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.

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.

Modulation of sympathetic nerve activity during posthandgrip muscle ischemia in humans

1994 ◽  
Vol 266 (1) ◽  
pp. H79-H83 ◽  
Author(s):  
C. A. Ray ◽  
N. H. Secher ◽  
A. L. Mark
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sensory Nerve ◽  
Vascular Occlusion ◽  
Voluntary Contraction ◽  
Central Command ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Muscle Ischemia

To evaluate modulation of muscle sympathetic nerve activity (MSNA) during posthandgrip muscle ischemia (PHGMI), subjects performed 2 min of isometric handgrip at 33% of maximal voluntary contraction (MVC) followed by 2 min of PHGMI produced by forearm vascular occlusion. The response to PHGMI was studied in the absence and again during the addition of contralateral rhythmic handgrip (RHG; 40 times/min) at 15% (n = 6) and 30% (n = 10) MVC during the second minute of the PHGMI. Additionally, to isolate the effect of central command, response to PHGMI was studied during attempted RHG after sensory nerve blockade (n = 5). RHG for 2 min at 15 and 30% MVC and attempted RHG for 2 min did not increase MSNA. Isometric handgrip elicited an 130 +/- 48% increase in MSNA (P < 0.05), which was maintained during PHGMI. RHG at 15 and 30% MVC elicited an attenuation of MSNA (-10 +/- 7% and -14 +/- 6%, respectively) when performed during the second minute of PHGMI (P < 0.05). In contrast, attempted RHG did not significantly affect MSNA during PHGMI. The findings demonstrate modulation of MSNA during activation of the muscle metaboreflex. The attenuation of metaboreceptor-mediated increases in MSNA appear to be the result of mechanosensitive muscle afferents and not central command.

scholarly journals Interindividual variability in muscle sympathetic responses to static handgrip in young men: evidence for sympathetic responder types?

2018 ◽  
Vol 314 (1) ◽  
pp. R114-R121 ◽  
Author(s):  
Anthony V. Incognito ◽  
Connor J. Doherty ◽  
Jordan B. Lee ◽  
Matthew J. Burns ◽  
Philip J. Millar
Keyword(s):  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Interindividual Variability ◽  
Muscle Sympathetic Nerve Activity ◽  
Voluntary Contraction ◽  
Response Patterns ◽  
Arterial Baroreflex ◽  
Muscle Metaboreflex ◽  
Time To Peak ◽  
Pressure Time

Negative and positive muscle sympathetic nerve activity (MSNA) responders have been observed during mental stress. We hypothesized that similar MSNA response patterns could be identified during the first minute of static handgrip and contribute to the interindividual variability throughout exercise. Supine measurements of multiunit MSNA (microneurography) and continuous blood pressure (Finometer) were recorded in 29 young healthy men during the first (HG1) and second (HG2) minute of static handgrip (30% maximal voluntary contraction) and subsequent postexercise circulatory occlusion (PECO). Responders were identified on the basis of differences from the typical error of baseline total MSNA: 7 negative, 12 positive, and 10 nonresponse patterns. Positive responders demonstrated larger total MSNA responses during HG1 ( P < 0.01) and HG2 ( P < 0.0001); however, the increases in blood pressure throughout handgrip exercise were similar between all groups, as were the changes in heart rate, stroke volume, cardiac output, total vascular conductance, and respiration (all P > 0.05). Comparing negative and positive responders, total MSNA responses were similar during PECO ( P = 0.17) but opposite from HG2 to PECO (∆40 ± 46 vs. ∆-21 ± 62%, P = 0.04). Negative responders also had a shorter time-to-peak diastolic blood pressure during HG1 (20 ± 20 vs. 44 ± 14 s, P < 0.001). Total MSNA responses during HG1 were associated with responses to PECO ( r = 0.39, P < 0.05), the change from HG2 to PECO ( r = −0.49, P < 0.01), and diastolic blood pressure time to peak ( r = 0.50, P < 0.01). Overall, MSNA response patterns during the first minute of static handgrip contribute to interindividual variability and appear to be influenced by differences in central command, muscle metaboreflex activation, and rate of loading of the arterial baroreflex.

Abstract 266: Neural Circulatory Responses to Isolated Muscle Metaboreflex Activation in Postmenopausal Women

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Jody L Greaney ◽  
Evan L Matthews ◽  
Paul J Fadel ◽  
William B Farquhar ◽  
Megan M Wenner
Keyword(s):  
Blood Pressure ◽  
Postmenopausal Women ◽  
Young Women ◽  
Blood Pressure Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Feedback Mechanism ◽  
Voluntary Contraction ◽  
Pressure Response ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex

Understanding the neural circulatory responses to exercise in postmenopausal women (PMW) is important given their greater risk for developing hypertension. During exercise, blood pressure is controlled, in part, by the exercise pressor reflex, which is a feedback mechanism originating in skeletal muscle and compromised of mechanically and metabolically sensitive afferents. A recent study reported an enhanced blood pressure response during exercise in normotensive PMW due to greater muscle metaboreflex activation, but the mechanism(s) underlying these responses are unknown. Herein, we tested the hypothesis that metaboreflex activation elicits exaggerated sympathetic nervous system responses in PMW compared to young women, contributing to the enhanced blood pressure response during exercise. Methods: Blood pressure (BP, Finometer) and muscle sympathetic nerve activity (MSNA, peroneal microneurography) were continuously measured in 7 PMW (age 59±2 years; BMI 24±1 kg/m 2 ) and 7 young women (age 23±2 years; BMI 22±2 kg/m 2 ) during 2-minutes of isometric handgrip exercise performed at 30% of maximal voluntary contraction followed by 3-minutes of forearm ischemia (post-exercise ischemia, PEI) to isolate muscle metaboreflex activation. Results: Resting mean arterial pressure (MAP) was similar between PMW (85±3 mmHg) and young women (82±2 mmHg; P>0.05). During exercise, the increase in MAP was greater in PMW (Δ18±2mmHg) compared to young women (Δ 12±2 mmHg; P<0.05), and this was maintained during PEI (Δ13±1 mmHg PMW vs. Δ 6±1 mmHg young women; P<0.05). Resting MSNA was higher in PMW (24±4 bursts/min) compared to young women (9±3 bursts/min; P<0.05). Interestingly, the increase in MSNA during exercise was comparable between groups (P>0.05), whereas during PEI, the increase in MSNA was approximately 50% greater in PMW compared to young women (Δ13±2 burst/min PMW vs. 7±2 bursts/min young women; P<0.05). Conclusions: These preliminary data suggest that compared to young women, PMW exhibit an exaggerated MSNA response to isolated muscle metaboreflex activation.

Modulation of the spontaneous beat-to-beat fluctuations in peripheral vascular resistance during activation of muscle metaboreflex

2007 ◽  
Vol 293 (1) ◽  
pp. H416-H424 ◽  
Author(s):  
Masashi Ichinose ◽  
Shunsaku Koga ◽  
Naoto Fujii ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Transfer Function ◽  
Vascular Resistance ◽  
High Frequency ◽  
Low Frequency ◽  
Regulatory Mechanisms ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Vascular Regulation ◽  
Arterial Blood ◽  
Transfer Function Analysis

Continuous measurement of leg blood flow (LBF) using Doppler ultrasound with simultaneous noninvasive mean arterial blood pressure (MAP) measurement permits beat-to-beat estimates of leg vascular resistance (LVR) in humans. We tested the hypothesis that the beat-to-beat fluctuations in LVR and the dynamic relationship between MAP and LVR are modulated by the activation of muscle metaboreflex. Twelve healthy subjects performed a 1-min isometric handgrip exercise at 50% maximal voluntary contraction, which was followed by a period of imposed postexercise muscle ischemia (PEMI). We then employed transfer function analysis to examine the dynamic relationships between MAP and LBF and between MAP and LVR, both at rest (control) and during PEMI. We found the following. 1) The spectral power for LBF and LVR in low-frequency (∼0.03–0.15 Hz) range significantly increased from control during PEMI without a significant change in the high-frequency (∼0.15–0.35 Hz) power. 2) During PEMI, the transfer function gains for MAP-LBF and MAP-LVR relationships in the low-frequency (∼0.05–0.15 Hz) range were significantly increased during PEMI (vs. control) but were unchanged in the high-frequency (∼0.2–0.3 Hz) range. 3) The phases for MAP-LBF and MAP-LVR relationships were not different during control and PEMI. The phase for MAP-LVR relationship revealed that changes in MAP were followed by directionally similar changes in LVR, which is consistent with the characteristics of intrinsic vascular regulatory mechanisms such as the myogenic response of the resistance arteries. We suggest that, in humans, modulation of the dynamic MAP-LVR relationship during activation of the muscle metaboreflex reflects complex interactions between intrinsic vascular regulatory mechanisms and sympathetic vascular regulation.

Muscle metaboreflex activation speeds the recovery of arterial blood pressure following acute hypotension in humans

2013 ◽  
Vol 304 (11) ◽  
pp. H1568-H1575 ◽  
Author(s):  
Masashi Ichinose ◽  
Kazuhito Watanabe ◽  
Naoto Fujii ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Maximum Voluntary Contraction ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Arterial Blood ◽  
Acute Hypotension

It has been suggested that the arterial baroreflex and muscle metaboreflex are both activated during heavy exercise and that they interact to modulate primary cardiovascular reflex responses. This proposed interaction and its consequences are not fully understood, however. The purpose of present study was to test our hypothesis that dynamic arterial baroreflex-mediated cardiovascular responses to acute systemic hypotension in humans are augmented when the muscle metaboreflex is active and that this results in a faster recovery of arterial blood pressure. Acute hypotension was induced nonpharmacologically in 12 healthy subjects by releasing bilateral thigh cuffs after 9 min of suprasystolic resting ischemia, with and without muscle metaboreflex activation via postexercise muscle ischemia (PEMI) after 1 min of isometric handgrip exercise at 50% maximum voluntary contraction. The thigh-cuff release evoked rapid reductions in mean arterial pressure (MAP) and increases in heart rate, cardiac output (Doppler), and total vascular conductance (TVC) under control conditions and during PEMI. The reductions in MAP from baseline were greater and the increases in TVC were smaller during PEMI than control. In addition, arterial baroreflex-mediated peripheral vasoconstriction was augmented during PEMI, as evidenced by a near doubling of the rate of recovery of MAP and TVC. These results show that when the muscle metaboreflex is activated in humans, arterial baroreflex-mediated peripheral vasoconstriction elicited in response to acute hypotension is augmented, which halves the time needed for MAP recovery. Such modulation of baroreflex function would be advantageous for maintaining an elevated arterial blood pressure during activation of the muscle metaboreflex.

Pressor responses to isometric biting are evoked by somatosensory receptors in periodontal tissue in humans

2009 ◽  
Vol 107 (2) ◽  
pp. 531-539 ◽  
Author(s):  
Yoshiyuki Okada ◽  
Yoshi-ichiro Kamijo ◽  
Kazunobu Okazaki ◽  
Shizue Masuki ◽  
Masaki Goto ◽  
...  
Keyword(s):  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Voluntary Contraction ◽  
Periodontal Tissue ◽  
Arterial Baroreflex ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Pressor Responses ◽  
Cutaneous Vascular Conductance

Jaw muscle contraction, such as mastication and biting (BT), is known to evoke pressor responses. We examined whether the responses were evoked by somatosensory receptors in periodontal tissue and, moreover, whether they were accompanied by altered arterial baroreflex sensitivity. In the first experiment, we measured mean arterial pressure, heart rate, and muscle sympathetic nerve activity from the peroneal nerve during 2-min isometric BT at 50% maximal voluntary contraction before [control (CNT)] and after pharmacological alveolar nerve block (BLK) in eight young men, while monitoring finger cutaneous vascular conductance, gingival vascular conductance (GVC), surface electromyogram of masseter muscle, and BT force. In the second experiment, cardiac and sympathetic baroreflex sensitivities were successfully determined in eight and five of the subjects, respectively, by the modified Oxford method during 5-min BT at 30% maximal voluntary contraction and also during resting without BT in CNT and BLK, respectively. In the first experiment, although BT in CNT and BLK significantly increased mean arterial pressure, heart rate, and total muscle sympathetic nerve activity (burst amplitude × burst incidence), and decreased finger cutaneous vascular conductance and GVC ( P < 0.05), all changes except GVC were markedly attenuated in BLK ( P < 0.05). There were no significant differences in integrated electromyogram and BT force among any trials. In the second experiment, although BT in CNT significantly decreased cardiac and sympathetic baroreflex sensitivities (both, P < 0.05), these changes disappeared in BLK. These results suggest that somatosensory receptors in periodontal tissue were involved in pressor responses to isometric BT, which was accompanied by decreased arterial baroreflex sensitivity.

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.

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.

Isometric handgrip training reduces arterial pressure at rest without changes in sympathetic nerve activity

2000 ◽  
Vol 279 (1) ◽  
pp. H245-H249 ◽  
Author(s):  
Chester A. Ray ◽  
Dario I. Carrasco
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Muscle Ischemia

The purpose of this study was to determine whether isometric handgrip (IHG) training reduces arterial pressure and whether reductions in muscle sympathetic nerve activity (MSNA) mediate this drop in arterial pressure. Normotensive subjects were assigned to training ( n = 9), sham training ( n = 7), or control ( n = 8) groups. The training protocol consisted of four 3-min bouts of IHG exercise at 30% of maximal voluntary contraction (MVC) separated by 5-min rest periods. Training was performed four times per week for 5 wk. Subjects' resting arterial pressure and heart rate were measured three times on 3 consecutive days before and after training, with resting MSNA (peroneal nerve) recorded on the third day. Additionally, subjects performed IHG exercise at 30% of MVC to fatigue followed by muscle ischemia. In the trained group, resting diastolic (67 ± 1 to 62 ± 1 mmHg) and mean arterial pressure (86 ± 1 to 82 ± 1 mmHg) significantly decreased, whereas systolic arterial pressure (116 ± 3 to 113 ± 2 mmHg), heart rate (67 ± 4 to 66 ± 4 beats/min), and MSNA (14 ± 2 to 15 ± 2 bursts/min) did not significantly change following training. MSNA and cardiovascular responses to exercise and postexercise muscle ischemia were unchanged by training. There were no significant changes in any variables for the sham training and control groups. The results indicate that IHG training is an effective nonpharmacological intervention in lowering arterial pressure.

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