Laboratory Report

Edward Mbanasor UB Number: 12007448 Dr. Morgan Denyer

1

Population Distributions

Date of experiment: Friday 24th January 2014

Name: Edward Mbanasor

Supervisor: Dr. Morgan Denyer

Laboratory Report submitted as part of the summative assessment for the module, Special Studies (Year 1)

CS-1001L

BSc Clinical Sciences/Medicine

Module Leader: Dr. Christine Beedham

Clinical Sciences

University of Bradford

UB Number: 12007448


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Introduction

The cardiovascular system comprises of the heart, blood and its corresponding vasculature.

The heart, made up of myogenic muscle, is the pump which circulates the blood throughout

the body to cells found in tissue for exchange of material, including waste, hormones and

nutrients1. Cardiac output is the volume of blood the heart ejects per minute (l/minute) and

its alteration is dependent on the requirement for oxygen and nutrients, especially glucose.

Determination of the cardiac output is influenced by stroke volume and heart rate. Heart

rate is the number of times the heart beats per minute (bpm) and stroke volume is the

volume of blood pumped (ml) from the left ventricle of the heart per beat2.

Heart rate is regulated by the sinoatrial node which is located in the wall of the right atrium

and it controls the rhythmicity of the heart. Furthermore, the sinoatrial node is innervated by

the sympathetic (thoracolumbar outflow) and parasympathetic (craniosacral outflow)

components of the autonomic nervous system (ANS). The thoracolumbar outflow, through

cardiac accelerator nerves causes an increase in heart rate through noradrenaline, which is a

positive inotropic agent that binds to beta-1 (β) receptors. The craniosacral outflow

decreases heart rate by decreasing the force of contraction through the neurotransmitter

acetylcholine via the vagus nerve. These activities are controlled by the cardiovascular

centre located in the medulla oblongata to modulate heart rhythm and force of contraction3.

During intense exercise, the demand for oxygen at a cellular level increases due to increased

lactate and carbon dioxide concentrations in the blood. This occurs when the muscles

undergo anaerobic respiration. The heart counteracts this by repaying the oxygen debt by

increasing the heart rate and stroke volume. Stroke volume can be modified by altering

preload or end-diastolic volume, myocardial contractility and afterload, which in turn

increases cardiac output. Thus, more blood is pumped to the muscles that require more

oxygen and nutrients for aerobic respiration. Blood flow is reduced to areas such as the

digestive system through the contraction of pre-capillary sphincters. Heart rate can be

measured in a number places throughout the body, but it is most commonly measured

through the brachial artery situated in the forearm4.

Factors such as physical fitness, age, height and gender can also affect heart rate. There is

evidence in literature to suggest that the height of an individual has a relationship with heart

size. Moreover, it suggests that tall individuals have a larger heart compared to shorter

individuals who have smaller hearts.


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This means that tall people have larger heart chambers so the ventricles have a greater end

diastolic volume. Hence there is a higher afterload resulting in a higher stroke volume and a

reduced heart rate because of a greater force of contraction due to thicker ventricles.

Consequently, there is less effort per cardiac cycle. This means more blood is pumped out

every cardiac cycle to supply oxygen to body tissues. Therefore, smaller subjects will have a

higher heart rate to meet metabolic demands5.

Null Hypotheses are a way of testing scientific theories. The first aim of this experiment was

to carry out an independent t-test to evaluate the Null Hypothesis stating that there is no

significant difference in heart rate between tall subjects and short subjects. The second

objective was to observe if there is a significant difference in heart rate before exercise and

15 and 30 minutes post-exercise. This was tested with the Null Hypotheses which stated

that there is no significant difference between resting heart rate before exercise and 15

minutes after exercise (Null Hypothesis 2) and that there is no significant difference in heart

rate at rest and heart rate 30 minutes post-exercise (Null Hypothesis 3). Null Hypotheses 2

and 3 were tested by a paired t-test6.

Methods

Refer to Laboratory Schedule.

Results

Data relating to height and heart rate during rest taken from the sample population (N=40)

included heart rate prior to exercise, directly after exercise and 1 minute, 5 minutes, 15

minutes and 30 minutes after exercise (Appendix 1). The resting heart rate ranged from 60

to 96 bpm and height ranged from 150 to 184.9 cm. The split data of class intervals with

widths of 10 bpm from 40 bpm 100 bpm is shown in Table 1. It was established that no

subjects had a resting heart rate of 40-50 bpm and 50-60 bpm. 8 subjects had a resting

heart rate between 60-70 bpm, 11 subjects had a resting heart rate between 70-80 bpm, 16

subjects had a resting heart rate between 80-90 bpm and 5 subjects had a resting heart

rate between 90-100 bpm. This data was plotted as a frequency distribution graph (Figure

1). Prior to plotting the data, it was expected that the distribution would be bimodal. The

range of subjects suggested that there would be a concentration at 2 class intervals; a

separate one for short individuals with a smaller heart and one for tall individuals with a

larger heart. Nevertheless, the frequency histogram did not support this expectation. The

only mode occurred at 80-90 bpm showing the data distribution to be unimodal.


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Resting class heart rate intervals (bpm) Frequency (Number of subjects in each heart rate class)

40-50 0

50-60 0

60-70 8

70-80 11

80-90 16

90-100 5 Table 1. Number of subjects in each heart rate interval ranging from 40 to 100 bpm.

The sample population was analysed and there was a median of 80 bpm, a mean of 78 bpm

and a mode of 80 bpm among 7 subjects. These values were expected as they lie within the

normal resting heart rate for an adult.

Null Hypothesis 1

This Null Hypothesis was tested by dividing the participants into two categories. 20 subjects

were in the short category (<170cm) and 20 were in the tall category (>171.2). The mean

of the short population and of the tall population, +/- their respective 95% confidence

interval (CI), are shown in Figure 2.

Figure 1. Frequency histogram showing the distribution of subjects in different heart rate

class intervals starting from 40 bpm and ending at 100 bpm with intervals of 10 bpm. The

distribution is a normal distribution or a Gaussian distribution.


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It was found that the short subjects had a mean resting heart rate of 79.20 bpm (95% CI:

+/- 3.96) and the tall subjects had a mean resting heart rate of 76.95 bpm (95% CI: +/-

5.22) (Table 2). The mean resting heart rate is lower for tall subjects with respect to the

short subjects by 2.25 bpm. However, this difference is small. In order to determine

whether Null Hypothesis 1 should be rejected or accepted, an independent t-test was carried

out to identify if there was a significant difference between the two data sets. The result

attained from the independent t-test was 0.72 which is less than the expected t-value of

2.02 at 38 degrees of freedom ((N1 + N2) - 2)). Hence, Null Hypothesis 1 must be accepted

proving that there is no significance difference in the resting heart rate between short

subjects and tall subjects.

Table 2. Summary of results from the independent t-test. The sample size (N), calculated values of

mean resting heart rate (bpm), the sum of squares for both short and tall subjects, the mean variance (s2),

the mean standard deviation (SD), the mean standard error (SE), the calculated t-value and the 95%

confidence intervals are displayed.

Height

Category

N

Mean

Resting Heart

Rate

(bpm)

Difference

between the means

(bpm)

Sum of

squares

s2 SD SE t-value

95%

CI

Short 20 79.20 1363.20

98.16

9.91

3.13

0.72

3.96

Tall 20 76.95 2366.95 5.22

Figure 2. Mean resting heart rate of short subjects and tall subjects +/- their 95% CI.

2.25


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Null Hypotheses 2 and 3

To explore these hypotheses the mean heart rate was calculated at 6 different time points

for the study population. For all the time points, except for resting heart rate and heart rate

directly after exercise a sample size of 39 subjects was used. For heart rate before exercise

a sample size of 40 subjects was used and directly after exercise a sample size of 37

subjects was used. The mean resting heart rate was 78.08 bpm (95% CI: +/- 3.15), heart

rate directly after exercise had a mean of 138.81 bpm (95% CI: +/- 8.86) and heart rate 1

minute after exercise had a mean of 113.36 bpm (95% CI: +/- 7.89). Furthermore, 5

minutes after exercise the mean heart rate was 96.08 bpm (95% CI: +/- 5.99), 15 minutes

after exercise the mean heart rate was 85.72 bpm (95% CI: +/- 5.02) and 30 minutes after

exercise the mean heart rate was 78.54 (95% CI: +/- 3.87). The mean heart rates and their

respective 95% confidence intervals against time are shown in Figure 3. Two paired t-tests

for 39 subjects (Appendices 2 and 3) were conducted to observe if there was a significant

difference between resting heart rate and heart rate at both 15 minutes and 30 minutes

after exercise. The paired t-test values were calculated in the same way for both Hypotheses

using 38 degrees of freedom (N-1) (Appendix 4).

Figure 3. Mean heart rate values and their respective 95% confidence intervals.


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There is a significant difference between the mean resting heart rate and the mean heart

rate directly after exercise. There is also a significant difference between the mean heart

rate at rest and the mean heart rate at 1 minute, 5 minutes and 15 minutes after exercise.

However, only the mean heart rate 30 minutes post-exercise depicts there to be no

significant difference with respect to the mean resting heart rate. This is due to the fact that

the mean heart rate directly after exercise and 1 minute, 5 minutes and 15 minutes after

exercise do not overlap with the 95% confidence interval of the mean heart rate at rest.

Nevertheless, the mean value of the heart rate at 30 minutes post-exercise lies within the

95% confidence interval of the resting heart rate, meaning that there is no significant

difference.

Null Hypothesis 2:

Table 3 shows the calculated t-value for Null Hypothesis 2 to be 3.86 which is higher than

the expected t-value of 2.02. Therefore, Null Hypothesis 2 must be rejected because there is

a significant difference between resting heart rate and heart rate 15 minutes post-exercise.

Mean

difference (x̄ )

Sum of

squares

s2 SD SE t-value 95% CI

7.79 6028.36 158.64 12.60 2.02 3.86 5.02

Table 3. Calculated mean difference (x̄ ), sum of squares, mean variance (s2), mean standard

deviation (SD), t-value and 95% CI values for Null Hypothesis 2.

Null Hypothesis 3:

With respect to the values in Table 4, it can be established that Null Hypothesis 3 should be

accepted, as the calculated t-value of 0.47 is lower than the expected t-value of 2.02. This

shows that there is no significant difference between heart rate at rest and heart rate 30

minutes post-exercise.

Mean difference (x̄ )

Sum of squares

Variance (s2) SD SE t-value 95% CI

0.62 2513.23 66.14 8.13 2.02 0.47 3.87

Table 4. Calculated mean difference (x̄ ), sum of squares, mean variance (s2), mean standard

deviation (SD), t-value and 95% CI values for Null Hypothesis 3.

Discussion

The collected results included height and heart rate which were continuous and discrete

variables respectively. The data obtained from 40 subjects was split into class widths to form

a frequency distribution histogram because the values were too large for categorisation as a

single class.


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The distribution was unimodal with the mode concentrated at the 80-90 bpm class interval,

which suggested that the data obtained did not come from multiple populations. The mean

resting heart rate was 78.08 bpm (95% CI: +/- 3.15), which was expected because the

normal resting heart rate for healthy adults is 50-90 bpm7.

The modal value of 80 bpm among 7 subjects was also expected as it falls within the normal

resting heart rate range. The median resting heart rate of 80 bpm also fell in the normal

resting heart rate range. These values are near the extreme end of the resting heart rate for

a healthy adult. Various reasons such as stress, dehydration and stimulants could have

caused deviation from the normal resting heart rate for each subject.

Some subjects had a very low resting heart rate of 60 bpm, which may be due to adaptions

from training, which meant that the participants were not at the same level of fitness. This

demonstrates that the mean was not a fair representation of the resting heart rate of the

study population. However, no subjects exhibited bradycardia (resting heart rate under 60

bpm) meaning that there were no athletes in the sample population8.

The confirmation of Null Hypothesis 1 has not been fully elucidated as research suggests

that smaller individuals generally have higher heart rates. This is because smaller individuals

are understood to have a higher surface area to volume ratio which increases heat loss9. On

the contrary, physical fitness could help those with smaller hearts to have a lower resting

heart rate due to hypertrophy of the left ventricle. This, in turn, increases stroke volume due

to adaptive changes to stress4.

The physical effect of a large heart may offer an explanation for the independent association

between height and resting heart rate. Tall stature is associated with slower heart rates and

prolonged return times for reflected waves and augmentation of the primary systolic pulses,

which relates to ventricular mass increases. This results in decreased central aortic

pressure10. This suggests that having a larger heart will result in a lower heart rate due to

an increased end-diastolic volume because of larger heart chambers which results in a larger

afterload. This means it is easier to overcome the aortic pressure. Individuals with large

hearts have a larger contraction, due to a greater amount of heart tissue that requires

stimulation. This means there is a lower acceleration and therefore a lower resting heart

rate. This is representative of the results acquired as the mean resting heart rate of tall

subjects was lower than that of short subjects.


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Short individuals have a heart with a smaller surface area compared to tall individuals

meaning they will have a higher resting heart rate. This is due to the fact that the time

periods for atrial and ventricular systole are decreased, due to a small volume of blood in

smaller heart chambers. In systemic circulation, blood leaving the left ventricle will have

shorter distance to travel before reaching the right atrium meaning a higher venous return11.

There are range of measurable factors which could have changed the result of the

experiment such as body mass index (BMI) which was not accounted for in this experiment.

BMI is calculated by dividing weight in kilograms by height in metres squared and gives an

idea about the body composition and physical state of an individual. A person with a high

BMI, who is mainly composed of fat tissue, has a higher resting heart rate in comparison to

an individual with a low BMI12. Another bound which could be explored is the resting heart

rates of the two genders. As females are smaller in stature than males they generally made

up the shorter population sample. In addition, females are largely genetically predisposed to

a higher resting heart rate13.

A factor which may have negatively influenced the gathered data were the determined limits

of the height categories. This could be seen as a personal assumption which may have led

to subjects who are normally deemed to be tall being on the upper bound of the short

category. This upper limit may be where height is a significant determinant of heart rate.

Another factor is the anticipatory response, whereby, before the start of exercise, the heart

rate of a subject usually increases above resting levels. This is due to the release of

noradrenaline from the adrenal medulla. The greatest anticipatory heart rate response is

observed in short sprint events. To rectify this for future experiments, the resting heart rate

should be gathered from subjects who are not anticipating any physical exercise. This will

ensure they are fully rested. Another major factor which was not controlled was the fitness

levels of the subjects as sedentary individuals are expected to have a higher resting heart

rate14.

Null Hypothesis 2 was rejected showing that there is a significant difference between resting

heart rate and heart rate 15 minutes post-exercise. On the other hand, Null Hypothesis 3

was accepted showing that there is no significant difference between resting heart rate and

heart rate 30 minutes after exercise. These results can be explained by the fact that heart

rate increases to meet the oxygen and metabolic requirements of working muscles, to form

adenosine triphosphate (ATP) for energy release, and to remove waste. This places an

increased demand on the cardiovascular system due to an increase in blood pressure.


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Chemoreceptors, located in the brain, detect a decrease in pH and increased carbon dioxide

concentrations. Baroreceptors, found in carotid bodies and aortic bodies, are sensitive to

blood pressure changes due to vasoconstriction. These receptors help restore homeostatic

conditions by initiating negative feedback mechanisms to meet metabolic demands.

Baroreceptors carry a generator potential to the cardiovascular centre in the medulla

oblongata to stimulate the release of noradrenaline which binds to β1 receptors in the

myocardium. This causes an influx of Ca2+ ions leading to an increased depolarisation rate in

the myogenic cells of the sinoatrial node.

In anaerobic conditions experienced during exercise there is a build-up of lactic acid because

of the need for short bursts of energy. The cells involved have low oxygen availability, which

means they cannot produce enough ATP via aerobic respiration. When this pathway is

blocked there is a build-up of H+ ions as NAD+ is unable to act as a proton acceptor. This

causes metabolic acidosis15.

Post-exercise, the heart increases its rate and force of contraction to make sure oxygenated

blood reaches cells at a faster rate. This allows time for the oxygen debt to be paid by

removing the excess of H+ ions and converting lactate into pyruvate, in order to restore the

normal balance. Immediately after exercise the mean heart rate was 138.81 bpm (95% CI:

+/- 8.86) and at 15 minutes post-exercise the mean heart rate fell significantly. This is

evidence that the body goes through recovery to repay oxygen debt by increasing the

ventilation rate and heart rate until normal conditions are restored. This ensures cells have

sufficient oxygen to undergo aerobic respiration16.

When normal conditions are restored and excess H+ ions and lactate are removed from the

muscle tissue, the elevated heart rate begins to decrease and return towards the resting

heart rate. This is supported by the fact that the mean heart rate 30 minutes post-exercise

of 78.54 bpm (95% CI: +/- 3.87) fell very close to the mean resting heart rate of 78.08 bpm

(95% CI: +/- 3.15).

Although these values are very close at 30 minutes post-exercise, it did not reach the mean

resting heart rate. This may due to the fact that subjects have different recovery times,

which is influenced by training-induced cardiac adaptations.

This could suggest that the sample population was generally physically unfit, therefore there

was a longer recovery phase. It is also possible that the body, by trying to restore normal

ATP levels, is consuming more glucose which requires more oxygen.


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Gender may have influenced the inability to reach the mean resting heart rate at 30 minutes

post-exercise. The sex differences in heart rate is largely a result of the greater percentage

of body fat in women and varying hormone levels. This means that differences in oxygen

requirements, cardiac output, and heart rate (which is generally greater in females than in

males) are important factors that alter heart rate. These factors should be controlled in

future investigations to give more accurate results17.

Conclusion

The investigation was conducted included observation of resting heart rate and the

differences between short and tall subjects. It also looked at the effect of exercise on heart

rate through three Null Hypotheses. Null Hypothesis 1, verified by the unpaired t-test, was

accepted which confirms that height does not dictate resting heart rate. The results can be

contested as it goes against many scientific findings, therefore further investigation is

required to provide a more informed confirmation or rejection of the results.

Null Hypothesis 2 was rejected, which disproves that 15 minutes after exercise is complete

resting heart rate returns to normal levels. Null Hypothesis 3 was accepted, which confirms

that resting heart rate levels are reached 30 minutes post-exercise. These were based on

the values obtained from the paired t-test. It was expected that the heart rate was to return

to normal levels because of homeostatic mechanisms, which help to maintain normal heart

rate by repaying the oxygen debt. Furthermore, 30 minutes is ordinarily enough time to

return to the resting heart rate. Varying physical fitness levels within the sample population

may have led to differences in the ability of the subjects to reach resting heart rate.

References

1. Kumar P, Clark M. Kumar & Clark's clinical medicine. 7th ed. Edinburgh: Saunders Limited, 2009.

2. Noble A. The cardiovascular system. Philadelphia: Elsevier Limited, 2005. 3. Naish J, Revest P, Court DS. Medical Sciences. Edinburgh: Churchill Livingstone, 2009. 4. Tortora GJ, Derrickson BH. Principles of anatomy and physiology: volume 2 –

maintenance and continuity of the human body. 13th ed. Chichester: Wiley, 2011. 5. Paajanen TA, Oksala NKJ, Kuukasjarvi P, Karhunen PJ. Short stature is associated with

coronary heart disease: a systematic review of the literature and a meta-analysis. Eur Heart J 2010;31: 1802-9.


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6. Chin R, Chin RY, Lee BY. Principles and practice of clinical trial medicine. UK: Academic Press, 2008.

7. Arnold JM, Fitchett DH, Howlett JG, Lonn EM, Tardif JC. Resting heart rate:

a modifiable prognostic indicator of cardiovascular risk and outcomes? Can J Cardiol 2008;24: 3-8.

8. Dewey FE, Rosenthal D, Murphy DJ, Froelicher VF, Ashley EA. Does size matter? Clinical

applications of scaling cardiac size and function for body size. Circulation 2008;117: 2279-87.

9. Samaras TT, Elrick H. Height, body size, and longevity: is smaller better for the human

body? West J Med 2002;176: 206-8. 10. Shimizu Y, Nakazato M, Sekita T, Kadota K, Arima K, Yamasaki H et al. Relationship

between adult height and body weight and risk of carotid atherosclerosis assessed in terms of carotid intima-media thickness: the Nagasaki Islands study. J Physiol Anthropol 2013;32: 19-26.

11. Atwal S, Porter J, Macdonald P. Cardiovascular effects of strenuous exercise in adult

recreational hockey: the hockey heart study. CMAJ 2002;166: 303-7. 12. Antelmi I, de Paula RS, Shinzato AR, Peres CA, Mansur AJ, Grupi CJ. Influence of age,

gender, body mass index, and functional capacity on heart rate variability in a cohort of subjects without heart disease. Am J Cardiol 2004;93: 381-5.

13. Sookan T, McKune AJ. Heart rate variability in physically active individuals: reliability

and gender characteristics. Cardiovasc J Afr 2012;23: 67-72. 14. Everson SA, Kaplan GA, Goldberg DE, Salonen JT. Anticipatory blood pressure response

to exercise predicts future high blood pressure in middle-aged men. Hypertension 1996;27: 1059-64.

15. Zanesco A, Antunes E. Effects of exercise training on the cardiovascular system:

pharmacological approaches. Pharmacol Ther 2007;114: 307-17. 16. Putman CT, Jones NL, Heigenhauser GJ. Effects of short-term training on plasma acid-

base balance during incremental exercise in man. J Physiol 2003;550: 585-603. 17. Zouhal H, Jacob C, Delamarche P, Gratas-Delamarche A. Catecholamines and the effects

of exercise, training and gender. Sports Med 2008;38: 401-23.


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Appendices

Height (cm)

Heart Rate

before

exercise (bpm)

Heart Rate directly

after

exercise (bpm)

Heart Rate 1 minute

after

exercise (bpm)

Heart Rate 5 minutes

after

exercise (bpm)


after

exercise (bpm)


after

exercise (bpm)

150 72 160 152 96 76 70

153 84 160 100 96 80 80

153.2 84

153.5 80 125 120 100 68 68

157 76 144 112 90 76 76

158.3 72 144 104 80 78 76

158.5 72 160 104 80 80 72

160 92 116 116 92 92 92

160 80 120 86 80 76 75

160.7 96 124 116 88 88

162 80 152 116 84 80 80

162.5 84 132 116 96 108 108

162.5 68 120 80 72 68 66

163 76 84 86 86 74 60

164.5 72 136 96 88 80 72

164.5 88 148 108 96 90 85

165 60 148 86 72 68 61

165 80 120 100 96 92 90

169 84 100 92 87 80 80

170 84 160 120 96 92 84

171.2 91 128 120 100 96 88

172 68 142 115 92 80 66

172 80 112 80 80 80

173.7 72 112 136 112 96 92

174 76 175 152 152 116 80

174.6 60 152 96 88 64 60

175.1 68 128 84 76 68 72

176 76 184 156 112 100 92

177 64 104 80 72 72 64

177.2 84 176 152 120 108 92

177.5 88 160 116 92 88 80

178.7 64 96 120 92 72 68

180.6 88 120 96 88 68 70

181 76 128 112 96 96 84

182 96 190 188 140 125 96

182.2 60 100 72 68 68 60

182.5 80 148 116 104 92 80

183 72 192 124 116 104 72

183.3 80 136 140 120 84 80

184.9 96 136 116 124 120 104 Appendix 1. Raw data collected from 40 subjects. Red: short subjects; Black: tall subjects.


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Subject Heart Rate before

exercise (bpm)

Heart Rate 15

minutes after exercise (bpm)

Mean difference

before and after exercise

1 72 76 7.79

2 84 80

3 80 68

4 76 76

5 72 78

6 72 80

7 92 92

8 80 76

9 96 88

10 80 80

11 84 108

12 68 68

13 76 74

14 72 80

15 88 90

16 60 68

17 80 92

18 84 80

19 84 92

20 91 96

21 68 80

22 80 80

23 72 96

24 76 116

25 60 64

26 68 68

27 76 100

28 64 72

29 84 108

30 88 88

31 64 72

32 88 68

33 76 96

34 96 125

35 60 68

36 80 92

37 72 104

38 80 84

39 96 120

Appendix 2. Summary of values used to calculate the t-value for Null Hypothesis 2.


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Subject Heart Rate before

exercise (bpm)

Heart Rate 30

minutes after exercise (bpm)

Mean

difference before and

after exercise

1 72 70 0.62

2 84 80

3 80 68

4 76 76

5 72 76

6 72 72

7 92 92

8 80 75

9 96 88

10 80 80

11 84 108

12 68 66

13 76 60

14 72 72

15 88 85

16 60 61

17 80 90

18 84 80

19 84 84

20 91 88

21 68 66

22 80 80

23 72 92

24 76 80

25 60 60

26 68 72

27 76 92

28 64 64

29 84 92

30 88 80

31 64 68

32 88 70

33 76 84

34 96 96

35 60 60

36 80 80

37 72 72

38 80 80

39 96 104

Appendix 3. Summary of values used to calculate the t-value for Null Hypothesis 3.


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N Mean

Heart

Rate

(bpm)

Sum of

squares

Variance

(s2)

Standard

Deviation

(s)

Standard

Error

(SE)

T-

value

95%

Confidence

Interval

Resting

Heart

Rate

(bpm)

40 78.08 3780.77 96.94 9.85 1.56 2.02 3.15

Heart

Rate

directly

after

exercise

(bpm)

37 138.81

25421.68 706.16 26.57 4.37 2.03 8.86

Heart

Rate 1

minute

after

exercise

(bpm)

39 113.36 22508.97 592.34 24.34 3.90 2.02 7.89

Heart

Rate 5

minutes

after

exercise

(bpm)

39 96.08 12968.77 341.28 18.47 2.96 2.02 5.99

Heart

Rate 15

minutes

after

exercise

(bpm)

39 85.72 9113.90 239.84 15.49 2.48 2.02 5.02

Heart

Rate 30

minutes

after

exercise

(bpm)

39 78.54 5403.69 142.20 11.92 1.91 2.02 3.87

Appendix 4. Summary of values used to compare resting heart rate to heart rate after exercise

at the 6 time points.

Laboratory Report

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