TFIE EFFECTS OF DORSAL; FACIAL AND WHOLE-HEAD IMMERSION ON TITE DIVE RESPONSE IN HUMANS
By
Dominique Gagnon
A Thesis Submitted to the Faculty of Graduate Studies In Partial Fulfillment of the Requirements For the Degree of
MASTER OF SCIENCE
Faculty of Kinesiology and Recreation Management University of Manitoba Winnipeg
Copyri ghtO2009 Dom inique Gagnon THE IINIVERSITY OF' MANITOBA
F'ACULTY OF GRADUATE STT]DIES coPYRrc;;ï"**rr.ro*
The Effects of Dorsal, Facial and Whole-Head Immersion on the Dive Response in Humans
BY
Dominique Gagnon
A Thesis/Practicum submitted to the Faculty of Graduate Studies of The University of
Manitoba in partial fulfillrnent of the requirement of the degree of
MASTER OF SCIENCE
Dominique Gagnon @ 2009
Permission has been granted to the University of Manitoba Libraries to lend a copy of this thesis/practicum, to Library and Archives Canada (LAC) to lend a copy of this thesis/practicum, and to LAC's agent (UMI/ProQuest) to microfilm, sell copies and to publish an abstract of this thesis/practicum.
This reproduction or copy of this thesis has been made available by authority of the copyright ovÍner solely for the purpose ofprivate study and research, and may only be reproduced and copied as permitted by copyright laws or with express written authorization from the copyright owner. ABSTRACT
The effects of regional influences of dorsal, facial and whole-head immersion on the dive response (DR) were studied in 7 subjects. Postural effects of supine and prone positions were also tested. Each subject performed three minute immersions in
iToC water, while breathing through a snorkel, under the following conditions: l) dorsum immersion in supine posture (DS), 2) facial immersion in prone posture (FP),
3) whole-head immersion in the supine posture (WS), and 4) whole-head immersion in the prone posture (WP). Bradycardia, a rise in systolic (SBP) and diastolic blood pressure (DBP) and a reduced finger tip skin blood flow (S¡BF) was seen in all conditions, although no intercondition differences were observed. No changes were
seen in acral and non-acral skin temperature during immersion. A rapid transient rise
in tidal volume (VÐ (P:0.005) after 20-sec of immersion and a decrease in respiratory
rate (RR) (P:0.028) after 60-sec was recorded. Baseline values showed a
significantly greater heart rate (HR) in both prone conditions compared to the supine
conditions (P<0.001) but no postural differences were observed during the immersion period. We concluded that the degree of stimulation of the trigeminal nerve between head dorsum, face, and whole head in 17oC water does not influence the magnitude of the DR during the frrst three minutes of immersion. Additionally, the ventilatory
component of the response seems to be composed of both a cold shock-like response
followed by a reduced drive. Finally, hemodynamic changes occurring with the
supine and the prone postures do not effect the DR and can be useful for future
studies. ACKNOWLEDGMENTS
I first would like to thank my advisor, Dr Gordon Giesbrecht for giving me the opportunity to work in his laboratory. His constant guidance and encouragements helped me gain critical scientific skills and, most importantly, the ability to carry out good research.
I also would like to express my gratitude towards the other two members of my thesis committee, Dr. Phillip Gardiner and Dr. Gerry Bristow. Their contribution was invaluable as they helped make this project something I am proud of.
My colleagues, Thea Pretorius, Gerren McDonald and Farrell Cahill continuously supported me with their time and advice. I wish you all the best in your future endeavors.
A special thanks to the 7 courageous subjects involved in the study. Despite being involved in some difficult trials, they all completed the study and made testing days that much more enjoyable.
I also would like to thank my family who regardless of the long distance made sure that I knew they loved and supported me no matter what.
Finally, thank you Sheila for being there every step of the way. TABLE OF CONTENTS
ABSTRACT...... I ACKNOWLEDGMENTS...... I TABLE OF CONTENTS...... ilI LIST OF FIGIIRES...... V LIST OF TABLES...... VI LIST OF APPENDICES...... VII LIST OF ABBREVIATIONS. ... VIII
CHAPTER 1: INTRODUCTION...... I Importance of the Study...... 4
Statement of Purpose...... 5 Hypotheses ...... 5
CIIAPTER 2: REVIEW OF LITERATIIRE...... 6 The Dive Response...... 7 The Elicitation of the Dive Response ...... 8 Face immersion...... 8 Breath-Holding...... 9 Physiological Effects of the Dive Response...... I I Bradycardia ...... I I
Increase in Mean Arterial Pressure...... 12 Vasoconstriction...... 12 Reflex Breath-Holding...... 14 Factors Modifying the Dive Response...... 16 Body Positioning...... 16
Water Temperature...... 17 Age...... 18 ApneaTraining...... 19 Fitness ...... 20
Emotional State...... 21 Summary...... 21
ilt CHAPTER 3: RESEARCH STIIDY .... 24 METHODS ...... 2s Subjects...... 25 Instrumentation...... 25 Head Immersion Tank ....27 ExperimentalProtocol...... 27
Protocol...... 30 DataAnalysis...... 31 RESULTS...... 33
Cardiovascular Responses...... 34
Blood Flow and Skin Temperature...... 38
Ventilation and Breathing Patterns...... 41
DISCUSSION ...... 46 Possible Mechanisms for the Results...... 47 Practical Implications forthe Results...... 5l Considerations...... 52
CHAPTER 4: SUMMARY AND CONCLUSION ...... 54 SUMMARY ...... 55 CONCLUSION...... 56
REFERENCES...... 57
IV LIST OF FIGURES
FIGURE l. Head Immersion Tank
FIGURE 2. changes in HR during 3 minutes of immersion and l0 minutes of recovery in all conditions.
FIGURE 3. changes in sBP during 3 minutes of immersion and l0 minutes of recovery in all conditions.
FIGURE 4. changes in DBP during 3 minutes of immersion and l0 minutes of recovery in all conditions
FIGURE 5. Changes in Acral Tr¡ during 3 minutes of immersion and 10 minutes of recovery in all conditions.
FIGURE 6. Changes in Non-Acral Tr¡ during 3 minutes of immersion and l0 minutes of recovery in all conditions.
FTGURE 7. changes in s¡BF during 3 minutes of immersion and 10 minutes of recovery in all conditions.
FIGURE 8. Changes in V s during 3 minutes of immersion and l0 minutes of recovery in all conditions.
FIGURE 9. Changes in RR during 3 minutes of immersion and l0 minutes of recovery in all conditions.
FIGITRE 10. Changes in V1 during 3 min of immersion and 10 min of recovery in all conditions.
V LIST OF TABLES
TABLE L. Absolute baseline values for HR, SBP, DBP, Acral Tr¡, Non-Acral Tr¡,
S¡BF, RR and V1
VI LIST OF APPENDICES
APPENDIX A. Anthropometric Data
APPENDIX B. Plan of Head Immersion Tank
APPEIIDIX C. Head Immersion Tank
APPENDIX D. Head Insertion in the Immersion Tank
APPENDIX E. Finapres Measurement Site
APPENDIX F. Acral Skin Temperature Measurement Sites (dorsal view)
APPENDIX G. Acral Skin Temperature and Laser Doppler Blood Flow
Measurement Sites (Palmar View)
APPENDIX H. Conditions
APPENDIX I. Order of Trials
vil LIST OF ABBREVIATIONS
BP Blood Pressure
CI Cardiac Index
CO Cardiac Output
CVP Central Venous Pressure
DBP Diastolic Blood Pressure
DR Dive Response
HR Heart Rate
IBM Involuntary Breathing Movements
MAP Mean Arterial Pressure
PBP Physiological Breaking Point
RR Respiratory Rate
SBP Systolic Blood Pressure
S¡BF Skin Blood Flow
SV Stroke Volume
Tsk Skin Temperature
úE Minute Ventilation
VR Venous Return
vr Tidal Volume
vill CHAPTER 1 : INTRODUCTION INTRODUCTION
The mammalian dive response (DR) is an important combination of reflexes that enhance survival during cold water immersion. The purpose of this response is to redirect a limited supply of oxygen to the brain (14, 26,54) to increase functional or survival time underwater. It is activated by facial immersion in cold water which stimulates facial cold receptors innervated by the trigeminal nerve (13, 17,59).
Stirnulation generates rapid changes in cardiac, respiratory and vascular responses including bradycardia with concomitant reduction in cardiac output (CO), breath- holding (apnea) and peripheral vasoconstriction (5, 26, 39, 54) paralleled with a redistribution of blood flow from the periphery to the core, including the brain (23,
39,54).
This response is predominantly seen in diving mammals such as seals and whales. The Weddell seal for example, demonstrates a heart rate (HR) reduction from
55 to 15 beats per minute, lower cardiac output from 40 to 6 liters per minute and a relatively constant blood pressure (BP) for dives up to 600 meters deep (32). Similar physiological adaptations allow the Bottlenosed whale to reach depths of more than
1000 meters (52). In humans, similar reflex adjustments have been observed albeit to a lesser extent (15, 54). Facial immersion causes a reflex apnea due to an inhibition in neural activity to the respiratory muscles (26). This is paralleled by reflex 'pacemaker bradycardia induced by vagal nerve stimuli to the cardiac (4).
Furthermore, Fagius and Sundlöf (15) reported that activation of facial cold receptors is a major factor in mediating sympathetic outflow, causing peripheral vasoconstriction. In contrast to diving mammals, humans demonstrate a reflex increase in BP during stimulation with values reaching as high as 2801200 mmHg (16). The sharp increase in BP may be associated with the sudden intense peripheral vasoconstriction (and consequent increase in total peripheral resistance) despite a decrease in cardiac output, that occurs in response to the immersion (54). With the redistribution of blood volume from the periphery towards the visceral organs and the brain, these adaptations are consistent with the oxygen conservation effect of the dive response when oxygen supply is limited.
Whereas some studies (54, 60) measured an inverse relationship between water temperature (5-35"C) in which the face is immersed and the magnitude of bradycardia in controlled settings (a decrease in water temperature will generate a stronger bradycardia), others found no relationship. Conversely, Hayward et al. (30) found the level of bradycardia was unrelated to water temperature when participants were fully submerged during simulated accidental cold water near-drowning.
Responses were compared in 160 participants using a wide range of water temperatures (0-35'C). Interestingly, they observed a decrease in breath-holding capacity with lower water temperatures.
Much of our understanding of the dive response stems from studies which have examined the reflex mediated. Most studies (2, 4, 6, 15, 37,38, 39, 44, 60) have examined facial immersion to study how the afferent stirnuli affect efferent activity since evidence was found that face immersion alone, without whole-body immersion, elicits the dive response (39). Since breath-holding itself can also be a stimulus in humans (16), studies have been conducted both during apnea (2,4,5,44,63) and/or while breathing through a snorkel (6,29,39,44). Schuitema and Holm (59) studied facial areas responsible for the dive response and found that the forehead has the most influence compared to other regions of the face. While this study provides valuable
information regarding the relative influence of regional stimuli on the reflex- adjustments associated with the diving response, the effects of whole-head and dorsal
immersions remain relatively unstudied. Some insight into this response may be obtained by those studies which have examined the thermoregulatory responses during different conditions of body and head immersions on core cooling rates (22,
41, 49, 50). Giesbrecht et al (22) reported that core cooling rate during whole-body
cold water immersion (12"C) is influenced by the exposure of the head to the water.
Relative to the head-out body immersion, core cooling rate increased by 40%o when dorsal head was also immersed. This difference was not observed when the body was not cold stressed. It is noteworthy that the increase of core cooling rate (40Yo), resulting from the inclusion of the dorsal head during immersion, was proportionally
greater than the increase in total heat loss (10%). Pretorius et al (49) reported
comparable results using whole-head immersion in l7"C water. When body
immersion was combined with the full immersion of the head, core cooling rate
increased by 39%. However, when the body was insulated, whole-head immersion
also significantly increased core cooling rate by 45%; an amount that was also
proportionally greater than the increase in total heat loss (10%). While the
mechanisms for these differences remain unresolved, these findings demonstrate the
importance of considering regional influences on the dive response.
Importance of the Study
While many studies (6,29, 39, 44) have examined the dive response while
breathing through a snorkel during facial immersion, cold-water drowning and/or
diving situations typically include immersion of the head dorsum. We are unaware of any work that has examined the individual and combined influences of facial and dorsal head cooling on the dive response.
Statement of Purpose
The purpose of this study is to determine regional influences of dorsal, facial, and whole-head immersion in 17oC water on the cardiovascular, peripheral blood flow and ventilatory drive components of the dive response in humans, tested in the horizontal position. Both a prone and supine position was required for facial and dorsum immersion, respectively. Although some studies demonstrated a faster HR
(51, 65, 69) and a higher MAP (69) in the prone than in the supine position, we are unaware of any work on differential responses to cold immersion stimuli in the two positions. For comparative purposes, whole-head immersion was conducted in both positions.
Hypotheses
We hypothesized that the dive reflexes would significantly increase from dorsal to facial to whole-head immersion, with no differences between prone and supine whole-head conditions. CFIAPTER 2: REVIEV/ OF THE LITERATURE REVIEW OF THE LITERATURE
This review of the literature will provide information on the role and functions of the dive response. It \ /ill cover how the response is initiated with details of its physiologicaleffects and factors that may potentially alter the degree of these effects.
The elicitation of the dive response involves interactions through the head and does not require the entire body under water. The methodology of this study focuses primarily on the head but a deep understanding of the response's mechanisms which occur throughout the entire body is essential. This review of the literature will provide a summary of relevant and curuent studies of the topic necessary to understand those mechanisms.
The Dive Response @R)
The dive response is an oxygen-conserving mechanism (4, 14) that enhances survival during cold water submersion in mammals. It increases anaerobic metabolism (2, 14) in order to save oxygen for hypoxia-sensitive tissues, as well as puts the body into a hypometabolic state (14) and is associated with the redistribution of blood flow. Facial immersion in cold water or voluntary/involuntary breath- holding alone can elicit the response (26, 54,60), but the combination of both stimuli creates a stronger and more pronounced response (60). The physiological responses include; bradycardia with decreased CO, an increase MAP, various levels of vasoconstriction in specific vascular beds, and reflex breath-holding and/or reduced ventilatory drive. The following section will describe the physiological effects of both stimuli and their implications in the response.
7 Elicitation of the Dive Response
Facial Immersion
The literature is contradictory as to which stimulus is the most important to
stimulate the dive response. According to some studies (10, 38, 60) the main stimulus
of the dive response is immersion of the face in cold water. Upon cold water
immersion, facial cold receptors send afferent sensory information to the trigeminal
nerve and then through the trigeminal-brainstem-vagal pathways to evoke the
response (39). Further confirmation of this stimulus has been demonstrated in a study
(13) that was conducted on mature rats with electrical stimulation of the trigeminal
ethmoid nerve which elicited some components of the dive response. Sensory
branches of the trigeminal nerve are the ophthalmic, maxillary, and mandibular
branches. They each provide facial sensory information. The sensory information
from these areas is then sent to the brainstem which regulates sympathetic and
parasympathetic activity of the dive response (34, 54). Shuitema and Holm (59)
found that the forehead, which is innervated by the ophthalmic branch, was the most
important area for elicitation of the dive response. Other important areas that evoke
the dive response found in this study were the eyes which are also innervated by the
ophthalmic branch. Allen et al. (l) found that dive response reflexes are almost
identical when comparing the cooling of the whole face or just the forehead. The minor additive cooling effect of the rest of the face seemed to demonstrate the prominent effect of the forehead over other facial areas in the response. Sterba and Lundgren (61) found that repetitive facial exposure to cold water
abolished the dive response. Their study involved 32 subjects performing several
breath-hold dives with 4 minutes rest between each. They suggested that it is possible
that facial cold receptors adapt with the abolishment of bradycardia, absence of CO
reduction and no change in forearm blood flow normally seen in the response.
Stimulation of facial cold receptors throughout dive response studies has been
done in many ways. Some studies (1, 59) have used ice bags or a cold water bag to the face to generate a dive response. It has nonetheless been demonstrated that the
separation of the skin from the cold stimuli reduces the magnitude of bradycardia (1).
Pressure in the eyeball causes an oculocardic reflex also generating bradycardia but is not related to the dive response (17). This is particularly important for methodological purposes when using ice bags or cold water bags around the eye region. Cool air against the face has also been used and has been associated with similar dive response reflexes compared to other methods (i5). Direct contact of the face with water seems, however, to be a more effective stimulus (26).
Breath-Holding
Voluntary breath-holding can independently elicit the dive response (4) but when it is combined with facial immersion in cold water, a stronger response is generated (26,42). Neural and mechanical cardiovascular adjustments associated with breath-holding include stimulation of the lung stretch receptors and an increasingly negative intrathoracic pressure (8). Stimulation of the lung stretch receptors (ex. breath-holding at total lung capacity) will inhibit cardiac vagal activity which will
accelerate HR (47). Decreased intrathoracic pressure will augment venous return (VR) from the inferior vena cava and increase SV as defined by the Frank-Starling
law of the heart which states that a greater blood volume entering the heart during diastole will generate a greater volume of blood ejected during systole. This increase
in VR will also activate the Bainbridge reflex, which by activating atrial receptors
located in the venoatrial junctions will accelerate the HR during the first instant of breath-holding (8).
A study by Andersson and Schagatay (3) determined that the degree of
inspiration before breath-holding will greatly affect the physiological changes of the response (3). Inspiring more than 60Yo of vital capacity increased maximum breath- holding time because of a slower rise in arterial CO2 (end-tidal COz) (3). However, they observed a reduction in bradycardia and MAP at greater lung volumes
demonstrating a decrease in dive response reflexes and its oxygen-conserving effects.
They concluded that an increase in intrathoracic pressure at higher lung volume would limit cardiac filling and attenuate the response. A prone position on a table was used during the study which, as will be discussed in a later section, could have modified the reflexes in this study.
The physiological breaking point (PBP), described as the point where the level
of arterial COz tension leads to excitation of respiratory muscles during breath- holding, increases involuntary breathing movements (IBM) (12). The period before
and after the PBP are respectively called the easy-going phase and the struggle phase
(12). Past the PBP, a progressively increasing urge to breathe which includes IBM is
seen until autonomic respiratory centers override voluntary control of respiration (5a).
However, Andersson and Schagatay (3) found that even during the struggling phase,
10 the involuntary breathing movements were too small to have an effect on the dive response.
Physiological Effects of the Dive Response
Bradvcardia
Many factors influence the HR during the dive response. Facial immersion and breath-holding have effects on HR through different pathways and at different time periods. As previously explained by the Frank-Starling law, an increase in VR from a decreased intrathoracic pressure will result in a greater SV. An increase in VR will also activate the Bainbridge reflex accelerating the HR. A greater SV and HR will consequently produce a rise in BP. This rise in BP will stimulate aortic and carotid baroreceptors (Baroreceptor reflex) which will increase parasympathetic vagal tone at the sinoatrial node (pacemaker of the heart) evoking bradycardia (47). This deceleration of HR is very fast and occurs within seconds. Another mechanism observed for bradycardia is the stimulation of facial cold receptors increasing cardiac vagal activify (29,39). This neurally-mediated delayed response occurs after about
1 0 seconds of imrnersio n @7). Finally, the short appearance of tachycardia occurring prior to bradycardia is due to a combination of activation of lung stretch receptors and of the Bainbridge reflex.
Journeay et al. (37) hypothesized that a reduced cardiac filling due to hypotension or lower body negative pressure would attenuate the HR, blood flow, and the MAP reflexes seen in the dive response. They indeed reported a reduced
11 bradycardia upon breath-holding with facial immersion in water when cardiac filling
was compromised. The MAP and blood flow responses, however, remained
unchanged from reduced cardiac filling compared to the control group suggesting that those responses are exerted separately. This study also demonstrated that bradycardia
during the dive response is mainly directed at reducing CO. When cardiac filling was
lowered, the reduced SV effected CO which limited the need of bradycardia.
Increased Mean Arterial Blood Pressure (MAP)
As a result of select peripheral and visceral vasoconstriction, a rise in MAP
attempts to maintain perfusion to oxygen-dependent tissues (26, 54). MAP values
between humans and diving mammals during the dive response can differ greatly
depending on the type of dive. While diving mammals can maintain their MAP at a
similar level during deep dives compared to shallow dives, humans can have a
significant increase where values as high as 2801200 mmHg have been observed (16).
As previously mentioned, negative intrathoracic pressure during breath-holding
facilitates cardiac filling which causes an increase in SV (a7). The increase in SV
produces a rise in MAP which has been observed in dive response studies (38, 47).
Vasoconstriction, discussed in the next section, also accounts for the rise in MAP with
a narrowing of blood vessels with concomitant blood flow redistribution towards core
organs and the brain. Another factor explaining the change in MAP could be the
excitation of peripheral chemoreceptors by progressive hypercapnia produced by the
rise in COz in the blood seen in specific tissues during vasoconstriction (60).
12 Vasoconstriction
Vasoconstriction is generated by sympathetic neural activity which stimulates nerves supplying specific vascular beds. Its main purpose is to redirect blood flow to hypoxia-sensitive tissue such as the brain and to limit the use of oxygen by muscles.
Vasoconstriction with the dive response is seen in the periphery of the limbs and
some visceral organs (54,71). Fagius and Sundlöf (15) suggested that
vasoconstriction is the primary physiological effect of the dive response. Many of their observations demonstrated that vasoconstriction appears prior to bradycardia,
playing a signif,rcant role in the response. Activation of facial cold receptors is
essential in the vasoconstrictor reflex of the dive response (15). Cooling of the skin
has also been shown to generate vasoconstriction in many vascular beds (71). Wilson
et al. (71) demonstrated that a strong pressor response is seen in both peripheral
(brachial artery, total forearm, cutaneous) and visceral (celiac, superior mesenteric,
and renal) vascular beds during whole-body skin surface cooling. Subjects of this
study were wearing a tube-lined suit filled with water at 15-18'C. Another important
finding of the Wilson et al. study, was the independence of the vasoconstrictive
response since no change was noticed in HR or CO. Furthermore, Brown et al. (9)
even demonstrated some cerebral vasoconstriction with cooling of the face. Cerebral
vasoconstriction was, however less than total peripheral vasoconstriction.
Nonetheless, cerebral oxygenation was maintained and even increased due to an
increase in cerebral blood flow. The authors of this study suggested that this increase
in cerebral perfusion could be due to trigeminal nerve stimulation which could have
partially offset the sympathetically-activated vasoconstriction of the cerebral vessels.
This pressor response indicates a strong tendency to maintain cerebral functions and
supports the Oz conservation theory during the dive response.
13 Two studies (22,41) investigated the effects of dorsal head immersion on core cooling rates in cold water in shivering (41) and non-shivering humans (22). Subjects were immersed in cold water for up to one hour. Investigators found that despite an increase of only 5Yo in heat loss from the head dorsum when the body was also immersed, core cooling rate increased by 87% (shivering) and by 40o/o (non- shivering). The redirection of blood volume to the core, including the brain, due to vasoconstriction, enhanced core cooling when the dorsal head was exposed to cold water. Interestingly, no increase in cooling rate was observed when only the head dorsum was exposed to the water. Similar studies were conducted by Pretorius e/ al.
(49,50) with the whole head submersed in cool (17"C) water. Comparable results were found in these studies as well. Unlike the dorsal head, however, whole-head submersion with and without whole-body immersion evoked an additional heat loss of
I l% while increasing core cooling rates by an average of 42%;o in non-shivering humans. When the same protocol was applied to shivering humans, similar results were observed. The latter study hypothesized that the differences in results between dorsal and whole head immersion could be explained by the role of the trigeminal nerve through the dive response and its vasoconstrictive effects. These disproportional differences between heat loss and core cooling rates were possibly due to an increase in peripheral vasoconstriction, mediated by the trigeminal nerve, resulting in a smaller thermal core (mass of tissue perfused). The whole-head immersion studies, by stimulating more of the trigeminal nerve, would have further reduced the size of the thermal core and consequently have a greafer effect on core cooling rate for a relative amount of heat loss.
14 Reflex Breath-Holdine
An interesting observation of the dive response is a reflex apnea upon wetting of the face. A decrease in neural activity to the respiratory muscles (diaphragm, intercostal muscles) from stimulation of the facial cold receptors consequently evokes reflex breath-holding (26): This was demonstrated in a study involving subjects submerged while breathing through a snorkel. They reported diffrculty for the subjects to breath normally upon entry into the water (28). Moreover, one of the most potent upper airway protective reflexes in mammals occurs during diving (13). In humans, the swallowing reflex, protecting the upper airways during swallowing, involves, in sequence: the vocal cords being approximated, closure of the epiglottis on top of the larynx, and deformation of the hypo-pharyngal muscles to allow food to pass down the esophagus (8). This protective sequence of events has yet to be thoroughly studied during simulated dives in humans. A study by Dutschmann (13) has, however demonstrated that electrical stimulation of the trigeminal ethmoidal nerve produced elements of the dive response including glottal constriction, preventing water from entering the trachea.
Mukhtar and Patrick (44) performed a series of tests to measure the ventilatory drive of humans during facial immersion in cold water. They concluded that a change in drive was part of the dive response as they observed enhanced maximal breath-hold duration and a PBP at higher alveolar PCOz. Decreased ventilatory drive was attributable to a lower sensitivity to the rise of COz in the body (44). While performing another series of trials with maintained breathing through a snorkel, facial immersion in 13"C water resulted in a reduced V s of 13%o also indicative of a reduced ventilatory drive. A previous study by the same group (43) showed that the
15 dive response is also accompanied by bronchoconstriction which is also mediated by vagal efferents. This study used forced expiratory flow at 40%;o and 25Yo of vital
capacity after apnea with and without facial immersion to determine the degree of
bronchoconstriction induced by these stimuli.
Factors Modiffing the Dive Response
Body Positioning
Cardiopulmonary and BP changes occur with postural change. Turning from
a supine to a prone position applies pressure on the thorax and increases intrathoracic
pressure, thus resulting in an increase in central venous pressure (CVP) (42, 66).
Because CVP is inversely proportional to VR, this added pressure consequently
reduces VR and CO (42). Many studies comparing the effects between supine and
prone positions have been conducted during general anesthesia for surgical purposes.
Most postural studies during anesthesia demonstrated a decrease in BP in the prone
position (48). These results are not, however, congruent with all literature as some
other studies showed no change in BP during anesthetic conditions (7,64,66). The
difference in the results of these studies could be attributed to the type of support used
in the prone position (66). A study by Backofen (7) found no difference in systemic
BP when measurements were taken on average 19 minutes after moving into the
prone position where another study by Poon et al. (a8) had a decrease in MAP l0
minutes after the change in position. The results for these studies need to be
interpreted carefully as the subjects used were part of the older population (65 + 12
16 yr. and 57 + 14 yr. respectively) and during anesthesia. A reduction in cardiac index
(CI) and SV in the prone position was also demonstrated in both studies.
Studies done with unanesthesized younger populations have shown discrepancies in regards to BP changes when moved from supine to prone position.
Three recent studies (51,65,69) have demonstrated different BP responses through time. A study by Tabara et al. (65) showed a significant decrease in brachial BP after
I minute following a change into prone position. Conversely, Watanabe et al. (69)
demonstrated a rise in BP but after 5 minutes while Pump et al. (51) found no change
during their t hour study where measurements were taken every 90 minutes. Since a
change in position can require a few minutes for cardiovascular adjustments (69), it is
possible that these studies simply reflect the different adaptation phases of the
increase in intrathoracic pressure produced by the prone position during
unanesthesized conditions. More importantly, these studies have, however, all
recorded an increase in HR.
Water Temperature
While some studies have shown that the magnitude of the dive response is
dependent on water temperature (56, 60, 70), others have concluded that cooling of
the face without direct contact with water elicits the response (60), or that temperature
has very minimal effect if at all (30). Temperature dependence of the dive response
has been observed with water temperatures ranging from cold (0"C) to above
thermoneutral (40'C) (19). Schagatay (56) concluded from a study performed on 23
subjects that the dive response was inversely proportional to water temperature within
a range determined by air temperature prior to immersion. They used temperatures of
17 10oC, 20oC and 30'C for both air and water. They found the most pronounced HR reduction was with ambient air temperature of 30oC and water temperature of 1OoC, the largest air-water temperature difference. The subjects of this study were lying prone on a mattress with only the instruction to put their face in a water basin near the mattress. Another study by Hayward (30), which did not find a signifrcant difference between water temperature and the dive response, had their subjects sliding into a large tank. The great movements and a change in the emotional state may have caused tachycardia affecting the results of the study. Although, it is possible that inhalation at different lung capacities from the subjects could have also altered the results.
Most current studies have observed a greater dive response with colder stimuli
(71). Interestingly, a recent study by Jay (35) demonstrated that water temperatures below 10oC reduce the oxygen-conservation effects of the dive response by predominance of the neurally mediated cold shock-like response. They examined an
increase in ventilation and a shorter breath-holding duration with water temperatures
at lO'C and 0"C. These changes did not affect bradycardia but demonstrated that
lower temperatures were limiting functional time underwater due to an increase in
stimulation of cutaneous temperature-sensitive neuronal drive to inspire, indicating a
cold shock-like response.
Ase
There is a decrease in diving bradycardia with increasing age which limits the
effects of the dive response (27) and can be fully abolished by the seventh or eighth
decade (24). The exact mechanism of this phenomenon has not been studied
18 thoroughly although Turner (67) suggests a reduction in parasympathetic tone in older people may be a cause for the decrease. Also, elderly individuals do not respond to thermal stimulation in the same fashion as younger people (36). Jennings et al. (36) studied the effect of age in a facial cooling study between a young (20 yr. old) and an old (80 yr. old) group. They used finger tip temperature cooling as an index of peripheral vasoconstriction and found a greater decrease in finger temperature in the young group. The main finding of their study was a reduced capability to retain heat
via peripheral vasoconstriction in the old group indicating thermoregulatory vulnerability in the elderly.
Apnea Training
Experienced divers train to remain underwater for long periods of time but very little research has been done in this area. More recently, several studies have
focused on the degree of the physiological adaptations seen in the response and the
duration of breath-holding. Some recent work has shown a clear relationship between
apneic time and HR reduction with longer apneic times occurring when the face was
immersed in water (55). The same relationship was also found between apneic time
and reduction in S¡BF (55). Valic et al. (68) determined that trained divers had a
more pronounced muscle oxygen desaturation, maintaining oxygen supply of vital
organs more effectively. Thus, this oxygen shift to hypoxia-sensitive organs allowed
the trained divers to remain underwater longer and demonstrated a clear oxygen
conserving effect of the dive response. Decreased ventilatory drive, reduced stress,
and a higher tolerance to COz build up may also contribute to an increase in apneic
time with training (58).
19 The Ama diving people in Japan are a very interesting study group for the dive
response as their profession involves constant repetitive dives. While some think this
group of individuals might have a very strong dive response, in order to better
perform their work, a study shows that the Ama divers have a comparable HR
response when compared to same age non-divers (54). They, however, are able to
remain underwater for longer periods of time compared to their non-diver peers (54).
This study demonstrated a multi-factorial aspect for breath-hold duration which is not
completely based on the dive response.
Fitness
Fitness level and its relationship to the dive response have been of interest for
many years. Conclusions are quite diverse with some literature claiming that physical
f,itness enhances the dive response (21), while others say it has no effect at all (63,
7l). Frey and Kenney (18) compared a group of competitive swimmers to a group cif
non-swimmers and found that the first group had a lower HR during apnea with and
without facial immersion trials. They attributed this difference to a greater
parasympathetic nervous vagal control in the trained group. No physical fitness
assessment was performed for the groups in study; the training regime alone was used
to categorize the groups. Contrary to that study, Stromme (63) found no relationship
between bradycardia and physical fìtness. Subjects were categorized into three fìtness
groups as determined by the Harvard step test. Some could argue that this particular
step test was an indirect method of assessing fitness levels which could prove to potentially be unreliable. More work needs to be done in this area in order to fully comprehend the effects of fitness and its fùnctions on the dive response.
20 Emotional State
Individual reactions from psychological stress differ greatly from person to person (40). It is acknowledged throughout the literature that higher brain functions have a large impact on the dive response (26). A study from Hughes et al. (33) concluded that distraction, preoccupation or harassment leads to a reduced bradycardia when the face is immersed. Interestingly however, the same study also confirmed that fear was accentuating the deceleration of HR and increasing other dive reflexes. A major element of the study was the large variation in responses from person to person under similar circumstances.
Additionally, a study by Zbrozyna (72) observed a combination of typical dive response reactions with "defense" reactions when subjects were holding their breath in 18"C water. "Defense" reactions consisted of increased HR as well as vasodilation in forearm and calf. "Defense" reactions subsided in most subjects experiencing them after multiple repetitions of the stimulus over a period of many weeks.
Summary
Literature about the dive response is vast with many unanswered questions.
Much research has been done in this fìeld but due to the level of complexity of the topic, many physiological elements of the response remain unclear. A more individualized approach to smaller elements of the response may be what is required to fully understand the dive response.
Bradycardia has been one of the very first elements of study with dive response research. Over the years it has been mostly studied in animals with breath-
21 holding combined with whole-head or whole-body immersion, and later on in humans with facial immersion only. Parasympathetic vagal fiber activity innervating the heart via the brainstem has so far been explained solely by stimulation of facial cold receptors when breathing was maintained. Confirmation of other areas of the head involved in the process has not, to our knowledge, been investigated as potential mechanisms in the bradycardic component of the dive response. So far, only some branches of the trigeminal nerve have mainly been used to explain this phenomenon.
The vasoconstriction effects of facial cooling and/or skin cooling in other areas than the head (ex. forearm, calf) on the dive response has received much impoftance in the literature. As these effects have neither been suppofted nor refuted with portions of the head other than the face, further information of blood flow patterns would be useful for additional knowledge concerning the dive response especially with respect to drowning and near-drowning incidents.
Many studies (2, 3, 4,5) have focused on gas analysis and neural activity to determine changes during the decrease in ventilatory drive when the dive response occurs. Literature is currently scarce concerning the effectors of this change in drive
1V u, RR, V¡. Also, other than facial cold receptors stimulation, no other dive response related stimulus has been used to determine changes in ventilatory drive.
The present study focuses on the respiratory patterns derived from this change in ventilatory drive, since very few studies emphasized this component of the dive response.
22 In conclusion, the multi-factorial aspects of the dive response need to be studied more specifically before large generalizations are made about its overall functional significance. The present study focuses on a novel approach examining the role and relationship of the regional influences of the head in the dive response which, to our knowledge, has never been studied before.
23 CHAPTER 3: RESEARCH STUDY
24 METHODS
Subjects
The protocol of this study was approved by the University of Manitoba
EducationÆ.{ursing Research Ethics Board. Seven male subjects provided written informed consent and were screened by a PAR-Q questionnaire for cardiovascular and respiratory diseases that could be aggravated by cold water exposure. Although the study was open to male and female subjects, only males volunteered. No deception was used and all information about the study was disclosed to the subjects prior to the first session. The study was conducted during the first week of May.
Each subject took part in one familiarization and four experimental sessions. Each
session was at least 24 hours apart and at the same time of day to control for circadian effects. Subjects were requested to abstain from the consumption of alcohol and caffeine, the use of tobacco and vigorous exercise for 72 h prior to each session.
They were instructed to consume a light meal before they arrived for the study.
The subjects were 34.1 + 7.7 yr old; 179.9 + 6.5 cm tall; weighed 79.5 + 8.3
kg; had 17.8 + 3.3% body fat and had a BSA of 1.99 + 0.1%. They were closely
monitored for any signs of distress during immersions.
Instrumentation
Heart rate (HR), systolic (SBP) and diastolic blood (DBP) pressure were
digitally measured using a plethysmographic finger cuff, around the intermediate
phalange on.the middle finger of the left hand (Finapres 2300, Ohmeda, Madison,
WI). This system allowed a non-invasive continuous beat-by-beat measurement and
25 collection. Many facial immersion studies (2,4,5,37) have used this system which
has previously demonstrated accurate BP and HR measurements.
Skin temperatures were measured at six acral and three non-acral sites. Acral
skin temperature was measured on the tip and base of each of the right thumb, index
and ring finger using t-type thermocouples (Mon-a-therm, Mallinckrodt Medical, St-
Louis, MO). Non-acral skin temperature was measured on the dorsal hand, mid-
forearm and upper arm using t-type thermocouples integrated into a heat-flow sensor
(Concept Engineering, Old Saybrook, CT) according to standard procedures (21).
Thermocouples on acral sites were attached using adhesive waterproof tape
(Leukoplast, Elastoplast, Guelph, Canada). Thermocouples on non-acral sites were
attached using hypoallergenic adhesive disks (3M Double Stick Disks 2181, London,
Canada). An index of finger tip skin blood flow (SkBF) was derived from measuring
red blood cell flux values by laser-Doppler flowmetry (periflux System 5000, Main
control unit; PF50l0 LDPM, operating unit; perimed AB, stockhohn, Sweden) at the
distal phalange of the middle hnger of the right hand. The laser-Doppler flow probe was affrxed with adhesive rings in a site that demonstrated high flux values and pulsatile activity under resting conditions.
Respiratory rate (RR) and tidal volume (V) were measured using a metabolic cart (v*u* 229 by sensormedics, Yorba Linda, cA) in the breath-by-breath mode.
Since part of each trial required breathing under water, subjects breathed through a snorkel which \ryas connected to the system's Mass Flow Sensor.
26 Head Immersion Tank
A head immersion tank (Fig. 1) (Appendix B, C) was specifically constructed for this study such that only the subject's head was exposed to the water. The tank was constructed from a flexible scrim-reinforced vinyl cylinder (42 cm diameter, 88 cm tall) with an open top and a closed bottom end. A dry suit vulcanized rubber neck seal was glued to a24 cm diameter hole, which was cut into the side of the tank (the center was 27 cm from the top). This allowed head insertion through a waterproof neck barrier. An internal frame (50 cm high) kept the top portion of the tank rigid
(including the neck seal section). The top of the frame was securely suspended from an external support. The bottom of the tank sat on a platform which was suspended
from an electrically-isolated hoist. Because the tank had flexible sides, elevating the platform raised the bottom of the tank only, thus the water level within the tank relative to the head, allowing part, or all, of the head to be immersed. During
immersion, the subjects were vigilantly observed at all times for any signs of distress.
If necessary, the platform could be quickly lowered. Water temperature was
controlled at 77+0.5oC with a pump which exchanged water befween the immersion
tank and a temperature controlled water bath (1250 L).
Experimental Protocol
On separate days, subjects participated in four experimental trials involving
either dorsal, face, or whole head immersion with the latter done in supine and prone
positions. The order of conditions was selected to achieve a balanced design
(Appendix I). The four conditions were (Appendix H): l) Dorsum Immersion in
supine posture (DS); Subjects lay supine on the mattress with the head through the
27 neck cuff. The water level was raised until the ears were completely immersed (thus immersing most of the surface area innervated by the cervical nerves); 2) Facial
Immersion in the prone posture (FP): Subjects lay prone on the mattress with the head through the neck cuff. The water level was raised to a point just anterior to the ear (thus immersing most of the surface area innervated by the trigeminal nerve),'3l
Whole Heød Immersion in the supine posture (lT¡S): Subjects lay supine on the mattress with the head through the neck cuff. The water level was raised to completely immerse the whole head; 4) Whole Head Immersion in the prone posture
(WP)'Subjects lay prone on the mattress with the head through the neck cuff. The water level was raised to completely immerse the whole head.
28 Neck Cuff
Figure 1. Head Immersion Tank system demonstrating water level during baseline and recovery (left) and during whole-head immersions (right) (For dorsal and face conditions, the tank would be positioned relatively between both components of the figure). Also demonstrates position of the neck cuff for insertion of the head on the right side of the tank. Protocol
One familiarization and four experimental trials were performed in a climatic chamber which was controlled at 29+05"C and at 20o/o relative humidity. This setting was just above thermoneutral conditions of 27"C (53). During the
familiarization trial, the subject's head dorsum, face and whole head in supine and prone postures were each immersed for approximately i minute. The purpose \ryas to reduce potential stress for subsequent trials and evaluate the capability ofthe subject to participate in the study.
For each experimentaltrial, the subjects sat for a conditioning period of 20-40 min in the climatic chamber until peripheral vasodilatation was observed in acral skin temperature. Vasodilatation was assumed when finger tip temperatures were higher than finger base temperatures (11, 58). The subjects were then instrumented while in
the supine posture. They then either remained in the supine position or assumed a
prone posture, after which they inserted their head through the neck seal of the Head
Immersion Tank. In order to support the head within the tank, the forehead or dorsum
rested on two styrofoam supports placed 6 cm apart, each with a surface area of 7.5
cmt 1i."., 1.5 cm laterally and 5 cm longitudinally). The two surfaces were slopped
inward at 45". Thus, <2o/o of the face or dorsum contacted the supports at any time.
The subject then breathed through the snorkel for 10-min of baseline recording. At
this point, the water was raised to the desired level for 3-min as defined for each of
the 4 conditions (ust anteriorly to the ears in dorsum supine and face prone postures,
and covering the entire head in both whole-head postures). Subjects remained resting
for the immersion period or until either the investigator or the subject terminated the
test for safety concerns. The immersion period was subsequently followed by a
30 recovery period of 1O-min with the water lowered away from the head and the subject remaining in the same position.
Data Analysis
All parameters were plotted as percentage of baseline except for temperatures, which were plotted as absolute change from baseline. Mean baseline values were calculated from the four-minute period between five minutes and one minute before
immersion. Values at time 0 were collected immediately before the application of the
stimulus and were not included in the statistical analysis. Mean recovery values were
calculated from the first (early recovery) and second (late recovery) five-rninute
periods following immersion. Mean finger tip temperature (T¡¡nr.r tip) was determined
using the mean of the three finger tip sites. Non-acral arm temperature (T.,n) was
determined from the average of the dorsal hand and two arm sites. Also, while
cardiovascular adjustments occur rapidly, other elements of the dive response take
approximately 30-sec to develop (3, 4). Hence, parameters were plotted and analyzed
at different time periods. Values during immersion were plotted as follows: for
cardiovascular measures (HR, SBP and DBP), averaged values over the immediately
preceding 1g-sec periods and were plotted at 10,30,90 and 180-sec of immersion;
for skin temperature and blood flow (T¡nr.r tip, Tarm and S¡BF), the immediately
preceding 30-sec periods were averaged and plotted at 30' 60,90 and 180-sec of
immersion; for respiration measures (RR, V1), the immediately preceding 10-sec
periods were averaged and plotted at20, 60, 120 and 180-sec of immersion.
Two-way repeated measures analyses of variance was used to analyze values
throughout immersion and recovery periods using the repeated factors of time (differ
31 between parameters as explained above) and conditions (levels: DS, Fp, ws, wp).
Separate one-\¡/ay repeated measures analyses of variance were carrie d to analyze baseline values. Results are reported as mean +SD. P<0.05 was used to identi$r statistical differences. Post-hoc analysis was conducted using Tukey's multiple comparison test. Since only whole head immersions could be done in both positions
(supine and prone), post hoc testing was also used to determine postural differences between WS and WP when intercondition differences were found.
32 RESULTS
One trial was aborted after the first few seconds of WP immersion as the subject abruptly stopped breathing. The subject later mentioned that as soon as the water covered his head, he could not bring himself to take a breath. The subject later returned and completed all four conditions successfully.
Baseline values for all parameters of the four conditions are given in Table 1.
Heart rate baseline measurements for both supine conditions (66 + 7 .5 DS and 69 t 5 beats/min WS) were less compared to prone conditions (77 + 7.6 FP and 78 + 4.7
beats/min WP) (P:0.029). Diastolic blood pressure in DS (73 + 10.4 mmHg) was
also less relative to FP (84 L 4.6 mmHg) (P:0.021). No other parameter baseline
values were signifi cantly different.
33 Measures WS WP
HR 66 (7.5)** 77 (7.6) 69 (5)** 78 (4.7)
SBP 123 (15) l3s (13.4) 131 (e.5) 137 (l l.s) DBP 73 (r0.4)* 84 (4.6) 76 (7.e) 82 (4.e)
SrBF s.89 (2.26) s.73 (2.38) s.s7 (2.te) s.s6 (1.8e)
Thnger tip 3s.7 (0.62) 3s.3 (0.79) 3s.4 (1.46) 34.9 (1.04) T*. 33.9 (0.87) 34.6 (0.86) 34.3 (0.s5) 34.2 (0.62)
14.0337 14.88739 15.08126 15.791 8 Vp
RR 16 (1.4) l8 (2.s) 16 (4) 18 (3.3) vr 0.82 (0.1) 0.85 (0.09) 0.e8 (0.26) 0.e4 (0.17)
Table L. Absolute baseline values for heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean finger tip temperature (T¡¡gs¡ 1ip), non-acral arm temperature (T**), skin blood flow (S¡BF), minute ventilation (V e), respiratory rate
(RR) and tidal volume (Vr). Values are means (SD) for 7 subjects. HR(beats/min);
SBP (mmHg); DBP (mmHg); S¡BF (laser-Doppler units); Tfins", tip ("C); T*'" (oC);
* ** V 6 (Umin) RR (breaths/min); V¡ (ml/breath). Lower than FP (P:0.021), Lower than FP and WP (P<0.001).
Cardiovascular Responses
Heart rate, SBP and DBP data, measured during the immersion and recovery
period, are presented in figures 2-4. HR changes during the immersion period were
influenced by tirne (P<0.001) but not by conditions (P:0.131) (Fig. 2). A significant
reduction in HR was observed from 90-sec to 180-sec relative to baseline and 10-sec
of immersion (P:0.002). Interaction between time and conditions (P<0.001) was also
measured. Heart rate for WP condition was signific4ntly less compared to DS
(P:0.032) at the end of immersion. WS was also greater than FP (P:0.016) and WP
34 (P:0.021) at 10-sec. No significant changes in HR were seen during recovery.
Furthermore, changes seen in SBP (Fig. 3) and DBP (Fig. 4) were both influenced by time (P<0.001) but not by conditions (P:0.534 and P:0.222, SBP and DBP respectively). An immediate rise in SBP was observed at l0-sec and was maintained during the full immersion period relative to baseline (P:0.004) and both recovery times (early recovery, P:0.017; late recovery, P:0.030). An increase in DBP relative to baseline was also measured during the immersion period except for a transient decrease at 30-sec. There were no interactions with either SBP (P:0.534) or DBP
(P:0.149). There were similar blood pressure responses in both prone conditions
(i.e., FP and WP). Alternatively, there was a tendency in the supine conditions (i.e.,
DS and WS) for values to be higher when the whole head was submersed, although these differences were not statistically significant.
35 ----¿- DS ---¡- FP ---r-- ws ----r- wP s o .Cõ oñØ Ëm É.8 Ëo oõ(Eq) ¡C oc) oL o-
Figure 2. Changes in HR during 3 minutes of immersion and 10 minutes of recovery in all conditions. t WS different from WP and FP (P<0.05). TT WP different from DS (P<0.05). * Lower than baseline (P<0.005). Error bars represent SE'
36 120 ---¿- DS +FP -+- WS 115 G- G) o\ L.v Jd) U'c '110 o:o0) Ë8 Eco 8b 105 68' t¡ -S oõ 100 äg >ì 0) u, a- 95
90 0 I 2 3 4 5 6 7 I I ',10 11 12 13 Time (min)
Figure 3. Changes in SBP during 3 minutes of immersion and 10 minutes of recovery in all conditions. * Greater than baseline and both recovery times (P<0.05). Emor bars represent SE.
37 120 ----+- DS +- FP 115 +ws -.+. WP LO\O\o oo) oc 110 ÀEEõ EP Oif õ o.¡ SE 96oo 100 .sb OL
.10 0 1 2 3 4 5 6 7 8 9 11 12 13 Time (min)
Figure 4. Changes in DBP during 3 minutes of immersion and l0 minutes of recovery ** in all conditions. Greater than baseline and 3O-sec (P<0.05). Error bars represent SE.
Blood Flow and Skin Temperature
The changes in s¡.BF (Fig. 5) during immersion were influenced by time
(P<0.001) but not by conditions (P:0.135). A rapid decrease in S¡BF was seen ar 30- sec and 60-sec relative to baseline, end of immersion and both recovery times.
Immersion at 90-sec also demonstrated lower values but only relative to baseline and late recovery. There were no interactions present (P:0.473).
38 Mean finger tip temperature (Fig. 6) had a similar tendency compared to S¡BF
with a decrease upon immersion but this difference was not statistically significant, thus there were no effects of either time (P:0.159) or conditions (P:0.235) during
immersion or recovery. There were no signihcant changes in T** during immersion
and recovery (Time P:0.095, Condition P:0.504). There were also no interactions for either Tfins", tip or T*-.
----¿- DS +FP +- ws WP G -r- 9ol=Ð l!.c oõoØ oÆ EË tro ðþ g'Þ CY iL8
012345678910111213 Time (min)
Figure 5. Changes in S¡BF during 3 minutes of immersion and l0 minutes of recovery in all conditions. * Lower than baseline, 180-sec, early recovery and late ** recovery (P<0.05). Lower than baseline and late recovery e<0.05). Error bars represent SE.
39 ----a-- DS +FP ----- WS o +WP J^ f! o- o.9õ- oo .sfi Fg OY troÞ)ts EP) cQ Eõ =
IMMERSION 012345678910111213 fime (min)
Figure 6. Changes in T¡nr", tip during 3 minutes of immersion and 10 minutes of recovery in all conditions. Eror bars represent SE.
40 ----^- DS _T FP +- ws o .+ WP J!^ /\ iEo 8.9 L_ l-(Ebg eCt <õ EÈ oo)t; o) IMMERSION 012345678910111213 lime (min) Figure 7. Changes in Tu,' during 3 minutes of immersion and l0 minutes of recovery in all conditions. Error bars represent SE. Ventilation and Breathing Pattern Minute ventilation (Fig. 8) had a rapid transient increase at 20-sec of immersion (P<0.005) which was achieved through aparallel increase in V1@<0.005) (Fig. 10). For the remainder of the immersion, V s decreased to or below baseline but was not statistically different at other times while V¡ progressively returned to baseline. RR (Fig. 9) was also influenced by tirne (P<0.001) with a decrease (-20%) 41 from 60-sec to the end of immersion. Neither ú s, RR or V1 were influenced by conditions (V E P<0.499, RR P<0.683, Vr P<0.592) and there were no interactions. Although there were no intercondition differences for ü s or RR, at 20-sec both supine and prone whole-head values were similar to each other and substantially higher than both partial-head values. Therefore, a subsequent analysis was performed after combining data for each of the whole-head and partial-head sub-conditions. In this case, an interaction was observed (V E P:0.006; RR P:0.01). A paired t-test indicated a significant difference between whole-head and partial-head values at 20- sec of immersion for both V s(P=0.022) and RR (P:0.025), 42 ----¿- DS -e FP +- WS +WP E oÈ-oL- iú ú) Ëc0 >õot Ë(soo) êC. EÞ o o- IMMERSION RECOVERY 567 Time (min) Figure 8. Changes in V s during 3 min of immersion and l0 min of recovery in all conditions. +* Greater than all other times (P<0.005). Error bars represent SE. 43 ----4- DS +FP +WS I -..F WP o) o.g Ë0) ô¿E >\ c0 oo õ0) .= H', oc)ØC É.? o) â- 012345678910111213 Time (min) Figure 9. Changes in RR during 3 minutes of immersion and l0 minutes of recovery * in all conditions. Lower than baseline (P<0.05). Error bars represent sE. 44 ----¿- DS +FP +ws +WP E 0) .E trõog =m >ooõ go 9# Fol Lo o) fL RECOVERY 0 't 2 3 4 5 6 7 I I '10 11 12 13 Time (min) Figure 10. Changes in Vt during 3 min of immersion and 10 min of recovery in all conditions. ** Greater than all other times (P<0.005). Error bars represent SE. 45 DISCUSSION This was the first study to compare the isolated effects of head dorsum, face and whole-head (supine and prone posture) immersion (17"C) on the dive response. Our findings are generally consistent with dive responses of other studies. We observed bradycardia in all conditions. However, a greater HR response was seen in WP compared to DS at the end of immersion. An increase in both SBP and DBP was also recorded. Finger tip skin blood flow had a transient decrease and then returned to baseline values. A transient increase was seen in V B before returning to baseline values with the effect being greater in whole-head compared to partial-head immersion conditions. This transient increase was accomplished via parallel changes in V1. Our results suggest no detectable differences between face and dorsum in any parameters of the dive response. Also, the initial respiratory response (V s) was greater in whole-head than either partial-head conditions. Finally, there were no effects of posture within either whole-head or partial-head sub-conditions. Previous dive response studies involving facial immersion in cool water while breathing have reported similar levels of bradycardia, increase in BP, and decrease in peripheral S¡BF. Andersson et al. (4) reported a decrease in HR of -l\Yo, increase in BP (MAP) of -5%o and a S¡BF decrease of -35Vo after 30 seconds of facial immersion in eupnea in 9-11'C water. Our results are also concurrent with previous ventilatory studies (35, 44) which demonstrated ventilatory drive changes at different time periods. In the early stages of immersion, Jay et al. (35) demonstrated an increase in ventilation (-10 L/min) during the first 60 seconds in 1OoC water compared to resting values. Later in the response, Mukhtar and Patrick (44) reported a reduction of l0%o 46 in ventilation after 2 minutes when subjects were breathing through a snorkel during face immersion in l3"C water. The differences in HR values between both supine and prone postures during our baseline measurements were comparable to previous postural studies indicating a faster HR in prone posture with no other stimuli (65,69). A study by Watanabe et al. (69) observed a decreas e of 7o/o in HR when subjects were turned form prone to supine whereas a l3Yo difference was observed in our study after 5 minutes allowing for cardiovascular adjustments. Possible Mechanisms for the Results The HR pattern during the dive response is affected by three components: l) an inspiratory tachycardia due to the stimulation of stretch receptors in the lungs; 2) breath-hold induced bradycardia activated by the baroreflex, originating from an decrease in intrathoracic pressure; and, 3) a time-dependent temperature-induced bradycardia elicited with activation of skin (i.e., face) cold thermoreceptors (47). In the present study, continous breathing was allowed. Despite an early increase in V1 (increase in pulmonary stretch receptor activity) in all conditions, only the WS condition presented tachycardia after 10 seconds of immersion. Heart rate for that condition was already elevated at ll7Yo before the onset of stimulation. Anticipation, leading to some tachycardia, is generally observed in dive studies but no other condition exhibited a similar HR response. This unexpected result may be due to a higher level of anxiety and stress towards the WS protocol as some subjects manifested some concerns about immersing their head while in the supine position despite the presence ofa snorkel and nose plug. Anxiety and stress has been used to explain tachycardia in other dive response studies (4,26). A study by Zybrozyna and 47 Westwood (72) reported tachycardia combined with vasodilation in subjects presenting anxiety during diving trials. While the degree of bradycardia observed in our study is similar to other studies, it was statistically observable only after 90 seconds of immersion. Other studies, with breathing maintained, demonstrated bradycardia sometimes as early as 10-15 seconds (4,47). These two studies invoked a greater cooling stirnulus using -10'C water. Another factor that could explain this phenomenon is the previously mentioned level of anxiety and stress demonstrated by some subjects. An early tachycardia most likely contributed to the delayed bradycardia. Additionally, the neck seal used for the Head Immersion Tank caused some pressure around the neck which may have led to some suppression of vagal tone. Some hemodynamic studies have previously observed that an increase in pressure of only 7 torr around the neck could increase both HR and BP 45, 46). The combination of a reduced cold stimulus, reduced vagal tone from the neck seal and anxiety towards the WS condition likely contributed to delay the bradycardia response. The intercondition heart rate difference at the end of the immersion period between DS and WP was possibly caused by postural effects during baseline measurements, and not by regional influences. Heart rate baseline values for WP were 12 beats/min higher than DS and 9 beats/min higher than WS and were significantly different to both. No difference was, however, observed between both whole-head conditions at 180 seconds of immersion. Since WP baseline HR was higher, a similar decrease to WS during immersion would prove to be a larger 48 percentage difference. In addition, reduced stimulation from the head dorsum cannot be ruled out as a reason for a higher HR in the DS condition. Significant decrease in finger S¡BF occurred within 30 seconds of immersion whereas significant bradycardia was delayed until 60 seconds of immersion. Previous studies suggested different times of emergence between vasoconstriction and bradycardia implying that since the former exhibits earlier signs, it is the most important reflex of the dive response. Fagius and Sundlöf (15) studied skin-nerve and muscle-nerve sympathetic activity (indicating vasoconstriction) during face immersion and found that the latter usually takes place before bradycardia. In the current study, the occurrence ofbradycardia after peripheral vasoconstriction supports the primary role of redistribution of blood flow to the core which acts as the first oxygen-conserving element of the response. The results of our study could not provide fufther indication on the possible role of the dive response on previous results on core cooling rates when head dorsum and whole head were immersed in cold water. Pretorius et al. (50) suggested that enhanced vasoconstriction, leading to a reduced mass of tissue being perfused, mediated by the trigeminal nerve could explain differences in core cooling rates during head dorsum and whole-head immersions. We could not confirm our main hypothesis that stimulation of the trigeminal nerve would lead to greater peripheral vasoconstriction. Water temperature is inversely proportional to the magnitude of the dive reflexes (56, 60). While this study has shown that 17"C water is enough to stimulate dive reflexes, we believe that longer immersion periods and/or lower water 49 temperatures may be required to elicit potential blood flow differences between facial and dorsum cooling. Although there were no significant changes in skin temperature during immersion, there was a tendency for T¡nr* rip to decrease in a similar pattern to S¡BF. This lack of significance in skin temperature response was likely due to the short duration of the trials which did not allow enough time for skin temperature to reflect blood flow redistribution. The ventilatory drive temporal shift from an early increase followed by a decrease was demonstrated by a swift rise in Yy at 20 seconds followed by a reduced RR from 60 seconds to the end of immersion. Previous studies reported different time periods for the ventilatory response during face immersions. Mukhtar and Patrick (44) observed a l3%o transient decrease in drive (V 6) from 2to 5 minutes following facial immersion in 13"C water. Ventilatory measurements of that study were only taken every minute for 5 minutes, however, and the rapid increase would have been missed. Jay et al. (35) reported similar results to our study; an increase in drive (V s) in 10'C water and colder, but in the early stages of immersion only. They concluded that facial immersion in that range of water temperature would generate a cold shock- like response, similar to whole body water immersion, over a reduction in ventilatory drive generally associated with the dive response. Similarly, Stewart et al. (62) recorded ventilatory increases when subjects immersed their face in 17oC water during 50 seconds of immersion. Trials performed in 35-37"C water showed little to no change indicating that temperature, and not water contact per se, has an effect on 50 the ventilatory component of the response. In connection with the previous studies, our results clearly demonstrates a temporal shift with an early ventilatory cold shock- like response followed by a reduced drive in the later stages of immersion in 17'C water leading us to believe that both components are parf of the dive response and are dependant on water temperature. Finally, we found minimal, if any, differences in responses between facial and dorsum stimulation. We expected the trigeminal nerve stimulation of facial immersion to elicit greater responses. It is noteworthy that the ear canal and the tympanic membrane (which are innervated by the vagus nerve) were not immersed with the face, but were immersed with the dorsum. Thus, vagal stimulation may have attenuated some of the differences that were expected between the two conditions. Practical Implications for Results The oxygen conserving mechanism of the dive response has been the subject of much debate regarding near-drowning accidents. The two main processes used to explain the increase of successful resuscitability in cold-water near drownings are: cooling of the brain with concomitant reduction in oxygen requirements and changes in post-anoxia lower levels of glutamate and dopamine (20); and, the circulatory adjustments of the dive response (20,24). Hayward (31) found a lower breath- holding time with colder water during simulated near-drowning accidents and emphasized a more important role of brain cooling for resuscitability. However, brain cooling becomes a more vital factor after l0 minutes of immersion in the absence of ventilation of water (25). In the first minutes of immersion, the rapid peripheral vasoconstrictive component of the dive response with dorsum, face, or whole-head 51 immersion is very influential and act as the first line of defense in preventing asphyxia of the brain and increasing survival time underwater. Our study demonstrates that even the small amount of stimulation generated by head dorsum exposure further reveals the importance of the dive response to increase resuscitability by exhibiting all elements of the response necessary to defend against near-drowning accidents. Concerning the postural component of this study, our findings could help future work on the dive response which will now be able to include supine and prone postures. Considerations As most of the immersed head dorsum is usually covered with hair, reduced stimulation of the dorsum compared to the other conditions could have limited the degree of the response. Real near-drowning situations, however, involving head dorsum would most likely include hair on the back of the head. Thus, we consider this factor negligible as it represents real-life scenarios. Additionally, the breathing unit could have limited ventilation as the modified snorkel with added tubing generated greater deadspace. The same breathing unit was, however, used for all conditions. Furthermore, the Head Immersion Tank permitted whole-head trials to be performed in both postures but did not allow the investigators to do the same with DS and FP trials. Proper water immersion of the head dorsum in the prone posture and of the face in the supine posture was not possible. The conclusions of this study regarding the effects of posture on the dive response consequently apply only to whole-head immersions. 52 In summary, there were no detectable differences between face and dorsum in any parameters of the response during the three minutes of immersion in 17oC. In addition, a temporal shift is seen in the ventilatory component of the response as indicated by a cold shock-like response in the first minute of immersion with increased Vt followed by a decrease in RR. Finally, the use of a supine or prone posture does not affect the reflexes of the dive response during whole-head immersions. Future studies should focus on stronger stimuli (colder water temperature and longer immersion period) to determine the precise effects of regional influences ofthe head on the dive response. 53 CHAPTER 4: SUMMARY AND CONCLUSION 54 ST]MMARY This study resulted in the emergence of three novel components to the widely studied dive response in humans. Firstly, when breathing is maintained, there are no detectable differences on the dive response reflexes between face and dorsum immersion in 17'C water during the three minutes of immersion. While some differences have been seen in other studies comparing branches of the trigeminal nerve on the face (59), our study found none when comparing the face to the dorsum. Since the dive response is inversely proportional to water temperature, it is possible that lower water temperatures and/or longer immersion periods may be helpful in determining potential regional differences. Secondly, it would seem that the ventilatory component of the response has a temporal shift and is composed of both a cold shock-like response in the early stages of immersion (expressed by an increase in V1) followed by a decrease in drive (expressed by a decrease in RR). A study by Stewart et al. (62) also demonstrated an increase in drive within the first minute of immersion in 17oC water but also indicated no ventilatory changes in warmer water. Future studies should focus on the temporal shift of the response with a wider range of water temperatures and with longer immersion periods. Finally, this was the first study to test the differences between supine and prone postures on the dive reflexes. Our baseline results were concurrent with other postural studies indicating higher heart rates in the prone posture compared to supine. More importantly, we found that the dive reflexes are not affected by postural change befween supine and prone positions. Even if most dive response studies used a prone position for methodological purposes, future research will be able to consider the supine posture as well. 55 CONCLUSION While this study brings new and interesting elements to the current literature, further research in the fìeld is needed. When breathing can be maintained, immersion periods of 10 minutes would more likely be more useful because of the stronger stimulus and of the realistic time frame, in which the dive response plays a primary role, before brain cooling occurs. It would also seem that research regarding water temperature effects could also further explain some dive response components. Lower temperatures would provide a stronger stimulus as well and could determine differences in breathing patterns when both component of the ventilatory response are considered. 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Clinical Automatic Research, 1992.2(4): p.225-233. 62 APPENDICES 63 APPENDIX A Anthropometric data Subiect Aqe (vr) Heiqht (cm) Mass (kq) BMI BSA (m2) A 29 181 82 25.0 2.03 J 32 182 85 25.7 2.06 D 38 183 83 24.8 2.05 S 29 188 84.5 23.9 2.11 W 32 172 72 24.3 1.85 c 29 170 64 22.1 1.74 G 50 183 86 25.7 2.08 MEAN 34.14 179.86 79.50 24.51 1.99 SD 7.7 6.9 8.5 1.2 0.1 Sum of Triceps Subscapular four skin % Body Subiect sf sf Biceps sf lliac/c sf folds Fat A 10.4 10.1 3.4 24 47.9 18.3 J 8.3 11 2.8 13.4 35.5 14.7 D 14.2 I 5.2 23.2 51.6 19.3 S 4.1 10.2 8.7 18.7 41.7 16.7 W 8.1 24.8 4 38.7 75.6 24 c .) 8.8 6.7 14.4 32.9 13.8 G NA NA NA NA NA 18 MEAN 8.02 12.32 5.13 22.07 47.53 17.83 SD 4.1 6.2 2.2 9.2 15.7 3.3 64 APPENDIX B PIan of the Head Immersion Tank 65 APPENDIX C Head Immersion Tank 66 APPENDIX D Head Insertion in the Immersion Tank 67 APPENDIX E Finapres Measurement Site N 68 APPENDIX F Acral Skin Temperature Sites @orsal View) 69 Appendix G Acral Skin Temperature and Laser Doppler Blood Flow Measurement Sites (Palmar View) 70 APPENDIX H Conditions Dorsum, Supine Baselile Lnrìter-sicltr Face, Prone Baseli¡re hruuersiorr Whole-Head, Supine Baseli'e Inlmersion Whole-Head, Prone B¿rselìne Iuullero-icut --l--E] I 71 APPENDIX I Order of Trials Subjects Day 1 Day 2 Day 3 Day 4 A WP WS F D W D WP WS F c F WP WS D D WS F D WP G WS WP F D J WP WS F D S WS D F WP 72 APPENDIX J Results Summary Table :':t,;.,';'t ",';T:,, ::t;',..,:' ; ,:ffit....^,','r, "$å, 1' €' ß € ñ A"NI ...:N: ì, i.:.ìi..rr-ì,r .i ."...:. .,- .', ..¡'NL:.:,'..: :.: t $- .€,-, € ..' .':.,' :,...:::'1.' : :.;:,tl;,.:': NNS :. NNS NNS t,tt ,t' .' ',1 ,', -'.' @' ..$,'.t,' . sLwNS \sz Þl NN &N @N ..€ ,ê:$ $ñ. ñ$ sw fw W & -,€$ ,.,,N $ r$