Enhanced corticospinal excitability with physiologically heightened sympathetic nerve activity

2013 ◽  
Vol 114 (4) ◽  
pp. 429-435 ◽  
Author(s):  
Vasiliy E. Buharin ◽  
Andrew J. Butler ◽  
Justin K. Rajendra ◽  
Minoru Shinohara

Corticospinal excitability is modulated differently with norepinephrine and dopamine agonists, although both monoamines are released with heightened sympathetic nerve activity. The purpose of this study was to investigate the influence of physiological heightening of sympathetic nerve activity on corticospinal excitability in healthy humans. Subjects were divided into control and experimental groups. In each participant, motor-evoked potentials (MEPs) were measured from the resting first dorsal interosseous muscle of the right hand with transcranial magnetic stimulation (TMS) in two trials separated by 1 h. In the experimental group, sympathetic nerve activity was physiologically heightened during the second trial by applying lower body negative pressure (LBNP). In the control group, sympathetic nerve activity was not altered between the two trials. MEP peak-to-peak amplitude increased from trial 1 to trial 2 in the experimental group only. This increase was evident at a TMS intensity of 130% resting motor threshold and higher. It was concluded that physiological heightening of sympathetic nerve activity with LBNP enhances corticospinal excitability.

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.


2002 ◽  
Vol 282 (6) ◽  
pp. H2210-H2215 ◽  
Author(s):  
Mazhar H. Khan ◽  
Allen R. Kunselman ◽  
Urs A. Leuenberger ◽  
William R. Davidson ◽  
Chester A. Ray ◽  
...  

Bed rest reduces orthostatic tolerance. Despite decades of study, the cause of this phenomenon remains unclear. In this report we examined hemodynamic and sympathetic nerve responses to graded lower body negative pressure (LBNP) before and after 24 h of bed rest. LBNP allows for baroreceptor disengagement in a graded fashion. We measured heart rate (HR), cardiac output (HR × stroke volume obtained by echo Doppler), and muscle sympathetic nerve activity (MSNA) during a progressive and graded LBNP paradigm. Negative pressure was increased by 10 mmHg every 3 min until presyncope or completion of −60 mmHg. After bed rest, LBNP tolerance was reduced in 11 of 13 subjects ( P < .023), HR was greater ( P< .002), cardiac output was unchanged, and the ability to augment MSNA at high levels of LBNP was reduced (rate of rise for 30- to 60-mmHg LBNP before bed rest 0.073 bursts · min−1 · mmHg−1; after bed rest 0.035 bursts · min−1 · mmHg−1; P < 0.016). These findings suggest that 24 h of bed rest reduces sympathetic nerve responses to LBNP.


2004 ◽  
Vol 287 (5) ◽  
pp. H2147-H2153 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Takeshi Ogawa ◽  
Keiji Hayashi ◽  
Narihiko Kondo ◽  
...  

We tested the hypothesis that orthostatic stress would modulate the arterial baroreflex (ABR)-mediated beat-by-beat control of muscle sympathetic nerve activity (MSNA) in humans. In 12 healthy subjects, ABR control of MSNA (burst incidence, burst strength, and total activity) was evaluated by analysis of the relation between beat-by-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (CON) and at two levels of lower body negative pressure (LBNP: −15 and −35 mmHg). At −15 mmHg LBNP, the relation between burst incidence (bursts per 100 heartbeats) and DAP showed an upward shift from that observed during CON, but the further shift seen at −35 mmHg LBNP was only marginal. The relation between burst strength and DAP was shifted upward at −15 mmHg LBNP (vs. CON) and further shifted upward at −35 mmHg LBNP. At −15 mmHg LBNP, the relation between total activity and DAP was shifted upward from that obtained during CON and further shifted upward at −35 mmHg LBNP. These results suggest that ABR control of MSNA is modulated during orthostatic stress and that the modulation is different between a mild (nonhypotensive) and a moderate (hypotensive) level of orthostatic stress.


2011 ◽  
Vol 110 (2) ◽  
pp. 352-358 ◽  
Author(s):  
Peizhen Zhang ◽  
Guoyuan Huang ◽  
Xiangrong Shi

Sympathetic nerve activity influences cerebral blood flow, but it is unknown whether augmented sympathetic nerve activity resets cerebral vasoreactivity to hypercapnia. This study tested the hypothesis that cerebral vasodilation during hypercapnia is restrained by lower-body negative pressure (LBNP)-stimulated sympathoexcitation. Cerebral hemodynamic responses were assessed in nine healthy volunteers [age 25 yr (SD 3)] during rebreathing-induced increases in partial pressure of end-tidal CO2 (PetCO2) at rest and during LBNP. Cerebral hemodynamic responses were determined by changes in flow velocity of middle cerebral artery (MCAV) using transcranial Doppler sonography and in regional cerebral tissue oxygenation (ScO2) using near-infrared spectroscopy. PetCO2 values during rebreathing were similarly increased from 41.9 to 56.5 mmHg at rest and from 40.7 to 56.0 mmHg during LBNP of −15 Torr. However, the rates of increases in MCAV and in ScO2 per unit increase in PetCO2 (i.e., the slopes of MCAV/PetCO2 and ScO2/PetCO2) were significantly ( P ≤0.05) decreased from 2.62 ± 0.16 cm·s−1·mmHg−1 and 0.89 ± 0.10%/mmHg at rest to 1.68 ± 0.18 cm·s−1·mmHg−1 and 0.63 ± 0.07%/mmHg during LBNP. In conclusion, the sensitivity of cerebral vasoreactivity to hypercapnia, in terms of the rate of increases in MCAV and in ScO2, is diminished by LBNP-stimulated sympathoexcitation.


Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 9 ◽  
Author(s):  
Kazuaki Ohara ◽  
Akane Misaizu ◽  
Yuji Kaneko ◽  
Takafumi Fukuda ◽  
Mika Miyake ◽  
...  

Hops, the immature inflorescences of the female hop plant (Humulus lupulus L.) are one of the main components of beer and provides flavor and bitterness. β-Eudesmol, an oxygenated sesquiterpene, is reported to accumulate in a particular hop cultivar. Recently, we revealed that β-Eudesmol ingestion affected autonomic nerve activity in an animal model. The effect on humans has not been elucidated, therefore, we investigated the effects of β-Eudesmol on reducing objective and subjective markers related to sympathetic nerve activity after the application of mental stress in healthy participants. Fifty participants (male and female aged 20 to 50 years) were randomly assigned to two groups. Five minutes before taking the Trier Social Stress Test (TSST) as a mental stressor, participants in each group ingested a beverage containing β-Eudesmol, the active beverage, or a placebo beverage that did not contain β-Eudesmol. Saliva 3-methoxy-4-hydroxyphenylglycol (MHPG), a major product of noradrenaline breakdown and a representative marker of sympathetic nerve activity, was significantly lower just after the TSST in the active group compared with the placebo group. Saliva cortisol, a marker of the endocrine stress response system, was not significantly different between the two groups. No adverse events related to test beverage ingestion were observed. This is the first experimental evidence of β-Eudesmol effect for mental stress in human.


2019 ◽  
Vol 121 (4) ◽  
pp. 1183-1194 ◽  
Author(s):  
Jason R. Carter

The technique of microneurography has advanced the field of neuroscience for the past 50 years. While there have been a number of reviews on microneurography, this paper takes an objective approach to exploring the impact of microneurography studies. Briefly, Web of Science (Thomson Reuters) was used to identify the highest citation articles over the past 50 years, and key findings are presented in a decade-by-decade highlight. This includes the establishment of microneurography in the 1960s, the acceleration of the technique by Gunnar Wallin in the 1970s, the international collaborations of the 1980s and 1990s, and finally the highest impact studies from 2000 to present. This journey through 50 years of microneurographic research related to peripheral sympathetic nerve activity includes a historical context for several of the laboratory interventions commonly used today (e.g., cold pressor test, mental stress, lower body negative pressure, isometric handgrip, etc.) and how these interventions and experimental approaches have advanced our knowledge of cardiovascular, cardiometabolic, and other human diseases and conditions.


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