Recent studies have demonstrated that muscle sympathetic nerve activity (MSNA) responses to isometric exercise differs between active and inactive limbs. Whether limb-dependent responses are characteristic of responses to the cold pressor test (CPT) remains to be established. Therefore, we tested the hypothesis that CPT-induced MSNA responses differ between affected and unaffected limbs such that MSNA in the affected lower limb is greater than MSNA responses in the contralateral lower limb and the upper limb. Integrated peroneal MSNA (microneurography) was measured in young healthy individuals (n = 10) at rest and during three separate 3-min CPTs: the microneurography foot, opposite foot, and opposite hand. Peak MSNA responses were extracted for further analysis, as well as corresponding hemodynamic outcomes including mean arterial pressure (MAP; Finometer). MSNA responses were greater when the microneurography foot was immersed in ice water than when the opposite foot was immersed (38 ± 18 vs 28 ± 16 bursts/100hb: P < 0.01). MSNA responses when the opposite hand was immersed were greater than both the microneurography foot (46 ± 22 vs 38 ± 18 bursts/100hb: P < 0.01) and opposite foot (46 ± 22 vs 28 ± 16 bursts/100hb: P ≤0.01). Likewise, MAP responses were greater during the hand CPT than the microneurography foot (99 ± 9 vs 96 ± 8 mmHg: P < 0.01) and opposite foot CPT (99 ± 9 vs 96 ± 9 mmHg: P < 0.01). These data indicate that (a) upper limbs and (b) immersed limbs elicit greater MSNA responses to the CPT than lower and/or non-immersed limbs.

Age and sex may alter the cerebral blood flow (CBF) responses to acute isometric exercise, via associated elevations in mean arterial pressure (MAP) and sympathetic activation. Our aim was to determine the relationships between age, sex, and exercise intensity on cerebrovascular responses to isometric handgrip exercise. In 78 healthy adults (18-80 yr, n = 42 females), cerebrovascular responses were assessed during 2-min isometric exercise bouts at three intensities [15, 30, 45% maximal voluntary contraction (MVC)]. Intracranial responses of the middle cerebral artery (MCA) and posterior cerebral artery (PCA) velocity (v) were measured using transcranial Doppler ultrasound. Extracranial responses of the internal carotid artery (ICA) and vertebral artery (VA) were assessed using Duplex ultrasound. Cardiopulmonary hemodynamic and neural parameters were measured throughout, including muscle sympathetic nerve activity, end-tidal carbon dioxide, and MAP. There were significant positive relationships between exercise intensity and the cerebral responses of the MCAv (P < 0.001) and PCAv (P = 0.005). There were no effects of intensity on ICA and VA responses (P > 0.05), despite intensity-dependent increases in MAP (P < 0.001). The increased MCAv response to exercise was blunted with advancing age (P = 0.01) with no influence of sex (P = 0.86). The present study provides data on age, sex, and intensity-specific relationships with intracranial and extracranial cerebrovascular responses to isometric exercise. Despite similar ICA, VA, and PCA responses, MCAv responses were attenuated with advancing age during handgrip exercise with no sex-dependent influence. Furthermore, intracranial responses were intensity dependent, whereas extracranial blood flow, shear-stress, and velocity responses were similarly increased at all intensities during handgrip exercise. NEW & NOTEWORTHY The influence of aging and sex on cerebral blood flow responses to isometric exercise are unknown. We observed intensity-dependent increases in velocity of the intracranial arteries, whereas the extracranial artery responses were similarly increased at all intensities during handgrip exercise in young and older individuals. Furthermore, we observed a blunted middle cerebral artery velocity response to handgrip exercise with advancing age, whereas the posterior circulation and extracranial responses were preserved across the lifespan in healthy individuals in males and females alike.

Background/Aims People living with rheumatoid arthritis (RA) tend to be less active than the general population which may be due to RA associated musculoskeletal pain, stiffness and fatigue. The health benefits of physical activity (PA) are widely recognised in the general population and studies in RA have also highlighted improvement in RA associated symptoms. However, encouraging increased PA in people living with RA is challenging and adherence to PA is usually low. Mobile health (mHealth) technology (i.e., fitness watches and apps) may provide an effective and economical solution to promoting PA in this high-risk population. The aims of the current study were to assess whether use of mHealth technology in RA i) increases PA levels and ii) reduces RA disease activity. Methods People with RA were randomised to either the MOTIVATE (mHealth intervention) or conventional care (CC) groups. The CC group were provided with online educational materials, as provided in routine care (e.g., PA information leaflets), to increase PA whereas the MOTIVATE group were provided with a personalised, progressive walking programme delivered via mHealth technology with ongoing, individualised support throughout the 12-week intervention. All participants received a self-testing kit, via mail, at baseline (week 0) and post-intervention (12 weeks). Measures included anthropometrics, blood pressure, PA monitoring, health questionnaires and all were requested to self-report RA disease activity using RADAI-5. Change data between weeks 0 and 12 were compared between groups using One-Way ANCOVA, controlling for baseline, and reported as mean difference (95% CI). Results Of 50 participants, 25 were randomised to the MOTIVATE group (age 50 +/- 11years; BMI 29 +/- 7kg/m2; females n=23), and 25 to CC (n=25, age 50 +/- 11years; BMI 26 +/- 6 kg/m2; females n=24). An increase in moderate-to-vigorous PA was observed in the MOTIVATE group, compared to a decrease in CC [81min (1, 160) vs. -35min (-123, 53); P=0.09)]. This was accompanied by an increase in steps per day in the MOTIVATE group, and a decrease in CC [763 (-432, 1957) vs. -76 (-1267, 1115); P=0.40]. A reduction in PHQ-9 depression score was evident in the MOTIVATE group whilst CC were unchanged [-2 (-2, -3) vs. 0 (-2, 0); P=0.07]. RADAI-5 decreased in the MOTIVATE group and stayed the same in CC [-2 (-2, 0) vs. 0(-2, 0), P=0.27]. Conclusion These findings identify the potential effectiveness of an mHealth PA programme to increase PA levels in people living with RA. Use of remote PA monitoring, with support from exercise specialists, may be an effective strategy to improve engagement in exercise and PA in the RA population. Data is suggestive this could improve RA related symptoms, although we did not observe statistical significance. Disclosure D.J. Bannell: Grants/research support; Research grant from the Aintree Arthritis Trust. M. France-Ratcliffe: None. K.L. Hesketh: None. M. Cocks: None. N. Goodson: None. C. Taylor: None. T. Pecanha: None. H. Jones: None. D.A. Low: None. V.S. Sprung: None.

In a sample of 191 normotensive young adults, we confirm that resting muscle sympathetic nerve activity is a poor predictor of resting blood pressure and now demonstrate that sympathetic baroreflex gain is associated with resting blood pressure in males but not females. In contrast, signal-averaged measures of sympathetic-blood pressure transduction are unrelated to resting blood pressure. These findings highlight sex differences in the neural regulation of blood pressure.

In cardiovascular research, sex and gender have not typically been considered in research design and reporting until recently. This has resulted in clinical research findings from which not only all women, but also gender-diverse individuals have been excluded. The resulting dearth of data has led to a lack of sex- and gender-specific clinical guidelines and raises serious questions about evidence-based care. Basic research has also excluded considerations of sex. Including sex and/or gender as research variables not only has the potential to improve the health of society overall now, but it also provides a foundation of knowledge on which to build future advances. The goal of this guidelines article is to provide advice on best practices to include sex and gender considerations in study design, as well as data collection, analysis, and interpretation to optimally establish rigor and reproducibility needed to inform clinical decision-making and improve outcomes. In cardiovascular physiology, incorporating sex and gender is a necessary component when optimally designing and executing research plans. The guidelines serve as the first guidance on how to include sex and gender in cardiovascular research. We provide here a beginning path toward achieving this goal and improve the ability of the research community to interpret results through a sex and gender lens to enable comparison across studies and laboratories, resulting in better health for all.

CVR is preserved in ageing adults, but the speed of the MCAv response is blunted in older and middle-aged adults compared to young adults. Utilizing dynamic onset responses reveal underlying differences in cerebral regulation with healthy ageing that were not detected by traditional methods.

Understanding the contribution of the autonomic nervous system to cerebral blood flow (CBF) control is challenging, and interpretations are unclear. The identification of calcium channels and adrenoreceptors within cerebral vessels has led to common misconceptions that the function of these receptors and actions mirror those of the peripheral vasculature. This review outlines the fundamental differences and complex actions of cerebral autonomic activation compared with the peripheral circulation. Anatomical differences, including the closed nature of the cerebrovasculature, and differential adrenoreceptor subtypes, density, distribution and sensitivity, provide evidence that measures on peripheral sympathetic nerve activity cannot be extrapolated to the cerebrovasculature. Cerebral sympathetic nerve activity seems to act opposingly to the peripheral circulation, mediated at least in part by changes in intracranial pressure and cerebral blood volume. Additionally, heterogeneity in cerebral adrenoreceptor distribution highlights region-specific autonomic regulation of CBF. Compensatory chemo- and autoregulatory responses throughout the cerebral circulation, and interactions with parasympathetic nerve activity are unique features to the cerebral circulation. This crosstalk between sympathetic and parasympathetic reflexes acts to ensure adequate perfusion of CBF to rising and falling perfusion pressures, optimizing delivery of oxygen and nutrients to the brain, while attempting to maintain blood volume and intracranial pressure. Herein, we highlight the distinct similarities and differences between autonomic control of cerebral and peripheral blood flow, and the regional specificity of sympathetic and parasympathetic regulation within the cerebrovasculature. Future research directions are outlined with the goal to further our understanding of autonomic control of CBF in humans.

Based on a collection of auto-ethnographic narratives that reflect our experiences as academic mothers at an Australian university, this paper seeks to illustrate the impact of COVID-19 on our career cycles in order to explore alternative feminist models of progression and practice in Higher Education. Collectively, we span multiple disciplines, parenting profiles, and racial/ethnic backgrounds. Our narratives (initiated in 2019) explicate four focal points in our careers as a foundation for analyzing self-definitions of professional identity: pre- and post-maternity career break; and pre- and post-COVID-19 career. We have modeled this research on a collective feminist research practice that is generative and empowering in terms of self-reflective models of collaborative research. Considering this practice and these narratives, we argue for a de-centering of masculinized career cycle patterns and progression pathways both now and beyond COVID-19. This represents both a challenge to neo-liberal norms of academic productivity, as well as a call to radically enhance institutional gender equality policies and practice.

We previously demonstrated that muscle sympathetic nerve activity (MSNA) increases to contracting muscle as well as to non-contracting muscle, but this was only assessed during isometric exercise at ∼10% of maximum voluntary contraction (MVC). Given that high-intensity isometric contractions will release more metabolites, we tested the hypothesis that the metaboreflex is expressed in the contracting muscle during high-intensity but not low-intensity exercise. MSNA was recorded continuously via a tungsten microelectrode inserted percutaneously into the right common peroneal nerve in 12 participants, performing isometric dorsiflexion of the right ankle at 10, 20, 30, 40, and 50% MVC for 2 min. Contractions were immediately followed by 6 min of post-exercise ischemia (PEI); 6 min of recovery separated contractions. Cross-correlation analysis was performed between the negative-going sympathetic spikes of the raw neurogram and the ECG. MSNA increased as contraction intensity increased, reaching mean values (± SD) of 207 ± 210 spikes/min at 10% MVC (P = 0.04), 270 ± 189 spikes/min at 20% MVC (P < 0.01), 538 ± 329 spikes/min at 30% MVC (P < 0.01), 816 ± 551 spikes/min at 40% MVC (P < 0.01), and 1,097 ± 782 spikes/min at 50% MVC (P < 0.01). Mean arterial pressure also increased in an intensity-dependent manner from 76 ± 3 mmHg at rest to 90 ± 6 mmHg (P < 0.01) during contractions of 50% MVC. At all contraction intensities, blood pressure remained elevated during PEI, but MSNA returned to pre-contraction levels, indicating that the metaboreflex does not contribute to the increase in MSNA to contracting muscle even at these high contraction intensities.

Purpose Sympathetic vasoconstriction plays a major role in the beat-to-beat control of blood pressure. To be effective and thus avoid dangerously high or low blood pressures, this mechanism relies upon transduction of sympathetic nerve activity at the level of the vasculature. However, recent evidence suggests that considerable variability exists in beat-to-beat vascular transduction, particularly between the sexes. Methods We reviewed the methods available for quantifying beat-to-beat transduction of muscle sympathetic nerve activity (MSNA) and explored the recent evidence for sex differences in vascular transduction. We paid specific attention to relationships between vascular transduction and factors such as resting levels of sympathetic nerve activity and baroreflex sensitivity. Results There are two dominant methods now available for the quantification of beat-to-beat transduction of muscle sympathetic nerve activity at rest. Whilst there is some evidence to suggest that young females exhibit lower levels of vascular transduction, results vary depending on the method used and the direction of change in MSNA. Evidence suggests that compensatory relationships may exist between key components of neurovascular control, such as vascular transduction and resting levels of MSNA. Also consistent is the presence of such relationships in young males but not young females. Conclusion The lack of significant relationships in young females may reflect the influence of vasodilator mechanisms that counteract sympathetic vasoconstriction. The assessment of vascular transduction following MSNA bursts and non-bursts in males and females, both young and older, may help to gain a mechanistic understanding of the prevalence of hypotensive and hypertensive disorders across the lifespan.

Sympathetic baroreflex sensitivity (BRS) is a measure of how effectively the baroreflex buffers beat-to-beat changes in blood pressure through the modulation of muscle sympathetic nerve activity (MSNA). However, current methods of assessment do not take into account the transduction of sympathetic nerve activity at the level of the vasculature, which is known to vary between individuals. In this study we tested the hypothesis that there is an inverse relationship between sympathetic BRS and vascular transduction. In 38 (18 men) healthy adults, continuous measurements of blood pressure, MSNA and superficial femoral artery diameter and blood flow (Doppler ultrasound) were recorded during 10 min of rest. Spontaneous sympathetic BRS was quantified as the relationship between diastolic pressure and MSNA burst incidence. Vascular transduction was quantified by plotting the changes in leg vascular conductance for 10 cardiac cycles following each burst of MSNA, and taking the nadir. In men, sympathetic BRS was inversely related to vascular transduction ( r = −0.49; P = 0.04). However, this relationship was not present in women ( r = −0.17; P = 0.47). To conclude, an interaction exists between sympathetic BRS and vascular transduction in healthy men, such that men with high sympathetic BRS have low vascular transduction and vice versa. This may be to ensure that blood pressure is regulated effectively, although further research is needed to explore what mechanisms are involved and examine why this relationship was not apparent in women. NEW & NOTEWORTHY Evidence suggests that compensatory interactions exist between factors involved in cardiovascular control. This study was the first to demonstrate an inverse relationship between sympathetic BRS and beat-to-beat vascular transduction. Those with low sympathetic BRS had high vascular transduction and vice versa. However, this interaction was present in young men but not women.

We have previously shown that the increase in muscle sympathetic nerve activity (MSNA) to contracting muscle during sustained isometric exercise is due primarily to central command and that contracting muscle does not express a metaboreceptor-driven increase in MSNA. Here we tested the hypothesis that MSNA increases to the contracting muscle also during rhythmic isotonic exercise, in which muscle metabolites will not accumulate because the contraction is performed without external load. MSNA was recorded from the common peroneal nerve in 10 participants, and negative-going sympathetic spikes were extracted during 50 cycles of sinusoidal (0.15 Hz) isotonic dorsiflexions of the ipsilateral or contralateral ankle. Electromyographic activity (EMG) was recorded from the tibialis anterior muscle on both sides. Cross-correlation analysis between MSNA and EMG revealed a marked cyclic modulation of MSNA to the contracting (ipsilateral) muscle. This modulation, in which MSNA increased during the contraction phase, was three times greater than that to the noncontracting muscle (modulation index = 27.4 ± 3.2% vs. 9.2 ± 1.5%; P < 0.002). There were no differences in either the intensity or the magnitude of modulation of EMG during ipsilateral and contralateral contractions. We conclude that central command increases MSNA to the contracting muscle during rhythmic isotonic exercise. NEW & NOTEWORTHY Muscle sympathetic nerve activity (MSNA) increases to contracting muscle during isometric exercise, but whether this occurs during rhythmic isotonic exercise is unknown. We recorded MSNA to the pretibial flexors during cyclic dorsiflexion of the ipsilateral or contralateral ankle. MSNA showed a cyclic increase during the contraction phase that was significantly higher to the contracting than the noncontracting muscle, supporting central command as the primary mechanism responsible for increasing MSNA.

Previous research indicates that greater sympathetic vasoconstrictor drive to skeletal muscle occurs during isometric upper limb exercise compared to lower limb exercise. However, potential disparity between blood flow and metaboreflex activation in contracting upper and lower limbs could contribute to the augmented sympathetic response during upper limb exercise. Therefore, the aim of this study was to examine MSNA responses during ankle dorsiflexion and handgrip exercise under ischaemic conditions, in order to standardize the conditions in terms of perfusion and metaboreflex activation. Eight healthy male subjects performed 4-min contractions of ischaemic isometric handgrip and ankle dorsiflexion at ∼10% maximal voluntary contraction, followed by 6 min of post-exercise ischaemia. MSNA was recorded continuously by microneurography of the common peroneal nerve of the non-contracting leg and quantified from negative-going sympathetic spikes in the neurogram, synchronized with the cardiac cycle. The time-course of MSNA exhibited parallel increases during exercise of the upper and lower limbs, rising throughout the contraction to peak at 4 min. This represented an increase of 100% relative to resting levels for handgrip exercise (66 ± 24 vs. 33 ± 7 spikes/min at rest) and 103% for dorsiflexion (63 ± 25 vs. 31 ± 8 spikes/min at rest; P < 0.01). In both conditions MSNA remained elevated during post-exercise ischaemia and returned to pre-contraction levels during recovery. These findings demonstrate that that the MSNA response to metaboreflex activation is similar for upper and lower limb exercise when perfusion is controlled for.

Journal of Sleep ResearchVolume 27, Issue 6 e12738 LETTER TO THE EDITOR Getting to the heart of cardiac autonomic dysfunction in insomnia Correction(s) for this article Corrigendum Volume 28Issue 1Journal of Sleep Research First Published online: January 17, 2019 Christopher J. Gordon, Corresponding Author Christopher J. Gordon christopher.gordon@sydney.edu.au orcid.org/0000-0003-2698-4864 Sydney Nursing School, University of Sydney, Sydney, NSW, Australia CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, Glebe, NSW, Australia Correspondence Christopher J. Gordon, Sydney Nursing School, The University of Sydney, Sydney, NSW 2006, Australia. Email: christopher.gordon@sydney.edu.auSearch for more papers by this authorKirsty L. Dodds, Kirsty L. Dodds CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, Glebe, NSW, AustraliaSearch for more papers by this authorNathaniel S. Marshall, Nathaniel S. Marshall orcid.org/0000-0002-9014-1397 Sydney Nursing School, University of Sydney, Sydney, NSW, Australia CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, Glebe, NSW, AustraliaSearch for more papers by this authorChristopher B. Miller, Christopher B. Miller orcid.org/0000-0002-2936-7717 Big Health Ltd, London, UKSearch for more papers by this authorChloe E. Taylor, Chloe E. Taylor School of Medicine, Western Sydney University, Sydney, NSW, AustraliaSearch for more papers by this authorCraig L. Philips, Craig L. Philips CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, Glebe, NSW, Australia Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, Sydney, NSW, Australia Sydney Medical School, University of Sydney, Sydney, NSW, AustraliaSearch for more papers by this author Christopher J. Gordon, Corresponding Author Christopher J. Gordon christopher.gordon@sydney.edu.au orcid.org/0000-0003-2698-4864 Sydney Nursing School, University of Sydney, Sydney, NSW, Australia CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, Glebe, NSW, Australia Correspondence Christopher J. Gordon, Sydney Nursing School, The University of Sydney, Sydney, NSW 2006, Australia. Email: christopher.gordon@sydney.edu.auSearch for more papers by this authorKirsty L. Dodds, Kirsty L. Dodds CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, Glebe, NSW, AustraliaSearch for more papers by this authorNathaniel S. Marshall, Nathaniel S. Marshall orcid.org/0000-0002-9014-1397 Sydney Nursing School, University of Sydney, Sydney, NSW, Australia CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, Glebe, NSW, AustraliaSearch for more papers by this authorChristopher B. Miller, Christopher B. Miller orcid.org/0000-0002-2936-7717 Big Health Ltd, London, UKSearch for more papers by this authorChloe E. Taylor, Chloe E. Taylor School of Medicine, Western Sydney University, Sydney, NSW, AustraliaSearch for more papers by this authorCraig L. Philips, Craig L. Philips CIRUS, Centre for Sleep and Chronobiology, Woolcock Institute of Medical Research, Glebe, NSW, Australia Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, Sydney, NSW, Australia Sydney Medical School, University of Sydney, Sydney, NSW, AustraliaSearch for more papers by this author First published: 31 July 2018 https://doi.org/10.1111/jsr.12738Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume27, Issue6December 2018e12738 RelatedInformation

Key points It is not clear how sympathetic activity to contracting muscle is controlled. We recorded muscle sympathetic nerve activity (MSNA) to the ipsilateral tibialis anterior muscle during 4 min of isometric dorsiflexion of the ankle and 6 min of post‐exercise ischaemia, which was repeated contralaterally. MSNA to the contracting muscle increased within 1 min of static exercise and returned to pre‐contraction levels at the end. Unlike the increase in MSNA seen in the non‐contracting muscle, post‐exercise ischaemia had no effect on MSNA to the contracted muscle. We conclude that central command is the primary mechanism responsible for increasing MSNA to contracting muscle and also that the metaboreflex is not expressed in contracting muscle. Abstract Both central command and metaboreflex inputs from contracting muscles increase muscle sympathetic nerve activity (MSNA) to non‐contracting muscle during sustained isometric exercise. We recently showed that MSNA to contracting muscle also increases in an intensity‐dependent manner, although whether this can be sustained by the metaboreflex is unknown. MSNA was recorded from the left common peroneal nerve and individual spikes of MSNA extracted from the nerve signal. Eleven subjects performed a series of 4 min dorsiflexions of the left ankle at 10% of maximum voluntary contraction under three conditions: without ischaemia, with 6 min of post‐exercise ischaemia, and with ischaemia during and after exercise; these were repeated in the right leg. Compared with pre‐contraction values, MSNA to the contracting muscles increased and plateaued in the first minute of contraction (50 ± 18 vs . 34 ± 10 spikes min −1 , P = 0.01), returned to pre‐contraction levels within 1 min of the contraction ending and was not influenced by ischaemia during or after contraction. Conversely, MSNA to the non‐contracting muscles was not different from pre‐contraction levels in the first minute of contraction (34 ± 9 vs . 32 ± 5 spikes min −1 , P = 0.48), whereas it increased each minute and was significantly greater by the second minute (44 ± 8 spikes min −1 , P = 0.01). Ischaemia augmented the MSNA response to contraction (63 ± 25 spikes min −1 after 4 min, P < 0.05) and post‐exercise ischaemia (63 ± 27 spikes min −1 after 6 min, P < 0.01) for the non‐contracting muscles only. These findings support our conclusion that the metaboreflex is not expressed in the contracting muscle during sustained static exercise.

Sympathetic baroreflex sensitivity (BRS) is a tool used to quantify how effectively the baroreflex buffers beat‐to‐beat changes in blood pressure. However, current methods of assessment do not take into account vascular transduction, i.e. the response of the peripheral vasculature to vasoconstrictor drive. The aim of the study was to investigate the relationship between sympathetic BRS and vascular transduction. Muscle sympathetic nerve activity (MSNA, microneurography), blood pressure, heart rate and superficial femoral artery blood flow (Doppler ultrasound) were recorded at rest for 5 min in 28 healthy adults (18–31yrs, 13 males, 15 females). Sympathetic BRS was quantified by plotting MSNA burst incidence against mean diastolic pressure using 3 mmHg bins. For vascular transduction, the % change in leg vascular conductance was determined for 15 cardiac cycles following each MSNA burst and the nadir of the response was calculated. Linear regression analysis was used to examine the relationship between sympathetic BRS and vascular transduction in males and females separately. Sympathetic BRS was not significantly different between males (−2.9± 1.8) and females (−3.2 ± 1.6 %bursts/mmHg, p=0.68). However, vascular transduction was significantly lower in males (−5.5 ± 4.1) compared with females (9.1 ± 4.7 %change in ml/min/mmHg, p=0.04). In males there was a significant inverse relationship between sympathetic BRS and vascular transduction (r=0.78, p=0.002), but in females there was no significant relationship (r=0.34, p=0.21). The results suggest that in males those with high sympathetic BRS have low vascular transduction, and vice versa. This may represent a compensatory effect to ensure that blood pressure is regulated effectively. However, this relationship between sympathetic BRS and vascular transduction was not apparent in young females.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.