Gender does not influence sympathetic neural reactivity to stress in healthy humans

1996 ◽  
Vol 270 (1) ◽  
pp. H350-H357 ◽  
Author(s):  
P. P. Jones ◽  
M. Spraul ◽  
K. S. Matt ◽  
D. R. Seals ◽  
J. S. Skinner ◽  
...  

Previous data support the idea of heightened sympathetically mediated cardiovascular reactivity in males. However, definitive conclusions cannot be made because of inconsistent reports, possibly stemming from imprecise measurement of sympathetic activity and/or failure to equate the stress stimuli between genders. The present study tested the hypothesis that males exhibit heightened sympathetic reactivity that is associated with heightened cardiovascular and plasma catecholamine responses. In 37 healthy adults (20 males, 17 females: age = 20-42 yr), direct recordings of skeletal muscle sympathetic nerve activity (MSNA), plasma catecholamines, heart rate, blood pressure, and perceived stress were measured before and during three laboratory stressors (isometric handgrip, cold pressor, and mental arithmetic). MSNA, catecholamine, and cardiovascular reactivity (defined as change from rest) were not consistently different between genders. For the isometric handgrip, when expressed as absolute unit changes, males had larger MSNA responses (P < 0.01), which were partially explained by greater contraction force; they did not differ in terms of percent change from baseline or in perceived stress. The responses to the cold pressor and mental arithmetic tasks were similar between genders. These findings indicate that stress-evoked vasoconstrictor neural excitation and the associated increases in blood pressure are not consistently influenced by gender.

2004 ◽  
Vol 13 (5) ◽  
pp. 287-294 ◽  
Author(s):  
Henrik Reims ◽  
Knut Sevre ◽  
Eigil Fossum ◽  
Aud Høieggen ◽  
Ivar Eide ◽  
...  

1985 ◽  
Vol 69 (3) ◽  
pp. 365-368 ◽  
Author(s):  
Pierre-Marc Bouloux ◽  
Ashley Grossman ◽  
Saad Al-Damluji ◽  
Timothy Bailey ◽  
Michael Besser

1. The effects of naloxone (8 mg) on the pressor and plasma catecholamine response to a standard cold-pressor test have been evaluated in six normal male subjects. Plasma catecholamines were estimated by high performance liquid chromatography coupled to electrochemical detection. 2. Cold stimulation induced significant elevations in plasma noradrenaline and adrenaline to reach mean peak levels 61% and 108% above their respective basal levels (P < 0.05). Systolic blood pressure increased by 23 ± 6.5 mmHg (P < 0.001), and heart rate increased by 7.5 ± 2.5 beats/min (P < 0.001). 3. Naloxone pretreatment significantly enhanced the plasma adrenaline response to the cold stimulus by 98% (P < 0.01) with concomitant changes in peak systolic blood pressure (peak increment 31 ± 6 mmHg) and pulse rate (12.5 ± 3.5 beats/min) responses (both P < 0.05). The mean plasma noradrenaline response to cold also increased after naloxone, but this failed to achieve significance. 4. Endogenous opioids are likely to be involved in the sympathoadrenal response to a mild acute stress in man.


2008 ◽  
Vol 294 (2) ◽  
pp. R458-R466 ◽  
Author(s):  
Jian Cui ◽  
Vernon Mascarenhas ◽  
Raman Moradkhan ◽  
Cheryl Blaha ◽  
Lawrence I. Sinoway

Based on animal studies, it has been speculated that muscle metabolites sensitize muscle mechanoreceptors and increase mechanoreceptor-mediated muscle sympathetic nerve activity (MSNA). However, this hypothesis has not been directly tested in humans. In this study, we tested the hypothesis that in healthy individuals passive stretch of forearm muscles would evoke significant increases in mean MSNA when muscle metabolite concentrations were increased. In 12 young healthy subjects, MSNA, ECG, and blood pressure were recorded. Subjects performed static fatiguing isometric handgrip at 30% maximum voluntary contraction followed by 4 min of postexercise muscle ischemia (PEMI). After 2 min of PEMI, wrist extension (i.e., wrist dorsiflexion) was performed. The static stretch protocol was also performed during 1) a freely perfused condition, 2) ischemia alone, and 3) PEMI after nonfatiguing exercise. Finally, repetitive short bouts of wrist extension were also performed under freely perfused conditions. This last paradigm evoked transient increases in MSNA but had no significant effect on mean MSNA over the whole protocol. During the PEMI after fatiguing handgrip, static stretch induced significant increases in MSNA (552 ± 74 to 673 ± 90 U/min, P < 0.01) and mean blood pressure (102 ± 2 to 106 ± 2 mmHg, P < 0.001). Static stretch performed under the other three conditions had no significant effects on mean MSNA and blood pressure. The present data verified that in healthy humans mechanoreceptor(s) stimulation evokes significant increases in mean MSNA and blood pressure when muscle metabolite concentrations are increased above a certain threshold.


2010 ◽  
Vol 299 (3) ◽  
pp. H925-H931 ◽  
Author(s):  
G. S. Gilmartin ◽  
M. Lynch ◽  
R. Tamisier ◽  
J. W. Weiss

Chronic intermittent hypoxia (CIH) is thought to be responsible for the cardiovascular disease associated with obstructive sleep apnea (OSA). Increased sympathetic activation, altered vascular function, and inflammation are all putative mechanisms. We recently reported (Tamisier R, Gilmartin GS, Launois SH, Pepin JL, Nespoulet H, Thomas RJ, Levy P, Weiss JW. J Appl Physiol 107: 17–24, 2009) a new model of CIH in healthy humans that is associated with both increases in blood pressure and augmented peripheral chemosensitivity. We tested the hypothesis that exposure to CIH would also result in augmented muscle sympathetic nerve activity (MSNA) and altered vascular reactivity contributing to blood pressure elevation. We therefore exposed healthy subjects between the ages of 20 and 34 yr ( n = 7) to 9 h of nocturnal intermittent hypoxia for 28 consecutive nights. Cardiovascular and hemodynamic variables were recorded at three time points; MSNA was collected before and after exposure. Diastolic blood pressure (71 ± 1.3 vs. 74 ± 1.7 mmHg, P < 0.01), MSNA [9.94 ± 2.0 to 14.63 ± 1.5 bursts/min ( P < 0.05); 16.89 ± 3.2 to 26.97 ± 3.3 bursts/100 heartbeats (hb) ( P = 0.01)], and forearm vascular resistance (FVR) (35.3 ± 5.8 vs. 55.3 ± 6.5 mmHg·ml−1·min·100 g tissue, P = 0.01) all increased significantly after 4 wk of exposure. Forearm blood flow response following ischemia of 15 min (reactive hyperemia) fell below baseline values after 4 wk, following an initial increase after 2 wk of exposure. From these results we conclude that the increased blood pressure following prolonged exposure to CIH in healthy humans is associated with sympathetic activation and augmented FVR.


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Mildred A. Pointer ◽  
Sadiqa Yancey ◽  
Ranim Abou-Chacra ◽  
Patricia Petrusi ◽  
Sandra J. Waters ◽  
...  

Although several studies have shown that enhanced cardiovascular reactivity can predict hypertension development in African Americans, these findings have not been consistent among all studies examining reactivity and hypertension susceptibility. This inconsistency may be explained by the influence of anxiety (state and trait) on the blood pressure response to stress. Therefore, this study sought to determine whether anxiety is associated with blood pressure response to cold pressor (CP) and anger recall (AR) stress tests in young healthy African Americans. Modeling using state and trait anxiety revealed that state anxiety predicts systolic (SBP) and diastolic blood pressure DBP response to CP and AR (P≤0.02). Interestingly, state anxiety predicted heart rate changes only to CP (P<0.01;P=0.3for AR). Although trait anxiety was associated with SBP response to AR and not CP, it was not a significant predictor of reactivity in our models. We conclude that anxiety levels may contribute to the variable blood pressure response to acute stressors and, therefore, should be assessed when performing cardiovascular reactivity measures.


2007 ◽  
Vol 103 (3) ◽  
pp. 835-842 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Cynthia S. Hogeman ◽  
Sadeq Quraishi ◽  
Latoya Linton-Frazier ◽  
Kristen S. Gray

Short-term intermittent hypoxia leads to sustained sympathetic activation and a small increase in blood pressure in healthy humans. Because obstructive sleep apnea, a condition associated with intermittent hypoxia, is accompanied by elevated sympathetic activity and enhanced sympathetic chemoreflex responses to acute hypoxia, we sought to determine whether intermittent hypoxia also enhances chemoreflex activity in healthy humans. To this end, we measured the responses of muscle sympathetic nerve activity (MSNA, peroneal microneurography) to arterial chemoreflex stimulation and deactivation before and following exposure to a paradigm of repetitive hypoxic apnea (20 s/min for 30 min; O2 saturation nadir 81.4 ± 0.9%). Compared with baseline, repetitive hypoxic apnea increased MSNA from 113 ± 11 to 159 ± 21 units/min ( P = 0.001) and mean blood pressure from 92.1 ± 2.9 to 95.5 ± 2.9 mmHg ( P = 0.01; n = 19). Furthermore, compared with before, following intermittent hypoxia the MSNA (units/min) responses to acute hypoxia [fraction of inspired O2 (FiO2) 0.1, for 5 min] were enhanced (pre- vs. post-intermittent hypoxia: +16 ± 4 vs. +49 ± 10%; P = 0.02; n = 11), whereas the responses to hyperoxia (FiO2 0.5, for 5 min) were not changed significantly ( P = NS; n = 8). Thus 30 min of intermittent hypoxia is capable of increasing sympathetic activity and sensitizing the sympathetic reflex responses to hypoxia in normal humans. Enhanced sympathetic chemoreflex activity induced by intermittent hypoxia may contribute to altered neurocirculatory control and adverse cardiovascular consequences in sleep apnea.


2010 ◽  
Vol 299 (1) ◽  
pp. R80-R91 ◽  
Author(s):  
Lindsay D. DeBeck ◽  
Stewart R. Petersen ◽  
Kelvin E. Jones ◽  
Michael K. Stickland

Previous research has suggested a relationship between low-frequency power of heart rate variability (HRV; LF in normalized units, LFnu) and muscle sympathetic nerve activity (MSNA). However, investigations have not systematically controlled for breathing, which can modulate both HRV and MSNA. Accordingly, the aims of this experiment were to investigate the possibility of parallel responses in MSNA and HRV (LFnu) to selected acute stressors and the effect of controlled breathing. After data were obtained at rest, 12 healthy males (28 ± 5 yr) performed isometric handgrip exercise (30% maximal voluntary contraction) and the cold pressor test in random order, and were then exposed to hypoxia (inspired fraction of O2 = 0.105) for 7 min, during randomly assigned spontaneous and controlled breathing conditions (20 breaths/min, constant tidal volume, isocapnic). MSNA was recorded from the peroneal nerve, whereas HRV was calculated from ECG. At rest, controlled breathing did not alter MSNA but decreased LFnu ( P < 0.05 for all) relative to spontaneous breathing. MSNA increased in response to all stressors regardless of breathing. LFnu increased with exercise during both breathing conditions. During cold pressor, LFnu decreased when breathing was spontaneous, whereas in the controlled breathing condition, LFnu was unchanged from baseline. Hypoxia elicited increases in LFnu when breathing was controlled, but not during spontaneous breathing. The parallel changes observed during exercise and controlled breathing during hypoxia suggest that LFnu may be an indication of sympathetic outflow in select conditions. However, since MSNA and LFnu did not change in parallel with all stressors, a cautious approach to the use of LFnu as a marker of sympathetic activity is warranted.


1992 ◽  
Vol 70 (1) ◽  
pp. 36-42 ◽  
Author(s):  
J. K. McLean ◽  
P. Sathasivam ◽  
K. MacNaughton ◽  
T. E. Graham

Two types of cold pressor tests were used to study gender differences in cardiovascular and plasma catecholamine responses. Ten male and ten female, young, healthy Caucasian subjects participated. The tests consisted of (1) 5 °C air blown at 3.5–4 m/s onto part of the face for 4 min and (2) the open right hand immersed to the wrist in water at 5 °C for 4 min. Heart rate, blood pressure (BP), and venous plasma norepinephrine were collected before, during, and 5 min after the 4 min of cold exposures. Test order was decided by a Latin square design, and the subjects rested in a quiet room for 30 min between the two tests. All parameters demonstrated significant (p < 0.01) increases from rest during the cold tests. Gender differences were significant (p < 0.01) in diastolic and systolic BP in each test with the males having a greater response, but gender differences were not found in heart rate or norepinephrine concentration. The study demonstrated that gender differences exist in the blood pressure responses to local cold, but that the mechanisms involved do not include a parallel difference in heart rate or venous plasma norepinephrine concentration.Key words: blood pressure, gender differences, stroke volume.


Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Jody L Greaney ◽  
Evan L Matthews ◽  
Paul J Fadel ◽  
William B Farquhar ◽  
Megan M Wenner

Understanding the neural circulatory responses to exercise in postmenopausal women (PMW) is important given their greater risk for developing hypertension. During exercise, blood pressure is controlled, in part, by the exercise pressor reflex, which is a feedback mechanism originating in skeletal muscle and compromised of mechanically and metabolically sensitive afferents. A recent study reported an enhanced blood pressure response during exercise in normotensive PMW due to greater muscle metaboreflex activation, but the mechanism(s) underlying these responses are unknown. Herein, we tested the hypothesis that metaboreflex activation elicits exaggerated sympathetic nervous system responses in PMW compared to young women, contributing to the enhanced blood pressure response during exercise. Methods: Blood pressure (BP, Finometer) and muscle sympathetic nerve activity (MSNA, peroneal microneurography) were continuously measured in 7 PMW (age 59±2 years; BMI 24±1 kg/m 2 ) and 7 young women (age 23±2 years; BMI 22±2 kg/m 2 ) during 2-minutes of isometric handgrip exercise performed at 30% of maximal voluntary contraction followed by 3-minutes of forearm ischemia (post-exercise ischemia, PEI) to isolate muscle metaboreflex activation. Results: Resting mean arterial pressure (MAP) was similar between PMW (85±3 mmHg) and young women (82±2 mmHg; P>0.05). During exercise, the increase in MAP was greater in PMW (Δ18±2mmHg) compared to young women (Δ 12±2 mmHg; P<0.05), and this was maintained during PEI (Δ13±1 mmHg PMW vs. Δ 6±1 mmHg young women; P<0.05). Resting MSNA was higher in PMW (24±4 bursts/min) compared to young women (9±3 bursts/min; P<0.05). Interestingly, the increase in MSNA during exercise was comparable between groups (P>0.05), whereas during PEI, the increase in MSNA was approximately 50% greater in PMW compared to young women (Δ13±2 burst/min PMW vs. 7±2 bursts/min young women; P<0.05). Conclusions: These preliminary data suggest that compared to young women, PMW exhibit an exaggerated MSNA response to isolated muscle metaboreflex activation.


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