Superficial venous vascular response of the resting limb during static exercise and postexercise muscle ischemia

2013 ◽  
Vol 38 (9) ◽  
pp. 941-946 ◽  
Author(s):  
Anna Ooue ◽  
Kohei Sato ◽  
Ai Hirasawa ◽  
Tomoko Sadamoto
Keyword(s):  
Recovery Period ◽  
Arterial Occlusion ◽  
Voluntary Contraction ◽  
Superficial Vein ◽  
Vascular Response ◽  
Upper Arm ◽  
Cross Sectional ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Exercise Induced

Superficial venous vascular response to exercise is mediated sympathetically, although the mechanism is not fully understood. We examined whether sympathetic activation via muscle metaboreflex plays a role in the control of a superficial vein in the contralateral resting limb during exercise. The experimental condition involved selective stimulation of muscle metaboreceptors: 12 subjects performed static handgrip exercises at 45% maximal voluntary contraction for 1.5 min followed by a recovery period with arterial occlusion of the exercise arm (OCCL). For the control condition (CONT), the same exercise protocol was performed except that the recovery period occurred without arterial occlusion. Heart rate (HR) and mean arterial blood pressure (MAP) were measured. The cross-sectional area of the basilic superficial vein (CSAvein) and blood velocity (Vvein) in the resting upper arm were measured by ultrasound while the cuff on resting upper arm was inflated constantly to a subdiastolic pressure of 50 mm Hg. Basilic vein blood flow (BFvein) was calculated as CSAvein × Vvein. During exercise under both OCCL and CONT, HR and MAP increased (p < 0.05), while CSAvein decreased (p < 0.05). During recovery under OCCL, HR returned to baseline, but the exercise-induced increase in MAP and decrease in CSAvein were maintained (p < 0.05). During recovery under CONT, HR, MAP, and CSAvein returned to baseline. BFvein did not change during exercise or recovery under either condition. These results suggest that sympathoexcitation via muscle metaboreflex may be one of the factors responsible for exercise-induced constriction of the superficial veins per se in the resting limb.

scholarly journals Altered mechanisms of sympathetic activation during rhythmic forearm exercise in heart failure

1998 ◽  
Vol 84 (5) ◽  
pp. 1551-1559 ◽  
Author(s):  
David H. Silber ◽  
Greg Sutliff ◽  
Qing X. Yang ◽  
Michael B. Smith ◽  
Lawrence I. Sinoway ◽  
...  
Keyword(s):  
Heart Failure ◽  
Matched Control ◽  
Circulatory Arrest ◽  
Voluntary Contraction ◽  
Control Group ◽  
Resonance Spectroscopy ◽  
Muscle Metaboreflex ◽  
Separate Control ◽  
Forearm Exercise ◽  
Exercise Induced

In congestive heart failure (CHF), the mechanisms of exercise-induced sympathoexcitation are poorly defined. We compared the responses of sympathetic nerve activity directed to muscle (MSNA) and to skin (SSNA, peroneal microneurography) during rhythmic handgrip (RHG) at 25% of maximal voluntary contraction and during posthandgrip circulatory arrest (PHG-CA) in CHF patients with those of an age-matched control group. During RHG, the CHF patients fatigued prematurely. At end exercise, the increase in MSNA was similar in both groups (CHF patients, n = 12; controls, n = 10). However, during PHG-CA, in the controls MSNA returned to baseline, whereas it remained elevated in CHF patients ( P < 0.05). Similarly, at end exercise, the increase in SSNA was comparable in both groups (CHF patients, n = 11; controls, n = 12), whereas SSNA remained elevated during PHG-CA in CHF patients but not in the controls ( P < 0.05). In a separate control group ( n = 6), even high-intensity static handgrip was not accompanied by sustained elevation of SSNA during PHG-CA. 31P-nuclear magnetic resonance spectroscopy during RHG demonstrated significant muscle acidosis and accumulation of inorganic phosphate in CHF patients ( n = 7) but not in controls ( n = 9). We conclude that in CHF patients rhythmic forearm exercise leads to premature fatigue and accumulation of muscle metabolites. The prominent PHG-CA response of MSNA and SSNA in CHF patients suggests activation of the muscle metaboreflex. Because, in contrast to controls, in CHF patients both MSNA and SSNA appear to be under muscle metaboreflex control, the mechanisms and distribution of sympathetic outflow during exercise appear to be different from normal.

scholarly journals Autonomic nervous system properties in migraine patients and nonmedication treatment in headache free period

2010 ◽  
Vol 64 (5-6) ◽  
pp. 209-214
Author(s):  
Daina Voita ◽  
Evita Vaļēviča ◽  
Anastasija Zakke ◽  
Juris Porozovs ◽  
Anda Kauliņa
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Recovery Period ◽  
Arterial Occlusion ◽  
Control Group ◽  
Training Methods ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
System Properties ◽  
And Gender

Autonomic nervous system properties in migraine patients and nonmedication treatment in headache free period The aim of the study was to characterise parameters of the autonomic nervous system in migraineurs and to find out and to adapt the optimal biofeedback (BFB) training methods. Heart rate (HR), arterial blood pressure and baroreflex sensitivity (BRS) at rest, static workload, arterial occlusion and during recovery period were measured. 22 migraineurs (female, average age 22.2 ± 2.4 years) and 14 healthy age and gender matched controls participated. Migraine patients were divided into two groups (M1 and M2) according to HR and BRS at rest. At rest 60% of migraine patients (group M1) had significantly decreased HR vs. control group (P< 0.01). The M2 group showed a tendency to decreased BRS at rest comparing to the control group and significantly (P< 0.01) differed in this parameter from the M1 group. In a 10 s precontraction period M1 group had a significantly lower HR increase comparing to other analysed groups (P< 0.01). HR was significantly decreased in the M1 group during the recovery period comparing to the control and M2 groups (P< 0.05). Both parts of autonomic nervous system, PNS and SNS branches, were impaired in migraineurs. The M2 group had most likely decreased PNS activity and impaired SNS activity. M1 group patients showed increased PNS activity. BFB training sessions reduced migraine attack frequency and need for medication in the M2 group.

scholarly journals Brain tissue acid-base changes during ischemia

1997 ◽  
Vol 2 (5) ◽  
pp. E5 ◽  
Author(s):  
William E. Hoffman ◽  
Fady T. Charbel ◽  
Guy Edelman ◽  
James I. Ausman
Keyword(s):  
Brain Tissue ◽  
Brain Temperature ◽  
Recovery Period ◽  
Arterial Occlusion ◽  
Extracellular Acidosis ◽  
Arterial Blood ◽  
Minute Period ◽  
Temporary Occlusion ◽  
Baseline Levels ◽  
Cerebrovascular Surgery

It is likely that brain tissue acidosis during ischemia is associated with neuronal injury. The authors measured brain extracellular H+, PCO2 and HCO3- concentrations during an ischemic event produced by temporary occlusion of the middle or anterior cerebral arterial distributions, with a 10-minute recovery period. Patients who were to undergo craniotomy for cerebrovascular surgery were recruited for the study. A probe that measures PCO2, pH, and temperature was inserted into tissue at risk for ischemia during temporary arterial occlusion. As a control for this treatment, PaCO2 was increased 10 mm Hg in five patients over a 10-minute period. Under baseline conditions, there was no difference in arterial blood pressure, blood gas levels, or brain temperature between patients who underwent temporary arterial occlusion or those in whom hypercapnia was induced. In patients in whom hypercapnia was induced, H+, PCO2, and HCO3- concentrations increased and all values returned to baseline levels within 10 minutes. In 10 patients who underwent a median 9-minute arterial occlusion, transient ischemia was seen with an increase in tissue H+ and PCO2 levels of 100% and 60%, respectively, and a 20% decrease in HCO3-levels. After a 10-minute postischemic recovery, only PCO2 had returned to baseline levels. These results are consistent with a rapid equilibration of lactic acidosis across the cell membrane during ischemia which decreases HCO3- concentration. After ischemia, extracellular acidosis may be prolonged because of the extrusion of H+ from the cell by membrane ion exchange.

scholarly journals Transfer function characteristics of the neural and peripheral arterial baroreflex arcs at rest and during postexercise muscle ischemia in humans

2009 ◽  
Vol 296 (5) ◽  
pp. H1416-H1424 ◽  
Author(s):  
Shigehiko Ogoh ◽  
James P. Fisher ◽  
Colin N. Young ◽  
Peter B. Raven ◽  
Paul J. Fadel
Keyword(s):  
Transfer Function ◽  
Muscle Sympathetic Nerve Activity ◽  
Voluntary Contraction ◽  
Arterial Baroreflex ◽  
Isometric Handgrip ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Muscle Ischemia ◽  
Transfer Function Gain

Previous studies have demonstrated an increase in the arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) during isolated activation of the muscle metaboreflex with postexercise muscle ischemia (PEMI). However, the increased ABR-MSNA control does not appear to manifest in an enhancement in the ABR control of arterial blood pressure (BP), suggesting alterations in the transduction of MSNA into a peripheral vascular response and a subsequent ABR-mediated change in BP. Thus we examined the operating gains of the neural and peripheral arcs of the ABR and their interactive relationship at rest and during muscle metaboreflex activation. In nine healthy subjects, graded isolation of the muscle metaboreflex was achieved by PEMI following isometric handgrip performed at 15% and 30% maximal voluntary contraction (MVC). To obtain the sensitivities of the ABR neural and peripheral arcs, the transfer function gain from BP to MSNA and MSNA to femoral vascular conductance, respectively, was analyzed. No changes from rest were observed in the ABR neural or peripheral arcs during PEMI after 15% MVC handgrip. However, PEMI following 30% MVC handgrip increased the low frequency (LF) transfer function gain between BP and MSNA (ABR neural arc; +58 ± 28%, P = 0.036), whereas the LF gain between MSNA and femoral vascular conductance (ABR peripheral arc) was decreased from rest (−36 ± 8%, P = 0.017). These findings suggest that during high-intensity muscle metaboreflex activation an increased ABR gain of the neural arc appears to offset an attenuation of the peripheral arc gain to help maintain the overall ABR control of systemic BP.

scholarly journals Augmented pressor and sympathetic responses to skeletal muscle metaboreflex activation in type 2 diabetes patients

2016 ◽  
Vol 310 (2) ◽  
pp. H300-H309 ◽  
Author(s):  
Seth W. Holwerda ◽  
Robert M. Restaino ◽  
Camila Manrique ◽  
Guido Lastra ◽  
James P. Fisher ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Neural Mechanism ◽  
Voluntary Contraction ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Sympathetic Responses

Previous studies have reported exaggerated increases in arterial blood pressure during exercise in type 2 diabetes (T2D) patients. However, little is known regarding the underlying neural mechanism(s) involved. We hypothesized that T2D patients would exhibit an augmented muscle metaboreflex activation and this contributes to greater pressor and sympathetic responses during exercise. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were measured in 16 patients with T2D (8 normotensive and 8 hypertensive) and 10 healthy controls. Graded isolation of the muscle metaboreflex was achieved by postexercise ischemia (PEI) following static handgrip performed at 30% and 40% maximal voluntary contraction (MVC). A cold pressor test (CPT) was also performed as a generalized sympathoexcitatory stimulus. Increases in MAP and MSNA during 30 and 40% MVC handgrip were augmented in T2D patients compared with controls ( P < 0.05), and these differences were maintained during PEI (MAP: 30% MVC PEI: T2D, Δ16 ± 2 mmHg vs. controls, Δ8 ± 1 mmHg; 40% MVC PEI: T2D, Δ26 ± 3 mmHg vs. controls, Δ16 ± 2 mmHg, both P < 0.05). MAP and MSNA responses to handgrip and PEI were not different between normotensive and hypertensive T2D patients ( P > 0.05). Interestingly, MSNA responses were also greater in T2D patients compared with controls during the CPT ( P < 0.05). Collectively, these findings indicate that muscle metaboreflex activation is augmented in T2D patients and this contributes, in part, to augmented pressor and sympathetic responses to exercise in this patient group. Greater CPT responses suggest that a heightened central sympathetic reactivity may be involved.

Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

2005 ◽  
Vol 288 (4) ◽  
pp. H1532-H1538 ◽  
Author(s):  
Masashi Ichinose ◽  
Takeshi Nishiyasu
Keyword(s):  
Dynamic Effect ◽  
Voluntary Contraction ◽  
Dynamic Responses ◽  
Arterial Baroreflex ◽  
Peripheral Vascular ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Neck Pressure

We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflex [as reflected by alterations in the dynamic responses shown by leg blood flow (LBF: by the ultrasound Doppler method), leg vascular conductance (LVC), mean arterial blood pressure (MAP), and heart rate (HR)] in humans. In 12 healthy subjects (10 men and 2 women), who performed sustained 1-min handgrip exercise at 50% maximal voluntary contraction followed immediately by an imposed postexercise muscle ischemia (PEMI), 5-s periods of neck pressure (NP; 50 mmHg) or neck suction (NS; −60 mmHg) were used to evaluate carotid baroreflex function both at rest (Con) and during PEMI. First, the decreases in LVC and LBF and the augmentation of MAP elicited by NP were all greater during PEMI than in Con (ΔLVC, −1.2 ± 0.2 vs. −1.9 ± 0.2 ml·min−1·mmHg−1; ΔLBF, −97.3 ± 11.2 vs. −177.0 ± 21.8 ml/min; ΔMAP, 6.7 ± 1.2 vs. 11.5 ± 1.4 mmHg, Con vs. PEMI; each P < 0.05). Second, in Con, NS significantly increased both LVC and LBF (ΔLVC, 0.9 ± 0.2 ml·min−1·mmHg−1; ΔLBF, 46.6 ± 9.8 ml/min; significant change from baseline: each P < 0.05), and, whereas during PEMI no significant increases in LVC and LBF occurred during NS itself (ΔLVC, 0.2 ± 0.1 ml·min−1·mmHg−1; ΔLBF, 10.8 ± 9.6 ml/min; each P > 0.05), a decrease was evident in each parameters at 5 s after the cessation of NS. Third, during PEMI, the decrease in MAP elicited by NS was smaller (ΔMAP, −8.4 ± 1.0 vs. −5.8 ± 0.4 mmHg, Con vs. PEMI; P < 0.05), and it recovered to its initial level more quickly after NS (vs. Con). Finally, however, the HR responses to NS and NP were not different between PEMI and Con. These results suggest that during muscle metaboreflex activation in humans, the arterial baroreflex dynamic effect on peripheral vascular conductance is modulated, as exemplified by 1) an augmentation of the NP-induced LVC decrease, and 2) a loss of the NS-induced LVC increase.

Effect of Whole-Body Periodic Acceleration on Exercise-Induced Muscle Damage after Eccentric Exercise

2014 ◽  
Vol 9 (6) ◽  
pp. 985-992 ◽  
Author(s):  
Daniel H. Serravite ◽  
Arlette Perry ◽  
Kevin A. Jacobs ◽  
Jose A. Adams ◽  
Kysha Harriell ◽  
...  
Keyword(s):  
Muscle Damage ◽  
Eccentric Exercise ◽  
Recovery Period ◽  
Voluntary Contraction ◽  
The Body ◽  
Whole Body ◽  
Protein Carbonyls ◽  
Control Group ◽  
Periodic Acceleration ◽  
Exercise Induced

Purpose:To examine the effects of whole-body periodic acceleration (pGz) on exercise-induced-muscle-damage (EIMD) -related symptoms induced by unaccustomed eccentric arm exercise.Methods:Seventeen active young men (23.4 ± 4.6 y) made 6 visits to the research facility over a 2-wk period. On day 1, subjects performed a 1-repetition-maximum (1RM) elbowflexion test and were randomly assigned to the pGz (n = 8) or control group (n = 9). Criterion measurements were taken on day 2, before and immediately after performance of the eccentric-exercise protocol (10 sets, 10 repetitions using 120% 1RM) and after the recovery period. During subsequent sessions (24, 48, 72, and 96 h) these data were collected before pGz or passive recovery. Measurements included isometric strength (maximal voluntary contraction [MVC]), blood markers (creatine kinase, myoglobin, IL-6, TNF-α, TBARS, PGF2α, protein carbonyls, uric acid, and nitrites), soreness, pain, circumference, and range of motion (ROM).Results:Significantly higher MVC values were seen for pGz throughout the recovery period. Within-group differences were seen in myoglobin, IL-6, IL-10, protein carbonyls, soreness, pain, circumference, and ROM showing small negative responses and rapid recovery for the pGz condition.Conclusion:Our results demonstrate that pGz can be an effective tool for the reduction of EIMD and may contribute to the training-adaptation cycle by speeding up the recovery of the body due to its performance-loss-lessening effect.

Evaluation of muscle metaboreflex function through graded reduction in forearm blood flow during rhythmic handgrip exercise in humans

2011 ◽  
Vol 301 (2) ◽  
pp. H609-H616 ◽  
Author(s):  
Masashi Ichinose ◽  
Stephane Delliaux ◽  
Kazuhito Watanabe ◽  
Naoto Fujii ◽  
Takeshi Nishiyasu
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Pressor Response ◽  
Muscle Blood Flow ◽  
Voluntary Contraction ◽  
Open Loop ◽  
Handgrip Exercise ◽  
Hemodynamic Responses ◽  
Muscle Metaboreflex ◽  
Arterial Blood

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.

Muscle cooling delays activation of the muscle metaboreflex in humans

1997 ◽  
Vol 273 (5) ◽  
pp. H2436-H2441 ◽  
Author(s):  
Chester A. Ray ◽  
Keith M. Hume ◽  
Kathryn H. Gracey ◽  
Edward T. Mahoney
Keyword(s):  
Heart Rate ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Voluntary Contraction ◽  
Muscle Temperature ◽  
Isometric Handgrip ◽  
Local Cooling ◽  
Muscle Metaboreflex ◽  
Muscle Cooling ◽  
Exercise Induced

Elevation of muscle temperature has been shown to increase muscle sympathetic nerve activity (MSNA) during isometric exercise in humans. The purpose of the present study was to evaluate the effect of muscle cooling on MSNA responses during exercise. Eight subjects performed ischemic isometric handgrip at 30% of maximal voluntary contraction to fatigue followed by 2 min of postexercise muscle ischemia (PEMI), with and without local cooling of the forearm. Local cooling of the forearm decreased forearm muscle temperature from 31.8 ± 0.4 to 23.1 ± 0.8°C ( P = 0.001). Time to fatigue was not different during the control and cold trials (156 ± 11 and 154 ± 5 s, respectively). Arterial pressures and heart rate were not significantly affected by muscle cooling during exercise, although heart rate tended to be higher during the second minute of exercise ( P = 0.053) during muscle cooling. Exercise-induced increases in MSNA were delayed during handgrip with local cooling compared with control. However, MSNA responses at fatigue and PEMI were not different between the two conditions. These findings suggest that muscle cooling delayed the activation of the muscle metaboreflex during ischemic isometric exercise but did not prevent its full expression during fatiguing contraction. These results support the concept that muscle temperature can play a role in the regulation of MSNA during exercise.

Ischemic exercise and the muscle metaboreflex

2000 ◽  
Vol 89 (4) ◽  
pp. 1432-1436 ◽  
Author(s):  
Jacob A. Cornett ◽  
Michael D. Herr ◽  
Kristen S. Gray ◽  
Michael B. Smith ◽  
Qing X. Yang ◽  
...  
Keyword(s):  
Maximum Voluntary Contraction ◽  
Random Order ◽  
Muscle Afferents ◽  
Voluntary Contraction ◽  
The Other ◽  
Reflex Response ◽  
Handgrip Exercise ◽  
Muscle Metaboreflex ◽  
Effort Level ◽  
Arterial Blood

In exercising muscle, interstitial metabolites accumulate and stimulate muscle afferents. This evokes the muscle metaboreflex and raises arterial blood pressure (BP). In this report, we examined the effects of tension generation on muscle metabolites and BP during ischemic forearm exercise in humans. Heart rate (HR), BP, Pi, H2PO4 −, and pH (31P-NMR spectroscopy) data were collected in 10 normal healthy men (age 23 ± 1 yr) during rhythmic handgrip exercise. After baseline measurements, the subjects performed rhythmic handgrip for 2 min. At 2 min, a 250-mmHg occlusion cuff was inflated, and ischemic handgrip exercise was continued until near fatigue (Borg 19). Measurements were continued for an additional 30 s of ischemia. This protocol was performed at 15, 30, 45, and 60% of the subjects' maximum voluntary contraction (MVC) in random order. As tension increased, the time to fatigue decreased. In addition, mean arterial pressure and HR were higher at 60% MVC than at any of the other lower tensions. The NMR data showed significantly greater increases in H2PO4 −, Pi, and H+at 60% than at 15 and 30% MVC. Therefore, despite the subjects working to the same perceived effort level, a greater reflex response (represented by BP and HR data) was elicited at 60% MVC than at any of the other ischemic tensions. These data are consistent with the hypothesis that, as tension increases, factors aside from insufficient blood flow contribute to the work effect on muscle metabolites and the magnitude of the reflex response.

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