scholarly journals Exaggerated sympathetic and pressor responses to handgrip exercise in older hypertensive humans: role of the muscle metaboreflex

2010 ◽  
Vol 299 (5) ◽  
pp. H1318-H1327 ◽  
Author(s):  
Erin P. Delaney ◽  
Jody L. Greaney ◽  
David G. Edwards ◽  
William C. Rose ◽  
Paul J. Fadel ◽  
...  

Recent animal studies have reported that exercise pressor reflex (EPR)-mediated increases in blood pressure are exaggerated in hypertensive (HTN) rodents. Whether these findings can be extended to human hypertension remains unclear. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and venous metabolites were measured in normotensive (NTN; n = 23; 60 ± 1 yr) and HTN ( n = 15; 63 ± 1 yr) subjects at baseline, and during static handgrip at 30 and 40% maximal voluntary contraction (MVC) followed by a period of postexercise ischemia (PEI) to isolate the metabolic component of the EPR. Changes in MAP from baseline were augmented in HTN subjects during both 30 and 40% MVC handgrip ( P < 0.05 for both), and these group differences were maintained during PEI (30% PEI trial: Δ15 ± 2 NTN vs. Δ19 ± 2 HTN mmHg; 40% PEI trial: Δ16 ± 1 NTN vs. Δ23 ± 2 HTN mmHg; P < 0.05 for both). Similarly, in HTN subjects, MSNA burst frequency was greater during 30 and 40% MVC handgrip ( P < 0.05 for both), and these differences were maintained during PEI [30% PEI trial: 35 ± 2 (NTN) vs. 44 ± 2 (HTN) bursts/min; 40% PEI trial: 36 ± 2 (NTN) vs. 48 ± 2 (HTN) bursts/min; P < 0.05 for both]. No group differences in metabolites were observed. MAP and MSNA responses to a cold pressor test were not different between groups, suggesting no group differences in generalized sympathetic responsiveness. In summary, compared with NTN subjects, HTN adults exhibit exaggerated sympathetic and pressor responses to handgrip exercise that are maintained during PEI, indicating that activation of the metabolic component of the EPR is augmented in older HTN humans.

1991 ◽  
Vol 260 (3) ◽  
pp. E379-E388 ◽  
Author(s):  
P. A. Farrell ◽  
T. J. Ebert ◽  
J. P. Kampine

The influence of an endogenous opioid peptide (EOP) antagonist (naloxone, 1.2 mg iv bolus) on muscle sympathetic nerve activity (MSNA, microneurography) was studied on 19 young male and female volunteers. Isometric handgrip, cold pressor test, and acute baroreceptor unloading with sodium nitroprusside (autonomic stresses) were carried out under two conditions, one group (n = 11) before (control responses) and after naloxone and another group (n = 8) before and after placebo saline. Monitored cardiovascular variables included heart rate, central venous pressure (jugular vein catheter), arterial blood pressure (radial artery catheter), circulating catecholamines, and forearm blood flow. At rest, cardiovascular variables and MSNA were not affected by either naloxone or saline. MSNA (total activity = burst frequency x burst amplitude/100 cardiac cycles) increased during isometric handgrip to a greater extent (30 +/- 6 vs. 16 +/- 5 arbitrary units) after naloxone compared with control trials (P less than 0.05). After naloxone, arterial systolic and diastolic blood pressures were higher during handgrip exercise. These augmented arterial pressures and MSNA responses were not evident during either the cold pressor test or the sodium nitroprusside stress. These data suggest that isometric muscle contraction elicits a sympathetic neural response that may be modified by EOP. This interaction is not evident during two other stresses, when sympathetic responses are equal to or greater than those provoked by isometric handgrip exercise.


2011 ◽  
Vol 301 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
Sara S. Jarvis ◽  
Tiffany B. VanGundy ◽  
M. Melyn Galbreath ◽  
Shigeki Shibata ◽  
Kazunobu Okazaki ◽  
...  

Sex differences in sympathetic neural control during static exercise in humans are few and the findings are inconsistent. We hypothesized women would have an attenuated vasomotor sympathetic response to static exercise, which would be further reduced during the high sex hormone [midluteal (ML)] vs. the low hormone phase [early follicular (EF)]. We measured heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) in 11 women and 10 men during a cold pressor test (CPT) and static handgrip to fatigue with 2 min of postexercise circulatory arrest (PECA). HR increased during handgrip, reached its peak at fatigue, and was comparable between sexes. BP increased during handgrip and PECA where men had larger increases from baseline. Mean ± SD MSNA burst frequency (BF) during handgrip and PECA was lower in women (EF, P < 0.05), as was ΔMSNA-BF smaller (main effect, both P < 0.01). ΔTotal activity was higher in men at fatigue (EF: 632 ± 418 vs. ML: 598 ± 342 vs. men: 1,025 ± 416 a.u./min, P < 0.001 for EF and ML vs. men) and during PECA (EF: 354 ± 321 vs. ML: 341 ± 199 vs. men: 599 ± 327 a.u./min, P < 0.05 for EF and ML vs. men). During CPT, HR and MSNA responses were similar between sexes and hormone phases, confirming that central integration and the sympathetic efferent pathway was comparable between the sexes and across hormone phases. Women demonstrated a blunted metaboreflex, unaffected by sex hormones, which may be due to differences in muscle mass or fiber type and, therefore, metabolic stimulation of group IV afferents.


2016 ◽  
Vol 310 (2) ◽  
pp. H300-H309 ◽  
Author(s):  
Seth W. Holwerda ◽  
Robert M. Restaino ◽  
Camila Manrique ◽  
Guido Lastra ◽  
James P. Fisher ◽  
...  

Previous studies have reported exaggerated increases in arterial blood pressure during exercise in type 2 diabetes (T2D) patients. However, little is known regarding the underlying neural mechanism(s) involved. We hypothesized that T2D patients would exhibit an augmented muscle metaboreflex activation and this contributes to greater pressor and sympathetic responses during exercise. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were measured in 16 patients with T2D (8 normotensive and 8 hypertensive) and 10 healthy controls. Graded isolation of the muscle metaboreflex was achieved by postexercise ischemia (PEI) following static handgrip performed at 30% and 40% maximal voluntary contraction (MVC). A cold pressor test (CPT) was also performed as a generalized sympathoexcitatory stimulus. Increases in MAP and MSNA during 30 and 40% MVC handgrip were augmented in T2D patients compared with controls ( P < 0.05), and these differences were maintained during PEI (MAP: 30% MVC PEI: T2D, Δ16 ± 2 mmHg vs. controls, Δ8 ± 1 mmHg; 40% MVC PEI: T2D, Δ26 ± 3 mmHg vs. controls, Δ16 ± 2 mmHg, both P < 0.05). MAP and MSNA responses to handgrip and PEI were not different between normotensive and hypertensive T2D patients ( P > 0.05). Interestingly, MSNA responses were also greater in T2D patients compared with controls during the CPT ( P < 0.05). Collectively, these findings indicate that muscle metaboreflex activation is augmented in T2D patients and this contributes, in part, to augmented pressor and sympathetic responses to exercise in this patient group. Greater CPT responses suggest that a heightened central sympathetic reactivity may be involved.


2001 ◽  
Vol 281 (5) ◽  
pp. H2028-H2035 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Cynthia S. Hogeman ◽  
Mazhar Khan ◽  
Derek S. Kimmerly ◽  
Lawrence I. Sinoway

We tested the hypothesis that differences in sympathetic reflex responses to head-up tilt (HUT) between males ( n = 9) and females ( n = 8) were associated with decrements in postural vasomotor responses in women. Muscle sympathetic nerve activity (MSNA; microneurography), heart rate, stroke volume (SV; Doppler), and blood pressure (Finapres) were measured during a progressive HUT protocol (5 min at each of supine, 20°, 40°, and 60°). MSNA and hemodynamic responses were also measured during the cold pressor test (CPT) to examine nonbaroreflex neurovascular control. SV was normalized to body surface area (SVi) to calculate the index of cardiac output (Qi), and total peripheral resistance (TPR). During HUT, heart rate increased more in females versus males ( P < 0.001) and SVi and Qi decreased similarly in both groups. Mean arterial pressure (MAP) increased to a lesser extent in females versus males in the HUT ( P < 0.01) but increases in TPR during HUT were similar. MSNA burst frequency was lower in females versus males in supine ( P < 0.03) but increased similarly during HUT. Average amplitude/burst increased in 60° HUT for males but not females. Both males and females demonstrated an increase in MAP as well as MSNA burst frequency, mean burst amplitude, and total MSNA during the CPT. However, compared with females, males demonstrated a greater neural response (ΔTotal MSNA) due to a larger increase in mean burst amplitude ( P < 0.05). Therefore, these data point to gender-specific autonomic responses to cardiovascular stress. The different MSNA response to postural stress between genders may contribute importantly to decrements in blood pressure control during HUT in females.


Author(s):  
Joseph C. Watso ◽  
Mu Huang ◽  
Luke Belval ◽  
Frank A. Cimino III ◽  
Caitlin P. Jarrard ◽  
...  

Our knowledge about how low-dose (analgesic) fentanyl affects autonomic cardiovascular regulation is primarily limited to animal experiments. Notably, it is unknown if low-dose fentanyl influences human autonomic cardiovascular responses during painful stimuli in humans. Therefore, we tested the hypothesis that low-dose fentanyl reduces perceived pain and subsequent sympathetic and cardiovascular responses in humans during an experimental noxious stimulus. Twenty-three adults (10F/13M; 27±7 y; 26±3 kg•m-2, mean ± SD) completed this randomized, crossover, placebo-controlled trial during two laboratory visits. During each visit, participants completed a cold pressor test (CPT; hand in ~0.4 °C ice bath for two minutes) before and five minutes after drug/placebo administration (75 μg fentanyl or saline). We compared pain perception (100 mm visual analog scale), muscle sympathetic nerve activity (MSNA; microneurography, 11 paired recordings), and beat-to-beat blood pressure (BP; photoplethysmography) between trials (at both pre- and post-drug/placebo time points) using paired, two-tailed t-tests. Before drug/placebo administration, perceived pain (p=0.8287), Δ MSNA burst frequency (p=0.7587), and Δ mean BP (p=0.8649) during the CPT were not different between trials. After the drug/placebo administration, fentanyl attenuated perceived pain (36 vs. 66 mm, p<0.0001), Δ MSNA burst frequency (9 vs. 17 bursts/minute, p=0.0054), and Δ mean BP (7 vs. 13 mmHg, p=0.0174) during the CPT compared to placebo. Fentanyl-induced reductions in pain perception and Δ mean BP were moderately related (r=0.40, p=0.0641). These data provide valuable information regarding how low-dose fentanyl reduces autonomic cardiovascular responses during an experimental painful stimulus.


2020 ◽  
Vol 318 (2) ◽  
pp. R311-R319
Author(s):  
Jennifer R. Vranish ◽  
Seth W. Holwerda ◽  
Jasdeep Kaur ◽  
Paul J. Fadel

Patients with type 2 diabetes (T2D) exhibit greater daytime blood pressure (BP) variability, increasing their cardiovascular risk. Given the number of daily activities that incorporate short-duration isometric muscle contractions (e.g., carrying groceries), herein we investigated BP and muscle sympathetic nerve activity (MSNA) responses at the onset of isometric handgrip (HG). We tested the hypothesis that, relative to control subjects, patients with T2D would exhibit exaggerated pressor and MSNA responses to the immediate onset of HG. Mean arterial pressure (MAP) and MSNA were quantified during the first 30 s of isometric HG at 30% and 40% of maximal voluntary contraction (MVC) and during a cold pressor test (CPT), a nonexercise sympathoexcitatory stimulus. The onset of 30% MVC HG evoked similar increases in MAP between groups ( P = 0.17); however, the increase in MSNA was significantly greater in patients with T2D versus control subjects with the largest group difference at 20 s ( P < 0.001). At the onset of 40% MVC HG, patients with T2D demonstrated greater increases in MAP (e.g., 10 s, T2D: 9 ± 1 mmHg, controls: 5 ± 2 mmHg; P = 0.04). MSNA was also greater in patients with T2D at 40% MVC onset but differences were only significant at the 20–30 s timepoint (T2D: 15 ± 3 bursts/min, controls: −2 ± 4 bursts/min; P < 0.001). Similarly, MAP and MSNA responses were augmented during the onset of CPT in T2D patients. These findings demonstrate exaggerated pressor and MSNA reactivity in patients with T2D, with rapid and robust responses to both isometric contractions and cold stress. This hyper-responsiveness may contribute to daily surges in BP in patients with T2D, increasing their short-term and long-term cardiovascular risk.


Author(s):  
Ryosuke Takeda ◽  
Abigail S.L. Stickford ◽  
Stuart A. Best ◽  
Jeung-Ki Yoo ◽  
Yu-Lun Liu ◽  
...  

Excessive salt intake is considered a risk factor for the development of hypertension. Additionally, aberrant neuro-circulatory responses to a cold stimulus are associated with an increased risk of hypertension. This study aimed to determine whether salt loading versus salt reduction would impact hemodynamic and sympathetic neural responses during the cold pressor test (CPT) in premenopausal women with a history of normal pregnancy. Nine healthy premenopausal women [42±3 (SD) yr] were given a standardized isocaloric high salt (HS; 250 mEq sodium/day) or low salt (LS; 50 mEq sodium/day) diet for 1-week each (~2 months apart with the order randomized), while water intake was ad libitum. Laboratory testing was performed following each HS and LS period in the mid-luteal phase of the menstrual cycle. Subjects were in the supine position and beat-by-beat blood pressure (BP), heart rate (HR) and muscle sympathetic nerve activity (MSNA) were continuously measured during 1-minute baseline followed by 2-minute CPT and 3-minute recovery. BP and HR increased during the CPT (both P<0.001); the responses were similar between HS and LS. MSNA increased during the CPT, but the increment (D) was greater during HS than LS (29±6 vs. 15±4 bursts/min; P<0.001). The transduction of MSNA for vasoconstriction during the CPT was lower in HS (P<0.05). Thus, salt loading augments sympathetic neural reactivity to the cold stimulus with similar pressor responses compared to salt reduction, which may be attributed to the blunted neurovascular transduction ─ a compensatory mechanism for hemodynamic homeostasis in premenopausal women with a history of normal pregnancy.


1995 ◽  
Vol 269 (2) ◽  
pp. R406-R412 ◽  
Author(s):  
J. S. Floras

I have previously documented an inhibitory effect of atrial natriuretic factor (ANF) on postganglionic muscle sympathetic nerve activity (MSNA) in normal subjects that was consistent with either a central or ganglionic sympathoinhibitory action. To test the latter hypothesis, I examined, in seven young normotensive men, the effect of saline (as vehicle) and ANF (50 micrograms, then 50 ng.kg-1.min-1), given on 2 separate days according to a random double-blind study design, on blood pressure, heart rate, and MSNA before and after ganglionic neurotransmission was stimulated with edrophonium (ED; 12 mg iv), a rapidly reversible acetylcholinesterase inhibitor without central nervous system effects, and during subsequent augmentation of central sympathetic outflow by a cold pressor test (CPT). In five of these subjects, the protocol was replicated during nitroprusside infusion (0.4 micrograms.kg-1.min-1). ED increased MSNA during vehicle (P < 0.005) and nitroprusside (P < 0.003) but not during ANF infusion. The sympathoneural response to the combined stimuli of ED and CPT was also attenuated by ANF compared with either saline or nitroprusside infusions. Conclusions were that 1) postganglionic MSNA is increased by ED, 2) this facilitative effect of ED is attenuated by ANF, and 3) modulation of ganglionic neurotransmission is one mechanism for the relative sympatho-inhibition observed when ANF is infused at this dose.


2018 ◽  
Vol 120 (4) ◽  
pp. 1516-1524 ◽  
Author(s):  
Jeann L. Sabino-Carvalho ◽  
André L. Teixeira ◽  
Milena Samora ◽  
Maurício Daher ◽  
Lauro C. Vianna

Patients with Parkinson’s disease (PD) exhibit attenuated cardiovascular responses to exercise. The underlying mechanisms that are potentially contributing to these impairments are not fully understood. Therefore, we sought to test the hypothesis that patients with PD exhibit blunted cardiovascular responses to isolated muscle metaboreflex activation following exercise. For this, mean blood pressure, cardiac output, and total peripheral resistance were measured using finger photoplethysmography and the Modelflow method in 11 patients with PD [66 ± 2 yr; Hoehn and Yahr score: 2 ± 1 a.u.; time since diagnosis: 7 ± 1 yr; means ± SD) and 9 age-matched controls (66 ± 3 yr). Measurements were obtained at rest, during isometric handgrip exercise performed at 40% maximal voluntary contraction, and during postexercise ischemia. Also, a cold pressor test was assessed to confirm that blunted cardiovascular responses were specific to exercise and not representative of generalized sympathetic responsiveness. Changes in mean blood pressure were attenuated in patients with PD during handgrip (PD: ∆25 ± 2 mmHg vs. controls: ∆31 ± 3 mmHg; P < 0.05), and these group differences remained during postexercise ischemia (∆17 ± 1 mmHg vs. ∆26 ± 1 mmHg, respectively; P < 0.01). Additionally, changes in total peripheral resistance were attenuated during exercise and postexercise ischemia, indicating blunted reflex vasoconstriction in patients with PD. Responses to cold pressor test did not differ between groups, suggesting no group differences in generalized sympathetic responsiveness. Our results support the concept that attenuated cardiovascular responses to exercise observed in patients with PD are, at least in part, explained by an altered skeletal muscle metaboreflex. NEW & NOTEWORTHY Patients with Parkinson’s disease (PD) presented blunted cardiovascular responses to exercise. We showed that cardiovascular response evoked by the metabolic component of the exercise pressor reflex is blunted in patients with PD. Furthermore, patients with PD presented similar pressor response during the cold pressor test compared with age-matched controls. Altogether, our results support the hypothesis that attenuated cardiovascular responses to exercise observed in patients with PD are mediate by an altered skeletal muscle metaboreflex.


2020 ◽  
Vol 318 (5) ◽  
pp. H1198-H1207 ◽  
Author(s):  
Jeung-Ki Yoo ◽  
Mark B. Badrov ◽  
Mu Huang ◽  
Ryan A. Bain ◽  
Raymond P. Dorn ◽  
...  

The novel findings of the present study are that women with posttraumatic stress disorder (PTSD) have an augmented pressor response to the sympathoexcitatory stimulus of a cold pressor test (CPT) compared with healthy control subjects. Although integrated muscle sympathetic nerve activity burst responses were not significantly different between groups, total sympathetic action potential discharge in response to the CPT was markedly elevated in women with PTSD exhibiting increased firing of low-threshold axons as well as the recruitment of latent subpopulations of larger-sized axons that are otherwise silent at baseline. Aberrant autonomic circulatory control in response to sympathoexcitatory stimulus may in part explain the propensity toward developing hypertension and cardiovascular disease in this population.


Sign in / Sign up

Export Citation Format

Share Document