Chemoreflex and metaboreflex control during static hypoxic exercise

Houssière, Anne; Najem, Boutaïna; Ciarka, Agniezka; Velez‐Roa, Sonia; Naeije, Robert; Borne, Philippe van de

doi:10.1152/ajpheart.01043.2004

Cited by 45 publications

(47 citation statements)

References 31 publications

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“…Metaboreflex activation selectively suppressed the peripheral sympathoinhibitotry effects of chemoreflex inhibition but left the cardiac inhibitory effects of hyperoxia unaffected. These results further extend our observation that MSNA and HR are regulated by different mechanisms during exercise (19).…”

Section: Discussionsupporting

confidence: 90%

“…This is due to an increase in metaboreflex sensitivity by hyperoxia that overrules the sympathoinhibitory and BP lowering effects of chemoreflex inhibition. This occurs despite a reduced lactic acid production.handgrip; muscle sympathetic nerve activity; metaboreceptors; chemoreceptors MUSCLE METABORECEPTORS regulate sympathetic activation during exercise (19,25). This reflex is activated by metabolites released from exercising skeletal muscle.…”

mentioning

confidence: 99%

“…This is because hyperoxia suppresses the resting chemoreflex drive in humans (8,26,38). The carotid and aortic chemoreceptors increase MSNA in response to reductions in arterial oxygen content (19,27,42). Short periods of 3-4 min of hyperoxia (38) or hyperoxia with a 50% inspired O 2 fraction (FI O 2 ) (12, 21) do not decrease BP.…”

mentioning

confidence: 99%

“…handgrip; muscle sympathetic nerve activity; metaboreceptors; chemoreceptors MUSCLE METABORECEPTORS regulate sympathetic activation during exercise (19,25). This reflex is activated by metabolites released from exercising skeletal muscle.…”

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confidence: 99%

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Hyperoxia enhances metaboreflex sensitivity during static exercise in humans

Houssière

Najem²,

Cuylits³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Houssière, Anne, Boutaina Najem, Nicolas Cuylits, Sophie Cuypers, Robert Naeije, and Philippe van de Borne. Hyperoxia enhances metaboreflex sensitivity during static exercise in humans. Am J Physiol Heart Circ Physiol 291: H210 -H215, 2006; doi:10.1152/ajpheart.01168.2005.-Peripheral chemoreflex inhibition with hyperoxia decreases sympathetic nerve traffic to muscle circulation [muscle sympathetic nerve activity (MSNA)]. Hyperoxia also decreases lactate production during exercise. However, hyperoxia markedly increases the activation of sensory endings in skeletal muscle in animal studies. We tested the hypothesis that hyperoxia increases the MSNA and mean blood pressure (MBP) responses to isometric exercise. The effects of breathing 21% and 100% oxygen at rest and during isometric handgrip at 30% of maximal voluntary contraction on MSNA, heart rate (HR), MBP, blood lactate (BL), and arterial O 2 saturation (SaO 2 ) were determined in 12 healthy men. The isometric handgrips were followed by 3 min of postexercise circulatory arrest (PE-CA) to allow metaboreflex activation in the absence of other reflex mechanisms. Hyperoxia lowered resting MSNA, HR, MBP, and BL but increased Sa O 2 compared with normoxia (all P Ͻ 0.05). MSNA and MBP increased more when exercise was performed in hyperoxia than in normoxia (MSNA: hyperoxic exercise, 255 Ϯ 100% vs. normoxic exercise, 211 Ϯ 80%, P ϭ 0.04; and MBP: hyperoxic exercise, 33 Ϯ 9 mmHg vs. normoxic exercise, 26 Ϯ 10 mmHg, P ϭ 0.03). During PE-CA, MSNA and MBP remained elevated (both P Ͻ 0.05) and to a larger extent during hyperoxia than normoxia (P Ͻ 0.05). Hyperoxia enhances the sympathetic and blood pressure (BP) reactivity to metaboreflex activation. This is due to an increase in metaboreflex sensitivity by hyperoxia that overrules the sympathoinhibitory and BP lowering effects of chemoreflex inhibition. This occurs despite a reduced lactic acid production.handgrip; muscle sympathetic nerve activity; metaboreceptors; chemoreceptors MUSCLE METABORECEPTORS regulate sympathetic activation during exercise (19,25). This reflex is activated by metabolites released from exercising skeletal muscle. Several substances, such as lactic acid, phosphate, K ϩ , H ϩ , adenosine, prostaglandins, and bradykinin, are now identified as stimulators of this pressor reflex (35,37,40).These metabolites stimulate group III and IV chemosensitive afferents in the working muscles (32). These afferent fibers can also be activated by injection of lactic acid or a hyperosmolar solution of potassium chloride, and their activity is modulated by endogenous nitric oxide in resting and contracting muscle (3,6,11,13,16). This activation in both nonexercising and exercising limbs (32) provokes a rise in cardiac output and vasoconstriction of the nonischemic vascular beds. As a result, blood pressure (BP) and perfusion pressure increase and correct blood flow deficits during exercise (32,35,40,43).There are several reasons to believe that hyperoxia may affect sympathetic regulation during exercise.First, hyp...

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Hyperoxia enhances metaboreflex sensitivity during static exercise in humans

Houssière

Najem²,

Cuylits³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…Other investigators focused on coactivation of the muscle metaboreflex and hypoxic chemoreflex and reported no interaction and no specific effect on blood pressure response (39,14). By contrast, we found that blood pressure was higher during HCAϩMMA than HCA or MMA alone, but that the increase in MAP was smaller than the sum of the HCA and MMA responses.…”

Section: R45contrasting

confidence: 72%

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

Delliaux

Ichinose

Watanabe

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Ten healthy males participated under three experimental conditions: 1) hypercapnia (HCA, PET CO 2 : ϩ10 mmHg, by inhalation of a CO 2-enriched gas mixture); 2) muscle metaboreflex activation (MMA, by 5 min of local circulatory occlusion after 1 min of 50% maximum voluntary contraction isometric handgrip under normocapnia); and 3) HCAϩMMA. We measured mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO); calculated stroke volume (SV), and total peripheral resistance (TPR); and evaluated myocardial oxygen consumption (MV O2) and cardiac work (CW) noninvasively. MAP increased in the three experimental conditions but HCAϩMMA led to the highest MAP, CO, and HR. Moreover, HCAϩMMA increased SV and was associated with the highest MV O2 and CW. HCA and MMA exhibited inhibitory interactions with MAP, HR, TPR, MV O2, and CW, increases of which were smaller during HCAϩMMA than the sum of the increases during HCA and MMA alone (MAP: ϩ28 Ϯ 2 vs. ϩ34 Ϯ 2 mmHg, P Ͻ 0.001; HR: ϩ15 Ϯ 2 vs. ϩ22 Ϯ 3 bpm, P Ͻ 0.01; TPR: ϩ1.1 Ϯ 1.4 vs. ϩ3.0 Ϯ 1.5 mmHg·l·min Ϫ1 , P Ͻ 0.05; MV O2: ϩ50.25 Ϯ 4.74 vs. ϩ59.48 Ϯ 5.37 mmHg·min Ϫ1 ·10 Ϫ2 , P Ͻ 0.01; CW: ϩ59.10 Ϯ 7.52 vs. ϩ63.67 Ϯ 7.71 ml mmHg·min Ϫ1 ·10 Ϫ4 , P Ͻ 0.05). Oppositely, HCA and MMA interactions were linearly additive for CO (ϩ2.3 Ϯ 0.4 l/min) and SV (ϩ13 Ϯ 4 ml). We showed that muscle metaboreflex and hypercapnia interact in healthy humans, reducing vasoconstriction but enhancing SV.hypercapnia; muscle metaboreflex; hypertension; stroke volume; myocardial oxygen consumption REGULATION OF ARTERIAL BLOOD pressure involves the integration of humoral, hormonal, and neurogenic components. For example, whereas hypercapnia has direct humoral vasodilatory effects (19,20), the neurally mediated central chemoreflex increases cardiovascular sympathetic nervous system activity, leading heart rate (HR), stroke volume (SV), cardiac output (CO), vascular resistance, and then blood pressure all to increase (31). During exercise, blood pressure is also regulated by muscle reflexes (2, 17). The muscle metaboreflex forms a second direct excitatory input for the neural control of cardiovascular function (21, 29, 42) that also stimulates sympathetic pathways (29,30,33) leading to increases in HR, SV, CO, vascular resistance, and then blood pressure.It is known that central chemoreflex and muscle metaboreflex signals converge to common areas in the brain (43) and exert similar excitatory effects through the cardiovascular autonomic nervous system. On the other hand, little is known about the hemodynamic effects of muscle metaboreflex activation during hypercapnia. Ponikowski (35) showed that muscle ergoreflex activation was an independent predictor of ventilation sensitivity to hypercapnia in chronic heart failure and argued for the existence of interactions between the muscle metaboreflex and hypercapnic chemoreflex. Despite the likelihood that these two reflexes interact during exercise, this topic received little direct attention before the pioneering work of Lykidis et al. (22,23),...

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Interaction of hypoxia and vascular occlusion on cardiorespiratory responses during exercise

et al. 2018

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Background:The interaction of group III/IV afferents and chemoreflex during exercise is critical in healthy adults during high altitude exercise or in clinical populations who experience hypoxia. Purpose: Investigate the cardiorespiratory response to simultaneous vascular occlusion (to activate group III/IV afferents) and hypoxia (to activate chemoreflex) during cycling exercise. Methods: 18 adults (9 women, 25 ± 5 years) attended two sessions. Session 1: maximal cycle ergometry test. Session 2: two 26-minute bouts (randomized between hypoxia, 12.5% FiO 2 and normoxia, 21% FiO 2 ). Participants cycled at 30% of peak workload for 3 minutes (control, CTL) followed by alternating 2 minute periods of bilateral vascular occlusion of the proximal thigh at pressures of 20, 40, 60, 80, 100 mm Hg in a randomized sequence. Results: Ventilation (V E ) increased from CTL to 100 mm Hg during hypoxia (39 ± 9 to 51 ± 16 L/min) and normoxia (31 ± 7 to 39 ± 9 L/min, P < 0.01). Respiratory rate increased with vascular occlusion (P < 0.05) but not hypoxia (P = 0.10). Tidal volume was greater during hypoxia (P < 0.05), with no influence of vascular occlusion (P = 0.40). Mean arterial pressure and heart rate increased more with hypoxia compared with normoxia (P < 0.05). Conclusions: Our findings suggest that vascular occlusion and hypoxia both increase V E , albeit via different mechanisms. While hypoxia increased tidal volume, vascular occlusion increased respiratory rate. K E Y W O R D Scirculatory occlusion, group III and IV muscle afferents, hypoxia, ventilation and blood pressure | 65 KELLER-ROSS Et aL.

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Chemoreflex and metaboreflex control during static hypoxic exercise

Cited by 45 publications

References 31 publications

Hyperoxia enhances metaboreflex sensitivity during static exercise in humans

Hyperoxia enhances metaboreflex sensitivity during static exercise in humans

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

Interaction of hypoxia and vascular occlusion on cardiorespiratory responses during exercise

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