Search

Purpose Serum erythropoietin (EPO) concentration is increased following static apnoea-induced hypoxia. However, the acute erythropoietic responses to a series of dynamic apnoeas in non-divers (ND) or elite breath-hold divers (EBHD) are unknown. Methods Participants were stratified into EBHD (n = 8), ND (n = 10) and control (n = 8) groups. On two separate occasions, EBHD and ND performed a series of five maximal dynamic apnoeas (DYN) or two sets of five maximal static apnoeas (STA). Control performed a static eupnoeic (STE) protocol to control against any effects of water immersion and diurnal variation on EPO. Peripheral oxygen saturation (SpO2) levels were monitored up to 30 s post each maximal effort. Blood samples were collected at 30, 90, and 180 min after each protocol for EPO, haemoglobin and haematocrit concentrations. Results No between group differences were observed at baseline (p > 0.05). For EBHD and ND, mean end-apnoea SpO2 was lower in DYN (EBHD, 62 ± 10%, p = 0.024; ND, 85 ± 6%; p = 0.020) than STA (EBHD, 76 ± 7%; ND, 96 ± 1%) and control (98 ± 1%) protocols. EBHD attained lower end-apnoeic SpO2 during DYN and STA than ND (p p p = 0.622). EBHD EPO increased from baseline (6.85 ± 0.9mlU/mL) by 60% at 30 min (10.82 ± 2.5mlU/mL, p = 0.017) and 63% at 180 min (10.87 ± 2.1mlU/mL, p = 0.024). Serum EPO did not change after the STA (EBHD, p = 0.534; ND, p = 0.850) and STE (p = 0.056) protocols. There was a significant negative correlation (r = − 0.49, p = 0.003) between end-apnoeic SpO2 and peak post-apnoeic serum EPO concentrations. Conclusions The novel findings demonstrate that circulating EPO is only increased after DYN in EBHD. This may relate to the greater hypoxemia achieved by EBHD during the DYN.

Introduction: Acute apnea evokes bradycardia and peripheral vasoconstriction in order to conserve oxygen, which is more pronounced with face immersion. This response is contrary to the tachycardia and increased blood flow to muscle tissue related to the higher oxygen consumption during exercise. The aim of this study was to investigate cardiovascular and metabolic responses of dynamic dry apnea (DRA) and face immersed apnea (FIA).Methods: Ten female volunteers (17.1 ± 0.6 years old) naive to breath-hold-related sports, performed a series of seven dynamic 30 s breath-holds while cycling at 25% of their peak power output. This was performed in two separate conditions in a randomized order: FIA (15°C) and DRA. Heart rate and muscle tissue oxygenation through near-infrared spectroscopy were continuously measured to determine oxygenated (m[O2Hb]) and deoxygenated hemoglobin concentration (m[HHb]) and tissue oxygenation index (mTOI). Capillary blood lactate was measured 1 min after the first, third, fifth, and seventh breath-hold.Results: Average duration of the seven breath-holds did not differ between conditions (25.3 s ± 1.4 s, p = 0.231). The apnea-induced bradycardia was stronger with FIA (from 134 ± 4 to 85 ± 3 bpm) than DRA (from 134 ± 4 to 100 ± 5 bpm, p < 0.001). mTOI decreased significantly from 69.9 ± 0.9% to 63.0 ± 1.3% (p < 0.001) which is reflected in a steady decrease in m[O2Hb] (p < 0.001) and concomitant increase in m[HHb] (p = 0.001). However, this was similar in both conditions (0.121 < p < 0.542). Lactate was lower after the first apnea with FIA compared to DRA (p = 0.038), while no differences were observed in the other breath-holds.Conclusion: Our data show strong decreases in heart rate and muscle tissue oxygenation during dynamic apneas. A stronger bradycardia was observed in FIA, while muscle oxygenation was not different, suggesting that FIA did not influence muscle oxygenation. An order of mechanisms was observed in which, after an initial tachycardia, heart rate starts to decrease after muscle tissue deoxygenation occurs, suggesting a role of peripheral vasoconstriction in the apnea-induced bradycardia. The apnea-induced increase in lactate was lower in FIA during the first apnea, probably caused by the stronger bradycardia.

Background: Successful cardiopulmonary resuscitation after drowning or avalanche is often attributed to hypothermia-induced decrease in metabolism, which adapts the oxygen demand to the amount supplied under cardiac compression. Four decades ago, we speculated if oxygen-sparing mechanisms like those found in marine mammals, may improve cerebral oxygenation during acute airway blockade in humans. We investigated hemodynamic changes during steady state ergometer cycling with intermittent periods of apnea and face immersion (AFI) in ice-cold water. During AFI, heart rate (HR) dropped by 58% whereas average blood velocity (ABV) determined by means of a Doppler ultrasound velocity meter (UNIDOP University of Oslo, Oslo, Norway) fell by 85% in the radial artery and rose by 67% in the vertebral artery. Similar changes occured in radial artery ABV, albeit more slowly, when the test subject only held his breath while cycling. When he breathed via a snorkel during face immersion, HR remained unchanged while radial artery ABV fell transiently and subsequently returned to its pre-immersion level. These findings later were confirmed by other investigators. Moreover, a recent study revealed that the seal even has a system for selective brain cooling during the dive. Conclusion: Our research has confirmed prioritized cerebral circulation during AFI in cold water. We hypothesize that these changes may improve brain oxygenation due both to greater blood flow and possibly also to faster brain cooling, as demonstrated in diving seals. Keywords: apnea, breath-hold, cardiopulmonary resuscitation, diving response, hypothermia

Most terrestrial animals demonstrate an autonomic reflex that facilitates survival during prolonged submersion under water. This diving response is characterized by bradycardia, apnea and selective increases in peripheral vascular resistance. Stimulation of the nose and nasal passages is thought to be primarily responsible for providing the sensory afferent signals initiating this protective reflex. Consequently, the primary objective of this research was to determine the central terminal projections of nerves innervating the external nose, nasal vestibule and nasal passages of rats. We injected wheat germ agglutinin (WGA) into specific external nasal locations, into the internal nasal passages of rats both with and without intact anterior ethmoidal nerves (AENs), and directly into trigeminal nerves innervating the nose and nasal region. The central terminations of these projections within the medulla were then precisely mapped. Results indicate that the internal nasal branch of the AEN and the nasopalatine nerve, but not the infraorbital nerve (ION), provide primary innervation of the internal nasal passages. The results also suggest afferent fibers from the internal nasal passages, but not external nasal region, project to the medullary dorsal horn (MDH) in an appropriate anatomical way to cause the activation of secondary neurons within the ventral MDH that express Fos protein during diving. We conclude that innervation of the anterior nasal passages by the AEN and nasopalatine nerve is likely to provide the afferent information responsible for the activation of secondary neurons within MDH during voluntary diving in rats.

This research was designed to investigate the role of the anterior ethmoidal nerve (AEN) during repetitive trained diving in rats, with specific attention to activation of afferent and efferent brainstem nuclei that are part of this reflexive response. The AEN innervates the nose and nasal passages and is thought to be an important component of the afferent limb of the diving response. Male Sprague-Dawley rats (N = 24) were trained to swim and dive through a 5 m underwater maze. Some rats (N = 12) had bilateral sectioning of the AEN, others a Sham surgery (N = 12). Twelve rats (6 AEN cut and 6 Sham) had 24 post-surgical dive trials over 2 h to activate brainstem neurons to produce Fos, a neuronal activation marker. Remaining rats were non-diving controls. Diving animals had significantly more Fos-positive neurons than non-diving animals in the caudal pressor area, ventral medullary dorsal horn, ventral paratrigeminal nucleus, nucleus tractus solitarius, rostral ventrolateral medulla, Raphe nuclei, A5, Locus Coeruleus, and Kölliker-Fuse area. There were no significant differences in brainstem Fos labeling in rats diving with and without intact AENs. Thus, the AENs are not required for initiation of the diving response. Other nerve(s) that innervate the nose and nasal passages, and/or suprabulbar activation of brainstem neurons, may be responsible for the pattern of neuronal activation observed during repetitive trained diving in rats. These results help define the central neuronal circuitry of the mammalian diving response.

A dramatic bradycardia is induced by underwater submersion in vertebrates. The location of parasympathetic preganglionic cardiac motor neurons driving this aspect of the diving response was investigated using cFos immunohistochemistry combined with retrograde transport of cholera toxin subunit B (CTB) to double-label neurons. After pericardial injections of CTB, trained rats voluntarily dove underwater, and their heart rates (HR) dropped immediately to 95 ± 2 bpm, an 80% reduction. After immunohistochemical processing, the vast majority of CTB labeled neurons were located in the reticular formation from the rostral cervical spinal cord to the facial motor nucleus, confirming previous studies. Labeled neurons caudal to the rostral ventrolateral medulla were usually spindle-shaped aligned along an oblique line running from the dorsal vagal nucleus to the ventrolateral reticular formation, while those more rostrally were multipolar with extended dendrites. Nine percent of retrogradely-labeled neurons were positive for both cFos and CTB after diving and 74% of these were found rostral to the obex. CTB also was transported transganglionically in primary afferent fibers, resulting in large granular deposits in dorsolateral, ventrolateral, and commissural subnuclei of the nucleus tractus solitarii (NTS) and finer deposits in lamina I and IV-V of the trigeminocervical complex. The overlap of parasympathetic preganglionic cardiac motor neurons activated by diving with those activated by baro- and chemoreceptors in the rostral ventrolateral medulla is discussed. Thus, the profound bradycardia seen with underwater submersion reinforces the notion that the mammalian diving response is the most powerful autonomic reflex known.

Pioneering studies by Per Scholander indicated that the diving response consists of reflexly induced apnea, bradycardia and an alteration of blood flow that maintains perfusion of the heart and brain. More recently field physiological studies have shown that many marine animals can adjust cardiorespiratory aspects of their diving response depending upon the behavioral situation. This could suggest that the very labile heart rate during diving is under direct cortical control. However, the final control of autonomic nervous system functioning resides within the brainstem and not the cortex. Many physiologists regard the brain as a “black box” where important neuronal functioning occurs, but the complexity of such functioning leaves systematic investigation a daunting task. As a consequence the central control of the diving response has been under-investigated. Thus, to further advance the field of diving physiology by understanding its central neuronal control, it would be first necessary to understand the reflex circuitry that exists within the brainstem of diving animals. To do this will require an appropriate animal model. In this review, two animals, the muskrat and rat, will be offered as animal models to investigate the central aspects of the diving response. Firstly, although these rodents are not marine animals, natural histories indicate that both animals can and do exploit aquatic environments. Secondly, physiological recordings during natural and simulated diving indicate that both animals possess the same basic physiological responses to underwater submersion that occur in marine animals. Thirdly, the size and ease of housing of both animals makes them attractive laboratory research animals. Finally, the enormous amount of scientific literature regarding rodent brainstem autonomic control mechanisms, and the availability of brain atlases, makes these animals ideal choices to study the central control of the mammalian diving response.

Humans share with seals the ability to contract the spleen and increase circulating hemat-ocrit, which may improve apneic performance by enhancing gas storage. Seals have large spleens and while human spleen size is small in comparison, it shows great individual variation. Unlike many marine mammals, human divers rely to a great extent on lung oxygen stores, but the impact of lung volume on competitive apnea performance has never been determined. We studied if spleen- and lung size correlated with performance in elite apnea divers. Volunteers were 14 male apnea world championship participants, with a mean (SE) of 5.8 (1.2)years of previous apnea training. Spleen volume was calculated from spleen length, width, and thickness measured via ultrasound during rest, and vital capacity via spirometry. Accumulated competition scores from dives of maximal depth, time, and distance were compared to anthropometric measurements and training data. Mean (SE) diving performance was 75 (4) m for constant weight depth, 5 min 53 (39) s for static apnea and 139 (13) m for dynamic apnea distance. Subjects' mean height was 184 (2) cm, weight 82 (3) kg, vital capacity (VC) 7.3 (0.3) L and spleen volume 336 (32) mL. Spleen volume did not correlate with subject height or weight, but was positively correlated with competition score (r = 0.57; P< 0.05). Total competition score was also positively correlated with VC (r = 0.54; PArt. No.: Article 173

The mammalian diving response is a powerful autonomic adjustment to underwater submersion greatly affecting heart rate, arterial blood pressure and ventilation. The bradycardia is known to be mediated by the parasympathetic nervous system, arterial blood pressure is mediated via the sympathetic system and still other circuits mediate the respiratory changes. In the present study we investigate the cardiorespiratory responses and the brainstem neurons activated by voluntary diving of trained rats, and, compare them to control and swimming animals which did not dive. We show that the bradycardia and increase in arterial blood pressure induced by diving were significantly different that induced by swimming. Neuronal activation was calculated after immunohistochemical processing of brainstem sections for Fos protein. Labeled neurons were counted in the caudal pressor area, the medullary dorsal horn, subnuclei of the nucleus tractus solitarii, the nucleus raphe pallidus, the rostroventrolateral medulla, the A5 area, the nucleus locus coeruleus, the Kölliker-Fuse area and the external lateral and superior lateral subnuclei of the parabrachial nucleus. All these areas showed significant increases in Fos labeling when data from voluntary diving rats were compared to control rats and all but the commissural subnucleus of the nucleus tractus solitarii, A5 area, and raphe pallidus were different from swimming rats. These data provide a substrate for more precise experiments to determine the role of these nuclei in the reflex circuits driving the diving response.

The diving response is characterized by bradycardia, apnea, and increased peripheral resistance. This reflex response is initiated by immersing the nose in water. Because the anterior ethmoidal nerve (AEN) innervates the nose, our hypothesis was that intact AENs are essential for initiating the diving response in voluntarily diving rats. Heart rate (HR) and arterial blood pressure (BPa) were monitored using implanted biotransmitters. Sprague-Dawley rats were trained to voluntarily swim 5 m underwater. During diving, HR decreased from 480 ± 15 to 99 ± 5 bpm and BPa increased from 136 ± 2 to 187 ± 3 mmHg. Experimental rats (N = 9) then received bilateral AEN sectioning, while Sham rats (N = 8) did not. During diving in Experimental rats 7 days after AEN surgery, HR decreased from 478 ± 13 to 76 ± 4 bpm and BPa increased from 134 ± 3 to 186 ± 4 mmHg. Responses were similar in Sham rats. Then, during nasal stimulation with ammonia vapors in urethane-anesthetized Experimental rats, HR decreased from 368 ± 7 to 83 ± 4 bpm, and BPa increased from 126 ± 7 to 175 ± 4 mmHg. Responses were similar in Sham rats. Thus, 1 week after being sectioned the AENs are not essential for initiating a full cardiorespiratory response during both voluntary diving and nasal stimulation. We conclude that other nerve(s) innervating the nose are able to provide an afferent signal sufficient to initiate the diving response, although neuronal plasticity within the medullary dorsal horn may be necessary for this to occur.

We previously observed that the spleen contracts during maximal apnea and stays contracted for prolonged period after series of apneas. The role of central mechanisms in the initial splenic contraction and cardiovascular responses during apnea is unknown. Now, we investigated changes occurring during short apneas lasting 15 s during which arterial O2 and CO2 levels are unchanged. We studied changes in splenic size and blood flow, as well as central and peripheral cardiovascular parameters before, during and after a single apnea both with and without forehead cold stimulation to isolate the effect of the diving response from the apnea. Splenic artery diameter and blood velocity were not significantly changed during apnea. Spleen volume was reduced by about 20% as early as 3 seconds after the start of apnea and was quickly recovered after cessation of the attempt. Heart rate increased early during the apnea, simultaneously with spleen volume change to compensate for reductions in stroke volume and arterial pressure. Heart rate recovered towards baseline levels later in each apnea as arterial pressure was restored in concert with a rise in peripheral resistance. Splenic contraction and cardiovascular changes were not influenced by facial cold stimulation. Results indicate that sympathetic nerve activation to spleen and heart occurs during initial stage of the diving.