Andersson, J P A, Biasoletto-Tjellström, G, and Schagatay, E K A
Effects of the human diving response on the alveolar gas exchange during apnea. In manuscript, 2002.

Andersson, J P A, Linér, M H, Fredsted, A, and Schagatay, E K A
Alveolar gas exchange and cardiovascular responses during apneas in exercising humans. In manuscript, 2002.

Schagatay, E, and van Kampen, M
Apneic snout immersion in trained pigs elicits a "diving response". Advances in Experimental Medicine and Biology 393:73-76, 1995.

 

Schagatay, E, van Kampen, M, and Andersson, J
Effects of repeated apneas on apneic time and diving response in non-divers. Undersea and Hyperbaric Medicine 26:143-149, 1999.

Abstract

Human breath-hold divers usually perform a series of dives with short intervals. Repeated apneas prolong apneic time, and an accentuated diving response has been suggested to be the cause. The aim of this study was to investigate the effect of repeated apneas on apneic time and diving response in humans. Forty-one subjects performed a series of five apneas with face immersion in water of 10 degrees Centigrade, separated by 2-min intervals. Apneas were performed at rest and to individual maximal duration. Heart rate, mean arterial pressure, skin capillary blood flow, and respiratory movements were recorded. Thirty-eight of the subjects were used for analysis of cardiovascular parameters, and in 23 subjects the physiological breaking point could be detected by the involuntary breathing movements. Heart rate reduction and blood pressure increase were most prominent during the first apneic face immersion, while skin capillary blood flow reduction was most intense in the second apneic face immersion. Blood pressure and skin capillary blood flow during recovery from apneic episodes also changed throughout the series. Repetition increased apneic time by 55% and postponed the occurrence of involuntary breathing movements by 27% in subjects passing the physiological breaking point. We conclude that both physiologic factors, associated with the accumulation of CO2, and psychologic factors, related to the capacity to withstand the respiratory drive, contribute to the prolongation of apneic time whereas an increased diving response does not contribute.

Published by courtesy of "Undersea and Hyperbaric Medicine".

Key words: diving reflex, bradycardia, vasoconstriction, arterial blood pressure, breath-holding time, short-term training.

Holm, B, Schagatay, E, and Andersson, J
A possible physiological role of the face as a thermosensor in an ancient water ape and in present day humans. Perpectives in Human Biology 4:41-46, 1999.

Schagatay, E, and Andersson, J
Diving response and apneic time in humans. Undersea and Hyperbaric Medicine 25:13-19, 1998.

Abstract

The aim of this study was to compare apneic time with the human diving response, defined as heart rate (HR) reduction and reduced skin blood flow, in groups with varying degrees of breath-hold diving experience. Apneic time and HR reduction at apneas in air and apneas with face immersion in cold water were thus recorded in nine groups. Skin capillary blood flow was recorded in six of the groups. All subjects received the same information on maximizing apneic duration, and no information about their progress during the apneas. The longest apneas and the most pronounced cardiovascular adjustments were found in the young, trained divers. It was found that apneic time was significantly correlated to HR reduction among the nine groups (r = 0.94, P < 0.001), and to skin capillary blood flow reduction among the six groups where the parameter was measured (r = 0.82, P < 0.05). The correlation between HR reduction and skin capillary blood flow reduction was also significant (r = 0.85, P < 0.05). When the difference in HR reduction and apneic time between apneas in air and apneas with face immersion were compared in the nine groups, it was found that all groups reacted with a more pronounced HR reduction during apneas with face immersion. All groups without prior breath-hold diving experience were found to perform shorter apneas with face immersion than apneas in air, or apneas of the same duration in both conditions, which has been reported in other studies. However, in all groups with diving experience, the apneic time was prolonged during apneas with face immersion. The results of this study suggest an oxygen-conserving effect of the diving response in trained apneic divers.

 Published by courtesy of "Undersea and Hyperbaric Medicine".

 Key words: breath-hold, face immersion, bradycardia, vasoconstriction, oxygen conservation.

Andersson, J, and Schagatay, E
Arterial oxygen desaturation during apnea in humans. Undersea and Hyperbaric Medicine 25:21-25, 1998b.

Abstract

We studied the effect of the human diving response, defined as bradycardia and reduced peripheral blood flow, on arterial hemoglobin desaturation. We induced a diving response of different magnitudes by using apnea in air and apnea with face immersion. Each of 21 subjects performed five apneas in air and five apneas with face immersion in 10 degrees Centigrade water. Periods of apnea in both conditions were of the same duration in any individual subject (average: 126.4 s) and the order of air and water was equally distributed among subjects. Heart rate, skin capillary blood flow, arterial blood pressure, arterial hemoglobin oxygen saturation during apneas, and end-tidal fractions of CO2 after apneas were recorded with non-invasive methods. The bradycardia and capillary blood flow reduction during apnea in air (7.8 and 37.7% change from control, respectively) were significantly potentiated by face immersion (13.6 and 55.9%, respectively). Arterial hemoglobin desaturated more during apnea in air (2.7%) compared to during apnea with face immersion (1.4%). We conclude that the potentiation of the human diving response with face immersion in cold water leads to a smaller decrease in arterial hemoglobin saturation, which may reflect an oxygen-conserving effect.

Published by courtesy of "Undersea and Hyperbaric Medicine".

Key words: breath-holding, face immersion, bradycardia, vasoconstriction, diving response, oxygen saturation.

Holm, B, Schagatay, E, Kobayashi, T, Masuda, A, Ohdaira, T, and Honda, Y
Cardiovascular change in elderly male breath-hold divers (Ama) and their socio-economical background at Chikura in Japan. Applied Human Science 17:181-187, 1998.

Gennser, M., E. Schagatay, J. Andersson, B. Lagercrantz, D. Benoni, and H. Örnhagen. (1999) Cardiorespiratory effects of apnoeic dives and free ascents in two classes of divers. In: Shupak, A., R. Lincoln, and Y. Grossman (eds.) XXV Annual Scientific Meeting of the European Underwater and Baromedical Society, Haifa and Eilat, Israel: 228-231.

Örnhagen, H., E. Schagatay, J. Andersson, E. Bergsten, P. Gustafsson, and S. Sandström. (1998) Mechanisms of “buccal pumping” (“lung packing”) and its pulmonary effects. In: Gennser, M. (ed.) XXIV Annual Scientific Meeting of the European Underwater and Baromedical Society. National Defence Research Establishment, Stockholm, Sweden. FOA Report: FOA-B--98-00342--721--SE: 80-83.

 

Andersson, J., and E. Schagatay. (1998) Effects of the human diving response on oxygen consumption. In: Gennser, M. (ed.) XXIV Annual Scientific Meeting of the European Underwater and Baromedical Society. National Defence Research Establishment, Stockholm, Sweden. FOA Report: FOA-B--98-00342--721--SE: 84-87.

INTRODUCTION

During diving, marine mammals redistribute blood flow and reduce heart rate by the “diving response”. This response is part of their complex adaptations to sustain apnoea. The diving response in some marine mammals is considered to reduce the rate of oxygen consumption. A reduced rate of oxygen consumption has been observed in some species as a lower post-dive oxygen uptake compared to the pre-dive uptake. A diving response similar to that found in diving mammals and birds is induced when humans are breath-holding. The human diving response is enhanced during breath-hold diving when, in addition to the apnoea, the upper part of the face is immersed (4). In humans, the most pronounced effects are a bradycardia and a selective vasoconstriction, resulting in a redistribution of the blood flow towards the hypoxia-sensitive organs (e.g. the heart and brain). The effect of the human diving response on the rate of oxygen consumption has been a matter of debate, some results suggesting an effect while others do not. In studies on several groups of subjects with varying degrees of breath-hold diving experience we have found that the most experienced subjects (i.e., native breath-hold divers and trained under-water rugby players) react with a very profound diving response during apnoea, while subjects without experience in breath-hold diving display a less pronounced diving response (3). There was a strong correlation between the magnitude of the diving response, when fully established, and the apnoeic duration. This indicates that the diving response may reduce the rate of oxygen consumption during apnoeas in humans.

This study is divided in two parts. The first aim was to investigate if there was any difference in the desaturation of arterial haemoglobin resulting from apnoeas of the same duration in air and with face immersion in cold water. A more pronounced diving response at apnoeas with face immersion might reduce the rate of oxygen consumption, which could be reflected in a smaller degree of arterial haemoglobin desaturation during apnoea with face immersion in cold water compared to during apnoea in air.

The second aim was to study the rate of oxygen uptake after apnoeas with face immersion in cold water. The increased oxygen uptake after apnoea could be considered as a repayment for the reduction in body oxygen stores during apnoea, and hence reflecting the amount of oxygen consumed during the apnoea. If the rate of oxygen consumption during apnoeas is the same as during quiet breathing the total oxygen uptake during apnoeas and an associated recovery period would be expected to be equal to the oxygen uptake before the apnoeas. A reduced oxygen uptake could indicate a reduced oxygen consumption during apnoeas.


METHODS

All experiments were conducted in conformity with the principles of the Declaration of Helsinki and with approval from the Medical Faculty’s Research Ethics Committee. Procedures and instruments were demonstrated, and the volunteers gave their informed consent for participation. Each subject was told not to hyperventilate and to make a deep, but not maximal, inspiration before breath-holding. The subject did not swallow nor expire and relaxed during breath-holding. The subject assumed a prone position on a mattress with the head on a rigid pillow placed above a water container and the forearms on each side of the container. Water temperature was 9.5-10.5°C and ambient air temperature was 22-26°C.

I) 21 healthy subjects of a mean age of 24 yr. participated. Each subject performed one series of five apnoeas in air and one series of five apnoeas with face immersion in cold water. Apnoeas were spaced apart by two minutes and series by fifteen minutes of rest. The individual breath-holding times were kept constant at a submaximal duration in all apnoeas performed by each subject (average: 126 sec). Half the number of subjects performed the series with apnoeas in air first. Heart rate (HR) and arterial blood pressure were continuously recorded on the middle finger by a photoplethysmometer (Finapres 2300, Ohmeda, Madison, Wisconsin, USA). Skin capillary blood flow (CBF) in the thumb was continuously measured with a laser Doppler flowmeter (Advanced Laser Flowmeter 21, Advance Company LTD, Tokyo, Japan). Arterial haemoglobin oxygen saturation (SaO2) was continuously measured on the index finger by a pulse oximeter (Biox 3700e, Ohmeda, Madison, Wisconsin, USA). Values were directly collected in a computer via an A/D-converter. The continuous recording started 120 sec before the first apnoea and continued until 120 sec after the last apnoeic episode. During apnoea in air, the subject had the face above the water, and during apnoeas with face immersion the entire face, including the chin and forehead, was immersed.

The relative change in HR and CBF during apnoea compared to pre-apnoeic values were calculated for each apnoea. Control values for SaO2 were calculated from the period 60-30 sec preceding each apnoea. The degree of arterial haemoglobin desaturation was calculated as the per cent change in saturation during the first 60 sec after apnoea, from the control values. The results were compared between apnoeas in air and apnoeas with face immersion using paired t-test. The level used for significance was P<0.05.

II) Five apnoeas with face immersions spaced by 2 min pauses were performed by 8 subjects (mean age: 27 yr.). HR and SaO2 were continuously measured with the finger pulse oximeter. CBF in the thumb was continuously measured with the laser Doppler flowmeter. Values were directly collected in a computer via an A/D-converter. Oxygen uptake was recorded with a breath-by-breath gasanalyser integrated with a computer system (CPX/D Cardiopulmonary Exercise System, Medical Graphics, MN, USA). Recordings began 15 min before the first apnoea, and ceased 30 min after the last apnoea. Venous blood samples were taken in 5 subjects. Control samples were collected at rest 10 minutes before apnoeas. Blood samples were then taken at the beginning and end of each apnoea and 2, 4, 10 and 30 min after the last apnoea. The lactate concentration in the blood samples was analysed immediately in triplicates with a lactate analyser (Yellow spring institute).

The relative change in HR and CBF during apnoea compared to pre-apnoeic values were calculated for each apnoea. Control values of resting oxygen uptake were calculated from the 15 min of rest before the apnoeas. Recovery values of oxygen uptake were calculated from onset of the first apnoea to the end of the 30 min recovery period after apnoeas. Control values of lactate concentration, just before the first apnoea, were compared with peak values after the series of apnoeas. The values were compared between control and recovery using paired t-test. The level used for significance was P<0.05.


RESULTS

Figure 1. Per cent change in heart rate and skin capillary blood flow during apnoea in air and apnoea with face immersion. Values are means with SEM for 21 subjects. [Modified from Andersson and Schagatay (1).]

I) During apnoeas in air, the HR-reduction was 7.8% and the CBF-reduction was 37.7% (Fig. 1). The diving response initiated by both apnoea and face immersion in cold water was more pronounced (P<0.001). During apnoeas with face immersion, the HR-reduction was 13.6% and the CBF-reduction was 55.9% (Fig. 1).

Figure 2. Arterial haemoglobin desaturation during apnoea in air (A) and apnoea with face immersion (AFI) in one subject breath-holding for 150 sec in both situations.

Figure 2 shows a typical recording of the continuous development of SaO2 during apnoeas in air and apnoeas with face immersion for one subject breath-holding for exactly 150 sec. As can be seen, SaO2 reaches a lower level after the apnoea in air than after the apnoea with face immersion. Mean haemoglobin saturation for all 21 subjects was reduced by 2.7% after apnoeas in air, and by 1.4% after apnoeas with face immersion (P<0.001).

II) Immediately after each apnoea, during the first 1-4 breaths, the rate of oxygen uptake was dramatically increased compared to the rate at rest before the apnoeas. Within 20 minutes after last apnoea the oxygen uptake had returned to the control level. In spite of the dramatic increase in oxygen uptake directly after the apnoeas, the over-all rate of oxygen uptake during the period of apnoeas and recovery was reduced by a mean of 9.0% compared to the rate at rest before the series (P<0.05). A reduced uptake could be seen in all subjects except one. Blood lactate increased from 0.5 mM before the apnoeas to 0.8 mM after the series (P<0.05).


CONCLUSIONS

After apnpeas with face immersion the arterial haemoglobin desaturated less than after apnoeas in air, which suggests that the body oxygen stores were less depleted after apnoeas with face immersion. In accordance was the finding of a reduced recovery oxygen uptake after a series of apnoeas with face immersion compared to the rate of oxygen uptake before the series. These results indicate the possibility that the human diving response may be oxygen conserving. The bradycardia could result in a lower metabolic demand of the cardiac muscle, and the pronounced vasoconstriction could reduce oxygen consumption in some tissues.

The observed increase in lactate concentration after the series of apnoeas is within the normal variation of lactate at rest. Åstrand and Rodahl (2) states that even at rest the blood lactate concentration is about 1 mM. Thus, the increase in this study from 0.5 to 0.8 mM obviously must be considered as a small increase. To be taken into account is the fact that all subjects showed an increase during the BH-series and the decline back to control level within 30 minutes. Those results imply that there might be an anaerobic part of the metabolism during apnoea. However, this is probably not the cause of the reduced oxygen uptake during the recovery period as the blood lactate has returned to control level within the 30 min. The aerobic energy requirements during removal of the lactic acid (gluconeogensis/oxidation) after apnoeas would have counteracted the anaerobic contribution to the reduced aerobic metabolism during apnoeas and recovery (2).


REFERENCES

1. Andersson, J. and E. Schagatay (1998). Arterial oxygen desaturation during apnea in humans. Undersea Hyperbar. Med. 25: 21-25.
2. Åstrand, P.-O. and K. Rodahl (1988). Textbook of work physiology: Physiological bases of exercise. Third edition. McGraw-Hill Book Co., Singapore. pp. 295-353.
3. Schagatay, E. and J. Andersson (1998). Diving response and apneic time in humans. Undersea Hyperbar. Med. 25: 13-19.
4. Schagatay, E., J. Andersson and B. Holm (1998). The triggering of the human diving response. This volume.



Published by courtesy of "European Underwater and Baromedical Society".

 

Schagatay, E., J. Andersson, and B. Holm. (1998) The triggering of the human diving response. In: Gennser, M. (ed.) XXIV Annual Scientific Meeting of the European Underwater and Baromedical Society. National Defence Research Establishment, Stockholm, Sweden. FOA Report: FOA-B--98-00342--721--SE: 88-91.

INTRODUCTION

A series of cardiovascular and respiratory adaptations permit aquatic air breathers to leave the surface for extended periods. Among them is the ”diving response”, which is shared by man. This adaptation, consisting of selective vasoconstriction and bradycardia, serves to limit over all oxygen consumption and protect the heart and brain from asphyxia (2). In humans the response is induced by breath-holding while immersing the face in cold water. The magnitude of heart rate reduction is an often used measure of the magnitude of the diving response. Trained human divers exhibit a bradycardia of 40-50%, which is in the range of the responses found in some semiaquatic mammals. As the response in man has often been reported to reach its maximum in 10°C of water, it has been concluded that the diving response in humans is not effective in diving, as most apneic diving occurs in relatively warm waters (4). The face has been recognized as the area involved in the triggering of the response, but the conclusions concerning the location of the cold receptors involved have varied. While chilling of the face evokes a parasympathetic effect on the heart, chilling of other areas of the body are known to trigger tachycardia (3). The study of the interactions between the diving response and other cardiovascular reflexes is limited. The aims of the studies reviewed here were to further investigate the neural mechanisms responsible for triggering the human diving response, specifically I) the influence of air and water temperature (5), II) the location of the facial cold receptors involved (7) and III) the interaction between the diving response and the response to chilling of the arm (6). A general aim was to make an evaluation of whether the response is triggered in the human apneic diver.


METHODS

Seventy healthy volunteers participated in these ethically approved studies. Experi-ments were performed with the subjects in a prone position, and the orders of the various exposures were randomized in all tests. The diving response was elicited by apnea and facial chilling by cold water bags or by immersion, sometimes in combination with arm immersion. Cardiovascular and respiratory parameters were continuously recorded non-invasively. To evaluate the magnitude of the diving response the main parameter was the reduction of the heart rate during apnea from the heart rate obtained prior to each apnea.

Study I) Twenty three volunteers were exposed for 1 h to 10, 20 and 30°C ambient air, after which they performed apnea and immersed the face in 10, 20 and 30°C of water in the climatic chamber.

Study II) The faces of 22 subjects were divided into six areas of equal size (Fig 2a.), which were chilled with cold water bags while the subjects performed apnea. In addition, apnea without immersion and apnea with full immersion of the face in cold water were performed.

Study III) While snorkel breathing, nine subjects performed immersions in 10°C water of 1) the arm, 2) the face 3) the arm and the face. Sixteen other subjects performed the same proceedures during simultaneous apnea.


RESULTS

Study I) Both air and water temperatures influenced the magnitude of the diving response developed. In 10 and 20°C ambient air, there were significant cold responses at face immersion in 10°C of water, but not at immersion in 20 or 30°C of water. However, in 30°C ambient air both 10 and 20°C triggered significant cold responses (Fig 1., adapted from 5).

Fig 1. Relationship between ambient air and water temperature in the triggering of the diving response.

Study II) When the reduction of the heart rate for chilling of each area was com-pared to the heart rate reduction at apnea alone, the only significant increase in heart rate reduction was found when the forehead or eye regions were chilled. When the responses from the forehead and eyes were added together they were equivalent to the response obtained when the whole face was immersed (Fig 2a., adapted from 7).

Study III) During breathing, simultaneous immersion of the face and arm in cold water resulted in a small tachycardia. During apnea, however, chilling of the arm had no effect on the magnitude of the bradycardia obtained when the face was immersed into cold water (Fig 3., adapted from 6).

Fig 3. Heart rate responses to chilling of face or arm or both, at eupnea and apnea.


CONCLUSIONS

We concluded that: I) The human diving response will be triggered also in a warm environment, as long as the water is colder than the ambient air. Thus the tropical diver in warm water is likely to develop a diving response if the ambient air to which the head is exposed between dives is warmer than the water. II) The elicitation of the diving response by cold stimulation is derived from the upper part of the face innervated by the ophthalmic part of the trigeminal nerve (forehead and eye area). This will ensure that the response is triggered during full facial immersion (diving, Fig 2c.) but not during swimming (Fig 2b). III) During breathing, the influence from cold stimulation of the extremity will dominate over the influence from the stimulation from the upper face, resulting in tachycardia, while during apnea the influence from the upper face will abolish the influence from the arm and produce bradycardia.This suggests that the diving response is triggered at apneic diving even with simultaneous body chilling.

The three studies indicate that the sensory inputs serve well for triggering of the diving response during human apneic diving and that this possibly oxygen con-serving response (1) may dominate over other cardiovascular reflexes during apnea.

REFERENCES
1) Andersson, J. and E.Schagatay (1998). Effects of the human diving response on oxygen consumption. This volume.
2) Elsner, R. and B. Gooden (1983). Diving and asphyxia: a comparative study of animals and man. Physiol. Society monograph 40. Cambridge Univ. Press, Cambridge.
3) Frey, M.A.B., E.A. Selm and J.W Walther (1980). Reflex cardiovascular responses to cold exposure of the face or foot. Jpn. Heart J. 21: 665-679.
4) Mukhtar, M.R. and J.M. Patrick (1986). Ventilatory drive during face immersion in man. J. Physiol. 370: 13-24.
5) Schagatay, E. and B. Holm (1996). The effects of water and ambient air temperatures on human diving bradycardia. Eur. J. Appl. Occup. Physiol. 73: 1-6.
6) Schagatay, E., J. Andersson and B. Holm (in press). The conflicting stimuli of chilling the face and the forearm on cardiovascular regulation. Proceedings from the International Symposium on Problems with Cold Work, Nov. 16-20, 1997, Stockholm, Sweden.
7) Schuitema, K.E. and B. Holm (1988). The role of different facial areas in eliciting human diving bradycardia. Acta Physiol. Scand. 132: 119-120.

Published by courtesy of "European Underwater and Baromedical Society".

Andersson, J., E. Schagatay, P. Gustafsson, and H. Örnhagen. (1998) Cardiovascular effects of “buccal pumping” in breath-hold divers. In: Gennser, M. (ed.) XXIV Annual Scientific Meeting of the European Underwater and Baromedical Society. National Defence Research Establishment, Stockholm, Sweden. FOA Report: FOA-B--98-00342--721--SE: 103-106.

INTRODUCTION

"Buccal pumping" is a technique by which some breath-hold divers voluntarily can increase their lung volume above their normal total lung capacity (TLC). After a completed maximum inspiration, the diver "gasps" air into the mouth while the glottis is closed. After the mouth has been closed, a positive oral pressure is created by a swallowing manoeuvre, while at the same time the glottis is opened. Thus, the air is pumped into the lungs. Thereafter the cycle is repeated until as much as 1.5 litres has been added to the TLC (7). Buccal pumping is used by these breath-hold divers to increase pre-dive lung volume and thereby supposedly also the theoretical diving depth.

Due to the elastic recoil of the chest wall, the intrathoracic pressure is increased during breath-holding at TLC with relaxed respiratory muscles. This reduces the venous return and thus cardiac output (4), which causes a transient reduction in arterial blood pressure (BP) during the first 20 s of breath-holding (1, 3). This reduction in BP would be expected to be accentuated by buccal pumping. Fainting has been reported to occur in association with buccal pumping by individual divers (personal communications).

This study was designed to elucidate the circulatory effects of this manoeuvre and to verify the hypothesis that fainting could be caused by a fall in BP due to the excessive intrathoracic pressure after buccal pumping.


METHODS

Subjects
This study was approved by the Research Ethics Committees at the Universities of Göteborg and Lund. Three subjects (Table 1), capable of buccal pumping at least 0.5 liters above TLC, volunteered for the study after being informed about the procedures. They all had significant experience from breath-hold diving.


Table 1. Subject characteristics.

Procedures
Each subject was sitting in a chair during all measurements. In order to obtain a standardised cardiopulmonary situation before each measurement, the subject stood up and bended knees after which he made a VC-manoeuvre in the sitting position. One minute of rest and spontaneous breathing then preceded each measurement. First a series of measurements at normal TLC was made. A mouthpiece with a computer regulated on/off valve was connected to a spirometer (Vicatest 5, Mijnhardts, The Netherlands). At TLC the subject took the mouthpiece in his mouth and relaxed his lungs against the closed valve for measurement of airway pressure. The valve was opened and 0.5 litres of air was allowed to passively pass out of the lungs, after which the valve was closed and relaxation pressure was measured again. The "apnoea" lasted for about 1 minute during which the lung volume was gradually lowered by passive exhalation to the subject's functional residual capacity and then actively to his residual volume through the valve controlled mouthpiece. This simulated to some extent a breath-hold dive with compression of pulmonary gas and elimination of the high intrathoracic pressure. In each subject 7-8 recordings were made both at TLC and TLC with additional buccal pumping (TLC + Bucc).

Cardiovascular and pulmonary parameters were continuously recorded and stored in a computer. Systolic and diastolic blood pressures were recorded with a photoplethysmograph (Finapres 2300, Ohmeda, Madison, Wisconsin), while heart rate was derived from an EKG-monitor (Micromon 7142, Kontron Instruments, Watford, U.K.). Arterial haemoglobin oxygen saturation (SaO2) was recorded with a pulse oximeter (Biox 3700, Ohmeda, Madison, Wisconsin). Heart rate and blood pressure values before the manoeuvres during quiet breathing (control) and at peak inspiration were compared both at TLC and at TLC+Bucc with a paired t test.


RESULTS

High intrathoracic pressures were produced by the buccal pumping. At TLC, the average relaxation airway pressure was 3.1 kPa. After buccal pumping at TLC, the relaxation airway pressure was increased to 6.1 kPa. For other pulmonary results, please see Örnhagen et al (7).

Systolic and diastolic blood pressures (BP) were reduced at both TLC and TLC+Bucc compared to values before the inspiration (Fig. 1). At TLC, average systolic and diastolic BP were reduced by 27% and 26%, respectively, while at TLC+Bucc they were reduced by 49% and 36%, respectively (Table 2). The lowest BP recorded at TLC+Bucc in subjects 2 and 3 were 26/24 mmHg and 49/44 mmHg, respectively, while in subject 1 it did not fall below the value at TLC.

After inspiration to TLC, heart rate increased by 8%. After buccal pumping heart rate increased by 24% compared to the control values (Table 2). The SaO2 never fell below 96% in any subject.


Table 2. Sitting mean heart rate and blood pressure during control (quiet breathing) and during apnoea at TLC and TLC+Bucc.

Values are means from 3 subjects. Differences compared to control values are indicated with ** (P<0.01) and *** (P<0.001), respectively.





Figure 1.  Click to enlarge the figure in a separate window. Arterial blood pressure during TLC (top) and TLC+Bucc (bottom) in subject 3. Arrows indicate start of inspiration and beginning of expiration. A.c. in top figure indicates autocalibration period of the Finapres.



CONCLUSIONS

During normal breath-holding after an inspiration to TLC, a brief transient tachycardia and fall in arterial BP develops (1). However, during continued breath-holding at TLC this initial drop develops into a rise in BP within the first 15 sec of apnoea (1, 3). A similar BP response was observed in this study after inspiration of TLC. During TLC the pulse pressure is still 45 mmHg which indicates that venous return was not completely impeded (Table 2). During buccal pumping the pulse pressure is dramatically reduced and the systolic pressure is gradually falling (Table 2, Fig. 1) indicating that venous return was impeded to a great extent by the high intrathoracic pressure. If the high intrathoracic pressure had been kept longer than 15 s as if a person had practised breath-holding after buccal pumping on land it is most likely that syncope had been the result. The very rapid gain in BP when intrathoracic pressure is relieved (Fig. 1) indicate that syncope from buccal pumping is a risk if the diver remains at the surface and not when diving, because already at 2 m depth the pulmonary "over-inflation" is eliminated due to compression of pulmonary gas.

Inspired and held lung volume during apnoea has been shown to affect the human diving response (i.e., bradycardia and vasoconstriction) by both mechanical and pulmonary stretch receptor effects (1). The mechanical effects are most pronounced in the beginning of breath-holding and similar to the effects observed in this study. The stretch receptor effects are probably effective during the entire apnoea if the lung volume is kept constant. It is not clear how these considerably high intrathoracic pressures affect the high pressure sensitive pulmonary J-receptors (2). Neither is it certain that the pulmonary J-receptors, if stimulated, affect the circulation in the normal way (i.e., reflex cardiac slowing and vasodilatation) upon stimulation during TLC+Bucc (5). Also, in our experiments the influence from pulmonary stretch receptors was most likely reduced towards the end of the apnoea when the lung volume and pressure were small.

The BP recorded during quiet breathing in the sitting young subjects were somewhat high and probably reflects the normal cardiovascular response to a new and demanding situation for the subjects. Digital artery blood pressure values recorded with the Finapres have also been reported to be slightly higher than brachial artery measurements (6).

Our results support the suggestion that reported cases of fainting among breath-hold divers performing buccal pumping, could have been caused by the excessive increase in intrathoracic pressure. The most dramatic reductions in BP observed at peak buccal pumping indicate that loss of consciousness must be considered as a risk, especially if the diver remains at the surface. One should also bear in mind that the levels of buccal pumping performed by the subjects in this study were not maximal since avoidance of syncope was pursued and it was a demanding protocol with several repetitions. In an authentic diving situation were buccal pumping is performed to a maximal or near maximal level, the cardiovascular effects are probably even more pronounced.


REFERENCES

1. Andersson, J. and E. Schagatay (1998). Effects of lung volume and involuntary breathing movements on the human diving response. Eur. J. Appl. Physiol. 77:19-24.
2. Kaufman, M.P., G.A. Iwamoto, J.H. Ashton and S.S. Cassidy (1982). Responses to inflation of vagal afferents with endings in the lung of dogs. Circ. Res. 51:525-531.
3. Kawakami, Y., B.H. Natelson and A.B. DuBois (1967). Cardiovascular effects of face immersion and factors affecting diving reflex in man. J. Appl. Physiol. 23:964-970.
4. Linér, M.H. (1994). Cardiovascular and pulmonary responses to breath-hold diving in humans. Acta Physiol. Scand. 151(Suppl 620):1-32.
5. Shepherd, J.T. (1981). The lungs as receptor sites for cardiovascular regulation. Circulation 63:1-10.
6. Stroud, M.A., D.P. James, D. Railton and P.J. Sowood (1994). Digital and brachial artery blood pressure measurements during peripheral, cold-induced vasoconstriction. Eur. J. Appl. Physiol. 68:134-138.
7. Örnhagen, H., E. Schagatay, J. Andersson, E. Bergsten, P. Gustafsson and S. Sandström (1998) Mechanisms of "buccal pumping" and its pulmonary effects. This volume.



Published by courtesy of "European Underwater and Baromedical Society".

Schagatay, E., J. Andersson, and B. Holm. (1997) The conflicting stimuli of chilling of the face and the forearm on cardiovascular regulation. In: Holmér, I., and K. Kuklane (eds.) International Symposia on Problems with Cold Work. National Institute for Working Life, Stockholm, Sweden. Arbete och Hälsa 18: 178-181.

Congress Abstracts

de Bruijn, R., Richardson, M., Schagatay, E. (2003) The function of the human diving response in the immersed diver.  Annual Meeting of the European Underwater and Baromedical Society, Copenhagen, Denmark.

Background: Much previous research has used apneic face immersion as a model for studying the diving response and its oxygen-conserving effect, however there are few direct comparisons to apneic face immersion with the body immersed. Therefore, it is not settled if the oxygen conserving effect revealed in the dry-body model persists in the immersed diver. In this study we compared the diving response and its effect on arterial oxygen saturation between apnea in horizontal dry-body and immersed-body conditions.

 Methods: Twelve individually determined near-maximal apneas of the same duration were completed by 17 healthy untrained subjects at rest. Three apneas in each of four categories were performed: dry-body apnea (DA), dry-body, face-immersion apnea (DFIA), immersed-body apnea (IA), and immersed-body, face-immersion apnea (IFIA), in a weighted order. For the face and body immersions, mean water temperature (± SD) was 23.1 ±0.12^oC and mean air temperature was 23.3 ±0.32^oC. Heart rate and arterial haemoglobin saturation were recorded non-invasively with a pulse oximeter.

Results: The diving response was similar for both the dry-body and the immersed body-categories. In all 4 categories the heart rate was reduced. The heart rate reduction in DFIA and IFIA categories was more pronounced than in the DA and IA categories. Heart rate reduction during DA and DFIA was 10% (±1.6) and 18% (±2.8) respectively (P<0.01), while heart rate reduction during IA and IFIA was 9% (±2.6) and 18% (±3.1) respectively (P<0.01).  In both the DFIA and IFIA categories there was less desaturation compared to the DA and IA categories (DA vs. DFIA P<0.001, IA vs. IFIA P<0.05).

 Conclusion: Face immersion enhances the apneic diving response both in the dry- and immersed-body conditions, and is associated with a less pronounced arterial oxygen desaturation. We conclude that the immersed diver may benefit from an oxygen conserving diving response. This study also shows that the dry-body model can be useful for studying the diving response.

Robert de Bruijn, Matt Richardson, Ulrica Milling, Hanna Lemon, Erika Schagatay. (2004).  Erythropoeitin production as a result of repeated apneas.  Annual meeting of the European Undersea and Baromedical Society, Ajaccio, Corsica, France.

Background: It has been known for decades that high altitude hypoxia will lead to increased erythropoiesis. Hypoxia in mainly the kidney results in an increased production of erythropoietin (EPO) stimulating erythropoiesis. High altitude natives display a higher haemoglobin concentration than sea level residents, which in turn increase their haemoglobin concentration as part of the adaptation to altitude. Another group of humans exposed to hypoxia is apneic divers, which may endure transient acute hypoxia, spaced by periods of normal breathing. We recently found higher haemoglobin levels in elite apneic divers, compared to groups of elite skiers and untrained subjects, suggesting that apnea training may induce erythropoiesis in humans. It is well known that diving mammals display high haemoglobin concentrations, and the beneficial effects are obvious: A larger oxygen store before diving prolongs the aerobic dive limit, and a higher haemoglobin concentration may speed up recovery after apneas and act as a buffer against acidosis during the dive. Although our group comparisons reveal a higher haemoglobin concentration in divers, it cannot be determined whether this is a training effect or genetically determined i.e. if individuals with higher concentrations of haemoglobin are more prone to take up apneic diving.

Methods: To investigate if apnea training can induce EPO production, 5 previously untrained volunteers (3 men and 2 women, mean age±SD 28 ±5.5 years) performed 15 maximal apneas in a horizontal position in air. The apneas were grouped in 3 series of 5 apneas and spaced by 2 minutes of which 1 minute was spent slightly hyperventilating, to produce apneas sufficiently long to induce hypoxia. Series were spaced by 10 minutes resting periods. To determine EPO levels, venous blood samples were taken before apneas and directly after the last apnea series, followed by samples 1, 2, 3 and 5 hours after the apneas.

Results: Mean baseline EPO before the apneas was 10.2 U/L. In all subjects EPO levels increased during the 5 hours period after the apneas. The time for EPO-peak values were different among individuals. The mean peak value occurred after 3 h, where the mean increase was 12 % of the pre apnea reference value.

Conclusion: The results suggest that apnea induced intermittent hypoxia could lead to increased erythropoiesis. The evaluation of these findings in a larger group of subjects, including measurements of the individual circadian variations in EPO production, is in progress.

Robert de Bruijn, Matt Richardson, Helena Haughey , HC Holmberg, Glenn Björklund, and Erika Schagatay (2004). Hemoglobin levels in elite divers, elite skiers and untrained humans. Annual meeting of the European Undersea and Baromedical Society, Ajaccio, Corsica, France.

Background: In diving mammals the oxygen storage capacity plays an important role in determining aerobic dive duration. This is therefore also likely to be of vital importance for performance in human apneic divers. In endurance athletes, oxygen carrying capacity is an important factor for maintaining a high oxygen supply to the working muscle. The amount of oxygen stored in the blood is largely determined by the hemoglobin concentration (Hb). Increased circulating Hb would prolong apneas by improving the gas storage and transportation capacity of the blood. This would increase the available oxygen during apnea, improve the CO₂ buffering capacity and provide faster recovery from hypoxia and hypercapnia during breathing intervals. We therefore aimed to investigate Hb levels in elite divers, compared to non divers and non diving endurance athletes.

Methods: We compared the Hb in 3 groups of male subjects: elite apneic divers, elite cross-country skiers and untrained subjects. The 13 apneic divers were all registered competitors for a world apnea championship, and trained apnea (mean+SE) for 7.3 ±1.2 h/week and related physical activities for 8.9 ±1.9 h/week. The 13 cross-country skiers were all members of the Swedish national team for their respective age groups and trained 13.5+1.0 hours per week of ski training or related physical activities, and were inexperienced in apneic diving. The 23 untrained subjects had little or no experience in breath-holding and none was a competitive athlete in any sport. The mean age for divers was 35±4 years, for skiers 20±1 years and for untrained subjects 29±1 years, weight and height were similar for all groups. After a period of 20 min of horizontal rest in order to account for posture-related effects on filtration, venous blood samples, or capillary samples obtained by finger puncture, were drawn and analysed for Hb using standard Hemocue-equipment.

Results: The apneic divers had higher Hb than both the untrained subjects (P<0.05) and the skiers (P<0.01). The Hb did not differ between the untrained subjects and the skiers (Figure).

Conclusion: Apneic divers displayed a higher Hb than endurance athletes and untrained subjects. We suggest that the specific apnea training, involving hypoxic periods, may lead to increased erythropoiesis, in a similar way as during high altitude exposure. The result in skiers is in accordance with earlier findings in endurance athletes, and may reflect that the blood volume, not specifically the Hb, has increased.

Richardson, M., Holmberg, H.-C., de Bruijn, R., Björklund, G., Haughey, H., Schagatay, E. (2004) Hemoglobin concentration after serial apneas in divers, skiers and untrained humans. 7th Scandiavian Congress on Medicine and Science in Sports, Stockholm, Sweden.

Introduction:  In addition to the human cardiovascular ‘diving response’, i.e., bradycardia and peripheral vasoconstriction during apnea, recent studies have shown that spleen contraction also occurs during repeated apneas.  This latter response may serve to expel erythrocytes into the circulation to promote gas transportation.  Both responses are highly individual, and while the cardiovascular diving response is known to be more pronounced after apnea training, no study has previously adressed the possible training effect on the spleen related hematological response. Spleen contraction has also been observed as a result of physical exercise, and its possible effects would be to increase aerobic capacity. The aim of the present investigation was to study the hematological responses to serial apneas performed during rest by elite apneic divers, by elite cross-country skiers and by untrained subjects.               

Methods: After 20 min of rest, 78 subjects (32 untrained subjects, 13 elite skiers, and 33 elite apneic divers) of both sexes performed three maximal apneas, each spaced by a two minute normal breathing interval. Blood samples were taken before, directly after, and 10 minutes after the apneic series and analyzed for haemoglobin (Hb) concentration.

Results: All groups responded to maximal apneas with an increase in hemoglobin concentration, which had disappeared after 10 min of recovery. The increase in hemoglobin concentration was more pronounced in the apneic divers (4g/L) than in skiers (3g/L) and untrained subjects (2g/L; P < 0.05). All groups prolonged their apneic times through the series, but the increase was most evident for the divers versus both the skiers (P < 0.05) and untrained subjects (P < 0.01).

Conclusions: Significant increases in Hb and Hct values occur immediately after a maximal apnea series, followed by a return towards baseline values after 10 minutes, regardless of physical activity level or training type.  These increases are likely due to spleen contraction as demonstrated in previous research.  However, of the three groups the elite apnea divers were responding most strongly. The results suggest that these responses could be more pronounced as a result of apnea training in comparison to high-intensity aerobic training.

Richardson, M., Haughey, H., de Bruijn, R., Andersson, J., Schagatay, E. (2003) Hematological Response pattern associated with maximal-duration Apnea series in untrained subjects. Annual Meeting of the European Underwater and Baromedical Society, Copenhagen, Denmark. 

Background:  In addition to the human cardiovascular ‘diving response’, i.e., bradycardia and peripheral vasoconstriction during apnea, recent studies have shown that spleen contraction also occurs during repeated apneas.  This latter response may serve to expel erythrocytes into the circulation to promote gas transportation.  However, prospective changes in blood parameters after repeated apneas have yet to be systematically described.  As is the case with diving response parameters, some individuals may have stronger haematological changes from performing apneic series than others. These variations need to be considered in future studies of the function of the spleen and blood components during apnea.  The present study was aimed to describe the haematological response pattern associated with repeated maximal apneas in healthy non-divers.               

Methods: After 20 min of rest, 46 healthy untrained subjects of both sexes performed three maximal apneas, spaced by two minutes rest and normal breathing. Blood samples were taken before, within 1 minute after, and 10 minutes after the apneic series and analyzed for changes in haemoglobin (Hb) concentration and hematocrit (Hct). 

Results: Pre-apnea Hb concentration (mean±SE) was normally distributed (147.1±1.6 g/L).  An increase of 2.1±0.3% in the Hb value was seen immediately post-series, followed by a decrease from this value of 1.8±0.3% at 10 minutes post-series.  Pre-apnea hematocrit (41.2±0.6 percent) showed a similar increase immediately post-series of 3.2±0.8% followed by a decrease of 1.6±0.4% from this value at 10 minutes post-series.  Classifying subjects as strong responders (above 75^th percentile) and weak responders (below 25^th percentile) resulted in mean increases in Hb and Hct above pre-apneic values of 4.7±0.4% and 7.1±2.1%, respectively for strong responders, and -0.5±0.4 and 0.5±0.6, respectively for weak responders.

Conclusion: Significant increases in Hb and Hct values occur immediately after a maximal apneic series, followed by a return towards baseline values after 10 minutes.  These increases may be due to the spleen contraction as demonstrated in previous research.  Furthermore, some subjects appear to respond more strongly than others, and pre-screening for these types of responders may be judicious in future testing.  The mechanism(s) underlying the strength of these haematological responses warrants further investigation.  

Schagatay, E., E. Rünow, and J. Andersson. (2001) Diving response and arterial desaturation during exercise and apnea. In: XXXIV International Congress of Physiological Sciences. International Union of Physiological Sciences, Christchurch, New Zealand.

Schagatay, E., J. Andersson, and B. Nielsen. (2001) Does facial chilling augment the hematocrit increase seen at human apneic diving? In: International Thermal Physiology Symposium. IUPS Commission on Thermal Physiology, Wollongong, Australia.

Andersson, J., J. Larsson, and E. Schagatay. (2000) Yoga-breathing, apnea, and alveolar gas exchange. Undersea Hyperb Med 27 (Suppl.).
 

BACKGROUND: Competitive breath-hold divers use different techniques to prepare both mentally and physically before diving. Long periods of slow, deep breathing have been reported to precede diving in elite breath-hold divers. We investigated how a specific, yoga inspired, pre-dive ventilation used by some Swedish elite breath-hold divers affect alveolar gas exchange and apneic ability.

METHODS: Four divers experienced in using yoga-techniques before breath-holding volunteered. They performed four breath-holds with face immersion in 10°C water during prone rest, spaced by >20 min of rest. The two last breath-holds were preceded by two 3-min periods of “yoga-breathing”, i.e., slow and deep breathing, separated by 5 min of rest. Apnea followed the end of the second yoga-breathing period. The apneic times in all four breath-holds were predetermined and kept equal. Respiratory and cardiovascular parameters were recorded non-invasively. The two phases of the apnea were identified by recording the thoracic movements and detecting the onset of involuntary breathing movements triggered by the increase in PaCO2.

RESULTS: The ventilation increased from 11.4 l*min-1 before the control apneas to 23.3 l*min-1 during the yoga-breathing (P<0.01). The pre-apneic PETCO2-values were lowered from 4.74 to 3.78 mmHg after yoga-breathing (P<0.05), and the RER were 1.03 and 1.44, respectively (P<0.05). The mean breath-holding time of the apneas was 161 s, and the duration of the first, “easy going phase” was 102 s in the control apneas. After yoga-breathing the duration of the “easy going phase” had dramatically increased (P<0.01), as no involuntary breathing movements appeared during the subsequent apneas.

CONCLUSIONS: The yoga-breathing performed by these divers was clearly a hyperventilation with profound physiological effects, and may be a risk factor in competitive apneic diving. This prolonged hyperventilation probably affects not only the CO2 stores of fast-equilibrating tissues, i.e., lungs and blood, but also that of slow tissues, i.e., muscles.

Published by courtesy of "Undersea and Hyperbaric Medicine".

Andersson, J., P. Tomberg, and E. Schagatay. (2000) Influence of volition on the human diving response. Undersea Hyperb Med 27 (Suppl.).

BACKGROUND: Some diving mammals have been shown to display cortical influence on the magnitude of the heart rate reduction during diving. Psychophysiological investigations show that the human diving response can be augmented by fear and attenuated if subjects perform mental arithmetic. Our aim was to study the possible volitional control of the human diving response by short and long apneas.

METHODS: The volunteers were twelve healthy subjects with a mean age of 25 yr, including four under water rugby players. Each subject performed two series of three apneas with face immersion in 10°C water, during prone rest. Three apneas were of a maximal duration while three were of a fixed, sub-maximal duration. Apneas were spaced by 10 min pauses. The series were randomly ordered. Mean arterial pressure (MAP), heart rate (HR) and skin capillary blood flow (SkBF) were recorded non-invasively. Cardiovascular data from the periods 90-30 sec before apnea and 30-60 sec during apnea were compared for effects of apneas. The responses to short and long duration apneas were compared using paired t-test.

RESULTS: Mean breath-holding times were 61 and 151 sec in the two series. The HR and SkBF reductions did not differ between the short and long apneas, but the increase in MAP was higher during the long apneas (P<0.05). The MAP increased from 99 and 103 mmHg before (NS), to 110 and 117 mmHg during the short and long apneas (P<0.001).

CONCLUSION: The HR and SkBF responses during apnea were not affected by anticipation. However, the higher MAP during the maximum duration apneas suggests a more pronounced selective vasoconstriction in some tissues during the long apneas. We conclude that there may be a cortical influence on components of the human diving response in humans, expressed as a stronger response during maximum duration apneas.


Published by courtesy of "Undersea and Hyperbaric Medicine".

Andersson, J., E. Schagatay, and B. Nielsen. (1999) Effects of apneas on alveolar gas exchange. Undersea Hyperb Med 26 (Suppl): 29.

INTRODUCTION: The breath-by-breath ventilation (end-tidal carbon dioxide and oxygen [PETCO2/O2] and tidal volume [VT]) during recovery following apneas were investigated.

METHODS: Five maximal duration apneas with face immersions spaced by 2 min pauses were performed by 3 subjects. Apneas were performed during prone rest after a deep inspiration. PETCO2/O2 and VT were recorded with a breath-by-breath flow- and gasanalyzer. Average values from the first apnea are presented.

RESULTS: The breath-holding time was 168 s. The PETCO2 and PETO2 in the first expiration after apneas were 40.3 and 81.3 mmHg, respectively. After 5-10 s of breathing the PETCO2 had decreased to 27.4 mmHg, while the PETO2 increased to 126.9 mmHg. After 30 s the PETCO2 and PETO2 were 36.6 and 115.1 mmHg, respectively. I.e., the PETCO2 values produced an approximately U-shaped curve during the initial 20-30 s of recovery. This was reflected by an inverse shape of the PETO2 curve. The average VT during the initial 15 s after apnea was 2.2 liters and gradually decreased so that after 30 s the VT was 1.1 liters.

CONCLUSIONS: During apnea there is a continuous O2 uptake from the lungs to the blood. However, it has been shown that a large portion of the CO2 does not enter the alveoli during normobaric apnea, but is buffered in the body, particularly in distal parts of the body, due to the reduced cardiac output (1). This is reflected by the roughly U-shaped curve of the PETCO2 values during the initial 20-30 s of recovery. In the first maximal expiration following the apnea the total lung CO2 content is expelled. The following breaths have lower PETCO2 values. As the cardiac output increases the distal CO2 pools are unloaded to the lungs and the PETCO2 increases again. Similarly, the increased cardiac output and perfusion of the lungs with blood of a low O2 content, causes reduced PETO2 values later in the recovery period. This could be considered as a ventilation-perfusion mismatch in the early recovery period.

REFERENCE: 1. Linér MH. Cardiovascular and pulmonary responses to breath-hold diving in humans. Acta Physiol Scand 1984; 151 (Suppl 620):1-32.

Published by courtesy of "Undersea and Hyperbaric Medicine".

Schagatay, E., and J. Andersson. (1999) The respiratory, circulatory and hematological effects of repeated apneas in humans. Undersea Hyperb Med 26 (Suppl): 29-30.

BACKGROUND: The natural way to dive for animals and man is to perform serial dives, with durations and surface intervals suitable to allow enough time at the profitable depth. Therefore, a relevant aspect of apneic diving physiology is to study the effect of one dive upon another. This is a preliminary report of three studies from our laboratory concerning the short term effects of serial apneas.

METHODS: 65 young, healthy non divers participated. Diving was simulated by apnea and facial immersion (AFI) in 10°C water by subjects at prone rest. Maximal duration apneas were spaced by 2 min of breathing. Series I (n=7) consisted of 12 AFI, series II (n=41) and III (n=17) of 5 AFI. Subjects were told to avoid hyperventilation and to perform apnea after a deep but not maximal inspiration. Recordings were done using standard, non invasive methods. Blood samples were drawn from a venous catheter in study III.

RESULTS:  Respiratory effects: Apneic duration increased until AFI6 (I). The physiological breaking point (determined by the PaCO2) was delayed until AFI3 (II; III). No difference was found between the five AFI in pre-apneic lung volume or end-tidal CO2 of the last breath before apnea (III).  Circulatory effects: The cardiovascular “diving response” was attenuated by the repetition (I-III). The reduction of heart rate and skin capillary blood flow, and the increase of mean arterial blood pressure from control were highest during AFI 1 or 2 (I-III), and the responses stabilized after 6 apneas (I).  Hematological effects: Hematocrit (Hct) and hemoglobin concentration (Hb) increased over AFI1-3, and had returned to control value ten minutes after the apneas (III). No change in the total protein content was observed.

CONCLUSIONS: Prolonged apneic duration by repetition of apneas was caused by both physiological and psychological factors. The physiological mechanisms involved in these studies were not increased lung volume, decreased PACO2 by hyperventilation or an increase of the diving response. Among the possible causes, a reversible increase in the blood gas storage capacity by increased Hct and Hb over series of dives could be considered. This change may be caused by splenic contraction.

Published by courtesy of "Undersea and Hyperbaric Medicine".

Andersson, J., E. Schagatay, and G. Biasoletto-Tjellström. (1999) The hypercapnic ventilatory response before and after a breath holding series. In: Shupak, A., R. Lincoln, and Y. Grossman (eds.) XXV Annual Scientific Meeting of the European Underwater and Baromedical Society, Haifa and Eilat, Israel: 232.

Introduction
The mechanisms behind the "short-term training effect", the increase in breath holding time (BHT) observed when apneas are repeated with short intervals, have not been elucidated. Analysis of the appearance of the "physiological breaking point", reached at a critical PaCO₂ level, reveals that both physiological and psychological factors are responsible for this effect. One possible contributing factor could be a reduced CO₂ chemosensitivity caused by repeated apneas.

Methods
Seven subjects volunteered (6 M/1 F; mean age 26 yr; height: 183 cm; weight: 77 kg). None of the subjects was a trained apneic diver. All subjects performed five apneas with face immersion in 10°C water spaced by two minutes pauses. The hypercapnic ventilatory response (HCVR) was tested with the rebreathing method of Read (1967) after normal breathing (control) and one minute after the series of apneas. The control HCVR test was performed either 30 min before (n=4) or 30 min after (n=3) the series of apneas. The initial gas mixture consisted of 7% CO₂, 50% O₂ and 43% N₂. Respiratory variables and end-tidal gas pressures were continuously recorded. The CO₂ chemosensitivity was expressed as the slope of the HCVR curve (dV_E^.dP_ETCO₂^-1).

Results
The mean BHT increased from 111 s in the first apnea to 151 s in the fifth apnea (P<0.05). Five subjects (mean BHT: 150 s) had a decreased HCVR after the series of apneas, while two subjects (mean BHT: 85 s) had an increased response. The average values for all subjects were 2.42 and 2.07 liters^.min^-1.mm Hg CO₂^-1 for the control and the post apnea HCVR, respectively (NS). For the 5 subjects with a reduced post apnea HCVR, the mean values were 2.52 and 1.66 liters^.min^-1.mm Hg CO₂^-1 (P<0.05), and for the 2 subjects with an increased response, they were 2.18 and 3.11 liters^.min^-1.mm Hg CO₂^-1 (NS).

Conclusions
We conclude that a reduced CO₂ chemosensitivity could be one contributing factor to the short-term training effect of repeated apneas.

Published by courtesy of "European Underwater and Baromedical Society".

Schagatay, E., and J. Andersson. (1998) The short term training effect of repeated apneas on haematocrit in humans. In: Gennser, M. (ed.) XXIV Annual Scientific Meeting of the European Underwater and Baromedical Society. National Defence Research Establishment, Stockholm, Sweden. FOA Report: FOA-B--98-00342--721--SE: 112.

INTRODUCTION
In some marine mammals, the spleen is believed to serve as a dynamic red blood cell reservoir, causing elevated haematocrit and haemoglobin concentrations during diving. A 20% decrease in splenic volume in working ama-divers after a three hours diving shift was found with an ultrasonic scanner (Hurford et al 1990). This was accompanied by a 10% increase in haematocrit (Hct) and haemoglobin concentration (Hb). Haemoconcentration due to diuresis was not excluded. Our aim was to investigate the effects of repeated breath-holds (BH) on Hct and Hb, to reveal if any observed change is reversible.


METHODS
Ten volunteers performed five maximal duration BH:s with face immersion in 10°C water. BH:s were performed in a prone position and spaced by 2 min of rest. Venous blood samples were taken immediately before the first BH (Sample no. 1), and directly after BH no. 1, 3 and 5 (Sample no. 2-4). Samples were also taken 3, 10 and 20 minutes after the BH-series (Sample no. 5-7).


RESULTS
Hct and Hb increased over the BH-series. Twenty minutes after the series, values had decreased from to the level before the BH-series.


Table 1. Hb and Hct before, during and after the BH-series.

Values are means±SEM, n=10.


CONCLUSIONS

Reversible increases in Hb and Hct occur during BH in man. This indicates that the increases in Hb and Hct found by Hurford et al (1990) were probably not only caused by increased diuresis, and that a possible cause could be the observed splenic contraction.


Reference
Hurford, W.E. Hong, S.K., Park, Y.S., et al. Splenic contraction during breath-hold diving in the Korean ama. J Appl Physiol 69: 932-936, 1990.

Published by courtesy of "European Underwater and Baromedical Society".

Gustafsson, P.M., S. Sandström, J. Andersson, E. Schagatay, and H. Örnhagen. (1998) Radiografisk beskrivning av hur överfyllning av lungorna åstadkoms med s k "buccal pumping" hos andhållnings-dykare. In: Svenska Läkaresällskapets Rikstämma, Göteborg, Sweden.

Örnhagen, H., E. Schagatay, J. Andersson, E. Bergsten, and P. Gustafsson. (1998) "Grodandning" eller "buccal pumping", en ny riskfaktor inom sportdykning? In: Svenska Läkaresällskapets Rikstämma, Göteborg, Sweden.

Andersson, J., and E. Schagatay. (1997) Arterial hemoglobin desaturation during apneas in humans. In: The Society for Experimental Biology Annual Meeting, Canterbury, England: 53.

Andersson, J., E. Schagatay, and B. Holm. (1997) Cardiovascular responses to arm and face immersion in cold water during apnea. In: XXXIII International Congress of Physiological Sciences. International Union of Physiological Sciences, St. Petersburg, Russia: PO58.30.

Andersson, J., and E. Schagatay. (1996) Effects of lung volume and involuntary breathing movements on the human diving response. The Physiologist 39: A28.

Schagatay, E., and J. Andersson. (1996) Effects of training on diving response and time in humans. The Physiologist 39: A28.

Other Papers

Andersson, J., and E. Schagatay. (1996) Människan som fridykare (In Swedish). UVM - Undervattensmagasinet 1: 46-47. Artikeln är utlagd i pdf-format. Läs om pdf här.

Schagatay, E., B. Holm, and J. Andersson. (1995) Dykning: Effekter av träning på människans dyktid och dykrespons (In Swedish). Svensk Idrottsforskning 3: 45-47.