Ventilation inhibits sympathetic action potential recruitment even during severe chemoreflex stress

Badrov, Mark B.; Barak, Otto; Mijačika, Tanja; Shoemaker, Leena N.; Borrell, Lindsay J.; Lojpur, Mihajlo; Drviš, Ivan; Dujić, Željko; Shoemaker, J. Kevin

doi:10.1152/jn.00381.2017

Cited by 22 publications

(32 citation statements)

References 43 publications

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“…Therefore, displaying AP latency as a function of AP cluster size indicates the shorter latency of larger AP clusters . Of note, repeated observations that the larger APs also express faster conduction velocity (Badrov et al 2015(Badrov et al , 2017 discount the potential problem that they simply represent axons that lie closer to the recording electrode.…”

Section: )mentioning

confidence: 95%

“…Concurrently, new clusters of larger APs emerged, representing a recruitment response. A second pattern observed was that the recruitment of new large APs progressed with the severity of the stress, be it apneas (Badrov et al 2017), isometric exercise (Badrov et al 2016b), or baroreceptor unloading (Badrov et al 2015;Salmanpour et al 2011a). Importantly, the appearance of larger APs observed during fatiguing handgrip persisted during a period of postexercise forearm ischemia highlighting the important role of peripheral muscle metaboreceptors in the recruitment of the latent AP pool.…”

Section: )mentioning

confidence: 95%

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Fifty years of microneurography: learning the language of the peripheral sympathetic nervous system in humans

Shoemaker

Klassen

Badrov

et al. 2018

Journal of Neurophysiology

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As a primary component of homeostasis, the sympathetic nervous system enables rapid adjustments to stress through its ability to communicate messages among organs and cause targeted and graded end organ responses. Key in this communication model is the pattern of neural signals emanating from the central to peripheral components of the sympathetic nervous system. But what is the communication strategy employed in peripheral sympathetic nerve activity (SNA)? Can we develop and interpret the system of coding in SNA that improves our understanding of the neural control of the circulation? In 1968, Hagbarth and Vallbo (Hagbarth KE, Vallbo AB. Acta Physiol Scand 74: 96-108, 1968) reported the first use of microneurographic methods to record sympathetic discharges in peripheral nerves of conscious humans, allowing quantification of SNA at rest and sympathetic responsiveness to physiological stressors in health and disease. This technique also has enabled a growing investigation into the coding patterns within, and cardiovascular outcomes associated with, postganglionic SNA. This review outlines how results obtained by microneurographic means have improved our understanding of SNA outflow patterns at the action potential level, focusing on SNA directed toward skeletal muscle in conscious humans.

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confidence: 95%

Section: )mentioning

confidence: 95%

Fifty years of microneurography: learning the language of the peripheral sympathetic nervous system in humans

Shoemaker

Klassen

Badrov

et al. 2018

Journal of Neurophysiology

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“…However, the former study did not show the influence of dynamic ventilation on MSNA at two matched chemical stressors. More recently, Badrov et al (2017) also demonstrated lower action potential recruitment when they matched a similar rebreathing protocol to maximal BHs at functional residual capacity within elite BH divers. Within our own findings, when stress is matched between rebreathing and our BH (end-inspiratory), rebreathing exhibited a markedly blunted MSNA response.…”

Section: Msna Response To Dynamic Ventilation Versus Static Lung Volumentioning

confidence: 96%

Mechanisms of sympathetic regulation during Apnea

et al. 2019

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Volitional Apnea produces a robust peak sympathetic response through several interacting mechanisms. However, the specific contribution of each mechanism has not been elucidated. Muscle sympathetic activity was collected in participants (n = 10; 24 ± 3 years) that performed four maximal volitional apneas aimed at isolating lung‐stretch (mechanical) and chemoreflex drive: (Ainslie and Duffin 2009) end‐expiratory breath‐hold, (Ainslie et al. 2013) end‐inspiratory breath‐hold, (Alpher et al. 1986) prehyperventilation breath‐hold, and (Andersson and Schagatay 1998) prehyperoxia breath‐hold. A final repeated rebreathe breath‐hold protocol was performed to measure the peak sympathetic response during successive breath‐holds at increasing chemoreflex stress. Finally, the influence of dynamic ventilation was assessed through asphyxic rebreathe. Muscle sympathetic activity was calculated as the change in burst frequency (burst/min), burst incidence (burst/100 heart‐beats), and amplitude (au) between baseline and prevolitional breakpoint. Rebreathe was analyzed at similar chemoreflex stress as inspiratory breath‐hold. All maneuvers increased muscle sympathetic activity compared to baseline (P < 0.01). However, prehyperoxia exhibited a smaller increase (+22.18 ± 9.13 burst/min; +25.52 ± 11.7 burst/100 heart‐beats) compared to inspiratory, expiratory, and prehyperventilation breath‐holds. At similar chemoreflex strain, rebreathe sympathetic activity was blunted compared to inspiratory breath‐hold (P < 0.01). Finally, muscle sympathetic activity was not different between the repeated rebreathe trials, despite elevated chemoreflex stress and lower breath‐hold duration with each subsequent breath‐hold. We have demonstrated an obligatory role of the peripheral, but not central, chemoreflex (prehyperventilation vs. prehyperoxia) in producing peak sympathetic responses. At similar chemoreflex stresses the act of dynamic ventilation, but not static lung stretch per se, blunts muscle sympathetic activity. Finally, similar peak sympathetic responses during successive repeated breath‐holds suggest a sympathetic ceiling may exist.

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“…Still, muscle sympathetic nerve activity (burst frequency and amplitude) markedly increases during a maximal dry static breath hold by an astounding ∼2000% from baseline (Heusser et al., ; Steinback et al., ). In part because the increase in sympathetic nerve activity is dependent on the duration of breath hold, the primary stimulus for the large sympathetic response during a maximal dry breath hold was initially suggested to result from chemostress (Heusser et al., ); however, it is more likely that mounting pulmonary nerve activity is largely responsible (Badrov et al., ). Thus, ventilation per se partly restrains sympathetic axonal recruitment even during extreme chemoreflex stress (Badrov et al., ).…”

Section: Cardiovascular Regulation and The Dive Responsementioning

confidence: 99%

“…In part because the increase in sympathetic nerve activity is dependent on the duration of breath hold, the primary stimulus for the large sympathetic response during a maximal dry breath hold was initially suggested to result from chemostress (Heusser et al., ); however, it is more likely that mounting pulmonary nerve activity is largely responsible (Badrov et al., ). Thus, ventilation per se partly restrains sympathetic axonal recruitment even during extreme chemoreflex stress (Badrov et al., ). Moreover, breath holds performed at different lung volumes will dramatically impact muscle sympathetic nervous activity (Breskovic, Steinback, Salmanpour, Shoemaker, & Dujic, ; Dujic et al., ; Heusser et al., , ; Steinback, Breskovic, Banic, Dujic, & Shoemaker, ; Steinback et al., ) and central blood flow distribution (Stembridge et al., ).…”

Section: Cardiovascular Regulation and The Dive Responsementioning

confidence: 99%

Physiology of static breath holding in elite apneists

Bain

Drviš

Dujić

et al. 2018

Experimental Physiology

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Breath-hold-related activities have been performed for centuries, but only recently, within the last ∼30 years, has it emerged as an increasingly popular competitive sport. In apnoea sport, competition relates to underwater distances or simply maximal breath-hold duration, with the current (oxygen-unsupplemented) static breath-hold record at 11 min 35 s. Remarkably, many ultra-elite apneists are able to suppress respiratory urges to the point where consciousness fundamentally limits a breath-hold duration. Here, arterial oxygen saturations as low as ∼50% have been reported. In such cases, oxygen conservation to maintain cerebral functioning is critical, where responses ascribed to the mammalian dive reflex, e.g. sympathetically mediated peripheral vasoconstriction and vagally mediated bradycardia, are central. In defence of maintaining global cerebral oxygen delivery during prolonged breath holds, the cerebral blood flow may increase by ∼100% from resting values. Interestingly, near the termination of prolonged dry static breath holds, recent studies also indicate that reductions in the cerebral oxidative metabolism can occur, probably attributable to the extreme hypercapnia and irrespective of the hypoxaemia. In this review, we highlight and discuss the recent data on the cardiovascular, metabolic and, particularly, cerebrovascular function in competitive apneists performing maximal static breath holds. The physiological adaptation and maladaptation with regular breath-hold training are also summarized, and future research areas in this unique physiological field are highlighted; particularly, the need to determine the potential long-term health impacts of extreme breath holding.

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Ventilation inhibits sympathetic action potential recruitment even during severe chemoreflex stress

Cited by 22 publications

References 43 publications

Fifty years of microneurography: learning the language of the peripheral sympathetic nervous system in humans

Fifty years of microneurography: learning the language of the peripheral sympathetic nervous system in humans

Mechanisms of sympathetic regulation during Apnea

Physiology of static breath holding in elite apneists

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