Juan Mejia

BIO 431

Prof. Muntzel

Dec. 23, 2015

Effect of Water Temperature on the Heart Rate, Blood Pressure, and Pulse Wave Velocity components of the Mammalian Dive

Reflex

Introduction

Apnea, the holding of breath elicits bradycardia, which is the slowing of the heart

rate. This response is given by the chemoreceptors in the body that detect the lack of

Oxygen and the buildup of Carbon Dioxide [1].

According to Hurwitz the dive reflex is defined as bradycardia by putting your

head underwater (while holding your breath of course) [2]. The physiological effects on

mammals include the slowing of the heart rate immediately after submersion and it is

maintained as long as the animal is under water [2]. Another effect is the redistribution of

blood, being that the blood s redirected as a priority to the brain and important organs,

while decreasing the blood flow to the extremities [2]. Furedy puts the dive reflex as a

response that redirects blood to more important organs and more sensitive to lack of

oxygen, while accompanied by “tonic peripheral constriction” with a heart rate

deceleration [3]. Andersson takes the dive reflex a little further, though his description of

the dive reflex supports Hurwitz and Furedy’s, he adds some physiological responses not

seen in the previous studies. He ads that in trained subjects blood lactate accumulate and

the uptake of O2 decreases [4]. A longer dive resulted in “less arterial O2 desaturation”

[4]. Also cardiac output decreases due to reductions in stroke volume and heart rate [4].

Shamsuzzaman gives the clearest description of the dive reflex. In which he states that

the dive reflex is just a response that allows birds and mammals to be underwater while

keeping the neural and cardiac system whole and healthy [5]. And lastly Eckert, who

shows the physiological effects of the dive reflex using a very simple but descriptive

image supports all of the other previous definitions and effects of the dive reflex. The

image shows the decrease in heart rate, the decrease in cardiac output, the increase of

CO2 and the decrease of O2, along with an immediate and drastic increase of blood

lactate right after breathing again [1]. Eckert talks about the chemoreceptors being a very

important cause of the physiological effects. The lack of breathing decreases the O2

concentration, which activates arterial receptors that elicit the vasoconstriction of the

arteries, and the decrease in heart rate and cardiac output [1].

Pulse Wave Velocity (PWV), which is the speed of the blood traveling the

arteries, is highly dependent on arterial stiffness, which increases the speed of the blood,

but also increases blood pressure [6,7]. Also in Seetho’s research correlating arterial

stiffness and sleep apnea, he found that the sleep apnea does increase pulse wave velocity

therefore arterial stiffness also increases [6]. To bring everything together that means that

apnea, which elicits the dive reflex, also elicits arterial stiffness, therefore as the heart

rate slows down and blood pressure goes up, the resistance goes down due to the arterial

stiffness allowing the blood to travel faster to vital organs. Temperature plays an

important role in the dive reflex because according to Furedy’s experiments the lower

(colder) the temperature the greater the bradycardia response. In other words the heart

rate slow down even more and the vasoconstriction is even greater. Therefore in this

experiment we hope to see the same results. The decreasing in temperature would also

play a role in the Systolic Blood Pressure (SBP) by increasing it. Shamsuzzaman tested

this out and found that with cold water the Mean Blood Pressure (MBP) increases even

higher than with regular room temperature water.

Methods

The equipment used to measure heart rate, systolic blood pressure, and pulse

wave velocity for this experiment were one plastic basin per group, dry paper towels, tap

water, ice, one thermometer per group, one stop watch per group or timer (you will need

to count 40 seconds), blood pressure cuff, finger pulse sensor, Powerlab program for

measurement of the heart rate and blood pressure. After the students were hooked up with

all the sensors and pressure cuff and did the experiment, the data, meaning the heart rate,

pulse wave velocity, and arterial blood pressure (which the systolic blood pressure could

be derived from). It took some manipulation of the graphs to get the data that we needed

for all 3 for example taking a range of 2-3 seconds on the graph to get the average and

include that average as one data point, or use it as one second in the data. There were 3

pressure cuffs, two hooked around the wrists and one right above the right ankle. The

subject also had a finger pulse sensor attached. The pressure cuffs were used to measure

the Systolic blood pressure, while the finger pulse sensor gave the heart rate, and pulse

wave velocity. The subject had all the equipment for all of the experiments, control,

apnea, and both dives.

To carry out the control procedure the subjects stood in front of the empty plastic

bucket. They were told to breathe normally for 40 seconds to acquire a representative

baseline. After the 40 seconds they were told to bend slowly and put their face in the

bucket with closed eyes, all of this while still breathing normally. The apnea procedure

went almost exactly the same as the control, the only absolute difference is when their

face went inside the bucket, the subjects had to hold their breath for at least 45 seconds.

The person timing the whole procedure would tap this person on the shoulder when they

were done. For the Dives at 10 and 40 degrees Celsius dives the water in the buckets

were either heated or had ice thrown in it. For the 10 degree Celsius dive the bucket was

filled with water and ice was placed inside and with a thermometer we waited until the

water reached to about 10 ± 1 degrees Celsius. Each time a student did the experiment the

cold water was remade. For the 40 degree Celsius water we had a water heater. We boiled

water and then mixed it with regular room temperature water until the two found

equilibrium at 40 degrees Celsius. Again, each time a student did the experiment the

water was remade.

Due to fear of the experiment being compromised by the facial receptors after one

of the dives, for example after the 10 degree Celsius dive, if the 40 degree dive was done

right after the facial temperature still would’ve been cold and therefore messed up the

results for the 40 degree Celsius dive, the students took a 20 minute break after one of the

dives to let the facial temperature go back to room temperature and reduce the mistakes

in the results. Students ate lunch while they waited for their face to go back to room

temperature.

Results

In the graph below we can see the results for the heart rate during the control,

apnea, and dive experiments. In the control line the heart rate stood fairly the same, it did

not fluctuate much. In the apnea we see a little more fluctuation but still the same with a

minor drop at the 25 sec mark. The heart rate at the 10 degrees Celsius dive showed a

good response as it decreased dramatically. The heart rate at the 40 degrees Celsius dive

shows a strange increase after the 15 sec mark.

The graph below pertains to the systolic blood pressure during the experiment. The

lowest pressure in the experiment was the control; pressure stood the same from the

baseline. Apnea follows as it ends right above the control during the dive, the pressure

decreased from the baseline. In the 10 degrees dive we can see how the SBP increased

from the baseline into the dive, it gave the biggest change in the graph. The pressure at 40

degrees also increased from the baseline not as high as the pressure for the 10 degrees.

The pulse wave velocity is the next graph. In the Apnea and control there was not much

change as we can see the fluctuations are minimal. However the pulse wave velocity in

the 10 degrees dive we can see how the speed of the blood rushes much faster through the

arteries at the beginning of the dive and then stabilizes at that speed. At the 40 degrees

dive the PWV definitely increases to the same point of the 10 degrees dive but then

decreases to it’s previous speed.

Discussion

A. From our results we found a few cardiovascular responses due to control,

apnea, and dive, and also how these would change given a change in temperature,

warmer and colder than room temperature. In the control part of the experiment the heart

rate, blood pressure, and pulse wave velocity don’t change much, HR averaged at 85

bpm, SBP averaged at about 110 mmHg, and PWV at about 3.6 m/sec. In apnea the heart

rate did not change much, it stood between 85-90 beats per minute (bpm) just like in

control. Blood pressure was higher in apnea, about +10 mmHg, and the apnea PWV

definitely showed greater variation than control PWV, reaching a full 0.1 m faster per

second. In the full dive all 3 cardiovascular responses being tested, HR, SBP, and PWV,

showed signs of change. HR decreased about 15 bpm less than the control @ 40 °C and

25 bmp @ 10 °C. SBP increased about 10 mmHg @ 40 °C and 20 mmHg @ 10 °C more

than the control. PWV was faster for the dives, increasing at both temperatures, about 0.5

m/sec more than the control.

B. The apnea HR did not deviate much from the control HR. This could have

been due to the sample size, which was very small so our data were not a true

representation of the effects of apnea on the heart rate. Which is to be reduced by around

18% [8]. In many of the experiments testing the breath hold (BH) in humans the results

were that apnea caused an obvious decrease in the HR [2,4,5]. But in our experiment we

did not get the same results. In the dive the HR was induced to a greater effect, which

supports previous experiments that tested the diving in mammals [2,3,4,5] and birds

[9,10]. This could be because the facial receptors were activated along with the chemo

stimuli, which is the increase in CO2 and the acidification of the blood [1]. Hurwitz

definitely supports this because he shows how the decrease in dive HR is way more

pronounced than in apneic HR [2]. Also in Hurwitz he states that while on dive, the HR

shows no signs of going back to it’s baseline (before the dive) HR [1] but Noren who

studied HR on bottled nose dolphin found out that the exercise response overrides the

dive reflex response, increasing the HR of the dolphins as they swam up and down, while

still being submerged [11]. The HR of the dolphins went back down when the dolphin

rested underwater [11]. Noren’s research agrees with Williams who studied the

physiological changes in seals while underwater, and the HR went up with stroke

frequency and went down when the stroke was reduced [12]. So dive has a lasting effect

on HR, as long as the facial receptors are being activated the heart rate would remain

slowed. Basically the dive HR results of our experiments supports the results that dive

HR elicits a response in the body to conserve oxygen [2,3,4,5]. In our results we found

that the colder temperatures elicits a stronger bradycardia in the cardiovascular system,

these results supports some of Furedy’s experiments. One of the results that it does

supports is that at 10 °C it’s where the lowest HR will be found (out of room temperature

and 40 °C). This is because Furedy’s suggests that cold-fiber activity is necessary for

eliciting a complete dive reflex. Furedy states that the effects of the 40 °C dive could be

comparable to the breath hold [3] but our results doesn’t show that. In fact the 40 °C

results are comparable to the 10 °C more than they are to the BH without dive. The heart

rate linearly decreases with temperature from high to low, and the lowest heart rates are

seen in the coldest of waters [13].

C. Our results show that the SBP increase in response to apnea. Supports both

Andersson and Shamsuzzaman results [4,5] along with Speck, who experimented with

varying apneic conditions and observed the heart rate along with the mean arterial blood

pressure [13]. Furedy explains that the BP increases due to the vasoconstriction of the

arteries, which are controlled mainly by alpha receptors [3]. Apnea elicits

vasoconstriction due to the changing in pH in the blood, which is an effect of the rising

CO2 levels leading to an increase in carbonic acid [1]. The vasoconstriction is more

pronounced in the dive than it is in the apnea without face immersion [4,5]. Andersson

shows how the dive mean arterial pressure (MAP) is higher than in the apnea MAP, while

Shamsuzzaman shows individually how the SBP is increased during the dive 4,5]. Our

results agree with both, during the dive the SBP of our subjects increased from the

control and were more pronounced than the apnea SBP. How fast this response came to

be, was tested by Panneton who claims that voluntarily diving rats BP does not change

abruptly, that’s so say not immediate after diving [14]. Our results agree because there

was a delay in the changing of SBP in our results. The blood pressure on our results, on

top of increasing due to the dive which could be augmented by the facial receptors, it

increased and were more pronounced in colder temperatures; higher pressure @ 10 °C

than @ 40 °C. This agrees with Choate experiments in which the percent change from

control in warm water was 10% while in cold water it was 27% [15]. She points out that

the reason why is because the signal sent to the medulla oblongata is reduced due to the

temperature of the water which elicits reduced sympathetic and parasympathetic activity

therefore not increasing the MAP as much as the colder waters [15].

D. The PWV in our results did not change during the apnea. In fact the apnea

PWV line overlapped a couple of times with the control PWV. This does not agree with

the experiment carried by Seetho in which he found that sleep apnea does in fact increase

arterial stiffness [6] but it doesn’t have to be sleep apnea to cause stiffness in the arteries,

regular breath hold can too [16]. During the dive the PWV definitely increased from the

control and apnea. It increased higher in the early stages of the dives and then it decreases

slightly. This happened in all of the 4 situations (control, apnea, and dive at 10 and 40

degrees). The way that temperature affected PWV was just as it affected HR and BP. It

augmented the response. In the early dive at 40 °C the PWV reached 4.2 almost identical

to the dive at 10 °C, but the 40 °C dive PWV quickly decreased in the late part reaching

as low as the control and apnea. This findings support Edwards findings, which were that

facial cooling does elicit a stronger response in the pulse wave velocity [17].

E. Some students couldn’t hold their breath for that long; they came out at around

30 to 35 seconds, which made the data incomplete for the graphs. Sample size was very

small in this experiment. There were 2 groups each consisting of 4 students max.

Sometimes 3 student per group participated, which means that just one student whose

results were way off could’ve skewed the data and graphs. And in fact there were such

students, whom heart rates were so low or so high that some of us believe that it was a

mistake. Which brings us to our next limitation. The electronics used were extremely

sensitive which are good and bad at the same time. Some of the students bumped their

finger sensors against the table during the experiments, which definitely could’ve

affected the results. Another thing to point out was that the taking of data from the

PowerLab graphs sometimes were difficult given the mouse of the computer didn’t work

therefore impatience led students to carelessly take irrelevant data to include in the

calculations. All in all it’s good to be honest with how the data could’ve been messed up

because that could lead us to make more careful procedures to gain better results that

really prove a hypothesis and not get false data that could be misleading.

F. A great next step into this is researching how does the whole body being

submerged changes anything. If it increases the BP even more or decreases the HR to a

lower extent. Maybe there’s other receptors in the body that augments the responses of

the dive reflex.

G. In conclusion it was found that there are immediate responses to the lack of

oxygen and increase in CO2 saturation in the body, which activate the chemoreceptors in

the arteries [1]. This causes a change in the HR, BP, and PWV. HR and BP during apneic

conditions and dives is a well studied subject and there’s no doubt that it’s response is

due to the apnea and is augmented by the facial receptors during a dive and is augmented

even more on colder water/temperature. PWV is an immediate dive reflex response,

which points that arterial stiffness therefore vasoconstriction is also immediate.

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