Static Apnea Research Articles

Effects of dietary inorganic nitrate on static and dynamic breath-holding in humans

Inorganic nitrate has been shown to reduce oxygen cost during exercise. Since the nitrate-nitrite-NO pathway is facilitated during hypoxia, we investigated the effects of dietary nitrate on oxygen consumption and cardiovascular responses during apnea. These variables were measured in two randomized, double-blind, placebo-controlled, crossover protocols at rest and ergometer exercise in competitive breath-hold divers. Subjects held their breath for predetermined times along with maximum effort apneas after two separate 3-day periods with supplementation of potassium nitrate/placebo.In contrast to our hypothesis, nitrate supplementation led to lower arterial oxygen saturation (SaO2, 77±3%) compared to placebo (80±2%) during static apnea, along with lower end-tidal fraction of oxygen (FETO2) after 4min of apnea (nitrate 6.9±0.4% vs. placebo 7.6±0.4%). Maximum apnea duration was shorter after nitrate (329±13s) compared to placebo (344±13s). During cycle ergometry nitrate had no effect on SaO2, FETO2 or maximum apnea duration. The negative effects of inorganic nitrate during static apnea may be explained by an attenuated diving response.

Fasting improves static apnea performance in elite divers without enhanced risk of syncope

In competitive apnea divers, the nutritional demands may be essentially different from those of, for example, endurance athletes, where energy resources need to be maximised for successful performance. In competitive apnea, the goal is instead to limit metabolism, as the length of the sustainable apneic period will depend to a great extent on minimising oxygen consumption. Many but not all elite divers fast before performing static apnea in competition. This may increase oxygen consumption as mainly lipid stores are metabolised but could also have beneficial effects on apneic duration. Our aim was to determine the effect of over-night fasting on apnea performance. Six female and seven male divers performed a series of three apneas after eating and fasting, respectively. The series consisted of two 2-min apneas spaced by 3 min rest and, after 5 min rest, one maximal effort apnea. Apneas were performed at supine rest and preceded by normal respiration and maximal inspiration. Mean (±SD) time since eating was 13 h (±2 h 43 min) for the fasting and 1 h 34 min (±33 min) for the eating condition (P < 0.001). Mean blood glucose was 5.1 (±0.4) mmol/L after fasting and 5.9 (±0.7) mmol/L after eating (P<0.01). Lung volumes were similar in both conditions (NS). For the 2-min apneas, nadir SaO2 during fasting was 95 (±1)% and 92 (±2)% (P < 0.001) on eating and ETCO2 was lower in the fasting condition (P < 0.01) while heart rate (HR) during apnea was 74 (±10) bpm for fasting and 80 (±10) bpm for eating conditions (P < 0.01). Maximal apnea durations were 4 min 41 s (±43 s) during fasting and 3 min 51 s (±37 s) after eating (P < 0.001), and time without respiratory contractions was 31 s (25%) longer after fasting (P < 0.01). At maximal apnea termination, SaO2 and ETCO2 were similar in both conditions (NS) and apneic HR was 63 (±9) bpm for fasting and 70 (±10) bpm for eating (P < 0.01). The 22% longer apnea duration after fasting with analogous end apnea SaO2 levels suggests that fasting is beneficial for static apnea performance in elite divers, likely via metabolism-limiting mechanisms. The oxygen-conserving effect of the more pronounced diving response and possibly other metabolism-limiting mechanisms related to fasting apparently outweigh the enhanced oxygen consumption caused by lipid metabolism.

Heart rate changes (HR) and oxygen saturation in blood (AO2) dependency in relation to the static apnea duration (STA)

Heart rate changes (HR) and oxygen saturation in blood (AO2) dependency in relation to the static apnea duration (STA)

Acute dietary nitrate supplementation improves dry static apnea performance

Acute dietary nitrate (NO3−) supplementation has been reported to lower resting blood pressure, reduce the oxygen (O2) cost of sub-maximal exercise, and improve exercise tolerance. Given the proposed effects of NO3− on tissue oxygenation and metabolic rate, it is possible that NO3− supplementation might enhance the duration of resting apnea. If so, this might have important applications both in medicine and sport. We investigated the effects of acute NO3− supplementation on pre-apnea blood pressure, apneic duration, and the heart rate (HR) and arterial O2 saturation (SaO2) responses to sub-maximal and maximal apneas in twelve well-trained apnea divers. Subjects were assigned in a randomized, double blind, crossover design to receive 70ml of beetroot juice (BR; containing ∼5.0mmol of nitrate) and placebo juice (PL; ∼0.003mmol of nitrate) treatments. At 2.5h post-ingestion, the subjects completed a series of two 2-min (sub-maximal) static apneas separated by 3min of rest, followed by a maximal effort apnea. Relative to PL, BR reduced resting mean arterial pressure by 2% (PL: 86±7 vs. BR: 84±6mmHg; P=0.04). The mean nadir for SaO2 after the two sub-maximal apneas was 97.2±1.6% in PL and 98.5±0.9% in BR (P=0.03) while the reduction in HR from baseline was not significantly different between PL and BR. Importantly, BR increased maximal apneic duration by 11% (PL: 250±58 vs. BR: 278±64s; P=0.04). In the longer maximal apneas in BR, the magnitude of the reductions in HR and SaO2 were greater than in PL (P≤0.05). The results suggest that acute dietary NO3− supplementation may increase apneic duration by reducing metabolic costs.

Size matters: spleen and lung volumes predict performance in human apneic divers.

Humans share with seals the ability to contract the spleen and increase circulating hematocrit, 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; P < 0.05). The three highest scoring divers had the greatest spleen volumes, averaging 538 (53) mL, while the three lowest-scoring divers had a volume of 270 (71) mL (P < 0.01). VC was also greater in the high-scorers, at 7.9 (0.36) L as compared to 6.7 (0.19) L in the low scorers (P < 0.01). Spleen volume was reduced to half after 2 min of apnea in the highest scoring divers, and the estimated resting apnea time gain from the difference between high and low scorers was 15 s for spleen volume and 60 s for VC. We conclude that both spleen- and lung volume predict apnea performance in elite divers.

Reply to Lundberg, Larsen, and Weitzberg

to the editor: The letter of Lundberg et al. ([12][1]) does not relate directly to any of the articles we published in this journal ([1][2], [2][3], [6][4]). Rather, the correspondents make a general point on the potential risks to athletes who might choose to supplement their diet with nitrate or (

Cardiovascular changes during underwater static and dynamic breath-hold dives in trained divers

Limited information exists concerning arterial blood pressure (BP) changes in underwater breath-hold diving. Simulated chamber dives to 50 m of freshwater (mfw) reported very high levels of invasive BP in two divers during static apnea (SA), whereas a recent study using a noninvasive subaquatic sphygmomanometer reported unchanged or mildly increased values at 10 m SA dive. In this study we investigated underwater BP changes during not only SA but, for the first time, dynamic apnea (DA) and shortened (SHT) DA in 16 trained breath-hold divers. Measurements included BP (subaquatic sphygmomanometer), ECG, and pulse oxymetry (arterial oxygen saturation, SpO₂, and heart rate). BP was measured during dry conditions, at surface fully immersed (SA), and at 2 mfw (DA and SHT DA), whereas ECG and pulse oxymetry were measured continuously. We have found significantly higher mean arterial pressure (MAP) values in SA (∼40%) vs. SHT DA (∼30%). Postapneic recovery of BP was slightly slower after SHT DA. Significantly higher BP gain (mmHg/duration of apnea in s) was found in SHT DA vs. SA. Furthermore, DA attempts resulted in faster desaturation vs. SA. In conclusion, we have found moderate increases in BP during SA, DA, and SHT DA. These cardiovascular changes during immersed SA and DA are in agreement with those reported for dry SA and DA.

Hypoxic Syncope in a Competitive Breath-Hold Diver with Elevation of the Brain Damage Marker S100B

Competitive breath-hold divers can accomplish previously unbelievable performances; e.g., the current world record for apnea during rest ("static apnea") is 11 min 35 s. However, whether such performances are associated with a risk for hypoxic brain damage has not been established. A breath-hold diver's competitive performance resulted in a loss of consciousness, after which he was subjected to a medical examination by the event physician. Blood samples were collected for analysis of the brain damage marker S100B in serum. The S100B in serum was 0.100 microg x L(-1) in the blood sample collected 15 min after the loss of consciousness. At 1 and 5 d after the incident it was 0.097 microg x L(-1) and 0.045 microg x L(-1) respectively. The elevated level of S100B, close to the upper reference limit (0.105 microg x L(-1)) indicates that the incident affected the integrity of the central nervous system. Even though this case does not establish that hypoxic brain damage is an inherent risk with loss of consciousness in competitive breathhold diving, the observation raises concerns. We suggest that it should be considered that repetitive exposures to prolonged apneas leading to severe hypoxia may be associated with negative long-term effects.

Don't Hold Your Breath

Competitive breath-holders can float face down in a pool for more than 4 minutes, and the world record is 11 minutes 35 seconds. That can't be good for their brains, right? To find out, researchers at Lund University in Sweden had nine trained breath-holders lie face-up on a couch and hold their breath to mimic the so-called static apnea pool competition. The breath-holders started with their normal warm-up routines: hyperventilation and “lung packing” (using tongue and throat muscles to force extra air into the lungs). Then they stopped breathing for an average of 5.5 minutes. The volunteers' blood oxygen levels dropped by almost 80%, and concentrations of the protein S100B—a standard marker for brain damage—increased by 37%, the researchers reported online 2 July in the Journal of Applied Physiology . S100B is normally found inside brain cells and fluid but seeps into the bloodstream when an injury disrupts the brain's protective blood-brain barrier. The breath-holders' concentrations were lower than those seen in stroke or traumatic brain injury patients, and the levels recovered after 2 hours. “We probably only saw a temporary opening of the blood-brain barrier,” says researcher Johan Andersson, but he warns that it is unclear if repeated barrier openings might produce long-term brain damage. Ralph Potkin, a pulmonologist at the Beverly Hills Center for Hyperbaric Medicine in Los Angeles, California, calls the findings “disconcerting.” But John Fitz-Clarke, a diving physiologist at Dalhousie University in Halifax, Canada, says that “it's way too premature to draw any conclusions about brain damage” from these findings.

Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations

The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., "static apnea" (average: 335 s, range: 281-403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O(2) and CO(2) (Pa(O(2)) and Pa(CO(2))) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with Pa(O(2)) and Pa(CO(2)) reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 microg/l at the start of apnea to 0.083 microg/l after the apnea (P < 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects.

Hypoxia and cardiac arrhythmias in breath-hold divers during voluntary immersed breath-holds

The incidence and nature of cardiac arrhythmias during static apnea were studied by monitoring the electrocardiogram (ECG) and oxygen saturation (SaO(2)) of 16 recreational breath-hold divers. All subjects completed a maximal apnea with a mean (+/-SD) breath-hold duration of 281 (+/-73) s without clinical complications. Both heart rate (HR) and SaO(2) decreased significantly with breath-hold duration. The decline in SaO(2) was inversely related to the decline in HR (r = -0.55, P < 0.05). Cardiac arrhythmias (supraventricular and ventricular premature complexes, right bundle branch block) occurred in 12/16 (77%) subjects and were related to breath-hold duration. Subjects with atrial premature complexes (n = 9) had a reduced BMI (P = 0.016) and a higher decline of the terminal SaO(2) (P = 0.01). In conclusion, ectopic arrhythmias were common during maximal static apneas for training purposes. The results indicate that the occurrence of ectopic beats is associated with individual factors such as the tolerable SaO(2) decrease.

Effects of Maximal Static Apnea on Antioxidant Defenses in Trained Free Divers

To investigate the effects of maximal static apnea on plasma antioxidant status, oxidative stress, and antioxidant enzyme activities in trained free divers. Blood was taken from apnea-trained (Tr) and control (Con) subjects at baseline (B) and after one (A1), three (A3), and five (A5) apneas. Trolox equivalent antioxidant capacity (TEAC), ferric reducing ability of plasma (FRAP), uric acid, and bilirubin assays assessed plasma antioxidant status and malondialdehyde (MDA) quantified the oxidative stress response. The activities of erythrocyte antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were determined at baseline and after the fifth apnea. TEAC was significantly higher in divers versus controls after A1 (P < 0.05). A group effect of SOD activity indicated higher activity throughout the protocol in Tr (mean +/- SD; Con, 43.2 +/- 10.1 U.g Hb; Tr, 50.1 +/- 7.3 U.g Hb; P = 0.04). With no other group differences, the groups' data were combined. Apnea significantly increased SOD (B, 44.1 +/- 11.1 U.g Hb; A5, 48.1 +/- 7.5 U.g Hb; P < 0.05) and GPx activity (B, 60.5 +/- 14.9 U.g Hb; A5, 70.1 +/- 16.0 U.g Hb; P = 0.02); however, CAT activity decreased (B, 5.25 +/- 0.59 U.mg Hb; A5, 5.00 +/- 0.53 U.mg Hb; P = 0.03). MDA was unaffected by apnea (P = 0.32). Trained free divers have increased SOD activity during apnea; however, there is little difference in their antioxidant and oxidative stress responses compared with controls. In both groups, acute changes in antioxidant enzyme activities suggest that they may protect from excessive antioxidant depletion and oxidative stress during apnea.

Static Apnea Effect on Heart Rate and Its Variability in Elite Breath-Hold Divers

The diving response includes cardiovascular adjustments known to decrease oxygen uptake and thus prolong apnea duration. As this diving response is in part characterized by a pronounced decrease in heart rate (HR), it is thought to be vagally mediated. In five professional breath-hold divers (BHDs) and five less-trained controls (CTL), we investigated whether the diving response is in fact associated with an increase in the root mean square successive difference of the R-R intervals (RMSSD), a time-domain heart rate variability (HRV) index. HR behavior and arterial oxygen saturation (SaO2) were continuously recorded during one maximal apnea. Short-term changes in SaO2, HR, and RMSSD were calculated over the complete apnea duration. BHDs presented bi-phasic HR kinetics, with two HR decreases (32 +/- 17% and 20 +/- 10% of initial HR). The second HR decrease, which was concomitant to the pronounced SaO2 decrease, was also simultaneous to a marked increase in RMSSD. CTL showed only one HR decrease (50 +/- 10% of initial HR), which appeared before the concomitant SaO2 and RMSSD changes. When all subject data were combined, arterial desaturation was positively correlated with total apnea time (r = 0.87, P < 0.01). This study indicates that baroreflex stimulation and hypoxia may be involved in the bi-phasic HR response of BHDs and thus in their longer apnea duration.

The modulation of antioxidant defences in response to maximal static apnea

Apneic behaviour can result in circulatory oxidative stress suggesting such practices could negatively affect human health. This study quantified the oxidative stress response in apnea trained and control subjects and determined changes in their antioxidant systems after five static apneas. Blood was taken at baseline (B) and after the first (A1), third (A3) and fifth (A5) apneas. Plasma antioxidant status was assessed using trolox equivalent antioxidant capacity (TEAC), ferric reducing ability of plasma (FRAP) and bilirubin assays. The activity of RBC antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidise (GPx) were determined and plasma malondialdehyde (MDA) assessed oxidative stress. Plasma bilirubin decreased from baseline to A1 (controls −17.2%; divers −17.8%; P<0.01) as did FRAP (controls −3.2%, divers −3.2%; P<0.03). Significant group differences in TEAC were noted at A1 (controls 1.76±0.18; divers 1.91±0.09 MEqu/Trolox/L; P<0.05). From baseline to A5, apnea increased SOD (controls 11.3%; divers 11.8%; P<0.05) and GPx activity (controls 14.8%; divers 17.7%; P<0.04), but decreased CAT activity (controls −7.3%; divers −2.0%; P<0.03). Apnea did not affect MDA (P>0.32). These data suggest there was no oxidative stress response to static apnea and that the modulation of antioxidant enzyme activity may be responsible for this protection.

Loss of Motor Control and/or Loss of Consciousness during Breath-Hold Competitions

Since the first official world championships in breath-hold diving (1996), a sport has developed where the athletes compete in various disciplines of breath-hold diving. One of the rules is that the diver should surface from a dive without showing any signs of hypoxia. Depending on the severity of hypoxia, a diver may suffer disqualifying signs such as loss of consciousness (LOC) or loss of motor control (LMC), the latter including signs such as confusion, affected postural control, spasms or speech problems. Data was collected from the results of the major international competitions following AIDA guidelines (Association International pour le Dévelopment de l'Apnée) in 1998, 2001-2004. The data was analyzed for frequency of LOC and LMC during constant weight diving and during static apnea. In constant weight diving, the diver swims down (and up) as deeply as possible along a vertically suspended rope (current record 105 m). In static apnea, the diver strives for maximum duration, floating motionless face down in a pool (current record 8.58 min). A total of 601 static apnea (SA) performances and 596 constant weight dives were judged in the six competitions. On average, 10 % of SA, and 11 % of CW performances were disqualified due to signs of hypoxia. For the competitions in 2002-2004, a distinction was made in the rules between LOC and LMC; of a total number of 355 SA performances, 1.1 % resulted in LOC, while 9.6 % resulted in LMC. For CW, the number was 344 with 6.1 % LOC and 6.1 % LMC. Despite the relatively high incidence of dramatic signs, it is noteworthy that there have been no reports of fatal accidents or permanent injuries from any of the above-mentioned competitions. This descriptive paper shows a relatively high incidence of disqualifications due to signs of hypoxia in breath-hold competitions 1998-2004.

Influence of lung volume, glossopharyngeal inhalation and P ET O2 and P ET CO2 on apnea performance in trained breath-hold divers

Breath-hold divers train and compete in maximal apnea performance. Glossopharyngeal inhalation (GI) is commonly used to increase lung volume above vital capacity (VC) prior to apnea. We investigated the hypothesis that this practice would increase apnea performance and relaxed airway pressure. Seven well-trained breath-hold divers performed maximal bouts of apnea at three different lung volumes (85% VC, VC and VC + GI) both at rest (dry static apnea) and during underwater swimming (dynamic apnea). Heart rate, apnea time and end tidal PCO(2) and PO(2) (P (ET) CO(2) and P (ET) O(2)) were recorded. In addition, relaxed airway pressure was measured after GI. Maximal GI increased lung volume by 1.59+/-0.57 l above VC and increased relaxed airway pressure to from 3.5+/-0.5 to 8.7+/-1.7 kPa. Dry static apnea time was higher at VC + GI (346+/-46 s) than at VC (309+/-38 s, P<0.05) and 85% VC (297+/-48 s, P<0.01). Likewise, dynamic apnea time was higher at VC + GI (97+/-27 s) than at VC (78+/-14 s, P<0.05) and 85% VC (71+/-17 s, P<0.05). P (ET) O(2) values reached 3.5+/-0.6 kPa at the end of dry static apnea bouts and this was not different from dynamic apnea when taking hydrostatic pressure at swimming depth into account (3.7+/-0.6 kPa, P=0.48). In conclusion, GI increases lung volume, relaxed airway pressure and apnea performance in well-trained breath-hold divers.

Effet d’une situation d’apnée statique sur les capacités individuelles d’estimation du temps

Introduction. – Apnea is known to induce specific physiological adaptation in order to protect brain and heart from hypoxia. During apnea, ability to accurately estimate time is the main factor to keep watch over it in order to perform safely. Therefore, the present study aimed to analyse the effect of static apnea on internal clock processes. Fact synthesis. – As expected, continuous heart rate monitoring appeared to be a good marker of biological activity. Five trials of time production (20 s) were performed by the subjects, in a sitting position using a chronometer. Time production was studied during three experimental conditions: at rest before static apnea, during five short static apneas (less than 1 min) and at rest after static apneas. Compared to rest, static apnea induced a bradycardia and an underestimation of time interval. Conclusion. – As previously reported in the literature, time processes and biological activity seemed to be connected. The apneic bradycardia could reflect a decrease in biological activity (primarily in order to decrease oxygen uptake) which might consequently influence time estimation mechanisms. If subjects underestimate time during static apnea, then any additional time spent in breath-hold condition could increase oxygen deficit and therefore lead to free diving accident.

Breath-hold training of humans reduces oxidative stress and blood acidosis after static and dynamic apnea.

Repeated epochs of breath-holding were superimposed to the regular training cycling program of triathletes to reproduce the adaptative responses to hypoxia, already described in elite breath-hold divers [Respir. Physiol. Neurobiol. 133 (2002) 121]. Before and after a 3-month breath-hold training program, we tested the response to static apnea and to a 1-min dynamic forearm exercise executed during apnea (dynamic apnea). The breath-hold training program did not modify the maximal performances measured during an incremental cycling exercise. After training, the duration of static apnea significantly lengthened and the associated bradycardia was accentuated; we also noted a reduction of the post-apnea decrease in venous blood pH and increase in lactic acid concentration, and the suppression of the post-apnea oxidative stress (increased concentration of thiobarbituric acid reactive substances). After dynamic apnea, the blood acidosis was reduced and the oxidative stress no more occurred. These results suggest that the practice of breath-holding improves the tolerance to hypoxemia independently from any genetic factor.

Oxygen consumption and carbon dioxide production during breath-hold diving.

ArticleOxygen consumption and carbon dioxide production during breath-hold diving.A B Craig Jr, and W L MeddA B Craig Jr, and W L MeddPublished Online:01 Feb 1968https://doi.org/10.1152/jappl.1968.24.2.190MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByBreath‐Hold Diving25 March 2018Blood biomarkers indicate mild neuroaxonal injury and increased amyloid β production after transient hypoxia during breath-hold diving7 July 2016 | Brain Injury, Vol. 30, No. 10Acute dietary nitrate supplementation improves dry static apnea performanceRespiratory Physiology & Neurobiology, Vol. 182, No. 2-3Lung compression effects on gas exchange in human breath-hold divingRespiratory Physiology & Neurobiology, Vol. 165, No. 2-3Physiological and Clinical Aspects of Apnea DivingClinics in Chest Medicine, Vol. 26, No. 3Reduced oxidative stress and blood lactic acidosis in trained breath-hold human diversRespiratory Physiology & Neurobiology, Vol. 133, No. 1-2Évaluation de la lactatémie au cours d’exercices en apnée: détermination d’une vitesse maximale de nageScience & Sports, Vol. 14, No. 2Hyperbaria: Breath‐hold Diving1 January 2011Energetics of underwater swimming with SCUBAMedicine & Science in Sports & Exercise, Vol. 28, No. 5Heart rate, alveolar gases and blood lactate during synchronized swimming14 November 2007 | Journal of Sports Sciences, Vol. 11, No. 2Gas Exchange in Hypoxia, Apnea, and Hyperoxia1 January 2011The Comparative Physiology of Diving in VertebratesRespiratory Physiology of Freely Diving Harbor Seals (Phoca vitulina)Physiological Zoology, Vol. 53, No. 4SOME COMMENTS ON A SKIN‐DIVING DEATH1 April 1971 | Medical Journal of Australia, Vol. 1, No. 15HEAT EXCHANGE BETWEEN MAN AND THE WATER ENVIRONMENTDas Verhalten der endexspiratorischen Atemgasdrucke, der O2-Aufnahme und CO2-Abgabe nach einfacher Apnoe im Wasser, an Land und apnoeischem TauchenPfl�gers Archiv European Journal of Physiology, Vol. 311, No. 4Pulmonary and Circulatory Adjustments Determining the Limits of Depths in Breathhold DivingScience, Vol. 162, No. 3857Depth limits of breath hold diving(an example of fennology)Respiration Physiology, Vol. 5, No. 1 More from this issue > Volume 24Issue 2February 1968Pages 190-202 https://doi.org/10.1152/jappl.1968.24.2.190PubMed5637682History Published online 1 February 1968 Published in print 1 February 1968 Metrics