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      The effect of various breath‐hold techniques on the cardiorespiratory response to facial immersion in humans

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          Abstract

          Repeated maximal breath‐holds have been demonstrated to induce bradycardia, increase haematocrit and haemoglobin and prolong subsequent breath‐hold duration by 20%. Freedivers use non‐maximal breath‐hold techniques (BHTs) to improve breath‐hold duration. The aim of this study was to investigate the cardiorespiratory and haematological responses to various BHTs. Ten healthy men (34.5 ± 1.9 years) attended five randomized experimental trials and performed a 40 min period of quiet rest or one of three BHTs followed by a maximal breath‐hold challenge during facial immersion in water at 30 or 10°C. Cardiovascular and respiratory parameters were measured continuously using finger plethysmography and breath‐by‐breath gas analysis, respectively, and venous blood samples were collected throughout. Facial immersion in cold water caused marked bradycardia (74.1 vs. 50.2 beats/min after 40 s) but did not increase breath‐hold duration compared with warm water control conditions. Facial immersion breath‐hold duration was 30.8–43.3% greater than the control duration when preceded by BHTs that involved repeated breath‐holds of constant duration ( P = 0.021), increasing duration ( P < 0.001) or increasing frequency ( P < 0.001), with no difference observed between BHTs. The increased duration of apnoea across all three BHT protocols was associated with a 6.8% increase in end‐tidal O 2 and a 13.1% decrease in end‐tidal CO 2 immediately before facial immersion. There were no differences in blood pressure, cardiac output, heart rate, haematocrit or haemoglobin between each BHT and control conditions ( P > 0.05). In conclusion, the duration of apnoea can be extended by manipulating blood gases through repeated prior breath‐holds, but changes in cardiac output and red blood cell mass do not appear essential.

          Abstract

          • What is the central question of this study?

            What is the effect of three repeated breath‐hold techniques routinely used by freedivers, thought to manipulate arterial partial pressures of O 2 and CO 2, on the cardiorespiratory and haematological response to breath‐holding during facial immersion?

          • What is the main finding and its importance?

            All three techniques increased breath‐hold by a similar duration, probably owing to the similar marked increase in end‐tidal O 2 and decrease in end‐tidal CO 2 observed in all three trials before facial immersion. These were the only cardiorespiratory changes that were consistently manipulated before the maximal breath‐hold. This would suggest that pronounced bradycardia and vasoconstriction of selective vascular beds are probably not obligatory for prolonging breath‐hold duration.

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          Most cited references24

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          The human diving response, its function, and its control.

          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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            Spleen volume and blood flow response to repeated breath-hold apneas.

            The purpose of this study was 1) to answer whether the reduction in spleen size in breath-hold apnea is an active contraction or a passive collapse secondary to reduced splenic arterial blood flow and 2) to monitor the spleen response to repeated breath-hold apneas. Ten trained apnea divers and 10 intact and 7 splenectomized untrained persons repeated five maximal apneas (A1-A5) with face immersion in cold water, with 2 min interposed between successive attempts. Ultrasonic monitoring of the spleen and noninvasive cardiopulmonary measurements were performed before, between apneas, and at times 0, 10, 20, 40, and 60 min after the last apnea. Blood flows in splenic artery and splenic vein were not significantly affected by breath-hold apnea. The duration of apneas peaked after A3 (143, 127, and 74 s in apnea divers, intact, and splenectomized persons, respectively). A rapid decrease in spleen volume ( approximately 20% in both apnea divers and intact persons) was mainly completed throughout the first apnea. The spleen did not recover in size between apneas and only partly recovered 60 min after A5. The well-known physiological responses to apnea diving, i.e., bradycardia and increased blood pressure, were observed in A1 and remained unchanged throughout the following apneas. These results show rapid, probably active contraction of the spleen in response to breath-hold apnea in humans. Rapid spleen contraction and its slow recovery may contribute to prolongation of successive, briefly repeated apnea attempts.
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              End-tidal and arterial carbon dioxide measurements correlate across all levels of physiologic dead space.

              End-tidal carbon dioxide (P(ETCO(2))) is a surrogate, noninvasive measurement of arterial carbon dioxide (P(aCO(2))), but the clinical applicability of P(ETCO(2)) in the intensive care unit remains unclear. Available research on the relationship between P(ETCO(2)) and P(aCO(2)) has not taken a detailed assessment of physiologic dead space into consideration. We hypothesized that P(ETCO(2)) would reliably predict P(aCO(2)) across all levels of physiologic dead space, provided that the expected P(ETCO(2))-P(aCO(2)) difference is considered. Fifty-six mechanically ventilated pediatric patients (0-17 y old, mean weight 19.5 +/- 24.5 kg) were monitored with volumetric capnography. For every arterial blood gas measurement during routine care, we measured P(ETCO(2)) and calculated the ratio of dead space to tidal volume (V(D)/V(T)). We assessed the P(ETCO(2))-P(aCO(2)) relationship with Pearson's correlation coefficient, in 4 V(D)/V(T) ranges. V(D)/V(T) was 0.7 for 54 measurements (11%). The correlation coefficients between P(ETCO(2)) and P(aCO(2)) were 0.95 (mean difference 0.3 +/- 2.1 mm Hg) for V(D)/V(T) 0.7. There were strong correlations between P(ETCO(2)) and P(aCO(2)) in all the V(D)/V(T) ranges. The P(ETCO(2))-P(aCO(2)) difference increased predictably with increasing V(D)/V(T).
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                Author and article information

                Contributors
                f.b.stephens@exeter.ac.uk
                Journal
                Exp Physiol
                Exp Physiol
                10.1111/(ISSN)1469-445X
                EPH
                expphysiol
                Experimental Physiology
                John Wiley and Sons Inc. (Hoboken )
                0958-0670
                1469-445X
                30 November 2022
                January 2023
                : 108
                : 1 ( doiID: 10.1113/eph.v108.1 )
                : 50-62
                Affiliations
                [ 1 ] Department of Sport and Health Sciences College of Life and Environmental Sciences University of Exeter Exeter UK
                Author notes
                [*] [* ] Correspondence

                Francis B. Stephens, Department of Sport and Health Sciences, College of Life and Environmental Sciences, St Luke's Campus, Heavitree Road, University of Exeter, Exeter EX1 2LU, UK.

                Email: f.b.stephens@ 123456exeter.ac.uk

                Author information
                https://orcid.org/0000-0001-6838-1020
                https://orcid.org/0000-0003-3597-8562
                https://orcid.org/0000-0002-1740-6248
                https://orcid.org/0000-0001-6312-5351
                Article
                EPH13276
                10.1113/EP090531
                10103768
                36448400
                71decdaa-f3cc-4124-8e98-708d4bf59c7f
                © 2022 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 April 2022
                : 07 November 2022
                Page count
                Figures: 7, Tables: 0, Pages: 13, Words: 6208
                Funding
                Funded by: Royal Navy
                Award ID: 680022329
                Categories
                Research Article
                Research Articles
                Environmental & Exercise
                Custom metadata
                2.0
                1 January 2023
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.4.0 mode:remove_FC converted:02.04.2024

                Anatomy & Physiology
                apnoea,breath‐hold,cardiovascular,end‐tidal,haemoglobin,respiratory
                Anatomy & Physiology
                apnoea, breath‐hold, cardiovascular, end‐tidal, haemoglobin, respiratory

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