β-Adrenergic Blockade and Metabo-Chemoreflex Contributions to ExerciseCapacity

Beloka, Sofia; Gujic, Marko; Deboeck, Gaël; Niset, Georges; Ciarka, Agnieszka; Argacha, Jean-François; Adamopoulos, Dionysios; Borne, Philippe van de; Naeije, Robert

doi:10.1249/mss.0b013e31817fbe11

Cited by 31 publications

(47 citation statements)

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“…Peripheral chemoreXex sensitivity was expressed as the ratio between the rise in V E and the reduction in oxygen saturation during hypoxia [ (V E hypoxia ¡ V E baseline )/ (SpO 2 hypoxia ¡ SpO 2 baseline )], and central chemosensitivity as the ratio between the rise in V E and P ET CO 2 during hypercapnia [ (V E hypoxia ¡ V E baseline )/ (P ET CO 2 hypoxia ¡ P ET CO 2 baseline )], as previously reported (Beloka et al 2008). …”

Section: Discussionmentioning

confidence: 91%

“…Muscle sympathetic nerve activity (MSNA) was recorded continuously by obtaining multiunit recordings of postganglionic sympathetic activity measured from a nerve fascicle in the peroneal nerve posterior to the Wbular head, as previously described (Velez-Roa et al 2003;Houssiere et al 2006;Beloka et al 2008). Electric activity in the nerve fascicle was measured using tungsten microelectrodes (shaft diameter 200 m, tapering to a non-insulated tip of 1-5 m).…”

Section: Chemorexex and Metaborexex Stimulationmentioning

confidence: 99%

“…ChemoreXex sensitivity was determined in resting conditions by the measurement of MSNA and V E during a period of 5-min exposure to hyperoxic hypercapnia (7% CO 2 , in O 2 , central chemoreXex sensitivity) and during a period of 5-min exposure to isocapnic hypoxia (10% O 2 in N 2 , peripheral chemoreXex sensitivity), as previously described (Beloka et al 2008). The order of the interventions was randomised, but kept constant for a given subject.…”

Section: Chemorexex and Metaborexex Stimulationmentioning

confidence: 99%

“…MetaboreXex sensitivity was estimated by the measurement of MSNA during a static voluntary contraction of the dominant forearm with a handgrip dynamometer, as previously described (Houssiere et al 2006;Beloka et al 2008). The maximal voluntary contraction was determined in triplicate before the start of each study.…”

Section: Chemorexex and Metaborexex Stimulationmentioning

confidence: 99%

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Effects of β2-adrenergic stimulation on exercise capacity in normal subjects

et al. 2011

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β2-Adrenergic receptor agonists are believed to present with ergogenic properties. However, how combined respiratory, cardiovascular and muscular effects of these drugs might affect exercise capacity remain incompletely understood. The effects of salbutamol were investigated in 23 healthy subjects. The study was randomised, placebo-controlled in double-blind and followed a cross-over design. Salbutamol was given at the dose of 10 μg/min in 11 subjects and 20 μg/min iv in the other 12 subjects. Measurements included muscle sympathetic nerve activity (MSNA), ventilatory responses to hyperoxic hypercapnia (7% CO(2) in O(2,) central chemoreflex), isocapnic hypoxia (10% O(2) in N(2), peripheral chemoreflex) and isometric muscle contraction followed by a local circulatory arrest (metaboreflex), cardiopulmonary exercise test (CPET) variables and isokinetic muscle strength. Salbutamol 10 μg/min increased heart rate and blood pressure, while MSNA burst frequency remained unchanged. Peripheral chemosensitivity increased, as evidenced by an increased ventilatory response to hypoxia, but ventilatory responses to hypercapnia or muscle ischaemia remained unchanged. The effects of salbutamol 20 μg/min were similar. Both doses of salbutamol did not affect CPET. Only the higher dose of salbutamol decreased the anaerobic threshold, but this was not associated with a change in VO(2) max. Salbutamol increased the slopes of ventilation as a function of VO(2) (P < 0.05) and VCO(2) (P < 0.001) during CPET. Maximal isokinetic muscle strength was not affected by salbutamol. In conclusion, the acute administration of either low or high dose salbutamol does not affect exercise capacity in normal subjects, in spite of an earlier anaerobic threshold and increased chemosensitivity.

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Section: Discussionmentioning

confidence: 91%

Section: Chemorexex and Metaborexex Stimulationmentioning

confidence: 99%

Section: Chemorexex and Metaborexex Stimulationmentioning

confidence: 99%

Section: Chemorexex and Metaborexex Stimulationmentioning

confidence: 99%

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Effects of β2-adrenergic stimulation on exercise capacity in normal subjects

et al. 2011

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“…Biscoe and Purvis (4) found that direct muscle afferent activity sensitized the carotid chemoreceptor (4); however, these findings were not supported in later studies (1,7). Some researchers have found that activation of cardiac afferents can also sensitize the carotid chemoreceptor (11), and similarly, that ␤-adrenergic blockade can decrease ventilation at any metabolic rate (2,41). Cardiac afferents can be activated by many factors including lactic acid, coronary occlusion (6,23), and an increase in HR (38).…”

Section: Discussionmentioning

confidence: 99%

Activation of the carotid chemoreflex secondary to muscle metaboreflex stimulation in men

Edgell

Stickland

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Edgell H, Stickland MK. Activation of the carotid chemoreflex secondary to muscle metaboreflex stimulation in men. Am J Physiol Regul Integr Comp Physiol 306: R693-R700, 2014. First published February 26, 2014 doi:10.1152 doi:10. /ajpregu.00472.2013 has shown that the carotid chemoreceptor (CC) contributes to sympathetic control of cardiovascular function during exercise, despite no evidence of increased circulating CC stimuli, suggesting enhanced CC activity/sensitivity. As interactions between metaboreceptors and chemoreceptors have been previously observed, the purpose of this study was to isolate the metaboreflex while acutely stimulating or inhibiting the CC to determine whether the metaboreflex increased CC activity/sensitivity. Fourteen young healthy men (height: 177.0 Ϯ 2.1 cm, weight: 85.8 Ϯ 5.5 kg, age: 24.6 Ϯ 1.1 yr) performed three trials of 40% maximal voluntary contraction handgrip for 2 min, followed by 3 min of postexercise circulatory occlusion (PECO) to stimulate the metaboreflex. In random order, subjects either breathed room air, hypoxia (target SPO 2 ϭ 85%), or hyperoxia (FIO 2 ϭ 1.0) during the PECO to modulate the chemoreflex. After these trials, a resting hypoxia trial was conducted without handgrip or PECO. Ventilation (V E), heart rate (HR), blood pressure, and muscle sympathetic nervous activity (MSNA) data were continuously obtained. Relative to normoxic PECO, inhibition of the CC during hyperoxic PECO resulted in lower MSNA (P ϭ 0.038) and HR (P ϭ 0.021). Relative to normoxic PECO, stimulation of the CC during hypoxic PECO resulted in higher HR (P Ͻ 0.001) and V E (P Ͻ 0.001). The ventilatory and MSNA responses to hypoxic PECO were not greater than the sum of the responses to hypoxia and PECO individually, indicating that the CC are not sensitized during metaboreflex activation. These results demonstrate that stimulation of the metaboreflex activates, but does not sensitize the CC, and help explain the enhanced CC activity with exercise. sympathetic nerve activity; ventilation; exercise EXERCISE is known to involve cardiovascular influences from metaboreceptors, mechanoreceptors, baroreceptors, and central command (25). The carotid chemoreceptor has been shown to be activated/sensitized during exercise (10,27,33,40). Previous work has provided evidence that the carotid chemoreceptor is enhanced with exercise despite no change in circulating carotid chemoreceptor stimuli (K ϩ , lactate, pH, PCO 2 , PO 2 ), and that carotid chemoreceptor inhibition with either dopamine or hyperoxia increases cardiac output and/or peripheral blood flow during exercise secondary to a reduction in sympathetic vasoconstrictor outflow (32-34). Similarly, rhythmic handgrip exercise in humans activates/sensitizes the carotid chemoreceptor despite no increase in blood lactate (34); however, the exact mechanism behind this activation/sensitization of the carotid chemoreceptor during exercise is unknown.Conflicting evidence exists concerning the role of muscle afferents on exercise-induced carotid chemorecepto...

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Disruption of adenylyl cyclase type 5 mimics exercise training

et al. 2017

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Exercise training is key to healthful longevity. Since exercise training compliance is difficult, it would be useful to have a therapeutic substitute that mimicked exercise training. We compared the effects of exercise training in wild type (WT) littermates with adenylyl cyclase type 5 knock out (AC5 KO) mice, a model of enhanced exercise performance. Exercise performance, measured by maximal distance and work to exhaustion, was increased in exercise trained WT to levels already attained in untrained AC5 KO. Exercise training in AC5 KO further enhanced their exercise performance. The key difference in untrained AC5 KO and exercise trained WT was the β-adrenergic receptor signaling, which was decreased in untrained AC5 KO compared to untrained WT but was increased in WT with exercise training. Despite this key difference, untrained AC5 KO and exercise trained WT mice shared similar gene expression, determined by deep sequencing, in their gastrocnemius muscle with 183 genes commonly up or down-regulated, mainly involving muscle contraction, metabolism and mitochondrial function. The SIRT1/PGC-1α pathway partially mediated the enhanced exercise in both AC5 KO and exercise trained WT mice, as reflected in the reduced exercise responses after administering a SIRT1 inhibitor, but did not abolish the enhanced exercise performance in the AC5 KO compared to untrained WT. Increasing oxidative stress with paraquat attenuated exercise performance more in untrained WT than untrained AC5 KO, reflecting the augmented oxidative stress protection in AC5 KO. Blocking nitric oxide actually reduced the enhanced exercise performance in untrained AC5 KO and trained WT to levels below untrained WT, demonstrating the importance of this mechanism. These results suggest that AC5 KO mice, without exercise training, share similar mechanisms responsible for enhanced exercise capacity with chronic exercise training, most importantly increased nitric oxide, and demonstrate more reserve with the addition of exercise training. A novel feature of the enhanced exercise performance in untrained AC5 KO mice is their decreased sympathetic tone, which is also beneficial to patients with cardiovascular disease.

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β-Adrenergic Blockade and Metabo-Chemoreflex Contributions to ExerciseCapacity

Cited by 31 publications

References 17 publications

Effects of β2-adrenergic stimulation on exercise capacity in normal subjects

Effects of β2-adrenergic stimulation on exercise capacity in normal subjects

Activation of the carotid chemoreflex secondary to muscle metaboreflex stimulation in men

Disruption of adenylyl cyclase type 5 mimics exercise training

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