 2 yr) participated in a controlled feeding study. Participants completed 7 days of a low-sodium diet (LS; 20 mmol sodium/day) and 7 days of a high-sodium diet (HS; 300 mmol sodium/day) in random order. All participants were salt resistant, defined as a ≤5-mmHg change in 24-h mean BP determined while on the LS and HS diets. Laser Doppler flowmetry was used to assess cutaneous vasodilation in response to local heating (42°C) during local delivery of Ringer's (n = 29), 20 mM ascorbic acid (AA; n = 29), 10 µM Tempol (n = 22), and 100 µM apocynin (n = 22). Additionally, endothelial cells were obtained in a subset of participants from an antecubital vein and stained for nitrotyrosine (n = 14). Cutaneous vasodilation was attenuated by the HS diet compared with LS [LS 93.0 ± 2.2 vs. HS 86.8 ± 2.0 percentage of maximal cutaneous vascular conductance (%CVCmax); P < 0.05] and was restored by AA during the HS diet (AA 90.7 ± 1.2 %CVCmax; P < 0.05 vs. HS). Cutaneous vasodilation was also restored with the local infusion of both apocynin (P < 0.01) and Tempol (P < 0.05) on the HS diet. Nitrotyrosine expression was increased on the HS diet compared with LS (P < 0.05). These findings provide direct evidence of dietary sodium-induced endothelial cell oxidative stress and suggest that NADPH-derived reactive oxygen species contribute to sodium-induced declines in microvascular function. NEW & NOTEWORTHY High-sodium diets have deleterious effects on vascular function, likely mediating, in part, the increased cardiovascular risk associated with a high sodium intake. Local infusion of apocynin and Tempol improved microvascular function in salt-resistant adults on a high-salt diet, providing evidence that reactive oxygen species contribute to impairments in microvascular function from high salt. This study provides insight into the blood pressure-independent mechanisms by which dietary sodium impairs vascular function. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/dietary-sodium-oxidative-stress-and-microvascular-function/ .

Bioelectrical impedance analysis does not detect an increase in total body water following isotonic fluid consumption.

PURPOSE: To determine if single-frequency foot-to-foot bioelectrical impedance analysis (BIA) can detect acute changes in total body water (TBW) following consumption of isotonic saline. All participants ate a sodium-free meal at 4 h prior to the data collection visit and had euhydration confirmed using urine specific gravity at the beginning of the experimental visit. Subjects drank 466 mL of isotonic saline (Na+ 140 mmol·L-1) following baseline measures. Blood sampling and BIA were performed at baseline and every 30 min for 3 h after saline consumption. Ten healthy participants completed this study. Plasma volume (5%Δ, p < 0.001) and serum sodium concentration (1%Δ, p < 0.001) increased by 60 min and 90 min, respectively. Body mass (p < 0.001) displayed a biphasic response increasing to a peak at 30 min (+0.38Δkg) and then decreasing to its minimum at 180 min (-0.35Δkg). BIA impedance (p = 0.678) was unaffected by the saline administration. BIA-derived TBW (p = 0.039) decreased from baseline starting at 150 min (0.21Δkg). Novelty Athletes and coaches wishing to achieve hyperhydration can do so through the consumption of isotonic fluid. 50 kHz foot-to-foot BIA-derived TBW is inadequate for measuring hyperhydration. Future studies should examine the physiological and performance effects of such a hyperhydration protocol.

Altered baroreflex sensitivity in young women with a family history of hypertension.

A positive family history of hypertension (+FH) is a risk factor for the future development of hypertension. Hypertension is associated with reductions in baroreflex sensitivity (BRS). Therefore, we hypothesized that young women with a +FH [ n = 12, 22 ± 1 yr, body mass index (BMI) 21 ± 1 kg/m2, mean arterial pressure (MAP) 79 ± 1 mmHg] would have lower BRS compared with young women without a family history of hypertension (-FH) ( n = 13, 22 ± 1 yr, BMI 21 ± 1 kg/m2, MAP 77 ± 2 mmHg, all P > 0.05 between groups). Continuous measurements of muscle sympathetic nerve activity, blood pressure, and electrocardiogram derived R-R interval were recorded at rest and during a Valsalva maneuver. Both cardiovagal BRS and vascular sympathetic BRS were assessed. Resting cardiovagal BRS was reduced in the +FH women (all sequences: -FH 32.3 ± 3.7 vs. +FH 20.2 ± 2.9 ms/mmHg, P = 0.02). Cardiovagal BRS during phase IV (-FH 16.5 ± 2.7 vs. +FH 7.6 ± 1.3 ms/mmHg, P < 0.01) but not phase II (-FH 5.5 ± 0.9 vs. +FH 5.0 ± 0.8 ms/mmHg, P = 0.67) of the Valsalva maneuver was also lower in the +FH women. Vascular sympathetic BRS at rest (-FH -2.38 ± 0.7 vs. +FH -2.33 ± 0.3 bursts· min-1·mmHg-1, P = 0.58) and during the Valsalva (-FH -0.74 ± 0.23 vs. +FH -0.66 ± 0.18 bursts·15 s-1·mmHg-1, P = 0.79) were not different between groups. These data suggest that healthy young women with a positive family history of hypertension have reduced cardiovagal BRS. This may be one mechanism contributing to the increased incidence of hypertension in this population later in life. NEW & NOTEWORTHY Having a family history of hypertension increases the risk of developing future hypertension. Reductions in baroreflex function have been demonstrated in hypertension and are an important marker for future cardiovascular disease. We show that young women with a family history of hypertension have lower cardiovagal baroreflex sensitivity. This alteration in autonomic function may be one mechanism contributing to the future incidence of hypertension in this patient population.

The influence of acute elevations in plasma osmolality and serum sodium on sympathetic outflow and blood pressure responses to exercise.

Elevated plasma osmolality (pOsm) has been shown to increase resting sympathetic nerve activity in animals and humans. The present study tested the hypothesis that increases in pOsm and serum sodium (sNa+) concentration would exaggerate muscle sympathetic nerve activity (MSNA) and blood pressure (BP) responses to handgrip (HG) exercise and postexercise ischemia (PEI). BP and MSNA were measured during HG followed by PEI before and after a 23-min hypertonic saline infusion (HSI-3% NaCl). Eighteen participants (age 23 ± 1 yr; BMI 24 ± 1 kg/m2) completed the protocol; pOsm and sNa+ increased from pre- to post-HSI (285 ± 1 to 291 ± 1 mosmol/kg H2O; 138.2 ± 0.3 to 141.3 ± 0.4 mM; P < 0.05 for both). Resting mean BP (90 ± 2 vs. 92 ± 1 mmHg) and MSNA (11 ± 2 vs. 15 ± 2 bursts/min) were increased pre- to post-HSI ( P < 0.05 for both). Mean BP responses to HG (106 ± 2 vs. 111 ± 2 mmHg, P < 0.05) and PEI (102 ± 2 vs. 107 ± 2 mmHg, P < 0.05) were higher post-HSI. Similarly, MSNA during HG (20 ± 2 vs. 29 ± 2 bursts/min, P < 0.05) and PEI (19 ± 2 vs. 24 ± 3 bursts/min, P < 0.05) were greater post-HSI. In addition, the change in MSNA was greater post-HSI during HG (Δ9 ± 2 vs. Δ13 ± 3 bursts/min, P < 0.05). A second set of participants ( n = 13, age 23 ± 1 yr; BMI 24 ± 1 kg/m2) completed a time control (TC) protocol consisting of quiet rest instead of an infusion. The TC condition yielded no change in resting sNa+, pOsm, mean BP, or MSNA (all P > 0.05); responses to HG and PEI were not different pre- to post-quiet rest ( P > 0.05). In summary, acutely increasing pOsm and sNa+ exaggerates BP and MSNA responses during HG exercise and PEI. NEW & NOTEWORTHY Elevated plasma osmolality has been shown to increase resting sympathetic activity and blood pressure. This study provides evidence that acute elevations in plasma osmolality and serum sodium exaggerated muscle sympathetic nerve activity and blood pressure responses during exercise pressor reflex activation in healthy young adults.

Blood pressure responses to dietary sodium: Association with autonomic cardiovascular function in normotensive adults.

Blood pressure responses to dietary sodium vary widely person-to-person. Salt sensitive rodent models display altered autonomic function, a trait thought to contribute to poor cardiovascular health. Thus, we hypothesized that increased salt sensitivity (SS) in normotensive humans would be associated with increased muscle sympathetic nerve activity (MSNA), decreased high frequency heart rate variability (HF-HRV), and decreased baroreflex sensitivity. Healthy normotensive men and women completed 1week of high (300mmol·day-1) and 1week of low (20mmol·day-1) dietary sodium (random order) with 24h mean arterial pressure (MAP) assessed on the last day of each diet to assess SS. Participants returned to the lab under habitual sodium conditions for testing. Forty-two participants are presented in this analysis, 19 of which successful MSNA recordings were obtained (n=42: age 39±2yrs., BMI 24.3±0.5kg·(m2)-1, MAP 83±1mmHg, habitual urine sodium 93±7mmol·24h-1; n=19: MSNA burst frequency 20±2 bursts·min-1). The variables of interest were linearly regressed over the magnitude of SS. Higher SS was associated with increased MSNA (burst frequency: r=0.469, p=0.041), decreased HF-HRV (r=-0.349, p=0.046), and increased LF/HF-HRV (r=0.363, p=0.034). SS was not associated with sympathetic or cardiac baroreflex sensitivity (p>0.05). Multiple regression analysis accounting for age found that age, not SS, independently predicted HF-HRV (age adjusted no longer significant; p=0.369) and LF/HF-HRV (age adjusted p=0.273). These data suggest that age-related salt sensitivity of blood pressure in response to dietary sodium is associated with altered resting autonomic cardiovascular function.

Rapid onset pressor response to exercise in young women with a family history of hypertension.

NEW FINDINGS: What is the central question of this study? Alterations in blood pressure control at exercise onset are apparent in older adults with established cardiovascular disease. It is currently not known whether these alterations are evident in young adults with a family history of hypertension. What is the main finding and its importance? We demonstrate that young women with a family history of hypertension display a larger change in blood pressure within the first 10 s of isometric exercise. These data suggest altered blood pressure control in young women with a family history of hypertension. Hypertensive adults demonstrate atypical increases in blood pressure (BP) and muscle sympathetic nerve activity (MSNA) at the immediate onset of static muscle contraction. However, it is unknown whether these abnormal responses occur in young, otherwise healthy adults at risk for developing future disease, such as those with a family history of hypertension (+FH). We tested the hypothesis that +FH young women have exaggerated increases in BP and MSNA at the onset of static muscle contraction compared with those without a family history of hypertension (-FH). We retrospectively examined beat-by-beat BP and MSNA during the initial 30 s of isometric handgrip exercise (30% of maximal voluntary contraction) in 16 +FH (22 ± 2 years old, 22 ± 3 kg m-2 ) and 16 -FH (22 ± 3 years old, 22 ± 3 kg m-2 ) women. Resting mean arterial pressure (+FH 80 ± 11 mmHg versus -FH 84 ± 13 mmHg), MSNA burst frequency (+FH 7 ± 3 bursts min-1 versus -FH 9 ± 5 bursts min-1 ) and burst incidence [+FH 12 ± 4 bursts (100 heart beats)-1 versus -FH 12 ± 8 bursts (100 heart beats)-1 ] were similar between groups (all P > 0.05). Within the first 10 s of exercise, changes in mean arterial pressure (+FH Δ8 ± 6 mmHg versus -FH Δ3 ± 2 mmHg, P < 0.05) and heart rate (+FH Δ8 ± 5 beats min-1 versus -FH Δ4 ± 4 beats min-1 , P < 0.05) were greater in +FH women. Absolute MSNA burst frequency during the first 30 s of exercise was not different between groups (-FH 7 ± 5 bursts min-1 versus +FH 9 ± 3 bursts min-1 ). Cardiovascular and sympathetic responses during the cold pressor test were not different between groups. These data demonstrate that young women at risk for developing cardiovascular disease exhibit greater changes in BP at the onset of static muscle contraction.

Peripheral venous distension elicits a blood pressure raising reflex in young and middle-aged adults.

Distension of peripheral veins in humans elicits a pressor and sympathoexcitatory response that is mediated through group III/IV skeletal muscle afferents. There is some evidence that autonomic reflexes mediated by these sensory fibers are blunted with increasing age, yet to date the venous distension reflex has only been studied in young adults. Therefore, we tested the hypothesis that the venous distension reflex would be attenuated in middle-aged compared with young adults. Nineteen young (14 men/5 women, 25 ± 1 yr) and 13 middle-aged (9 men/4 women, 50 ± 2 yr) healthy normotensive participants underwent venous distension via saline infusion through a retrograde intravenous catheter in an antecubital vein during limb occlusion. Beat-by-beat blood pressure, muscle sympathetic nerve activity (MSNA), and model flow-derived cardiac output (Q), and total peripheral resistance (TPR) were recorded throughout the trial. Mean arterial pressure (MAP) increased during the venous distension in both young (baseline 83 ± 2, peak 94 ± 3 mmHg; P < 0.05) and middle-aged adults (baseline 88 ± 2, peak 103 ± 3 mmHg; P < 0.05). MSNA also increased in both groups [young: baseline 886 ± 143, peak 1,961 ± 242 arbitrary units (AU)/min; middle-aged: baseline 1,164 ± 225, peak 2,515 ± 404 AU/min; both P < 0.05]. TPR (P < 0.001), but not Q (P = 0.76), increased during the trial. However, the observed increases in blood pressure, MSNA, and TPR were similar between young and middle-aged adults. Additionally, no correlation was found between age and the response to venous distension (all P > 0.05). These findings suggest that peripheral venous distension elicits a pressor and sympathetic response in middle-aged adults similar to the response observed in young adults.

High dietary sodium reduces brachial artery flow-mediated dilation in humans with salt-sensitive and salt-resistant blood pressure.

Recent studies demonstrate that high dietary sodium (HS) impairs endothelial function in those with salt-resistant (SR) blood pressure (BP). The effect of HS on endothelial function in those with salt-sensitive (SS) BP is not currently known. We hypothesized that HS would impair brachial artery flow-mediated dilation (FMD) to a greater extent in SS compared with SR adults. Ten SR (age 42 ± 5 yr, 5 men, 5 women) and 10 SS (age 39 ± 5 yr, 5 men, 5 women) healthy, normotensive participants were enrolled in a controlled feeding study consisting of a run-in diet followed by a 7-day low dietary sodium (LS) (20 mmol/day) and a 7-day HS (300 mmol/day) diet in random order. Brachial artery FMD and 24-h BP were assessed on the last day of each diet. SS BP was individually assessed and defined as a change in 24-h mean arterial pressure (MAP) of >5 mmHg between the LS and HS diets (ΔMAP: SR -0.6 ± 1.2, SS 7.7 ± 0.4 mmHg). Brachial artery FMD was lower in both SS and SR individuals during the HS diet (P < 0.001), and did not differ between groups (P > 0.05) (FMD: SR LS 10.6 ± 1.3%, SR HS 7.2 ± 1.5%, SS LS 12.5 ± 1.7%, SS HS 7.8 ± 1.4%). These data indicate that an HS diet impairs brachial artery FMD to a similar extent in adults with SS BP and SR BP.

Sympathetic reactivity in young women with a family history of hypertension.

Young adults with a family history of hypertension (+FH) have increased risk of developing hypertension. Furthermore, the blood pressure (BP) response to sympathoexcitatory stimuli in young adults can predict the future development of hypertension. Therefore, we hypothesized young women with a +FH would have exaggerated cardiovascular and sympathetic reactivity compared with young women without a family history of hypertension (-FH). Beat-by-beat mean arterial pressure (MAP) and muscle sympathetic nerve activity (MSNA) were measured in 14 women +FH (22 ± 1 yr, 21 ± 1 kg/m(2), MAP 80 ± 2 mmHg) and 15 women -FH (22 ± 1 yr, 22 ± 1 kg/m(2), MAP 78 ± 2 mmHg) during acute sympathoexcitatory maneuvers: cold pressor test, 2 min of isometric handgrip (HG) exercise at 30% of maximal voluntary contraction, and 3 min of postexercise ischemia (PEI; isolated activation of the skeletal muscle metaboreflex). During cold pressor test, the increase in BP was greater in women +FH (ΔMAP: +FH 16 ± 2 vs. -FH 11 ± 1 mmHg, P < 0.05), which was accompanied by an exaggerated increase in MSNA (ΔMSNA: +FH 17 ± 2 vs. -FH 8 ± 2 burst/min, P < 0.05). The increase in BP was greater in +FH during the last minute of HG (ΔMAP: +FH 23 ± 3 vs. -FH 12 ± 1 mmHg, P < 0.05) and during PEI (ΔMAP: +FH 17 ± 3 vs. -FH 9 ± 2 mmHg, P < 0.05). Similarly, the increase in MSNA was greater in +FH during both HG (ΔMSNA: +FH 12 ± 2 vs. -FH 6 ± 2 burst/min, P < 0.05) and PEI (ΔMSNA: +FH 16 ± 2 vs. -FH 4 ± 2 burst/min, P < 0.05). These data demonstrate that +FH women have greater BP and sympathetic reactivity compared with -FH women.

Exaggerated exercise pressor reflex in adults with moderately elevated systolic blood pressure: role of purinergic receptors.

The neurocirculatory responses to exercise are exaggerated in hypertension, increasing cardiovascular risk, yet the mechanisms remain incompletely understood. The aim of this study was to examine the in vitro effectiveness of pyridoxal-5-phosphate as a purinergic (P2) receptor antagonist in isolated murine dorsal root ganglia (DRG) neurons and the in vivo contribution of P2 receptors to the neurocirculatory responses to exercise in older adults with moderately elevated systolic blood pressure (BP). In vitro, pyridoxal-5-phosphate attenuated the ATP-induced increases in [Ca(2+)](i) (73 ± 15 vs. 11 ± 3 nM; P < 0.05). In vivo, muscle sympathetic nerve activity (MSNA; peroneal microneurography) and arterial BP (Finometer) were assessed during exercise pressor reflex activation (static handgrip followed by postexercise ischemia; PEI) during a control trial (normal saline) and localized P2 receptor blockade (pyridoxal-5-phosphate). Compared with normotensive adults (63 ± 2 yr, 117 ± 2/70 ± 2 mmHg), adults with moderately elevated systolic BP (65 ± 1 yr, 138 ± 5/79 ± 3 mmHg) demonstrated greater increases in MSNA and BP during handgrip and PEI. Compared with the control trial, local antagonism of P2 receptors during PEI partially attenuated MSNA (39 ± 4 vs. 34 ± 5 bursts/min; P < 0.05) in adults with moderately elevated systolic BP. In conclusion, these data demonstrate pyridoxal-5-phosphate is an effective P2 receptor antagonist in isolated DRG neurons, which are of particular relevance to the exercise pressor reflex. Furthermore, these findings indicate that exercise pressor reflex function is exaggerated in older adults with moderately elevated systolic BP and further suggest a modest role of purinergic receptors in evoking the abnormally large reflex-mediated increases in sympathetic activity during exercise in this clinical population.