The Human Dive Reflex
The dive reflex is portrayed as bradycardia caused by submerging an individual’s head underwater. In diving vertebrates this occurs in a remarkable manner than compared to humans (Hurwitz & Furedy 1986). A diving seal where baseline heart rate rises 100 beats to 10 beats per minute when diving would be an example of this (Hurwitz & Furedy 1986). Bradycardia is stated as slow resting heart rate or pulse rate (Tortara & Derrickson 2009). Accompanied bradycardia response to breath hold is advantageous for vertebrate as well as humans because it permits physiological processes to adjust to environmental change by redistributing blood flow from periphery (non-essential organs) to brain and other essential organs (Hurwitz et al 1986 & Gooden 1994 ) The dive reflex depends on the autonomic control of the heart to begin proper responses, the sympathetic nervous system (SNS) sends impulses through the cardiac accelerator nerve and starts release of norephrine which increases contractility and heart rate. However parasympathetic nervous system (PNS) works through vagus nerves which end in heart decreasing contractility of the heart by decreasing rate of spontaneous depolarization (Tortara & Derrickson 2009). Producing bradycardia response requires the sympathetic nervous system and parasympathetic nervous system to work antagonistically (Hurwitz & Furedy 1984). Dive reflex consists of two stimuli; the stimulation of facial receptors which are responsive to cold and wetness (pressure receptors), and the voluntary or involuntary termination of breathing or a decrease PO2 (Gooden 1994). Facial stimulus travels through the trigeminal to integrated respiratory centre and cardiovascular centre inside medulla oblongata. Inhibitory neural signals generated by facial receptors inhibits respiratory centre consequently triggers termination of respiratory muscles such as the diaphragm and intercostals causing reflex apnoea in order to inhibit aspiration of water (Hiebert & Burch 2003). In addition, inhibition of respiratory centre stimulates cardiovascular centre and therefore increases parasympathetic activity via vagus nerve to start bradycardia , and as well stimulates sympathetic activity to vasoconstrict arterioles in limbs and non essential organs for instance the skin, intestines, and kidney causing them to rely on anaerobic conditions (Hiebert & Burch 2003).This non essential organ vasoconstriction allows the redirection of blood flow to the brain and heart, this guards the brain from injury by supplying as much as oxygen that is needed , and reducing the brains requirement for oxygen by cooling (Hiebert & Burch 2003).The decrease in PO2 is sensed by the arterial chemoreceptor’s from involuntary or voluntary breath hold , stimulates the cardiovascular centre to signal the SNS and PNS to complete the same antagonist functions completed in respiratory inhibition stimulus(Hiebert & Burch 2003). Also the expected Bradycardia when simulating dive can be unsuccessful due to emotional reasons such as fear, being distracted, being embarrassed, or in eagerness to submerge out of water could induce tachycardia response (Gooden 1994). In addition the experiments accomplished will show the stimulus in dive reflex and the physiological reasons behind those reflexes will be discussed.
First of all the investigation was accomplished using a subject seated on lab stool with the same posture, with their head down, and elbows resting on the bench. Chart 5 was setup and a finger transducer was connected to the subject’s index finger. The subject sat quietly to rest heart rate and distractions were kept to smallest amount to avoid false recordings .The subjects palms were facing up to diminish finger movement as a result reducing signal dampening of finger transducer while recording . Prior to undertaking the diving experiments the subject practiced their breath hold; the subject took two deep breaths but not maximal breaths before holding their breath for 30 seconds. Every experiment lasted 1 and half minutes with recordings showing heart rate per min at: rest, 1st 15 seconds of breath hold, 2nd 15 seconds of breath hold, and recovery. For each dive stimulation, this was expected. Prior to the experiments it was noted not to force the subject from simulating a dive or breath hold if they feel unpleasant doing so. The effect of diving was experimented on using different water temperatures, and snorkelling equipment. The water basin was positioned in front of the subject seated in appropriate posture staying motionless (it was furthermore important for the subject to remain motionless during the experiment as this triggered further signal dampening while recording heart rate) .the subject would take a deep breath and exhale to some extent and submerge their face in water up to cheeks, and yet again heart rate would be recorded for 30 seconds.
These events were used for every breath hold dive simulation. For a more detailed method refer to MEDSCI 205 laboratory manual page 35-39.
For the analysis of results % change in heart rate was calculated using the equation below:
The above graph shows the percentage change in heart rate from the effect of apnoea caused by water temperature and pressure changes.
The graph above shows the effect of apnoea only on heart rate of the subject which indicates that holding breath has a apparent change in heart rate compared to holding breath in cold water.
The above graph represents the percentage change in heart rate due to the effects of temperature.
Investigating all data gathered from the experiments draw together the fact that bradycardia was observed in most of them. In table 3 the subject showed an increase in heart rate in snorkelling, the standard dive and holding breathing in warm water. As reviewed in the introduction the reason may be due anxiety or distractions which lead to the beginning of tachycardia (Gooden 1994). Snorkelling (shown on table 3) showed a noteworthy increase in heart rate instead of a bradycardia response, the fact that literature proposes on immersing face in water the body must begin reflex apnoea and diving bradycardia (Gooden 1994). Also in resting pulse 1st standard dive the 1st 15 seconds showed an increase in heart rate followed by significant decrease to 69.68 beats per min. The rapid decrease in the 2nd 15 seconds was due to the importance of the body adapting to retain oxygen reserve to supply vital organs (Hurwitz & Furedy 1984).
Analysing breathing in water with snorkel vs. Holding breath in cold water showed there were not such significant heart rate differences between the two experiments conducted .In breathing in water with a snorkel, there was a steady increase and decrease in heart rate from 7.9 % – 16.1% change, but these heart rate measurements were in range if of resting pulse 55.82 beats per min measured at the start of the experiment. In comparison holding breath in cold water showed expected decrease in heart rate from resting pulse by 7.8% decrease in first 15 seconds to 16.6% decrease in second 15 seconds. This experiment shows that voluntary apnoea by itself causes bradycardia through the decreasing levels of PO2 which triggers arterial chemoreceptors ,that sends stimulating the cardiovascular centre to start appropriate responses via the parasympathetic and sympathetic pathways working destructively (Hurwitz & Furedy 1984).
Snorkelling showed a change in heart rate by 7.9 % and 16.1%, but the reaction was an increase in heart rate than a likely decrease as assumed in literature (Hiebert & Burch 2003). Voluntary facial immersions in water according to literature should usually stimuli pressure receptors in face and obstruct respiratory muscles to begin reflex apnoea and in addition stimuli sympathetic to constrain blood flow and stimuli cardiovascular centre to begin bradycardia during the dive is model (Hiebert & Burch 2003). Additionally the simulated dive with cold water demonstrated a likely bradycardia response with a decrease change in heart by 7.8% and 16.6% this implies that the sensitivity of cold wet receptors on the face can add to Bradycardia, in effort to reduce oxygen expenditure (Hiebert & Burch 2003).While evaluating heart rate values obtained from snorkelling and breath hold in cold water, the experiment showed the stabilizer effects of cold water on decreasing the heart rate and that facial immersion should show a Bradycardia response. (Hiebert & Burch 2003) (Pauler, Pokorski, Honda, Ahn et al 1990.
From the analysis of results it can be agreed upon that holding breath in warm water has to some level, less change in heart rate, in the first 15 seconds heart rate increased by 1.3% and decreased by 0.79% in second 15 seconds with a significant 13.1% increase in heart rate in recovery phase well over the normal resting pulse 62.0 beats per min a probable cause may have been anticipation to submerge out of water (Hiebert & Burch 2003). Cold water, in comparison demonstrated the expected Bradycardia by illustrating significant change in heart rate from resting pulse by 7.8% in first 15 seconds to 12.3% in second 15 seconds, then restoring back to the resting pulse in the recovery phase. This experiment additionally confirmed that facial receptors are sensitive to cold and that immersion in cold water will constantly associate with a strong decrease in heart rate (Pauler, Pokorski, Honda, Ahn et al 1990). Also the variation in heart rate between warm water and cold water dive simulations point out that cold water has additive effects on heart rate reduction by apnoea (Hiebert & Burch 2003).
Cold water demonstrated the majority of significant change in heart rate compared to other cues. The probable cause of this would be facial immersion in cold water, as this leads to reducing metabolic functions in an effort to lower the oxygen demand to peripheral tissue caused from hypoxia and tissue cooling (Hiebert &Burch 2003). It has been stated by literature, that the higher the temperature the lower bradycardia responses expected the lower the temperature the higher the bradycardia responses expected (Gooden 1994). The second highest change in heart rate was shown in snorkelling which was not expected. The expected result was a small decrease in heart rate to explain pressure / wet receptors stimuli bradycardia (Hiebert &Burch 2003).Holding breath in air showed the expected change in heart rate. The other cues experimented showed the added effects to breath hold will increase bradycardia compared to breath hold alone. Also warm water had showed small change in heart rate this proposed that it has little or no added effect to dive reflex response.
In conclusion in all cues experimented with breath hold and facial immersion a commencement bradycardia was observed this proposed that breath hold or apnoea plays an important role in the dive reflex. In addition facial immersion in cold water was established to be the most powerful stimulus of dive reflex.