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Muscle sympathetic nerve activity (MSNA) responsiveness to mental stress is highly variable between individuals. Although stress perception has been posited as a contributor to the MSNA variability during mental stress, prior studies have been inconclusive. Furthermore, the importance of stress appraisal and coping on MSNA reactivity to mental stress has not been investigated. We hypothesize that appraisal of mental stress as a threat (i.e., perceived demands of stress exceed coping resources) versus a challenge (i.e., perceived coping resources sufficient for demands of stress) would be associated with greater MSNA reactivity. Twenty healthy adults (11 males, 9 females, 21 ± 3 yr, 23 ± 3 kg/m 2 ) participated. Beat-by-beat blood pressure (finger plethysmography), heart rate (electrocardiography), and MSNA (microneurography) were recorded during a 10-min quiet rest followed by the Trier Social Stress Test (TSST). After each phase of the TSST (i.e., speech prep, speech, and mental arithmetic), participants reported threat versus challenge appraisal. Endorsement of a threat appraisal was positively associated with changes in MSNA burst frequency ( r = 0.548, P = 0.018), burst incidence ( r = 0.599, P = 0.009), and total MSNA ( r = 0.697, P = 0.037) during the speech stress period. Moreover, increases in threat appraisal across tasks was associated with elevated MSNA burst frequency ( r = 0.531, P = 0.023), incidence ( r = 0.512, P = 0.030), and total MSNA ( r = 0.727, P = 0.027) responsiveness. These findings support an association between stress appraisal processes and postganglionic sympathetic neural reactivity to psychosocial stress and may partially explain interindividual variability in MSNA responses to mental stress. NEW & NOTEWORTHY The present study investigated the association between stress appraisal and muscle sympathetic nerve activity (MSNA) reactivity to the Trier Social Stress Test. Appraisal of the stress task as a threat (i.e., perceived inability to cope with the demands of the task) was associated with exaggerated MSNA reactivity to mental stress in humans. Threat appraisal is associated with exaggerated sympathetic reactivity to stress, potentially underlying the commonly observed interindividual variability in MSNA responsiveness to mental stress.

Background: Alcohol consumption is associated with cardiovascular disease, and the sympathetic nervous system is a suspected mediator. The present study investigated sympathetic transduction of muscle sympathetic nerve activity to blood pressure at rest and in response to cold pressor test following evening binge alcohol or fluid control, with the hypothesis that sympathetic transduction would be elevated the morning after binge alcohol consumption., Methods: Using a randomized, fluid-controlled (FC) crossover design, 26 healthy adults (12 male, 14 female, 25±6 years, 27±4 kg/m 2 ) received an evening binge alcohol dose and a FC. All participants underwent next-morning autonomic-cardiovascular testing consisting of muscle sympathetic nerve activity, beat-to-beat blood pressure, and heart rate during a 10-minute rest period and a 2-minute cold pressor test. Sympathetic transduction was assessed at rest and during the cold pressor test in both experimental conditions., Results: Evening alcohol increased heart rate (FC: 60±9 versus alcohol: 64±9 bpm; P =0.010) but did not alter resting mean arterial pressure (FC: 80±6 versus alcohol: 80±7 mm Hg; P =0.857) or muscle sympathetic nerve activity (FC: 18±9 versus alcohol: 20±8 bursts/min; P =0.283). Sympathetic transduction to mean arterial pressure (time×condition; P =0.003), diastolic blood pressure (time×condition; P =0.010), and total vascular conductance (time×condition; P =0.004) was augmented after alcohol at rest. Sympathetic transduction during the cold pressor test was also elevated after evening binge alcohol consumption ( P =0.002)., Conclusions: These findings suggest that evening binge alcohol consumption leads to augmented morning-after sympathetic transduction of muscle sympathetic nerve activity to blood pressure, highlighting a new mechanism whereby chronic or excessive alcohol consumption contributes to cardiovascular disease progression via altered end-organ responsiveness to sympathetic neural outflow., Registration: URL: https://clinicaltrials.gov/study/NCT03567434; Unique identifier: NCT03567434., Competing Interests: None.

Short and insufficient sleep are prevalent and associated with cardiovascular disease, with the sympathetic nervous system as a suspected mediator. The purpose of the present study was to investigate the association between objective, actigraphy-based total sleep time (TST), sleep efficiency (SE), and cardiovascular and sympathetic regulation in healthy adults. We hypothesized that short TST and low SE would be associated with elevated resting blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA). Participants included 94 individuals [46 males, 48 females, age: 30 ± 15 yr, body mass index (BMI): 26 ± 4 kg/m 2 ]. All participants underwent at least 7 days of at-home, wristwatch actigraphy monitoring (avg: 10 ± 3 days). Seated blood pressures were assessed using brachial blood pressure measurements, followed by a 10-minute supine autonomic testing session consisting of continuous HR (electrocardiogram), beat-by-beat blood pressure (finger plethysmograph), and MSNA (microneurography) monitoring. Partial correlations were used to determine the relationship between sleep and cardiovascular parameters while accounting for the influence of age, sex, and BMI. TST was not associated with MAP ( R = -0.105, P = 0.321), HR ( R = 0.093, P = 0.383), or MSNA burst frequency (BF; R = -0.168, P = 0.112) and burst incidence (BI; R = -0.162, P = 0.124). Similarly, SE was not associated with MAP ( R = -0.088, P = 0.408), HR ( R = -0.118, P = 0.263), MSNA BF ( R = 0.038, P = 0.723), or MSNA BI ( R = 0.079, P = 0.459). In contrast to recent preliminary findings, our results do not support a significant association between actigraphy-based sleep duration or efficiency and measures of resting blood pressure, heart rate, and MSNA. NEW & NOTEWORTHY The present study investigated the independent association between actigraphy-based sleep duration, efficiency, and measures of blood pressure, heart rate, and muscle sympathetic nerve activity (MSNA) in adult males and females. Contrary to our hypothesis, the findings do not support an independent association between habitual sleep and cardiovascular or sympathetic neural activity. However, these findings do not preclude a potential association between these parameters in populations with sleep disorders and/or cardiovascular disease.

Post-traumatic stress disorder (PTSD) is associated with increased cardiovascular disease (CVD) risk. Compared with males, females are twice as likely to develop PTSD after trauma exposure, and cardiovascular reactivity to stress is a known risk factor for CVD. We aimed to examine hemodynamic responses to acute mental stress in trauma-exposed females with and without a clinical diagnosis of PTSD. We hypothesized that females with PTSD would have higher heart rate (HR), blood pressure (BP), and lower blood flow velocity (BFV) responsiveness compared with controls. We enrolled 21 females with PTSD and 21 trauma-exposed controls. We continuously measured HR using a three-lead electrocardiogram, BP using finger plethysmography, and brachial BFV using Doppler ultrasound. All variables were recorded during 10 min of supine rest, 5 min of mental arithmetic, and 5 min of recovery. Females with PTSD were older, and had higher BMI and higher resting diastolic BP. Accordingly, age, BMI, and diastolic BP were covariates for all repeated measures analyses. Females with PTSD had a blunted brachial BFV response to mental stress (time × group, p = 0.005) compared with controls, suggesting greater vasoconstriction. HR and BP responses were comparable. In conclusion, our results suggest early impairment of vascular function in premenopausal females with PTSD., (© 2024 The Author(s). Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Our laboratory has previously reported that total sleep deprivation (TSD) modifies muscle sympathetic neural activity (MSNA) differently in young men and women. Because postmenopausal women are among the highest risk for hypertension, this study compares MSNA responses with TSD in older men and women. We hypothesized that TSD would alter MSNA in older adults, with greater sympathoexcitation in postmenopausal women. Twenty-seven participants (14 men and 13 women) between the ages of 55 and 75 yr were tested twice, once after 24-h TSD and once after normal sleep (randomized, crossover design). Our primary outcome measure of MSNA (microneurography) was successful across both conditions in 20 participants (10 men and 10 women). Secondary outcome measures included seated blood pressure, heart rate, and fasting plasma testosterone, estradiol, and progesterone. Age (60 ± 1 vs. 61 ± 2 yr) and BMI (27 ± 1 vs. 26 ± 1 kg/m 2 ) were not different between groups. TSD increased systolic blood pressure in both men (124 ± 5 to 130 ± 4 mmHg) and women (107 ± 5 to 116 ± 4 mmHg), but the increases were not different between groups (condition, P = 0.014; condition × sex, P > 0.05). In contrast, TSD elicited divergent MSNA responses in older men and women. Specifically, MSNA burst frequency increased in postmenopausal women (28 ± 3 to 34 ± 3 burst/min), but not older men (38 ± 3 to 35 ± 3 bursts/min; condition × sex, P = 0.032). In conclusion, TSD elicited sympathoexcitation in postmenopausal women but not age-matched men. These findings provide new mechanistic insight into reported links between sleep deprivation and hypertension. NEW & NOTEWORTHY Epidemiological studies report that sleep deprivation is more strongly associated with hypertension in women than in men. In the present study, 24-h total sleep deprivation (TSD) increased blood pressure in postmenopausal women and age-matched men. In contrast, only women demonstrated increases in muscle sympathetic nerve activity after TSD. The sympathoexcitation observed in postmenopausal women suggests a potential contributing mechanism for epidemiological observations and advances our understanding of the complex relations between sleep, sex, and hypertension.

Insufficient sleep and circadian rhythm disturbances have been each associated with adverse cardiovascular outcomes in epidemiological studies, but experimental evidence for a causal link is scarce. The present study compares the impact of circadian misalignment (CM) to circadian alignment (CA) on human autonomic function using a nonrandomized parallel group design to achieve the same total sleep time in both conditions. After baseline assessments (3 days with 10-hour bedtimes), 26 healthy young adults were assigned to sleep restriction (SR; eight 5-hour bedtimes) with either fixed nocturnal bedtimes (CA; n=13) or bedtimes delayed by 8.5 hours on 4 of the 8 days (CM; n=13). Daytime ambulatory blood pressure and heart rate (HR; CA, n=11; CM, n=10) and 24-hour urinary norepinephrine levels (CA, n=13; CM, n=13) were assessed at baseline and the end of SR. Nocturnal HR and HR variability were analyzed during sleep at baseline and during the fourth and seventh nights of SR (CA, n=8; CM, n=12). SR resulted in a significant increase in daytime HR in both groups, without changes in blood pressure. SR increased 24-hour urinary norepinephrine in the CM group (30±4 versus 21±2 μg), but not in the circadian alignment group (group×condition, P=0.005). In contrast to the lack of detectable impact of CM on daytime autonomic function, SR with CM elicited greater increases in nocturnal HR, as well as greater reductions in vagal indices of HR variability, than SR without CM (group×condition, P<0.05). In conclusion, SR and CM both result in impaired autonomic function that could lead, under chronic conditions, to enhanced cardiovascular risk., (© 2016 American Heart Association, Inc.)

Positive airway pressure (PAP) treatment has been shown to have a modest effect on ambulatory blood pressure (BP) in patients with obstructive sleep apnea (OSA). However, there is a paucity of data on the effect of PAP therapy on rapid, yet significant, BP swings during sleep, particularly in obesity hypoventilation syndrome (OHS). The present study hypothesizes that PAP therapy will improve nocturnal BP on the first treatment night (titration PAP) in OHS patients with underlying OSA, and that these improvements will become more significant with 6 wk of PAP therapy. Seventeen adults (7 men, 10 women; age 50.4 ± 10.7 years, BMI 49.3 ± 2.4 kg/m(2)) with OHS and clinically diagnosed OSA participated in three overnight laboratory visits that included polysomnography and beat-to-beat BP monitoring via finger plethysmography. Six weeks of PAP therapy, but not titration PAP, lowered mean nocturnal BP. In contrast, when nocturnal beat-to-beat BPs were aggregated into bins consisting of at least three consecutive cardiac cycles with a >10 mmHg BP surge (i.e., Δ10-20, Δ20-30, Δ30-40, and Δ>40 mmHg), titration, and 6-wk PAP reduced the number of BP surges per hour (time × bin, P < 0.05). PAP adherence over the 6-wk period was significantly correlated to reductions in nocturnal systolic (r = 0.713, P = 0.001) and diastolic (r = 0.497, P = 0.043) BP surges. Despite these PAP-induced improvements in nocturnal beat-to-beat BP surges, 6 wk of PAP therapy did not alter daytime BP. In conclusion, PAP treatment reduces nocturnal beat-to-beat BP surges in OHS patients with underlying OSA, and this improvement in nocturnal BP regulation was greater in patients with higher PAP adherence., (Copyright © 2016 the American Physiological Society.)

Background: Non-dipping of nocturnal blood pressure (BP) is associated with target organ damage and cardiovascular disease. Obstructive sleep apnoea (OSA) is associated with incident non-dipping. However, the relationship between disordered breathing during rapid eye movement (REM) sleep and the risk of developing non-dipping has not been examined. This study investigates whether OSA during REM sleep is associated with incident non-dipping., Methods: Our sample included 269 adults enrolled in the Wisconsin Sleep Cohort Study who completed two or more 24 h ambulatory BP studies over an average of 6.6 years of follow-up. After excluding participants with prevalent non-dipping BP or antihypertensive use at baseline, there were 199 and 215 participants available for longitudinal analysis of systolic and diastolic non-dipping, respectively. OSA in REM and non-REM sleep were defined by apnoea hypopnoea index (AHI) from baseline in-laboratory polysomnograms. Systolic and diastolic non-dipping were defined by systolic and diastolic sleep/wake BP ratios >0.9. Modified Poisson regression models estimated the relative risks for the relationship between REM AHI and incident non-dipping, adjusting for non-REM AHI and other covariates., Results: There was a dose-response greater risk of developing systolic and diastolic non-dipping BP with greater severity of OSA in REM sleep (p-trend=0.021 for systolic and 0.024 for diastolic non-dipping). Relative to those with REM AHI<1 event/h, those with REM AHI≥15 had higher relative risk of incident systolic non-dipping (2.84, 95% CI 1.10 to 7.29) and incident diastolic non-dipping (4.27, 95% CI 1.20 to 15.13)., Conclusions: Our findings indicate that in a population-based sample, REM OSA is independently associated with incident non-dipping of BP., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Endogenous female sex hormones influence muscle sympathetic nerve activity (MSNA), a regulator of arterial blood pressure and important factor in hypertension development. Although ≈80% of American women report using hormonal contraceptives sometime during their life, the influence of combined oral contraceptives (OCs) on MSNA and systemic hemodynamics remains equivocal. The goal of this study was to determine whether women taking OCs have altered MSNA and hemodynamics (cardiac output and total peripheral resistance) at rest during the placebo phase of OC use compared with women with natural menstrual cycles during the early follicular phase. We retrospectively analyzed data from studies in which healthy, premenopausal women (aged 18-35 years) participated. We collected MSNA values at rest and hemodynamic measurements in women taking OCs (n=53; 25±4 years) and women with natural menstrual cycles (n=74; 25±4 years). Blood pressure was higher in women taking OCs versus those with natural menstrual cycles (mean arterial pressure, 89±1 versus 85±1 mm Hg, respectively; P=0.01), although MSNA was similar in both groups (MSNA burst incidence, 16±1 versus 18±1 bursts/100 heartbeats, respectively; P=0.19). In a subset of women in which detailed hemodynamic data were available, those taking OCs (n=33) had similar cardiac output (4.9±0.2 versus 4.7±0.2 L/min, respectively; P=0.47) and total peripheral resistance (19.2±0.8 versus 20.0±0.9 U, respectively; P=0.51) as women with natural menstrual cycles (n=22). In conclusion, women taking OCs have higher resting blood pressure and similar MSNA and hemodynamics during the placebo phase of OC use when compared with naturally menstruating women in the early follicular phase., (© 2015 American Heart Association, Inc.)

Blunted dipping of nocturnal systolic arterial pressure (SAP) and heart rate (HR) are independent risk factors for hypertension and all-cause mortality. While several epidemiological studies report a significant association between short sleep duration and hypertension, associations between sleep efficiency and the nocturnal drop of SAP remain controversial. Moreover, relations between sleep efficiency and HR diurnal patterns have been overlooked. We hypothesized that low sleep efficiency (<85%) would be associated with blunted nocturnal SAP and HR dipping. Twenty-two normotensive subjects (13 men, 9 women; age: 18-28 yr) wore an actigraphy watch for 7 days and nights, and an ambulatory blood pressure monitor for 24 h on a nonactigraph night. There were no differences in age, sex, body mass index, mean sleep time, number of awakenings, or 24-h blood pressure between the low (n = 12) and high (n = 10) sleep efficiency groups. However, the low sleep efficiency subjects demonstrated a blunted dip of nocturnal SAP (10 ± 1% vs. 14 ± 1%, P = 0.04) and HR (12 ± 3% vs. 21 ± 3%, P = 0.03) compared with the high sleep efficiency group. The low sleep efficiency group also demonstrated a higher mean nocturnal HR (63 ± 2 vs. 55 ± 2 beats/min; P = 0.02). These findings support growing evidence that sleep efficiency, independent of total sleep time, may be an important cardiovascular risk factor., (Copyright © 2014 the American Physiological Society.)

Introduction: Spontaneous analysis techniques and Valsalva's maneuver (VM) are often used as a non-pharamcological approach to assess both sympathetic (sBRS) and cardiovagal (cBRS) baroreflex sensitivity. Despite their wide utilization, no studies have assessed the intra-individual reliability between these analysis techniques. Accordingly, we hypothesized that spontaneous BRS would be positively correlated to VM BRS., Methods: Heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 26 healthy subjects (age, 22 ± 1 year; 14 men and 12 women) during 10 min supine rest and 3 VM at 40 mmHg expiratory pressure (15 s, 1 min recoveries). For spontaneous BRS, relations between diastolic BP and MSNA were used to determine sBRS, while relations between systolic BP and R-R interval were used to determine cBRS. During VM, sBRS was the ratio of MSNA and the maximum diastolic BP reduction during early phase II, and cBRS was derived from linear relations between systolic BP and R-R interval during early phase II (i.e., hypotensive stimulus) and phase IV (i.e., hypertensive stimulus)., Results: Spontaneous sBRS was significantly correlated to VM sBRS (r = 0.516, p = 0.036). In contrast, spontaneous cBRS from up-up sequence was not correlated to VM phase IV cBRS (r = 0.274, p = 0.109). Similarly, spontaneous cBRS from down-down sequence was not correlated to VM phase II cBRS (r = 0.199, p = 0.207)., Conclusion: In conclusion, our findings demonstrate positive association between spontaneous sBRS and VM sBRS, but there is no correlation between spontaneous and VM cBRS.

The antihypertensive influence of fish oil is controversial, and the mechanisms remain unclear. Because the inverse relation between fish oil and hypertension appears to be partially dependent on the degree of hypertension, we tested the hypothesis that fish oil would elicit more dramatic reductions in mean arterial pressure (MAP) and muscle sympathetic nerve activity (MSNA) in prehypertensive (PHT) compared with normotensive (NT) subjects. Resting MAP, MSNA, and heart rate (HR) were examined before and after 8 wk of fish oil (9 g/day; 1.6 g eicosapentaenoic acid and 1.1 g docosahexaenoic acid) or placebo (olive oil; 9 g/day) in 38 NT (19 fish oil; 19 placebo) and 29 PHT (15 fish oil; 14 placebo) volunteers. Fish oil did not alter resting MAP, MSNA, or HR in either NT (80 ± 1 to 80 ± 1 mmHg; 11 ± 2 to 10 ± 1 bursts/min; 71 ± 2 to 71 ± 2 beats/min) or PHT (88 ± 2 to 87 ± 1 mmHg; 11 ± 2 to 10 ± 2 bursts/min; 73 ± 2 to 73 ± 2 beats/min) subjects. When NT and PHT groups were consolidated, analysis of covariance confirmed that pretreatment resting MAP was not associated with changes in MSNA after fish oil. In contrast, pretreatment resting HR was correlated with changes in MSNA (r = 0.47; P = 0.007) and MAP (r = 0.42; P < 0.007) after fish oil but not placebo. In conclusion, fish oil did not alter sympathetic neural control in NT or PHT subjects. However, our findings suggest that fish oil is associated with modest sympathoinhibition in individuals with higher resting heart rates, a finding that is consistent with a recent meta-analysis examining the relations among fish oil, HR, and the risk of cardiovascular disease.

The menstrual cycle has been reported to alter mean arterial pressure (MAP), but not muscle sympathetic nerve activity (MSNA), during vestibular activation. Specifically, MAP responses to head-down rotation (HDR) are augmented during the mid-luteal (ML) phase compared to the early follicular (EF) phase in young, eumenorrheic women. The purpose of the present study was to determine if the menstrual cycle influences vestibular-mediated changes in limb blood flow. MSNA, MAP, heart rate, and limb blood flow responses to HDR were measured in 12 healthy women. Resting MSNA, MAP, heart rate, forearm blood flow and calf blood flow were not altered by the menstrual cycle. HDR elicited similar increases in MSNA during the EF (Delta3+/-1 bursts/min; P<0.05) and ML (Delta2+/-1 bursts/min; P<0.05) phase, but only increased MAP during the ML phase (Delta4+/-2 mmHg; P<0.05). HDR did not change heart rate during either the EF or ML phase. HDR elicited similar increases in calf vascular resistance during the EF (Delta6+/-2 mmHg/mL/100 mL/min; P<0.05) and ML (Delta7+/-2 mmHg/mL/100mL/min; P<0.05) phases of the menstrual cycle. In contrast, HDR increased forearm vascular resistance during the ML phase (Delta4+/-2 mmHg/mL/100mL/min; P<0.05), but not the EF phase (Delta0+/-2 mmHg/mL/100mL/min). These findings suggest an increased transduction of sympathetic nerve activity into forearm vascular resistance during the ML phase, and reveal the first recorded divergent vascular response to vestibular excitation in human limbs., (2009 Elsevier B.V. All rights reserved.)

Mental stress consistently increases heart rate (HR) and blood pressure (BP) in humans, despite inconsistent sympathetic neural responses that include increases, decreases, or no change in muscle sympathetic nerve activity (MSNA). The purpose of the present study was to examine associations between MSNA, BP, and HR responses to mental stress. Leg MSNA, BP, HR, and perceived stress levels were recorded during 3-5 min of mental arithmetic in 82 subjects (53 men and 29 women). Subjects were divided into positive responders (>or=Delta3 bursts/min; n = 40), negative responders (

Sympathetic neural responses to mental stress are well documented but controversial, whereas sympathetic neural responses to emotional stress are unknown. The purpose of this study was to investigate neural and cardiovascular responses to emotional stress evoked by negative pictures and reexamine the relationship between muscle sympathetic nerve activity (MSNA) and perceived stress. Mean arterial pressure (MAP), heart rate (HR), MSNA, and perceived stress levels were recorded in 18 men during three randomized trials: 1) neutral pictures, 2) negative pictures, and 3) mental stress. MAP and HR increased during mental stress (Delta14 +/- 2 mmHg and Delta15 +/- 2 beats/min, P < 0.001) but did not change during viewing of negative or neutral pictures. MSNA did not change during viewing of neutral (Delta1 +/- 1 burst/min, n = 16) or negative (Delta0 +/- 1 burst/min, n = 16) pictures or during mental stress (Delta1 +/- 2 burst/min, n = 13). Perceived stress levels were higher during mental stress (3 +/- 0 arbitrary units) than during viewing negative pictures (2 +/- 0 arbitrary units, P < 0.001). Perceived stress levels were not correlated to changes in MSNA during negative pictures (r = 0.10, P = 0.84) or mental stress (r = 0.36, P = 0.23). In conclusion, our results demonstrate robust increases in MAP and HR during mental stress, but not during emotional stress evoked by negative pictures. Although the influence of mental stress on MSNA remains unresolved, our findings challenge the concept that perceived stress levels modulate MSNA during mental stress.

The effects of resistance training on arterial blood pressure and muscle sympathetic nerve activity (MSNA) at rest have not been established. Although endurance training is commonly recommended to lower arterial blood pressure, it is not known whether similar adaptations occur with resistance training. Therefore, we tested the hypothesis that whole body resistance training reduces arterial blood pressure at rest, with concomitant reductions in MSNA. Twelve young [21 +/- 0.3 (SE) yr] subjects underwent a program of whole body resistance training 3 days/wk for 8 wk. Resting arterial blood pressure (n = 12; automated sphygmomanometer) and MSNA (n = 8; peroneal nerve microneurography) were measured during a 5-min period of supine rest before and after exercise training. Thirteen additional young (21 +/- 0.8 yr) subjects served as controls. Resistance training significantly increased one-repetition maximum values in all trained muscle groups (P < 0.001), and it significantly decreased systolic (130 +/- 3 to 121 +/- 2 mmHg; P = 0.01), diastolic (69 +/- 3 to 61 +/- 2 mmHg; P = 0.04), and mean (89 +/- 2 to 81 +/- 2 mmHg; P = 0.01) arterial blood pressures at rest. Resistance training did not affect MSNA or heart rate. Arterial blood pressures and MSNA were unchanged, but heart rate increased after 8 wk of relative inactivity for subjects in the control group (61 +/- 2 to 67 +/- 3 beats/min; P = 0.01). These results indicate that whole body resistance exercise training might decrease the risk for development of cardiovascular disease by lowering arterial blood pressure but that reductions of pressure are not coupled to resistance exercise-induced decreases of sympathetic tone.