Relative Contributions of Voluntary Apnoea, Exposure to Cold and Face Immersion in Water to Diving Bradycardia in Humans

Marsh, Neville; Askew, Debra; Beer, K De; Gerke, Michelle B.; Müller, D; Reichman, Coral

doi:10.1111/j.1440-1681.1995.tb01957.x

Cited by 22 publications

(14 citation statements)

References 6 publications

(5 reference statements)

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“…The heart rate reduction and selective vasoconstriction elicited by apnoea without immersion were augmented by immersion of the face in cold water, as reported previously (Kawakami et al 1967;Hurwitz and Furedy 1986;Marsh et al 1995;Andersson and Schagatay 1998a). However, forearm immersion did not aect the cardiovascular responses during apnoea as it did during eupnoea (i.e.…”

Section: Discussionmentioning

confidence: 50%

Cardiovascular responses to cold-water immersions of the forearm and face, and their relationship to apnoea

Andersson¹,

Schagatay²,

Gislén

et al. 2000

European Journal of Applied Physiology

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Apnoea as well as cold stimulation of the face or the extremities elicits marked cardiovascular reflexes in humans. The purpose of this study was to investigate whether forearm immersion in cold water has any effect on the cardiovascular responses to face immersion and apnoea. We recorded cardiovascular responses to coldwater immersions of the forearm and face in 19 (part I) and 23 subjects (part II). The experimental protocol was divided in two parts, each part containing four tests: I1, forearm immersion during eupnoea; I2, face immersion during eupnoea; I3, forearm and face immersion during eupnoea; I4, face immersion during apnoea; II1, apnoea without immersion; II2, forearm immersion during apnoea; II3, face immersion during apnoea; and II4, forearm and face immersion during apnoea. The water temperature was 9-11 degrees C. Cold-water immersion of either the forearm or face was enough to elicit the most pronounced thermoregulatory vasoconstriction during both eupnoea and apnoea. During eupnoea, heart rate responses to forearm immersion (3% increase) and face immersion (9% decrease) were additive during concurrent stimulation (3% decrease). During apnoea, the heart rate responses were not affected by the forearm immersion. The oxygen-conserving diving response seems to dominate over thermoregulatory responses in the threat of asphyxia. During breathing, however, the diving response serves no purpose and does not set thermoregulatory adjustments aside.

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Section: Discussionmentioning

confidence: 50%

Cardiovascular responses to cold-water immersions of the forearm and face, and their relationship to apnoea

Andersson¹,

Schagatay²,

Gislén

et al. 2000

European Journal of Applied Physiology

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“…In this study by Schagatay and Holm (1996), subjects' faces were immersed in water at a temperature of 10 and 20 1C while the ambient air temperature was 30 1C; the results showed that a water temperature of 20 1C also augments diving bradycardia at warmer air temperatures. Occurring together, apnea, face immersion in water, and cold exposure have a synergistic effect on diving bradycardia, which is greater than the sum of each individual response (Marsh et al, 1995).…”

Section: Face Immersionmentioning

confidence: 96%

The human diving response, its function, and its control

Foster

Sheel

2005

Scandinavian Med Sci Sports

214

233

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The purpose of this review is to outline the physiological responses associated with the diving response, its functional significance, and its cardiorespiratory control. This review is separated into four major sections. Section one outlines the diving response and its physiology. Section two provides support for the hypothesis that the primary role of the diving response is the conservation of oxygen. The third section describes how the diving response is controlled and provides a model that illustrates the cardiorespiratory interaction. Finally, the fourth section illustrates potential adaptations that result after regular exposure to an asphyxic environment. The cardiovascular and endocrine responses associated with the diving response and apnea are bradycardia, vasoconstriction, and an increase in secretion of suprarenal catecholamines. These responses require the integration of both the cardiovascular system and the respiratory system. The primary role of the diving response is likely to conserve oxygen for sensitive brain and heart tissue and to lengthen the time before the onset of serious hypoxic damage. We suggest that future research should be focused towards understanding the role of altered ventilatory responses in human breath-hold athletes as well as in patients suffering from sleep-disordered breathing.

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“…First, swimming combines exertion, voluntary apnea, possible cold-water exposure, and face immersion, resulting in increased sympathetic and parasympathetic activity through activation of the "dive reflex." 24,25 This concomitant activation of both the sympathetic and parasympathetic autonomic system may explain why swimming seems to precipitate premature ventricular contractions. 26 Second, cold-water face immersion has been demonstrated to lengthen QT intervals in normal subjects and occasionally induce T-wave alternans.…”

Section: Discussionmentioning

confidence: 99%

Spectrum and Frequency of Cardiac Channel Defects in Swimming-Triggered Arrhythmia Syndromes

Choi¹,

Kopplin²,

Tester³

et al. 2004

Circulation

243

121

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Background-Swimming is a relatively genotype-specific arrhythmogenic trigger for type 1 long-QT syndrome (LQT1).We hypothesize that mimickers of concealed LQT1, namely catecholaminergic polymorphic ventricular tachycardia (CPVT), may also underlie swimming-triggered cardiac events. Methods and Results-Between August 1997 and May 2003, 388 consecutive, unrelated patients were referred specifically for LQTS genetic testing. The presence of a personal and/or family history of a near-drowning or drowning was determined by review of the medical records and/or phone interviews and was blinded to genetic test results.Comprehensive mutational analysis of the 5 LQTS-causing channel genes, KCNQ1 (LQT1), KCNH2 (LQT2), SCN5A (LQT3), KCNE1 (LQT5), and KCNE2 (LQT6), along with KCNJ2 (Andersen-Tawil syndrome) and targeted analysis of 18 CPVT1-associated exons in RyR2, was performed with the use of denaturing high-performance liquid chromatography and direct DNA sequencing. Approximately 11% (43 of 388) of the index cases had a positive swimming phenotype. Thirty-three of these 43 index cases had a "Schwartz" score (Ն4) suggesting high clinical probability of LQTS. Among this subset, 28 patients (85%) were LQT1, 2 patients (6%) were LQT2, and 3 were genotype negative. Among the 10 cases with low clinical probability for LQTS, 9 had novel, putative CPVT1-causing RyR2 mutations. Conclusions-In contrast to previous studies that suggested universal LQT1 specificity, genetic heterogeneity underlies channelopathies that are suspected chiefly because of a near-drowning or drowning. CPVT1 and strategic genotyping of RyR2 should be considered when LQT1 is excluded in the pathogenesis of a swimming-triggered arrhythmia syndrome.

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Relative Contributions of Voluntary Apnoea, Exposure to Cold and Face Immersion in Water to Diving Bradycardia in Humans

Cited by 22 publications

References 6 publications

Cardiovascular responses to cold-water immersions of the forearm and face, and their relationship to apnoea

Cardiovascular responses to cold-water immersions of the forearm and face, and their relationship to apnoea

The human diving response, its function, and its control

Spectrum and Frequency of Cardiac Channel Defects in Swimming-Triggered Arrhythmia Syndromes

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