Sympathetic regulation of coronary circulation during handgrip exercise and isolated muscle metaboreflex activation in men

2021 ◽  
Author(s):  
Eliza Prodel ◽  
Thiago Cavalcanti ◽  
Helena N. M. Rocha ◽  
Maitê L. Gondim ◽  
Pedro A. C. Mira ◽  
...  

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Eliza Prodel ◽  
Helena Nely Miguens Rocha ◽  
Maitê Lima Gondim ◽  
Thiago Cavalcanti ◽  
Luis Felipe Olveira ◽  
...  


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Jordan B. Lee ◽  
Karam Notay ◽  
Jeremy D. Seed ◽  
Massimo Nardone ◽  
Lucas J. Omazic ◽  
...  


2014 ◽  
Vol 306 (2) ◽  
pp. H251-H260 ◽  
Author(s):  
Kazuhito Watanabe ◽  
Masashi Ichinose ◽  
Rei Tahara ◽  
Takeshi Nishiyasu

We tested the hypotheses that, in humans, changes in cardiac output (CO) and total peripheral vascular resistance (TPR) occurring in response to isometric handgrip exercise vary considerably among individuals and that those individual differences are related to differences in muscle metaboreflex and arterial baroreflex function. Thirty-nine healthy subjects performed a 1-min isometric handgrip exercise at 50% of maximal voluntary contraction. This was followed by a 4-min postexercise muscle ischemia (PEMI) period to selectively maintain activation of the muscle metaboreflex. All subjects showed increases in arterial pressure during exercise. Interindividual coefficients of variation (CVs) for the changes in CO and TPR between rest and exercise periods (CO: 95.1% and TPR: 87.8%) were more than twofold greater than CVs for changes in mean arterial pressure (39.7%). There was a negative correlation between CO and TPR responses during exercise ( r = −0.751, P < 0.01), but these CO and TPR responses correlated positively with the corresponding responses during PEMI ( r = 0.568 and 0.512, respectively, P < 0.01). The CO response during exercise did not correlate with PEMI-induced changes in an index of cardiac parasympathetic tone and cardiac baroreflex sensitivity. These findings demonstrate that the changes in CO and TPR that occur in response to isometric handgrip exercise vary considerably among individuals and that the two responses have an inverse relationship. They also suggest that individual differences in components of the pressor response are attributable in part to variations in muscle metaboreflex-mediated cardioaccelerator and vasoconstrictor responses.



Author(s):  
Byung-Sun Lee ◽  
Kyung-Ae Kim ◽  
Jong-Kyung Kim ◽  
Hosung Nho

Studies found that cardiovascular responses to exercise are enhanced in individuals with obesity and are associated with a greater cardiac output (CO) response compared to normal weight controls. However, the mechanisms underlying these altered responses during dynamic exercise are not clear. We investigated whether the cardiovascular responses mediated by the muscle metaboreflex (MMR) activation are augmented in obese men during both static and dynamic exercise. Twenty males (10 obese (OG) and 10 non-obese (NOG)) were studied. Changes in CO, mean arterial pressure (MAP), and total vascular conductance (TVC) were compared between the two groups during dynamic handgrip exercise (DHE), post-exercise muscular ischemia (PEMI), and dynamic exercise corresponding to 40%, 60% and 80% workloads. Subjects completed 2 min of DHE at 30% of MVC, followed by 2 min of PEMI. MAP, CO, and TVC responses to DHE and dynamic exercise were significantly higher in OG, whereas there were no differences during PEMI. Increases in CO and MAP during mild to heavy dynamic exercise were seen in both groups, but the changes in these variables were greater in the OG. There were no significant differences in TVC between the two groups. Compared to NOG, the augmented blood pressure response to DHE and dynamic exercise in OG was associated with a greater increase in CO. Thus, the augmented CO and MAP responses were not associated with the activation of the MMR. Consequently, additional factors specific to obesity, such as the mechanoreflex, may have been involved.



2001 ◽  
Vol 280 (3) ◽  
pp. H969-H976 ◽  
Author(s):  
Catherine F. Notarius ◽  
Deborah J. Atchison ◽  
John S. Floras

Peak oxygen uptake (V˙o 2 peak) in patients with heart failure (HF) is inversely related to muscle sympathetic nerve activity (MSNA) at rest. We hypothesized that the MSNA response to handgrip exercise is augmented in HF patients and is greatest in those with lowV˙o 2 peak. We studied 14 HF patients and 10 age-matched normal subjects during isometric [30% of maximal voluntary contraction (MVC)] and isotonic (10%, 30%, and 50% MVC) handgrip exercise that was followed by 2 min of posthandgrip ischemia (PHGI). MSNA was significantly increased during exercise in HF but not normal subjects. Both MSNA and HF levels remained significantly elevated during PHGI after 30% isometric and 50% isotonic handgrip in HF but not normal subjects. HF patients with lower V˙o 2 peak (<56% predicted; n = 8) had significantly higher MSNA during rest and exercise than patients withV˙o 2 peak > 56% predicted ( n = 6) and normal subjects. The muscle metaboreflex contributes to the greater reflex increase in MSNA during ischemic or intense nonischemic exercise in HF. This occurs at a lower threshold than normal and is a function ofV˙o 2 peak.



2001 ◽  
Vol 281 (3) ◽  
pp. H1312-H1318 ◽  
Author(s):  
C. F. Notarius ◽  
D. J. Atchison ◽  
G. A. Rongen ◽  
J. S. Floras

Adenosine (Ado) increases muscle sympathetic nerve activity (MSNA) reflexively. Plasma Ado and MSNA are elevated in heart failure (HF). We tested the hypothesis that Ado receptor blockade by caffeine would attenuate reflex MSNA responses to handgrip (HG) and posthandgrip ischemia (PHGI) and that this action would be more prominent in HF subjects than in normal subjects. We studied 12 HF subjects and 10 age-matched normal subjects after either saline or caffeine (4 mg/kg) infusion during isometric [30% of maximal voluntary contraction (MVC)] and isotonic (10%, 30%, and 50%) HG exercise, followed by 2 min of PHGI. In normal subjects, caffeine did not block increases in MSNA during PHGI after 50% HG. In HF subjects, caffeine abolished MSNA responses to PHGI after both isometric and 50% isotonic exercise ( P < 0.05) but MSNA responses during HG were unaffected. These findings are consistent with muscle metaboreflex stimulation by endogenous Ado during ischemic or intense nonischemic HG in HF and suggest an important sympathoexcitatory role for endogenous Ado during exercise in this condition.



2002 ◽  
Vol 103 (3) ◽  
pp. 295-301 ◽  
Author(s):  
Daisaku MICHIKAMI ◽  
Atsunori KAMIYA ◽  
Qi FU ◽  
Yuki NIIMI ◽  
Satoshi IWASE ◽  
...  

Although angina pectoris in patients with coronary heart disease often occurs when their forearms are in an elevated position for a prolonged period, and sympathetic activation is a major cause of this condition, little is known about the physiological effects of forearm elevation on sympathetic activity during forearm exercise. We hypothesized that forearm elevation augments sympathetic activation during the static handgrip exercise in humans. A total of 10 healthy male volunteers performed 2min of static handgrip exercise at 30% of maximal voluntary contraction followed by 2min of post-exercise muscle ischaemia (PEMI; specific activation of the muscle metaboreflex) with two forearm positions: the exercising forearm was elevated 50cm above the heart (forearm-elevated trial) or fixed at the level of the heart (heart-level trial). Muscle sympathetic nerve activity (MSNA), blood pressure and heart rate were monitored. MSNA increased during handgrip exercise in both forearm positions (P<0.001); the increase was 51% greater in the forearm-elevated trial (516±99 arbitrary units) than in the heart-level trial (346±44units; P<0.05). The increase in mean blood pressure was 8.4mmHg greater during exercise in the forearm-elevated trial (P<0.05), while changes in heart rate were similar in both forearm positions. The increase in MSNA during PEMI was 71% greater in the forearm-elevated trial (393±71 arbitrary units/min) than in the heart-level trial (229±29units/min; P<0.05). These results support the hypothesis that forearm elevation augments sympathetic activation during handgrip exercise. The excitatory effect of forearm elevation on exercising MSNA may be mediated primarily by increased activation of the muscle metaboreflex.





2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Antti M. Kiviniemi ◽  
Mikko P. Tulppo ◽  
Maria F. Frances ◽  
Maxim Rachinsky ◽  
Rosemary Craen ◽  
...  


2011 ◽  
Vol 301 (2) ◽  
pp. H609-H616 ◽  
Author(s):  
Masashi Ichinose ◽  
Stephane Delliaux ◽  
Kazuhito Watanabe ◽  
Naoto Fujii ◽  
Takeshi Nishiyasu

Hypoperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex. Our aim was to determine the muscle metaboreflex threshold and gain in humans by creating an open-loop relationship between active muscle blood flow and hemodynamic responses during a rhythmic handgrip exercise. Eleven healthy subjects performed the exercise at 5 or 15% of maximal voluntary contraction (MVC) in random order. During the exercise, forearm blood flow (FBF), which was continuously measured using Doppler ultrasound, was reduced in five steps by manipulating the inner pressure of an occlusion cuff on the upper arm. The FBF at each level was maintained for 3 min. The initial reductions in FBF elicited no hemodynamic changes, but once FBF fell below a threshold, mean arterial blood pressure (MAP) and heart rate (HR) increased and total vascular conductance (TVC) decreased in a linear manner. The threshold FBF during the 15% MVC trial was significantly higher than during the 5% MVC trial. The gain was then estimated as the slope of the relationship between the hemodynamic responses and FBFs below the threshold. The gains for the MAP and TVC responses did not differ between workloads, but the gain for the HR response was greater in the 15% MVC trial. Our findings thus indicate that increasing the workload shifts the threshold for the muscle metaboreflex to higher blood flows without changing the gain of the reflex for the MAP and TVC responses, whereas it enhances the gain for the HR response.



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