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1 Center for Research and Education in Special Environments, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York 14214; 2 Department of Anesthesia, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; 3 Department of Physiology, Centre Medical Universitaire, Universite de Geneve, 1211 Geneva 4, Switzerland; and 4 Medical Service, Department of Veterans Affairs Medical Center, Buffalo, New York 14214
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Ferrigno, Massimo, Guido Ferretti, Avery Ellis, Dan
Warkander, Mario Costa, Paolo Cerretelli, and Claes E. G. Lundgren. Cardiovascular changes during deep breath-hold dives in
a pressure chamber. J. Appl. Physiol.
83(4): 1282-1290, 1997.
Electrocardiogram, cardiac output, and
blood lactate accumulation were recorded in three elite breath-hold
divers diving to 40-55 m in a pressure chamber in thermoneutral
(35°C) or cool (25°C) water. In two of the divers, invasive
recordings of arterial blood pressure were also obtained during dives
to 50 m in cool water. Bradycardia during the dives was more pronounced
and developed more rapidly in the cool water, with heart rates dropping
to 20-30 beats/min. Arrhythmias occurred, particularly during the
dives in cool water, when they were often more frequent than sinus
beats. Because of bradycardia, cardiac output decreased during the
dives, especially in cool water (to <3 l/min in 2 of the divers).
Arterial blood pressure increased dramatically, reaching values as high
as 280/200 and 290/150 mmHg in the two divers, respectively. This
hypertension was secondary to peripheral vasoconstriction, which also
led to anaerobic metabolism, reflected in increased blood lactate
concentration. The diving response of these divers resembles the one
described for diving animals, although the presence of arrhythmias and
large increases in blood pressure indicate a less perfect adaptation in
humans.
apnea; arrhythmias; bradycardia; cardiac output; arterial blood
pressure; lactate
INTRODUCTION THE CLASSIC DIVING RESPONSE in diving animals consists
mainly of bradycardia, decreased cardiac output (CO), and peripheral vasoconstriction (for a review, see Ref. 9). Blood flow is redistributed preferentially to vital organs, and lactate accumulates in unperfused muscles. A diving response, although attenuated or
modified, has also been described in humans during diving simulated by
apneic face immersion at the surface (for a review, see Ref. 31).
Most of the studies in humans during actual breath-hold dives have
focused on the diving bradycardia. Electrocardiographic (ECG)
recordings have been performed during dives to modest depths (10-20 m), either in a pool or in a pressure chamber (e.g., Ref. 14) or at sea (e.g., Ref. 29). A few suboptimal ECG recordings were
also obtained at sea during deep breath-hold dives performed by elite
sport divers (8, 13, 28), who have been able to reach depths exceeding
100 m (23). Whereas most of these studies have confirmed the presence
of diving bradycardia in human divers, no information on the
hemodynamic aspects of breath-hold dives in humans is available, with
the exception of one study in which CO was found to increase (in
contrast to the classic diving response) during dives to 20 m (14).
These dives were performed by untrained subjects in thermoneutral water
in a pressure chamber. On the other hand, high blood lactate
concentration
([La]b) values were recently observed in three elite divers at the end of breath-hold dives
down to 65 m at sea, even though the rate of energy expenditure during
those dives was only slightly higher than at rest (11). This evidence
of anaerobic metabolism, in the absence of an elevated metabolism, was
attributed to a marked peripheral vasoconstriction, probably resulting
in a decreased blood flow and oxygen delivery to muscles. This study
was conducted to obtain a more complete picture of the diving response
in well-trained breath-hold divers during simulated dives, which
closely resembled dives performed at sea.
ECG recordings, measurements of CO, arterial blood pressure (BP), and
[La]b accumulation
were obtained during several breath-hold dives to 40-55 m
performed in a pressure chamber by three elite divers, from whom our
group had earlier obtained ECG recordings during dives to 45-65 m
at sea (13). The dives were simulated in the submersed
condition, thus closely resembling diving in the ocean, while allowing
optimal physiological monitoring. The water temperature was either
thermoneutral (35°C) or cool (25°C). The cool water is a
stronger stimulus for the dive response (6), and it was used to more
closely simulate dives at sea. Deep breath-hold dives are typically
performed by using a weight that pulls the diver down during descent
and an inflatable flotation device that brings him or her to the
surface (23). Thus exertion and oxygen consumption are minimized. To
simulate this condition, our subjects were resting during the dives in
the chamber.
METHODS
RESULTS
Because only three subjects participated in this study, no attempts at
statistical treatment of the results were made. Because the
cardiovascular parameters measured during the dives showed a consistent
pattern of changes, data from a few representative dives by each of the
three divers are shown in Figs. 1, 2, 3, 4. HR values,
frequencies of arrhythmias, and CO values were averaged for each 10 m
of change in depth during descent and ascent, as well as for the entire
bottom stay in each dive.
HR. For calculation of HR, both sinus beats and arrhythmic beats were counted. After an initial tachycardia, bradycardia was observed during the dives, and it was more pronounced and developed more rapidly in the cool water, with HR values of 20-30 beats/min at or near the bottom (Fig. 1). The longest R-R intervals were also recorded during the dives in 25°C water (Fig. 2): 7.2 s for PM (at 30 m during descent), 4.6 s for EM (at 25 m during descent), and 2.5 s for RM (at 25 m during ascent), corresponding to instantaneous HR values of 8, 13, and 24 beats/min, respectively. During the dives in thermoneutral water, the longest R-R intervals were 1.7 s for PM (at 10 m during ascent), 3.8 s for EM (at 40 m during ascent), and 1.8 s for RM (at 10 m during ascent). The corresponding instantaneous HR values were 35, 16, and 33 beats/min, respectively. Heart rhythm. In both EM and PM, more arrhythmias, with an earlier onset, were observed in the dives in cool-water than in the thermoneutral-water dives. Also, in RM, more arrhythmias were present in the cool-water dives, but they tended to start later, i.e., not until the bottom had been reached. Often, during the dives in cool water, arrhythmias were more frequent than sinus beats. As can be seen in Fig. 3, no predominance of any one type of dysrhythmia was noted. Typically, the arrhythmias continued for 10-20 s during the recovery period. No arrhythmias were noted during control measurements. CO. Because SV did not change appreciably during the dives, the variations in CO were mostly due to changes in HR. As a consequence, at the beginning of the dive and early during descent, CO was higher than its control value (Fig. 4). Then, it decreased to control levels or, in the cool water, to even lower levels. Thus, as shown for PM and RM in the course of dives in cool water, their CO fell to <3 l/min compared with control levels of ~6.4 and 8.8 l/min, respectively. BP. The BP recordings obtained on subjects EM and RM during a dive to 50 m in 25°C water are shown in Fig. 5, together with the ECG and the depth-time profiles.
The sphygmomanometric BP of RM during the predive physical examination was 115/75 mmHg. Her BP (invasive measurement) while standing in the cool water to the waist was 150/75 mmHg. During the hyperventilation, immediately before the dive, it was ~185/120 mmHg (Fig. 5B). About 5 s after the beginning of breath holding and submersion, and coincident with the beginning of compression, her BP rose within 15 s to a maximum of ~280/200 mmHg. A slow decrease then followed to a minimum of ~150/50 mmHg, which occurred early during ascent. Then, her BP started to rise gradually, and, during the 47-s-long continued breath hold at the surface, her BP reached 240/115 mmHg. Thereafter, it decreased slowly to 165/95 mmHg in ~2 min. A similar pattern was observed in EM (Fig. 5A), whose BP during physical examination was 145/90 mmHg. After he entered the cool water, it was 160/80 mmHg, and it did not change appreciably during predive hyperventilation. During compression, his BP showed variations due to an irregular heart beat but reached a maximum, sustained over many beats, of 290/150 mmHg, with occasional systolic peaks reaching 345 mmHg. The variability in his BP continued during the bottom and ascent phases of the dive, with values ranging from 225/110 to 265/155 mmHg. After he reached the surface, during the 33-s-long continued breath hold, his BP was ~250/105 mmHg. Thereafter, it gradually decreased to 150/75 mmHg in ~3 min. A comparison of the simultaneous ECG and BP tracings showed that all the arrhythmias generated pulse pressures of at least 50 mmHg, and, therefore, the arrhythmias were arbitrarily considered hemodynamically effective. By application of this criterion, the HR obtained from the BP tracing was identical to the HR from the ECG. [La]b. The [La]b was always higher in the recovery period compared with the resting control values, indicating net lactate accumulation during the dives. In particular, during two dives to 50 m by EM, [La]b increased from 1.07 and 0.93 mM predive to 2.26 and 3.97 mM postdive, respectively. In PM, during a dive to 40 m and one to 45 m, [La]b increased from 1.92 and 1.67 mM predive to 3.05 and 2.49 mM postdive, respectively. Finally, during two dives to 50 m by RM, [La]b increased from 1.29 and 0.87 mM predive to 5.30 and 1.41 mM postdive, respectively.
DISCUSSION
40
cmH2O in
EM and 20
cmH2O in
RM) (33), which probably augmented
redistribution of blood from the periphery into the chest. As a result,
the heart may have been distended even more, contributing to
dysrhythmogenesis. In agreement with these concepts is our observation
that arrhythmias were more frequent in cool water, at depth, and early
in the ascent.
It is noteworthy that arrhythmias have only rarely been observed in
diving animals (9). From a description by Elsner and colleagues (10) of
the inferior vena cava sphincter in seals, it may be inferred that this
sphincter reduces venous return during dives and protects against
overdistension of the heart and consequent arrhythmias. Furthermore,
the aortic bulb in the seal not only helps to maintain arterial
pressure during diastole at very low HR but also reduces the increase
in left ventricular afterload, which would be expected secondary to
peripheral vasoconstriction during diving (9). This protective
mechanism would tend to decrease myocardial oxygen consumption. By
contrast, the large increases in BP that we recorded during the present
dives (see BP below) may have caused
some subendocardial ischemia. This could also have played a role in the
occurrence of arrhythmias. Ischemic ECG changes were described by
Oliveira and Gomez Patiño (25) in subjects emerging from
breath-hold dives down to 16 m. Finally, a high vagal tone in our
divers may have contributed to dysrhythmogenesis, as we have previously
suggested (12).
In a recent study, Tipton and colleagues (32) found frequent
arrhythmias including supraventricular and ventricular premature beats
that were similar to the ones described in the present study and
confirmed our preliminary, previously published results
(12). However, in their study, arrhythmias were observed
predominantly just before the termination of breath holding and within
the following 10 s. In the present study, most of the arrhythmias
occurred during the dives, possibly due to the larger intrathoracic
blood redistribution caused by the much greater depths reached by our
elite divers.
Even when the many arrhythmic beats are counted, bradycardia was
present, particularly in the cool water, during the breath-hold dives
in this study. Tachycardia just before and at the beginning of the
dives was similar in the cool and the thermoneutral water and may have
been due to anticipatory excitement and hyperventilation. However, the
more rapid onset of bradycardia and the lower HR values during the
dives in cool compared with thermoneutral water point to water
temperature as the most important factor in eliciting bradycardia in
our experiments. Depth by itself did not appear to affect HR because
diving bradycardia developed slowly and to a similar extent in both the
chamber dives in thermoneutral water (independent of maximal depth) and
the breath holds at the surface performed in a dry environment by the
same subjects during an earlier study (13).
CO.
Although there are several studies of CO during breath holding at the
surface with and without face immersion (for a review, see Ref. 15), to
our knowledge, only one study has looked at CO during actual
breath-hold diving in both the dry and submersed condition in
thermoneutral water (14). In that study, breath holding by the subjects
with large lung volume at the surface, just before they dove, decreased
cardiac index by 20.8% in the dry condition and 24.4% in the
submersed condition. This was thought to be due to a high
intrathoracic pressure impeding venous return. When the subjects dove
to 20 m, cardiac index returned to the control values, probably
secondary to a fall in intrathoracic pressure improving venous return.
Those changes in cardiac index reflected similar changes in SV because
no changes in HR were observed in those untrained subjects. A different
picture was observed in the present study involving elite divers. Both
bradycardia and many hemodynamically effective arrhythmias influenced
CO, which overall showed a tendency to decrease in the dives in the cool water. Changes in CO were caused by concomitant changes in HR
because SV showed no significant variations. The presence of a diving
response, that is, bradycardia with reduction of CO, in the present
study may have been due to the colder water, the deeper depths, and the
higher level of training in the elite divers compared with the subjects
of the study mentioned above (14).
BP.
To our knowledge, no information was available in the literature about
BP in humans during breath-hold diving. Before this study, measurements
of BP had been done either during apneic or nonapneic face immersion at
the surface (3, 17, 21, 31) or during breath holding just below the
surface (5, 18, 27, 30). Most of these studies showed no or only a
modest and gradual increase in BP. An exception is the study by
Bjertnæs et al. in 1984 (3), in which mean arterial pressures as high
as 25.33 kPa (~190 mmHg) were observed at the end of the experiments
involving apnea, face immersion in ice water, and exercise.
The very large and sudden increases in BP at the beginning of the
dives, up to 280/200 mmHg in RM and
290/150 mmHg (with occasional systolic peaks reaching 345 mmHg) in
EM, are by far the highest values
reported in the diving literature. These increases may have been due to
a combination of factors, besides apnea and submersion in cool water. A
markedly accentuated vasoconstrictor response may have developed
secondary to the subjects' training, which involves frequent deep
dives. Similarly, in the study by Campbell et al. (5), 1 of the 18 subjects, who was a competitive swimmer, showed consistently higher BP
responses than did the other subjects when performing breath holds in
and out of the water. Excitement, similar to what probably
happens during our divers' record attempts, may have also played a
role, particularly in the case of RM,
who exhibited high BP already during the last part of the predive hyperventilation.
The high BP recorded during the early part of the two dives was caused
primarily by peripheral vasoconstriction because CO, after a
short-lasting initial increase, tended to be at or below the predive
level. The drop in BP that developed as the dives continued appears to
have been due, at least in part, to lowered CO secondary to bradycardia
(presumably elicited by baroreceptor stimulation). The many arrhythmic
beats, which proved to be hemodynamically effective, contributed to
variations in BP during the dives. After the subjects surfaced, the
rise in BP during the continued breath holding may have been due to an
accentuation of peripheral vasoconstriction reflex caused by hypoxia,
which commonly occurs at the end of deep breath-hold dives (11).
The slow drop in pulse pressure, particularly evident at low HR, is
suggestive of intense peripheral vasoconstriction, similar to what
happens in the seal. A vasoconstrictor response has been described in
humans performing dives simulated by breath holding with face immersion
(18). However, in the seal, large increases in BP are prevented by a
concomitant reduction in CO (9), much greater than the one recorded in
our divers. Furthermore, humans lack the "aortic bulb," which not
only reduces systolic pressures during peripheral vasoconstriction (as
mentioned in HR and heart rhythm above) but also helps to
maintain BP during prolonged diastolic intervals (9).
Peripheral vasoconstriction implies a reliance of peripheral tissues on
anaerobic metabolism, conducive to accumulation of lactate. In fact, an
increase in [La]b has
been described after breath-hold diving in both diving animals (e.g.,
Ref. 9) and humans (e.g., Refs. 27 and 30). Furthermore, an increase in [La]b was found after
both the present chamber dives and some dives at sea performed by the
same subjects (11). This accumulation of lactate occurred despite the
low metabolic cost of diving, which was calculated for the dives at
sea. That level of metabolism should not have been accompanied by any
lactate accumulation during ordinary dynamic exercise. On the other
hand, whereas prolonged dry breath holds by the same subjects led to a
large fall in arterial oxygen pressure, they still did not cause
accumulation of blood lactate, probably because there was no intense
peripheral vasocontriction (11). In the present study, there must
have been a marked reduction of limb blood flow preventing oxygen
delivery to the muscles, thus inducing anaerobic metabolism. Support
for such a mechanism is offered by earlier observations in our
laboratory of a >50% reduction in forearm blood flow when subjects
held their breath at one atmosphere while their faces were flushed with
water at 20°C (31).
Despite the frequent prolonged R-R intervals, no clinical signs of a
failing circulation were observed and no symptoms were reported by the
divers. This is in sharp contrast to the light-headedness or even
syncope occurring in patients after only 5-10 s of absent or
ineffective cardiac contraction (16). Similarly, Arnold (2) described
cases of extreme, still asymptomatic, diving bradycardia elicited by
apneic facial immersion in ice water, with the longest R-R interval
being 10.8 s. An important factor in protecting cerebral perfusion
during the accentuated diving bradycardia is the intense peripheral
vasoconstriction, which helps to maintain cerebral perfusion pressure.
In conclusion, it appears that human elite breath-hold divers exhibit
an intense diving response. The cardiovascular changes of the elite
divers in this study, that is, bradycardia, a reduction in CO, and
peripheral vasoconstriction, resemble the ones described for diving
animals, in which they supposedly have an adaptive value. Yet, the
divers also showed other reactions, including many arrhythmias and very
high BP during their dives. These phenomena are possibly due to
anatomic differences from the diving animals, and, if encountered in a
clinical setting, they would be cause for considerable alarm. However,
in our subjects, these cardiovascular aberrations were not related to
any apparent cardiovascular disease and did not cause any signs or
symptoms; still, they point to some imperfections in the human response
to deep breath-hold diving. Finally, because our three subjects
belonged to the same family, these observations may be the expression
of genetic factors rather than representing a physiological adaptation,
and they may not apply to other human breath-hold divers.
ACKNOWLEDGEMENTS
We gratefully acknowledge the technical assistance of Andrew Barth, Donald Hartmayer, Bruce Laraway, Dean Marky, and David Suggs. Their enthusiasm was exceeded only by their attention to safety. The donation of pressure transducers by COBE Cardiovascular, Inc. is also gratefully acknowledged.
FOOTNOTES
Address for reprint requests: M. Ferrigno, Brigham and Women's Hospital, Dept. of Anesthesia, 75 Francis St., Boston, MA 02115 (E-mail: mferrigno{at}bics.bwh.harvard.edu).
Received 11 October 1996; accepted in final form 15 May 1997.
REFERENCES
| 1. | Arborelius, M., Jr., U. I. Balldin, B. Lilja, and C. E. G. Lundgren. Hemodynamic changes in man during immersion with the head above water. Aerospace Med. 43: 592-598, 1972[Medline]. |
| 2. | Arnold, R. W. Extremes in human breath-hold, facial immersion bradycardia. Undersea Biomed. Res. 12: 183-190, 1985[Medline]. |
| 3. | Bjertnæs, L., A. Hauge, J. Kjekshus, and E. Soyland. Cardiovascular responses to face immersion and apnea during steady state muscle exercise. A heart catheterization study on humans. Acta Physiol. Scand. 120: 605-612, 1984. [Medline] |
| 4. | Bonneau, A., F. Friemel, and D. Lapierre. Electrocardiographic aspects of skin diving. Eur. J. Appl. Physiol. 58: 487-493, 1989. |
| 5. |
Campbell, L. B.,
B. A. Gooden,
and
J. D. Horowitz.
Cardiovascular responses to partial and total immersion in man.
J. Physiol. (Lond.)
202:
239-250,
1969 |
| 6. |
Craig, A., Jr.
Heart rate responses to apneic underwater diving and to breath-holding in man.
J. Appl. Physiol.
18:
854-862,
1963.
|
| 7. |
Craig, A. B., Jr.,
and
M. Dvorak.
Thermal regulation during water immersion.
J. Appl. Physiol.
21:
1577-1585,
1966 |
| 8. | Data, P. G. Cardiac response to deep breath-hold diving (Abstract). FASEB J. 4: A854, 1990. |
| 9. | Elsner, R., and B. Gooden. Metabolic conservation by cardiovascular adjustments. In: Diving and Asphyxia. A Comparative Study of Animals and Man. New York: Cambridge Univ. Press, 1983, p. 14-29. |
| 10. | Elsner, R., W. N. Hanafee, and D. D. Hammond. Angiography of the inferior vena cava of the harbor seal during simulated diving. Am. J. Physiol. 220: 1155-1157, 1971. |
| 11. |
Ferretti, G.,
M. Costa,
M. Ferrigno,
B. Grassi,
C. Marconi,
C. E. G. Lundgren,
and
P. Cerretelli.
Alveolar gas composition and exchange during deep breath-hold diving and dry breath-holds in elite divers.
J. Appl. Physiol.
70:
794-802,
1991 |
| 12. | Ferrigno, M., A. Ellis, C. E. G. Lundgren, P. Cerretelli, G. Ferretti, D. Warkander, and M. Costa. Cardiac arrhythmias during deep breath-hold diving (Abstract). Undersea Biomed. Res. 19, Suppl.: 86-87, 1992. |
| 13. | Ferrigno, M., B. Grassi, G. Ferretti, M. Costa, C. Marconi, P. Cerretelli, and C. E. G. Lundgren. Electrocardiogram during deep breath-hold dives by elite divers. Undersea Biomed. Res. 19: 81-91, 1991. |
| 14. |
Ferrigno, M.,
D. D. Hickey,
M. H. Linér,
and
C. E. G. Lundgren.
Simulated breath-hold diving to 20 meters: cardiac performance in humans.
J. Appl. Physiol.
62:
2160-2167,
1987 |
| 15. | Ferrigno, M., M. H. Liner, and C. E. G. Lundgren. Cardiac performance during breath-hold diving in man: an overview. In: The Physiology of Breath-Hold Diving, edited by C. E. G. Lundgren, and M. Ferrigno. Bethesda, MD: Undersea Hyperbaric Med. Soc., 1987, p. 174-184. |
| 16. | Fowler, N. O. Syncope. In: Cardiac Diagnosis and Treatment. New York: Harper & Row, 1980, p. 1205-1213. |
| 17. | Gross, P. M., R. L. Terjung, and T. G. Lohman. Left ventricular performance in man during breath-holding and simulated diving. Undersea Biomed. Res. 3: 351-360, 1976. [Medline] |
| 18. |
Heistad, D. D.,
F. M. Abboud,
and
J. W. Eckstein.
Vasoconstrictor response to simulated diving in man.
J. Appl. Physiol.
25:
542-549,
1968 |
| 19. |
Hong, S. K.,
S. H. Song,
P. K. Kim,
and
C. S. Suh.
Seasonal observations on the cardiac rhythm during diving in the Korean ama.
J. Appl. Physiol.
23:
18-22,
1967 |
| 20. | Jung, K., and W. Stolle. Behaviour of heart rate and incidence of arrhythmia in swimming and diving. Biotelemetry Patient Monitoring 8: 228-239, 1981. |
| 21. |
Kawakami, Y.,
B. H. Natelson,
and
A. B. DuBois.
Cardiovascular effects of face immersion and factors affecting diving reflex in man.
J. Appl. Physiol.
23:
964-970,
1967 |
| 22. | Kurss, D. I., C. E. G. Lundgren, and A. J. Pasche. Effect of water temperature on vital capacity during head-out immersion. In: Proceedings of the Seventh Symposium on Underwater Physiology, edited by A. J. Bachrach, and M. M. Matzen. Bethesda, MD: Undersea Med. Soc., 1981, p. 297-301. |
| 23. | Maiorca, E. Depth records: practical considerations. In: The Physiology of Breath-Hold Diving, edited by C. E. G. Lundgren, and M. Ferrigno. Bethesda, MD: Undersea Hyperbaric Med. Soc., 1987, p. 291-298. |
| 24. | McDonough, J. R., J. P. Barutt, and J. C. Saffron. Cardiac arrhythmias as a precursor to drowning accidents. In: The Physiology of Breath-Hold Diving, edited by C. E. G. Lundgren, and M. Ferrigno. Bethesda, MD: Undersea Hyperbaric Med. Soc., 1987, p. 212-229. |
| 25. | Oliveira, E., and N. G. Gomez Patiño. Cambios electrocardiograficos inducidos por la immersion. Rev. Española Cardiol. 30: 11-15, 1977. |
| 26. | Olsen, C. R., D. D. Fanestil, and P. F. Scholander. Some effects of breath-holding and apneic underwater diving on cardiac rhythm in man. J. Appl. Physiol. 7: 461-466, 1962. |
| 27. |
Olsen, C. R.,
D. D. Fanestill,
and
P. F. Scholander.
Some effects of apneic underwater diving on blood gases, lactate, and pressure in man.
J. Appl. Physiol.
17:
938-942,
1962.
|
| 28. | Ravara, A., M. Lupi, C. Camerieri, and S. Caponnetto. Modificazioni crono-morfologiche dell' ECG dell' uomo in immersione in apnea. Boll. Soc. Ital. Biol. Sper. 51: 214-219, 1975[Medline]. |
| 29. | Sasamoto, H. The electrocardiogram pattern of the diving ama. In: Physiology of Breath-Hold Diving and the Ama of Japan, edited by H. Rahn, and T. Yokoyama. Washington, DC: Natl. Res. Counc., Natl. Acad. Sci., 1965, p. 1271-1280. (Publ. 134) |
| 30. |
Scholander, P. F.,
H. T. Hammel,
H. LeMessurier,
E. Hemmingsen,
and
W. Garey.
Circulatory adjustment in pearl divers.
J. Appl. Physiol.
17:
184-190,
1962.
|
| 31. | Sterba, J. A., and C. E. G. Lundgren. Breath-hold duration in man and the diving response induced by face immersion. Undersea Biomed. Res. 15: 361-375, 1988[Medline]. |
| 32. | Tipton, M. J., P. C. Kelleher, and F. Golden. Supraventricular arrhythmias following breath- hold submersions in cold water. Undersea Hyperb. Med. 21: 305-313, 1994[Medline]. |
| 33. | Warkander, D. E., M. Ferrigno, M. Ferretti, M. Costa, C. E. G. Lundgren, and P. Cerretelli. Respiratory mechanics during deep breath-hold diving (Abstract). Undersea Biomed Res. 21, Suppl.: 151, 1994. |
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J. P. A. Andersson, M. H. Liner, A. Fredsted, and E. K. A. Schagatay Cardiovascular and respiratory responses to apneas with and without face immersion in exercising humans J Appl Physiol, March 1, 2004; 96(3): 1005 - 1010. [Abstract] [Full Text] [PDF]
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J. P. A. Andersson, M. H. Liner, E. Runow, and E. K. A. Schagatay Diving response and arterial oxygen saturation during apnea and exercise in breath-hold divers J Appl Physiol, September 1, 2002; 93(3): 882 - 886. [Abstract] [Full Text] [PDF]
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P. Lindholm, P. Sundblad, and D. Linnarsson Oxygen-conserving effects of apnea in exercising men J Appl Physiol, December 1, 1999; 87(6): 2122 - 2127. [Abstract] [Full Text] [PDF]
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