Interaction between the muscle metaboreflex and the arterial baroreflex in control of arterial pressure and skeletal muscle blood flow

Kaur, Jasdeep; Álvarez, Alberto; Hanna, Hanna W.; Krishnan, Abhinav C.; Senador, Danielle; Machado, Tiago M.; Altamimi, Yasir H.; Lovelace, Abe T.; Dombrowski, M.; Spranger, Marty D.; O’Leary, Donal S.

doi:10.1152/ajpheart.00501.2016

Cited by 24 publications

(24 citation statements)

References 39 publications

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“…While studies examining interactions between the EPR and the baroreflex (Kaur et al 2016;Hureau et al 2018) and between the CR and the baroreflex (Katayama et al 2014(Katayama et al , 2016 have revealed interactive influences on the circulatory response to exercise, investigations on the haemodynamic consequences of the EPR:CR interaction are scarce and rather indirect. McCoy and colleagues (1987) found the EPR-evoked increases in blood pressure to inhibit the discharge of aortic chemoreceptors in anaesthetised cats.…”

Section: Introductionmentioning

confidence: 99%

The exercise pressor reflex and chemoreflex interaction: cardiovascular implications for the exercising human

Wan

Weavil

Thurston

et al. 2020

The Journal of Physiology

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Key points Although the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcitatory effect, the cardiovascular implication of their interaction remains elusive. We quantified the individual and interactive cardiovascular consequences of these reflexes during exercise and revealed various modes of interaction. The EPR and hypoxia‐induced CR interaction is hyper‐additive for blood pressure and heart rate (responses during co‐activation of the two reflexes are greater than the summation of the responses evoked by each reflex) and hypo‐additive for peripheral haemodynamics (responses during co‐activation of the reflexes are smaller than the summated responses). The EPR and hypercapnia‐induced CR interaction results in a simple addition of the individual responses to each reflex (i.e. additive interaction). Collectively, EPR:CR co‐activation results in significant cardiovascular interactions with restriction in peripheral haemodynamics, resulting from the EPR:CR interaction in hypoxia, likely having the most crucial impact on the functional capacity of an exercising human. Abstract We investigated the interactive effect of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exercise. Eleven healthy participants (5 females) completed a total of six bouts of single‐leg knee‐extension exercise (60% peak work rate, 4 min each) either with or without lumbar intrathecal fentanyl to attenuate group III/IV afferent feedback from lower limbs to modify the EPR, while breathing either ambient air, normocapnic hypoxia (SaO2 ∼79%, PaO2 ∼43 mmHg, PaCO2 ∼33 mmHg, pH ∼7.39), or normoxic hypercapnia (SaO2 ∼98%, PaO2 ∼105 mmHg, PaCO2 ∼50 mmHg, pH ∼7.26) to modify the CR. During co‐activation of the EPR and the hypoxia‐induced CR (O2‐CR), mean arterial pressure and heart rate were significantly greater, whereas leg blood flow and leg vascular conductance were significantly lower than the summation of the responses evoked by each reflex alone. During co‐activation of the EPR and the hypercapnia‐induced CR (CO2‐CR), the haemodynamic responses were not different from the summated responses to each reflex response alone (P ≥ 0.1). Therefore, while the interaction resulting from the EPR:O2‐CR co‐activation is hyper‐additive for blood pressure and heart rate, and hypo‐additive for peripheral haemodynamics, the interaction resulting from the EPR:CO2‐CR co‐activation is simply additive for all cardiovascular parameters. Thus, EPR:CR co‐activation results in significant interactions between cardiovascular reflexes, with the impact differing when the CR activation is achieved by hypoxia or hypercapnia. Since the EPR:CR co‐activation with hypoxia potentiates the pressor response and restricts blood flow to contracting muscles, this interaction entails the most functional impact on an exercising human.

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Section: Introductionmentioning

confidence: 99%

The exercise pressor reflex and chemoreflex interaction: cardiovascular implications for the exercising human

Wan

Weavil

Thurston

et al. 2020

The Journal of Physiology

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show abstract

“…Nonetheless, the current study cannot sufficiently address the exact nature of the interaction (additive, occlusive or facilitative) between these two reflexes, which is intimately dependent on the haemodynamic parameter being investigated (Kaur et al . ).…”

Section: Discussionmentioning

confidence: 97%

Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

Hureau

Weavil

Thurston

et al. 2018

The Journal of Physiology

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This study sought to comprehensively investigate the role of metabolically and mechanically sensitive group III/IV muscle afferents in carotid baroreflex responsiveness and resetting during both electrically evoked (EVO, no central command) and voluntary (VOL, requiring central command) isometric single-leg knee-extension (15% of maximal voluntary contraction; MVC) exercise. Participants (n = 8) were studied under control conditions (CTRL) and following lumbar intrathecal fentanyl injection (FENT) to inhibit μ-opioid receptor-sensitive lower limb muscle afferents. Spontaneous carotid baroreflex control of mean arterial pressure (MAP) and heart rate (HR) were assessed following rapid 5 s pulses of neck pressure (NP, +40 mmHg) or suction (NS, -60 mmHg). Resting MAP (87 ± 10 mmHg) and HR (70 ± 8 bpm) were similar between CTRL and FENT conditions (P > 0.4). In terms of spontaneous carotid baroreflex responsiveness, FENT did not alter the change in MAP or HR responses to NP (+13 ± 5 mmHg, P = 0.85; +9 ± 3 bpm; P = 0.99) or NS (-13 ± 5 mmHg, P = 0.99; -24 ± 11 bpm; P = 0.49) at rest or during either exercise protocol, which were of a remarkably similar magnitude to rest. In contrast, FENT administration reduced the exercise-induced resetting of the operating point for MAP and HR during both EVO (116 ± 10 mmHg to 100 ± 15 mmHg and 93 ± 14 bpm to 82 ± 10 bpm) and VOL (107 ± 13 mmHg to 100 ± 17 mmHg and 89 ± 10 bpm to 72 ± 10 bpm) exercise bouts. Together, these findings document that group III/IV muscle afferent feedback is critical for the resetting of the carotid baroreflex MAP and HR operating points, independent of exercise-induced changes in central command, but not for spontaneous carotid baroreflex responsiveness.

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“…Therefore, the baroreflex nearly completely prevents the metaboreflex from causing substantial peripheral vasoconstriction. As workload rises, the skeletal muscle vasculature progressively becomes the largest fraction of the total vascular conductance and therefore substantial pressor responses via peripheral vasoconstriction could only occur via constriction of the active muscle (O’Leary, 1991; Kaur et al, 2016, 2018). This could engender a positive feedback, vicious cycle where further metaboreflex activation causes further skeletal muscle vasoconstriction.…”

Section: Baroreflex – Metaboreflex Interaction In Hypertensionmentioning

confidence: 99%

“…This could engender a positive feedback, vicious cycle where further metaboreflex activation causes further skeletal muscle vasoconstriction. Indeed, recent studies have shown that there is some vasoconstriction within the active skeletal muscle during metaboreflex activation and this serves as an amplifier of the original response (Kaur et al, 2016). After induction of HF, this vasoconstriction in skeletal muscle is substantially greater perhaps due to depressed ability of the baroreflex to buffer metaboreflex-induced peripheral vasoconstriction (Kim et al, 2005a; Kaur et al, 2018).…”

Section: Baroreflex – Metaboreflex Interaction In Hypertensionmentioning

confidence: 99%

Neural Control of Cardiovascular Function During Exercise in Hypertension

2018

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During both static and dynamic exercise hypertensive subjects can experience robust increases in arterial pressure to such an extent that heavy exercise is often not recommended in these patients due to the dangerously high levels of blood pressure sometimes observed. Currently, the mechanisms mediating this cardiovascular dysfunction during exercise in hypertension are not fully understood. The major reflexes thought to mediate the cardiovascular responses to exercise in normotensive healthy subjects are central command, arterial baroreflex and responses to stimulation of skeletal muscle mechano-sensitive and metabo-sensitive afferents. This review will summarize our current understanding of the roles of these reflexes and their interactions in mediating the altered cardiovascular responses to exercise observed in hypertension. We conclude that much work is needed to fully understand the mechanisms mediating excessive pressor response to exercise often seen in hypertensive patients.

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Interaction between the muscle metaboreflex and the arterial baroreflex in control of arterial pressure and skeletal muscle blood flow

Cited by 24 publications

References 39 publications

The exercise pressor reflex and chemoreflex interaction: cardiovascular implications for the exercising human

The exercise pressor reflex and chemoreflex interaction: cardiovascular implications for the exercising human

Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

Neural Control of Cardiovascular Function During Exercise in Hypertension

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