Cardiopulmonary reflexes do not modulate exercise pressor reflexes during isometric exercise in humans

1993 ◽  
Vol 74 (5) ◽  
pp. 2559-2565 ◽  
Author(s):  
J. A. Arrowood ◽  
P. K. Mohanty ◽  
C. McNamara ◽  
M. D. Thames
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Isometric Exercise ◽  
Lower Body ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Pressor Reflexes ◽  
The Relationship ◽  
Exercise In Humans

Previous studies that measured reflex vasoconstrictor responses during isometric exercise have suggested that these responses were modulated by arterial and cardiopulmonary baroreflexes. The purpose of these experiments was to determine forearm vasoconstrictor responses to isometric handgrip alone and during two levels of cardiopulmonary baroreceptor unloading with lower body negative pressure (-5 and -10 mmHg LBNP). Handgrip combined with -5 mmHg LBNP produced vasoconstrictor responses that were significantly greater than the algebraic sum of the separate responses to handgrip and LBNP alone, thus confirming earlier studies. However, with -10 mmHg LBNP, the vasoconstrictor responses to LBNP plus handgrip were not different from the algebraic sum of the separate response to LBNP and handgrip alone. These results indicate that when the influence of cardiac baroreceptors was reduced to a greater degree (-10 mmHg LBNP) than in previous studies, no interaction was observed, whereas with less reduction (-5 mmHg LBNP) an apparent interaction was noted. These data, together with recent studies in which sympathetic nerve activity to the lower leg was measured during similar protocols, suggest nonlinearities in the relationship between sympathetic nerve activity and vasoconstrictor responses.

Modulation of control of muscle sympathetic nerve activity during orthostatic stress in humans

2004 ◽  
Vol 287 (5) ◽  
pp. H2147-H2153 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Takeshi Ogawa ◽  
Keiji Hayashi ◽  
Narihiko Kondo ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
Orthostatic Stress ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Burst Strength

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.

Time-dependent modulation of arterial baroreflex control of muscle sympathetic nerve activity during isometric exercise in humans

2006 ◽  
Vol 290 (4) ◽  
pp. H1419-H1426 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Time Dependent ◽  
Operating Pressure ◽  
Dependent Manner ◽  
Arterial Baroreflex ◽  
Isometric Handgrip ◽  
Nerve Activity

We investigated the time-dependent modulation of arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) that occurs during isometric handgrip exercise (IHG). Thirteen healthy subjects performed a 3-min IHG at 30% maximal voluntary contraction, which was followed by a period of imposed postexercise muscle ischemia (PEMI). The ABR control of MSNA (burst incidence and strength and total activity) was evaluated by analyzing the relationship between spontaneous variations in diastolic arterial pressure (DAP) and MSNA during supine rest, at each minute of IHG, and during PEMI. We found that 1) the linear relations between DAP and MSNA variables were shifted progressively rightward until the third minute of IHG (IHG3); 2) 2 min into IHG (IHG2), the DAP-MSNA relations were shifted upward and were shifted further upward at IHG3; 3) the sensitivity of the ABR control of total MSNA was increased at IHG2 and increased further at IHG3; and 4) during PEMI, the ABR operating pressure was slightly higher than at IHG2, and the sensitivity of the control of total MSNA was the same as at IHG2. During PEMI, the DAP-burst strength and DAP-total MSNA relations were shifted downward from the IHG3 level to the IHG2 level, whereas the DAP-burst incidence relation remained at the IHG3 level. These results indicate that during IHG, ABR control of MSNA is modulated in a time-dependent manner. We suggest that this modulation of ABR function is one of the mechanisms underlying the progressive increase in blood pressure and MSNA during the course of isometric exercise.

scholarly journals Microneurography and sympathetic nerve activity: a decade-by-decade journey across 50 years

2019 ◽  
Vol 121 (4) ◽  
pp. 1183-1194 ◽  
Author(s):  
Jason R. Carter
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
The Past ◽  
Thomson Reuters ◽  
The Impact

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.

Effect of morphine on sympathetic nerve activity in humans

2002 ◽  
Vol 93 (5) ◽  
pp. 1764-1769 ◽  
Author(s):  
Jason R. Carter ◽  
Charity L. Sauder ◽  
Chester A. Ray
Keyword(s):  
Opioid Receptor ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Cardiovascular Responses ◽  
Endogenous Opioids ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Trial Drug

There are conflicting reports for the role of endogenous opioids on sympathetic and cardiovascular responses to exercise in humans. A number of studies have utilized naloxone (an opioid-receptor antagonist) to investigate the effect of opioids during exercise. In the present study, we examined the effect of morphine (an opioid-receptor agonist) on sympathetic and cardiovascular responses at rest and during isometric handgrip (IHG). Eleven subjects performed 2 min of IHG (30% maximum) followed by 2 min of postexercise muscle ischemia (PEMI) before and after systemic infusion of morphine (0.075 mg/kg loading dose + 1 mg/h maintenance) or placebo (saline) in double-blinded experiments on separate days. Morphine increased resting muscle sympathetic nerve activity (MSNA; 17 ± 2 to 22 ± 2 bursts/min; P < 0.01) and increased mean arterial pressure (MAP; 87 ± 2 to 91 ± 2 mmHg; P < 0.02), but it decreased heart rate (HR; 61 ± 4 to 59 ± 3; P < 0.01). However, IHG elicited similar increases for MSNA, MAP, and HR between the control and morphine trial (drug × exercise interaction = not significant). Moreover, responses to PEMI were not different. Placebo had no effect on resting, IHG, and PEMI responses. We conclude that morphine modulates cardiovascular and sympathetic responses at rest but not during isometric exercise.

scholarly journals Muscle sympathetic nerve activity during intense lower body negative pressure to presyncope in humans

2009 ◽  
Vol 587 (20) ◽  
pp. 4987-4999 ◽  
Author(s):  
William H. Cooke ◽  
Caroline A. Rickards ◽  
Kathy L. Ryan ◽  
Tom A. Kuusela ◽  
Victor A. Convertino
Keyword(s):  
Negative Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Lower Body ◽  
Nerve Activity

Baroreflex modulation of muscle sympathetic nerve activity during posthandgrip muscle ischemia in humans

2001 ◽  
Vol 91 (4) ◽  
pp. 1679-1686 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Manabu Shibasaki ◽  
Nicole A. Hodges ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Muscle Ischemia ◽  
The Relationship

To identify whether muscle metaboreceptor stimulation alters baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA, beat-by-beat arterial blood pressure (Finapres), and electrocardiogram were recorded in 11 healthy subjects in the supine position. Subjects performed 2 min of isometric handgrip exercise at 40% of maximal voluntary contraction followed by 2.5 min of posthandgrip muscle ischemia. During muscle ischemia, blood pressure was lowered and then raised by intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure was more negative ( P < 0.001) during posthandgrip muscle ischemia (−201.9 ± 20.4 units · beat−1 · mmHg−1) when compared with control conditions (−142.7 ± 17.3 units · beat−1 · mmHg−1). No significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. However, both curves shifted during postexercise ischemia to accommodate the elevation in blood pressure and MSNA that occurs with this condition. These data suggest that the sensitivity of baroreflex modulation of MSNA is elevated by muscle metaboreceptor stimulation, whereas the sensitivity of baroreflex of modulate heart rate is unchanged during posthandgrip muscle ischemia.

Effects of graded LBNP on MSNA and interstitial norepinephrine

2002 ◽  
Vol 283 (5) ◽  
pp. H2038-H2044 ◽  
Author(s):  
Mazhar H. Khan ◽  
Lawrence I. Sinoway ◽  
David A. MacLean
Keyword(s):  
Nervous System ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Vastus Lateralis ◽  
Muscle Sympathetic Nerve Activity ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Nerve Activity ◽  
Sympathetic Nervous ◽  
The Relationship

Exposure to lower body negative pressure (LBNP) leads to an increased activation of the sympathetic nervous system (SNS) and an increase in muscle sympathetic nerve activity (MSNA). In this study, we examined the relationship between MSNA and interstitial norepinephrine (NEi) concentrations during LBNP. Twelve healthy volunteers were studied (26 ± 6 yr). Simultaneous MSNA and microdialysis data were collected in six of these subjects. Measurements of MSNA (microneurography) and NEi (microdialysis, vastus lateralis) were performed at rest and then during an incremental LBNP paradigm (−10, −30, and −50 mmHg). MSNA rose as a function of LBNP ( P < 0.001, n = 12). The plasma norepinephrine (NEp) concentration was 0.9 ± 0.1 nmol/l at rest ( n = 12). NEi measured in six subjects rose from 5.2 ± 0.8 nmol/l at rest to 17.0 ± 1.7 nmol/l at −50 mmHg ( P < 0.001). Of note, the rise in NEp with LBNP was considerably less compared with the changes in NEi (Δ21 ± 6% vs. Δ197 ± 52%, n = 6, P < 0.015). MSNA and NEi showed a significant linear relationship ( r = 0.721, P < 0.004). Activation of the SNS increased MSNA and NEi levels. The magnitude of the NEi increase was far greater than that seen for NEp suggesting that NE movement into the circulation decreases with baroreceptor unloading.

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