scholarly journals High-Intensity Interval Training Decreases Muscle Sympathetic Nerve Activity in Men With Essential Hypertension and in Normotensive Controls

2020 ◽  
Vol 14 ◽  
Author(s):  
Thomas Svare Ehlers ◽  
Yrsa Sverrisdottir ◽  
Jens Bangsbo ◽  
Thomas Petursson Gunnarsson
Keyword(s):  
Essential Hypertension ◽  
Sympathetic Nerve ◽  
High Intensity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
Nerve Activity ◽  
High Intensity Interval

scholarly journals The Role of Central Command in the Increase in Muscle Sympathetic Nerve Activity to Contracting Muscle During High Intensity Isometric Exercise

2021 ◽  
Vol 15 ◽  
Author(s):  
Daniel Boulton ◽  
Chloe E. Taylor ◽  
Simon Green ◽  
Vaughan G. Macefield
Keyword(s):  
Sympathetic Nerve ◽  
High Intensity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Dependent Manner ◽  
Nerve Activity ◽  
Contracting Muscle ◽  
Tungsten Microelectrode ◽  
The Right

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.

Muscle pump-induced inhibition of sympathetic vasomotor outflow during low-intensity leg cycling is attenuated by muscle metaboreflex activation

2020 ◽  
Vol 128 (1) ◽  
pp. 1-7
Author(s):  
Keisho Katayama ◽  
Thales C. Barbosa ◽  
Jasdeep Kaur ◽  
Benjamin E. Young ◽  
Damsara Nandadeva ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
High Intensity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Muscle Metaboreflex ◽  
Muscle Pump ◽  
Low Intensity ◽  
Leg Cycling ◽  
Cardiopulmonary Baroreflex

Muscle sympathetic nerve activity (MSNA) decreases during leg cycling at low intensity because of muscle pump-induced increases in venous return and loading of the cardiopulmonary baroreceptors. However, MSNA increases during leg cycling when exercise is above moderate intensity or for a long duration, suggesting that the sympathoinhibitory effect of the cardiopulmonary baroreflex can be overridden by a powerful sympathoexcitatory drive, such as the skeletal muscle metaboreflex. Therefore, we tested the hypothesis that high-intensity muscle metaboreflex activation attenuates muscle pump-induced inhibition of MSNA during leg cycling. MSNA (left radial nerve) was recorded during graded isolation of the muscle metaboreflex in the forearm with postexercise ischemia (PEI) after low (PEI-L)- and high (PEI-H)-intensity isometric handgrip exercise (20% and 40% maximum voluntary contraction, respectively). Leg cycling (15–20 W) was performed alone and during each PEI trial (PEI-L+Cycling, PEI-H+Cycling). Cycling alone induced a significant decrease in MSNA burst frequency (BF) and total activity (TA). MSNA BF and TA also decreased when cycling was performed during PEI-L. However, the magnitude of decrease in MSNA during PEI-L+Cycling [∆BF: –19 ± 2% ( P < 0.001), ∆TA: –25 ± 4% ( P < 0.001); mean ± SE] was less than that during cycling alone [∆BF: –39 ± 5% ( P = 0.003), ∆TA: –45 ± 5% ( P = 0.002)]. More importantly, MSNA did not decrease during cycling with PEI-H [∆BF: –1 ± 2% ( P = 0.845), ∆TA: +2 ± 3% ( P = 0.959)]. These results suggest that muscle pump-induced inhibition of sympathetic vasomotor outflow during low-intensity leg cycling is attenuated by muscle metaboreflex activation in an intensity-dependent manner. NEW & NOTEWORTHY There are no available data concerning the interaction between the sympathoinhibitory effect of muscle pump-induced cardiopulmonary baroreflex loading during leg cycling and the sympathoexcitatory influence of the muscle metaboreflex. In this study, muscle metaboreflex activation attenuated the inhibition of muscle sympathetic nerve activity (MSNA) during leg cycling. This may explain, in part, the response of MSNA to graded-intensity dynamic exercise in which low-intensity leg cycling inhibits MSNA whereas high-intensity exercise elicits graded sympathoexcitation.

Impaired baroreflex changes in muscle sympathetic nerve activity in adolescents who have a family history of essential hypertension

1988 ◽  
Vol 6 (4) ◽  
pp. S525-528 ◽  
Author(s):  
Yutaka Yamada ◽  
Eiji Miyajima ◽  
Osamu Tochikubo ◽  
Toshiyoshi Matsukawa ◽  
Hiroshi Shionoiri ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Family History ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
History Of

Effects of expiratory muscle work on muscle sympathetic nerve activity

2002 ◽  
Vol 92 (4) ◽  
pp. 1539-1552 ◽  
Author(s):  
P. Alexander Derchak ◽  
A. William Sheel ◽  
Barbara J. Morgan ◽  
Jerome A. Dempsey
Keyword(s):  
Sympathetic Nerve ◽  
High Intensity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Motor Output ◽  
Time Dependent ◽  
Nerve Activity ◽  
Task Failure ◽  
Expiratory Muscle ◽  
Expiratory Muscles

We hypothesized that contractions of the expiratory muscles carried out to the point of task failure would cause an increase in muscle sympathetic nerve activity (MSNA). We measured MSNA directly in six healthy men during resisted expiration (60% maximal expiratory pressure) leading to task failure with long [breathing frequency (fb) = 15 breaths/min; expiratory time (Te)/total respiratory cycle duration (Tt) = 0.7] and short (fb = 30 breaths/min; Te/Tt = 0.4) Te. Both of these types of expiratory muscle contractions elicited time-dependent increases in MSNA burst frequency that averaged +139 and +239%, respectively, above baseline at end exercise. The increased MSNA coincided with increases in mean arterial pressure (MAP) for both the long-Te (+28 ± 6 mmHg) and short-Te (+22 ± 14 mmHg) trials. Neither MSNA nor MAP changed when the breathing patterns and increased tidal volume of the task failure trials were mimicked without resistance or task failure. Furthermore, very high levels of expiratory motor output (95% maximal expiratory pressure; fb = 12 breaths/min; Te/Tt = 0.35) and high rates of expiratory flow and expiratory muscle shortening without task failure (no resistance; fb = 45 breaths/min; Te/Tt = 0.4; tidal volume = 1.9 × eupnea) had no effect on MSNA or MAP. Within-breath analysis of the short-expiration trials showed augmented MSNA at the onset of and throughout expiration that was consistent with an influence of high levels of central expiratory motor output. Thus high-intensity contractions of expiratory muscles to the point of task failure caused a time-dependent sympathoexcitation; these effects on MSNA were similar in their time dependency to those caused by high-intensity rhythmic contractions of the diaphragm and forearm muscles taken to the point of task failure. The evidence suggests that these effects are mediated primarily via a muscle metaboreflex with a minor, variable contribution from augmented central expiratory motor output.

Reduced baroreflex changes in muscle sympathetic nerve activity during blood pressure elevation in essential hypertension

1991 ◽  
Vol 9 (6) ◽  
pp. 537-542 ◽  
Author(s):  
Toshiyoshi Matsukawa ◽  
Eiji Gotoh ◽  
Osamu Hasegawa ◽  
Hiroshi Shionoiri ◽  
Osamu Tochikubo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Blood Pressure Elevation ◽  
Pressure Elevation

scholarly journals Altered respiratory related bursting of muscle sympathetic nerve activity in humans with essential hypertension

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
James P Fisher ◽  
David B McIntyre ◽  
William B Farquhar ◽  
Anthony E Pickering ◽  
Gregory Y H Lip ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity
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