Harrison_Amelia_RP_Word

The Cardiovascular Effects of Caffeine Ingestion During Rest in, Habitual High Versus Habitual Low Drinkers.

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Department of Exercise and Sport Science, Manchester Metropolitan University, Crewe, Cheshire, United Kingdom. BSc Exercise and Sport Science

Amelia Molly Harrison

Abstract:

Caffeine has social acceptance with widespread use with 90% of people consuming it in the

form of a coffee beverage in the United States of America (Burke, 2008). Caffeine has mainly

been used for its stimulant properties in daily life and in an athletic population as it’s been

shown to increase wakefulness and motor skills including attention and increase time to

exhaustion. Although caffeine is said to have varying effects both in a cognitive,

physiological and cardiovascular way performance results have been inconsistent partially

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due to exceedingly too high dosages or too low, Furthermore many studies have not

accounted for other factors such as age, gender, habitual usage, smoking and dietary intake.

The primary aim of the present study was to investigate caffeine’s effects on cardiovascular

parameters at rest, comparing habitual high versus habitual low consumers who drink either

black tea or coffee. Seven participants were segregated based on their consumption habits,

habitual low = (0-1 cup/day) and habitual high = 92-3+/day), and reported for testing on two

occasions. The single blind study involved collecting blood pressure (BP), Blood glucose and

blood flow vascular kinetic changes using colour Doppler ultrasound method. (FV1, RI, IMT

and Vm) at 0, 10, 20, 30 and 60 minutes post ingestion. Heart rate (HR) data was obtained

every three minutes. One session contained a caffeinated beverage and the other a

decaffeinated beverage (placebo) based on a 6mg/Kg body weight dosage. No significant

differences were found between Treatment, History or Time*History*treatment. This may be

partially due to small sample sizes or methodological issues within the study which should be

considered in future studies.

Acknowledgements:

I would like to thank all of my participants who gave up their time to take part in this

research project, my supervisor Gladys Ombele Pearson for all the help and support during

my final year and throughout my dissertation. Finally, I would like to thank my parents and

friends for their undivided love and support through this stressful year.

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Table of ContentsAbstract:............................................................................................................................................2

Acknowledgements:..........................................................................................................................2

Key words.............................................................................................................................................3

Introduction:......................................................................................................................................3

Method..............................................................................................................................................6

Subjects and ethics............................................................................................................................6

Procedures:.......................................................................................................................................7

Statistical analysis:...........................................................................................................................10

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Results:............................................................................................................................................10

Discussion:...........................................................................................................................................16

Limitations:..........................................................................................................................................21

Statistical difference tests:..................................................................................................................22

Conclusion:..........................................................................................................................................23

References:..........................................................................................................................................23

Key words:

Caffeine, Coffee, Habitual, High, Low, Rest.

1. Introduction:

The drug caffeine is commonly consumed by the global population with reports suggesting

90% of adults consuming it in their everyday diets (Burke, 2008). The average consumption

of coffee within adults is equivalent to approximately two to three cups or 272 milligrams

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(mg) per day (Corti et al. 2002). The gastrointestinal track absorbs caffeine rapidly and peak

plasma caffeine concentrations are reached within 30-60 minutes after ingesting the beverage

(Greer, 1998).

The stimulating effects of caffeine on improving daily performance such as motivation and

attention have been targeted, not only by athletes but by shift workers, long-haul truck

drivers, and members of the armed forces. These individuals regularly need to fight fatigue

and prolong their capacity to undertake their occupational activities during stressful

conditions (Burke, 2008). Although caffeine is consumed for the taste in the form of coffee

and tea, many consume it for its stimulant properties. Previous research has indicated that

caffeine may be a beneficial ergogoenic aid for athletes in various exercise modes, intensities

and durations (Douglas et al. 2002). It must be noted, however, that many studies have not

focused on testing participants in solely resting conditions, as well as this studies have not

investigated habitual high and habitual low history during rest. This may be helpful when

looking at the interaction between coffee consumption and tolerance levels over a specified

time period within different groups of people. Jackman et al. (1996) suggested that one key

benefit sort after by athletes is the delayed feeling of fatigue. Increased time to exhaustion

and increased fatty acid oxidation has also been reported to be a beneficial effect of

consuming caffeine (Chad and Quinele, 1989). Furthermore, previous research has also

shown that antioxidants found in coffee, such as chlorogenic acids have been recognised to

improve glucose metabolism and insulin sensitivity (Vandam, 2013). Not only this, but

coffee has been also demonstrated to have cardiovascular effects such as increased blood

pressure (BP) (by up to 14mmHg) in normative subjects under resting conditions (Robertson

et al. 1987). Previous authors Mahmud and Freely. (2001), stated that in males, caffeine

increases BP by increasing vascular resistance with no effect on cardiac output (Q). Hearltey

et al. (2004), stated that the vascular resistance increase is consistent with the blockage of

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vascular adenosine receptors in caffeine, which enhances the action of noradrenalin (Hatano

et al.1995). Several effects are thought to be correlated with high caffeine drinking on

cardiovascular parameters such as increased HR, vascular resistance (RI) and BP. Not only

this, but caffeine has also been found to impact on physiological parameters such as,

potassium (K+) accumulation. The increase in K+ has the effect of inhibiting muscle

contractions as caffeine interferes with the uptake of calcium (CA2+) by the sarcoplasmic

reticulum in striated muscle. This action can account for observations, that such

concentrations of caffeine increase the strength of contractions in both skeletal and cardiac

muscle (Graham, 2001). Fat metabolism has also been shown to increase with the

consumption of caffeine (O’keefe et al. 2013). In resting conditions, caffeine causes increases

in BP (Robertson et al. 1978; Sung et al. 1990) and systemic vascular resistance (Sung et al.

1990). Moreover, caffeine has been shown to produce increases in plasma rennin activity

(Robertson et al. 1978; Van Soeren et al. 1993) and it has been further hypothesised that this

is through a plasma Angiotensin II (ANG II) concentration response (Daniels et al. 1988).

Although Lane and Williams (1985), suggest potential caffeine stress interactions, the results

were obtained from subjects who were not regularly exposed to caffeine. However, Lane et

al. (1987), reported that the regular caffeine consumer would be at a greater risk from

caffeine stress interactions, due to their increased exposure. Moreover, one could however

argue that regular use of caffeine might lead to the development of drug tolerance that could

lead to a reduction, or eliminate the caffeine-stress interactions seen to date (Lane et al.

1987).

In view of these factors, this study sought to compare high habitual caffeine drinkers (two +

cups of coffee/tea) versus low caffeine drinkers (one cup or less). The intervention was

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provided through the ingestion of a coffee beverage in one session, and a de-caffeinated

coffee beverage (placebo) in the second session, separated from the first session by seven

days. It should be noted that although the decaffeinated beverage served the purpose of a

placebo condition it does in fact contain a small dosages of caffeine. Where decaffeinated

coffee contains around 2mg per cup and instant caffeinated cup contains 27mg (Suleman et

al. 1994). The primary aim of this study was to determine the acute effects of caffeine on

cardiovascular parameters. These included blood flow kinetics. And the effects over a period

of 60 minutes, within habitual high versus habitual low populations. The secondary second

aim of the study was to investigate the metabolic effects of caffeine ingestion and blood

glucose level and indirect calorimetry. It was hypothesised that ingestion of caffeine would

increase BP, heart rate (HR) and blood plasma volume. It was also hypothesised that through

the ingestion of caffeine, vasoconstriction will occur more so in habitual low consumers.

2. Method:

2.1 Subjects and Ethics

This study was granted ethical approval by the Manchester metropolitan university taught

programmes Ethics committee TPEC prior to testing beginning. Seven healthy active males

who participated in physical activity over 30 minutes weekly, were recruited to participate in

this study. Participants were informed of the procedures, methods, benefits and possible risks

(slight headaches and minimal bruising from the finger tip sample) during a familiarisation

session before written consent was obtained.

Of the seven recruited participants, two participants withdrew from the study creating an

attrition rate of 29% .The remaining five participants were split into two groups according to

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their habitual consumption of coffee or black tea beverages. The two groups being Habitual

high (2-3+ cups) n=3 versus Habitual low drinkers (0-1) n=2.

2.2 Inclusion Criteria:

The following inclusion criteria were applied. Participants were between the ages of 18-25,

physically active at least three times weekly, non resistance trained. Participants were also

free of any underlying health conditions such as diabetes and must have been injury free for

three months prior to testing.

Participants were asked to abstain from alcohol, caffeine and exercise 24 hours prior to

testing although they must have drank coffee on a regular basis three times a week

consuming either 0-1 coffee/tea (habitual low n=2) or consume 2+ cups daily (habitual high

n=3) these constraints were constructed in order to minimise any experimental error and for

the purpose of group habitual segregation.

2.3 Procedures:

Baseline measurements of body height and mass were collected using a wall mounted

Stadiometer ( 222 stadiometer, Seca, Birmingham) and balance scales (711, Seca,

Birmingham), respectively. These measures were obtained prior to testing in order to

determine the dosage required based on 6mg/Kg of body weight dosage with 250ml of hot

water (Daniel’s et al. 1989). During the single blind study, participants reported to the

laboratory at the Manchester Metropolitan Cheshire campus, on two occasions with a seven

day wash out period. During the first session participants were provided with a decaffeinated

(placebo – rich roast decaffeinated instant coffee granules, the co-operative, Manchester)

beverage and given five minutes time to consume it. During the second session participants

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were provided with a caffeinated (fair-trade rich roast caffeinated instant coffee granules, the

co-operative, Manchester) beverage and as per session one participant’s were given a five

minute consumption time. Both tests were preceded by a standardized five minute rest period

for rest HR collection.

In order to reduce the effects of circadian variations and physiological responses to the

environment (i.e. excitement owing to lighting and/or noise) both sessions were conducted at

the same time of day in as close to the same laboratory environmental conditions as possible.

Resting cardiovascular (CV) kinetics was obtained. These included, Heart rate using a (Polar

FTI 90037558, Polar Oulu, Finland HR monitor), BP using a manual blood pressure

sphygmanomomeitor (Omron M2 Basic digital automatic BP monitor Hoofddorp,

Netherlands) and blood glucose using finger tip sampling methods (Accutrend Roche Bascel,

Switzerland). The (AU5 Harmonic colour Doppler ultrasound Genoa, Italy) the ultrasound

scanning was conducted colour Doppler mode. The probe was placed on the carotid artery as

parallel as each participant’s vasculature would 1cm distal from the carotid node; the depth of

the scanning was 55.3mm with a frequency of US beams of 27 of to note any vascular kinetic

changes were obtained using a 60 º inclination angle. The vasculature kinetic measurements

obtained via ultrasound methods included (FV1),VM2, intermedial thickness (IMT) and RI

index. All stated tests were performed pre consumption of the beverages and then 10, 20, 30

and 60 minutes post ingestion, with the exception of HR data which was collected every three

minutes for 45 continuous minutes.

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2.4 Statistical Analysis:

Data compiled was analysed and checked for parametricity based on the four parametric

assumptions. Homogeneity of variance was tested using a Shapiro Wilkes, with sphercity

tested using Mauchley’s test of sphercity given the repeated measures design of the study.

Normality of distribution was assessed using the Levenes test and the data was known to be

ratio or interval and independently collected. Having followed these procedures, Thus data

was found to be parametric (DBP and Vm) and non-parametric (SBP, HR, RI, IMT, FV1,

Blood glucose). In the case of non-parametric data a Friedman’s signed rank test was

performed in. Where data was parametric a repeated measures analysis of variance

(ANOVA) was performed across both the decaffeinated and caffeinated conditions, as well as

between habitual high and habitual low participants. Data was analysed in statistical package

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Figure 1. Indicating the set up of the testing protocol

before the consumption of either beverage. Pre tests at

0 minutes had been performed

Figure 2. Colour Doppler AU5 ultrasound on

the carotid artery after the consumption of the

caffeinated beverage. (A) Vessel dimensions

including intermal diameter and IMT thickness.

Figure 3. Indicates blood flow kinetics. These included the capture of the vascular flow integral peaks

with the Fv1, RI and Vm data for one participant after a caffeinated beverage. An average was taken

after 15 peak traces, at each phase of the intervention

A


for the social sciences (SPSS) Data are presented as mean ± Standard Deviations (Mean ±

SD). A significant Alpha was set at P<0.05 95%.

3. Results:

Mean ± SDHistory N Height (cm) Weight (KG) Age (yrs)

Habitual High Drinkers 3 175.5± 1.15 71.0± 11.1 20 ± 1.15

Habitual Low Drinkers 2 185.6 ± 10.9 71.2 ± 10.9 22 ±1.41Table 1. Indicates Anthropometric Demographic Data. Height (cm), Mass (Kg), Age (yrs)

collected from the study cohort.

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Figure 4. Indicates mean and SD error bars for both treatment conditions, for BP Diastolic (mmHg). Square represents Caffeine beverage and triangles denotes the Decaf condition.

0 10 20 30 40 50 6050

55

60

65

70

75

80

85

90

Habitual High

Habitual Low

Time (m)

DBP

Deca

ffina

ted

(mm

Hg)

0 10 20 30 40 50 6050

60

70

80

90

100

110

120

Habitual High

Habitual Low

Time (m)

DBP

Caffe

ine

(mm

Hg)


A Repeated measures ANOVA was conducted on diastolic blood pressure (DBP) with no

statistical significance found between treatment conditions, time and history. Within the time

element, there were no significance in DBP F (1, 4) =.899 P>0.05. Analysing history between

habitual high and low consumers found no significant difference F (1, 4 =) 2.095 P<0.05.

Treatment also indicated no significant effect F=.200 P>0.05 There were also no significant

interaction between the interaction within treatment and history F (1, 4) =.705 P>0.05

Nonetheless it is interesting to note that the caffeine condition DBP peaked at 30 minutes

post ingestion with a mean 80.8 +9.25 mmHg, where as during the Decaffeinated condition

DBP peaked at 10 minutes post ingestion mean value 80.6 +6.10mmHg (Figure 4).

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0 10 20 30 40 50 60110

112

114

116

118

120

122

124

126

128

130

Habitual HighHabitual Low

Time (m)

SBP

caffi

nate

d (m

mHg

)

0 10 20 30 40 50 60100

105

110

115

120

125

130 Habitual High

Habitual Low

Time (m)

SBP

Deca

ffina

ted

(mm

Hg)


Mean average results for the decaffeinated condition indicate the largest decline was 10

minutes post ingestion. Whereas in the caffeine condition, results show a slower progression

with no immediate drop in systolic blood pressure (SBP) until 30 minutes post ingestion. The

largest declines in SBP between the caffeinated and decaffeinated condition was 5% and the

difference in the highest reported results in both treatments were 0.8%. There was no

statistical difference between SBP and interaction between time, treatment, history nor

time*history interactions. Decaffeinated treatment χ2 (4) =6.833 p>0.05, caffeine treatment

χ2 (4) = .330 P>0.05. Within the History there were no significant interactions. High history

χ2 (4) = 2.345 P>0.05, Low history χ2 (4) = 2.359 P>0.05

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Figure 5. Mean and SD error bars for SBP values, across the elected five time periods, for both treatment conditions.


A Friedman’s signed rank test was conducted on treatment conditions. No significant

interactions were found between HR and treatment conditions, in the decaffeinated condition

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0 10 20 30 6050.0

55.0

60.0

65.0

70.0

75.0

80.0

85.0

90.0

Habitual High

Habitual low

Time (m)

Hear

t Rat

e (B

PM) c

affei

ne

0 10 20 30 6050.0

55.0

60.0

65.0

70.0

75.0

80.0

85.0

90.0

95.0

100.0

Habitual high

Habitual low

Time (m)

Hear

t Rat

e (B

PM) D

ecaffi

nate

d

Indicates mean values with SD error bars, HR (BPM) over a period of

five time intervals. The Grey bars represent the Caffeine condition and the black

represents Decaf condition (placebo)


χ2 (4) = 4.939 p>0.05or the caffeinated condition χ2 (4) = 5.388 p>0.05. A one way repeated

measures ANOVA was conducted based on the participant’s history F (1,4) =.148 p>0.05and

no significant effect was found.

Table 2. Indicates the (mean ± SD) vascular kinetics obtained from the AU5 colour Doppler ultrasound during both conditions, segregated by habitual consumption of caffeinated drinks.

No significant interaction was found between any of the independent variables (Table 2). RI

indicated no significance between treatment conditions with decaffeinated χ2 (4) = 4.960

p>0.05 and caffeinated conditions χ2 (4) = 2.720 P<0.05 There was also no effect between

treatment condition, in habitual high drinkers χ2 (4) =5.600 p<0.05 and habitual low χ2 (4)

= .800 P>0.05.

IMT showed no significant interaction between treatment condition, time, or history. For the

treatment conditions the decaffeinated condition χ2 (4) = 8.383 p>0.05 and caffeinated

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Vascular Kinetics

Habitual High (n=3) Habitual Low (n=2)

Decaffeinated (placebo) Caffeine

Decaffeinated (placebo) Caffeine

FV1 (m) 0.18 ± 0.03 0.23 ± 0.08 0.11 ± 0.14 0.14 ± 0.06

IMT 0.47 ± 0.09 0.52 ± 0.11 0.50 ± 0.13 0.70 ± 0.16

RI 0.45 ± 0.27 0.99 ± 0.65 0.89 ± 0.35 0.66 ± 0.72

Vm 19.03 ±4.59 20.65 ± 6.69 8.76 ±4.20 14.94 ± 8.04


indicated χ2 (4) = 6.612 p>0.05. Within the history component, there was also no significance

for habitual high χ2 (4) = 3.593 p>0.05 and habitual low χ2 (4) = 4.821 P>0.05

No significant interaction occurred in blood flow between treatment, history or time. Within

the treatment conditions the decaffeinated condition indicated χ2 (4) = 4.583 P>0.05 and the

caffeinated condition χ2 (4) = 6.424 P>0.05 Participants history failed to reach significance

as habitual high was χ2 (4) = 8.339 p>0.05 and habitual low was χ2 (4) = 4.400 p>0.05.

There was statistically no significant effect of Vm on history F (1, 4) = 9.304 P>0.05. There

was no significant interaction between Vm and treatment conditions F (1,4) =2.219 p>0,05,

the ANOVA also conducted tests looking at the effect between history and time although

there was a significant interaction between history based on habitual high and habitual low

conditions there was no significant effect shown

F (1,4) = .758 P>0.05.

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0 10 20 30 600.0

1.0

2.0

3.0

4.0

5.0

6.0

Habitual High

Habitual Low

Time (m)

Bloo

d gl

ucos

e De

caffi

nate

s (m

mol

/L)

0 10 20 30 600.0

1.0

2.0

3.0

4.0

5.0

6.0

7.0Habitual High

Habitual low

Time (m)

BLoo

d Gl

ucos

e Ca

ffina

ted

(mm

ol/L

)


When assessing Glucose in the treatment conditions the decaffeinated condition indicated no

statistical interaction over the five time periods χ2 (4) = 3.958 P>0.05 and in the caffeinated

condition χ2 (4) = 1.933 P>0.05. History also had no significant interaction between the five

time periods χ2 (4) = 4.385 p>0.05 and habitual low χ2 (4) = 2.187 P>0.05.

Within the two treatment conditions the change of caffeine from the decaffeinated condition

showed an 11.2% increase in Blood glucose scores. Within the two treatment conditions

habitual high consumers in the caffeinated condition showed a 12% increase compared to the

habitual Low group. When looking at the decaffeinated condition, Habitual High and a 9%

increase over the habitual low counterparts.

4. Discussion:

The primary aim of this study was to determine the effects of caffeine on cardiovascular

parameters, in habitual high and habitual low coffee/tea drinkers over a period of 60 minutes.

The secondary aim of this study was to compare the clearing time of caffeine on the studied

populations. It was hypothesised that the ingestion of caffeine would increase BP as a result

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Mean ± SD Blood Glucose scores for all participants over five time periods in the decaffeinated condition.


of vasoconstriction. As a consequence of this increased BP, caffeine would also increase HR,

and blood plasma volume. Finally it was hypothesised that these effects would be more

noticeable in habitual low caffeine drinkers as a result of caffeine stress interactions and a

reduced tolerance.

Within this study HR, BP (both systolic and diastolic), blood glucose, FV1, IMT, RI and Vm

were found to be non significant when consuming the caffeinated and decaffeinated

beverages, which is in contrast to some epidemiological studies. (Robertson et al. 1989) In

these cases the sample size for the current study was likely to be insufficient to provide

statistical power, making direct comparisons difficult to conclude on. Methodological issues

within the study may also have been an impacting factor such as, the allowance for caffeine

to digest into the blood stream, to notice significant changes within blood glucose and other

hemodynamic variables. Peak volumes are assumed to occur at 60 minutes as suggested by

Daniels et al. (1988). There is, however, considerable interindividual variability in the rate of

absorption. Some studies such as Robertson et al. (1978), have suggested that waiting three

hours may be more optimal, as the caffeine induced effect of lipolyis is larger than at earlier

times after ingestion. The peak plasma concentrations of caffeine are usually obtained

between 30 -2 hours after the consumption of an oral beverage. The results of this study are

in accordance to that of Robertson et al. (1978) and state that performance may be improved

3–4 h after the ingestion of caffeine, as this time would correspond with elevated free fatty

acids (FFA) levels.

However, other inconsistent findings have been reported in the literature, this is possibly due

to the doses of the drug that have either been too low or exceedingly high (Glade et al. 2010).

The decision to use a 6mg/Kg body weight dosage was selected, on the basis of its similarity

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doses of 3-6mg/Kg of body weight, previously shown to increase BP at rest or during

exercise, without provoking side effects, intolerance or decrease in exercise performances

(Sung et al. 1998). Although this has been suggested across many studies, there was no

significant change over time owing to caffeine, found within any of the variables in the

current study having used a 6mg/Kg of body weight dosage. This may not be due to a

function of dosage, but when considering that the participants were habitual consumers, it

may be due to other confounding factors such as tolerance or added additives and lifestyle

habits such as smoking, dietary habits, and medication. All of these factors in turn can play a

part in the interaction of caffeine absorption and effects. The difference in tolerance after

taking the beverage through oral and intravenous administrations of caffeine may be another

view of the situational specificity of tolerance. Previous research indicates that drug tolerance

is due to the environment, interceptive and exproceptive stimuli that participants are exposed

to (Siegel et al. 2013). That is, drug tolerance is more pronounced when normal cues are

present such as smell and taste (Siegel et al. 2013). Finally, caffeine given in coffee is self-

administered where the participant administers the caffeine/coffee to themselves. In contrast,

intravenous caffeine is provided and given by the experimenter not the participant, which was

the process within the current study. If a drug is self-administered, response cues are

concurrent with the drug’s effects. Results of various studies indicate that greater tolerance is

displayed when self administering due to normal cues than to the same dose of an

experimenter providing the beverage, (externally received) (Siegel et al, 2000). This effect of

the self-administration contingency on tolerance has been demonstrated with a variety of

drugs, including cocaine, caffeine, nicotine, and alcohol in rats. Situational specificity of

tolerance has been implicated in tolerance to a variety of effects of many drugs, including

opiates, alcohol, nicotine, immunoenhancing drugs, cholecystokinin, carisoprodol,

haloperidol, and several benzodiazepines (Siegal et al. 2000). Given that caffeine is a drug

19


that operates in similar fashion to the previously listed drugs, though the effects are currently

unknown in the literature they must be considered. The effects of self administration and

situational specificity must be considered.

Within the BP variable, no significant interaction between time, history and treatment was

found (P > 0.05). Within history, habitual consumption of coffee or caffeine was associated

with elevated SBP at 60 minutes post consumption of the caffeinated beverage not the

decaffeinated beverage. However, many of the epidemiological studies showed no relation,

and some even showed a small inverse relationship between self reported coffee consumption

and BP (Nurminen et al. 1999). It must be noted that habitual high consumers may need

higher dosages of caffeine to induce the same effects of caffeine witnessed in habitual low

consumers because of the resistance build up to caffeine which can occur after 3-5 days of

consumption. (O’Keefe et al. 2013). It seems that caffeine is the active component for this

effect given that placebo conditions have demonstrated no effect which is also in line with the

results of this study. It is also interesting to note that within the results of SBP within the

habitual high group, they responded more to the caffeine at 60 minutes than the habitual low

group. SBP decreased in the habitual high group to 118 mmHg compared to 127mmHg in

Habitual low consumers which was a 9mmHg decrease. This may be due to greater

absorption rates in those habitual high drinkers as it also indicated their SBP peaked at 20

minutes, 10 minutes earlier than the habitual low consumers who peaked at 30 minutes post

ingestion. (Table 2) indicates large differences between the two groups at baseline; this may

be due to a function of habitual consumption and the long term adaptations that take place.

Those who drink small amounts of caffeine have higher SBP than those who consume more.

The regular consumption of caffeine is also associated with an increase of the number of

adenosine receptors within the brain, as a result of these effects of adenosine receptor

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blockage including the release of adrenaline, it has been stated that these are key mechanisms

which may explain the ergogenic effect of the drug (Bell and Mclellean, 2002), on high

versus low consumers of a caffeinated beverage and the figures in (Table 2).

In a study of 15 volunteers (including 6 habitual consumers) it was demonstrated that coffee

drinking increases BP, however habitual consumers showed no increase in BP (Daniels et al.

1998). In this study by Greer et al. (2010) there was also no effect on BP when using a

250mg dosage which is equivalent to two cups of coffee the authors concluded that caffeine

is not solely responsible for the CV effects associated with short and long term coffee

consumption, as caffeine is one compound of 1,000 components At 60 minutes post ingestion

for habitual consumers the change was not significant (0.73.4mmHg, t4 4.4, P0.012), even

though there was a significant and linear time interaction for coffee, in both conditions (Greer

et al. 2010). Corti et al. (2002), suggested that the development of tolerance during habitual

consumption may explain why drinking coffee in some epidemiological studies, did not have

a clear effect on BP with negative results. The observed results in some of the studies have

been inconsistent due to some individuals being more sensitive than others. It could also be

that inconsistencies are of a result of gender, body mass index (BMI) and smoking.

This study has suggested that HR results also showed no significant interaction (P> 0.05),

although the previously mentioned statistical limitations must be noted. It has been indicated

that men have a greater vascular resistance indicating a vasodilator effect (Sung et al. 1994),

However, it must be noted that the present study did not investigate gender effects. The

presser effect has often been accompanied by small decreases in HR (Nurimen et al. 1999). In

the present study, the caffeine condition HR showed more variability than the decaffeinated

condition. These results are in agreement with the previous findings of other studies

(Heartley, 2004; Nurmien et al. 1990).

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Caffeine was consumed in the form of coffee mainly due to accessibility and prevalence

within the world. In the United States of America, 90% of the population consume coffee,

with energy drinks only equating to 50% of the population (Burke, 2008) Coffee therefore,

represented the most ecologically valid modality for provision of caffeine within the study

cohort. Other administrative forms could have been used such as chewing gum, energy drinks

or in the form of a caffeine content spray. Energy drinks were not administered in the present

study due to them having other substances including taurine, ginseng and vitamin B12. To

date research has yet to investigate the effects of these substances on the CV system, which

could make CV effects more pronounced than just caffeine itself. In a separate study

conducted by. Emily Fletcher of the David Grant Air Force Medical Centre, healthy

volunteers experienced a greater increase in BP after they consumed an energy drink

compared to when they drank coffee which contained the same amount of caffeine. This

result, suggests that ingredients in energy drinks other than caffeine combine to produce

greater increase in BP. This is not to say, however, that caffeine has other unrecognisable

compounds and was found to be less effective when administered in an anhydrous form

(Graham et al.1998). A liquid form of consuming caffeine is the best delivery method as it

represents the most efficient process of absorbing caffeine with the most caffeine being

absorbed in the least amount of time (examine.com 2014) 99% of the caffeine contained

within a coffee beverage is available to be absorbed compared to 90% in capsules and 77% in

chewing gum. (Caffeine informer 2012: online) Whilst caffeine contained in gum is absorbed

quicker the volume of caffeine absorbed when compared to liquid forms is less overall.

Circadian variations when drinking coffee may also have an effect upon BP readings (Guo &

Stein, 2003). The highest levels of BP occur after 10am with a peak around noon following

this from noon until 6pm BP plateaus, and in the majority of people BP increases by up to

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20/15mmHg (Pickering, 1990). As a consequence of circadian variations it is suggested that

participants may require increased dosages of caffeine when testing in the morning in order to

increase their peak BP more than those who were tested from noon onwards (Pickering,

1990). Although participants were asked to abstain from any caffeinated beverages, exercise

and alcohol for 24 hours prior to testing, it has been previously stated that those who

consume coffee habitually, may also consume other dietary products such as cream, sugar or

other foods that have a diluting effect of caffeine (Live science, 2015: online).

No significant effect was found between blood glucose at any point during the protocol.

However, when observational analysis was conducted, blood glucose seemed to peak earlier

than the caffeine condition. In the decaffeinated treatment blood glucose peaked at 20

minutes where as the caffeine condition peaked at 60 minutes. Greer et al. (2001), reported

that a physiological concentration of caffeine resulted in a 20-25% decrease in glucose uptake

in a rodent contracting perfusion. In a separate study conducted by Greer et al. (1998), that

there was no effect of treatment on blood glucose concentration, at any time during the

protocol. it is important to note, that the changes may not be entirely due to caffeine. Caffeine

ingestion usually increases the plasma concentration of adrenaline, a hormone with

widespread effects. Caffeine is formed of a Trimethylxanthine which descends into three

Dimethylxanthines ( i.e. Paraxanthyne, Theophylline and Theobromine) The concentrations

of these metabolites increase in the plasma, as the caffeine concentration declines. Thus, as a

result of the complexities presented by the chemical makeup of caffeine it is difficult to

identify which tissues are affected (Graham and Spriet, 1996).

4.1 Limitations:

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The most notable limitation to the present study was that such a small sample size created a

loss of power, as a small population doesn’t reliably reflect the population mean and lacks

representation of a phenomenon occurring, which increases the likelihood of outliers and

extreme observations (Field, 2010). Although a power analysis was conducted, which stated a

sample size of 26 was needed, due to limited time and resources of an undergraduate research

project only five participants could be recruited. One of the primary aims of the study was to

investigate the influences of caffeine consumption and history. In this study these were

defined as habitual high and habitual low consumers. The sample size for the study did not

provide statistical power making direct comparisons between the habitual high and habitual

low groups difficult to conclude on due to differing sample numbers within each group

(habitual high n=3, habitual low n=2). Other methodological defects also lie within the study

including the design. This study utilised a single blind protocol where by all participants were

unaware of the condition they were undertaking at the time of testing. However, as the

experimenter was aware of the condition this may have created unintentional external error

and bias. It is noted that Randomized double blind placebo control (RDBPC) studies are

considered the “gold standard” of epidemiologic studies. (Misra, 2012). RDBPC studies

eliminate the influence of immeasurable cofounding variables that may lead to an under or

over estimation of the treatment effect and bias (Misra, 2012). By blinding the participants

and experimenter this study design type eliminates the possibility that the observed effects

are due to the use of other treatment conditions. Participants were asked to abstain from

alcohol, caffeine and exercise 24 hours prior to testing, so the effects of the treatments and

other substances would be accurate and nothing other than diet would interact with the

mechanisms by which caffeine works. Although factors such as age, gender, smoking and

habitual consumption of caffeine were monitored and accounted for, it is not always possible

to 100% control these factors as supervision was not constant between experimental sessions.

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Therefore, participants may have consumed caffeine in other sources which they may have

not known about such as chocolate or chewing gum. Having not fasted this increased the

likelihood that glucose results would be inaccurate, or not solely due to the effects of

caffeine. Other factors that would have affected the internal validity of the study would have

been that participants were not tested under the same resting environments. In some testing

sessions the laboratories contained other experimenters carrying out various other studies.

Furthermore, differing rooms may have influenced the variation in results as some had

brighter lighting which may have caused more excitement within the participants. Future

studies should consider more strict regimes of monitoring environmental factors than those

utilised in the current study (e.g. use of a Lux meter).

4.2 Statistical Difference tests:

Statistical analysis differences within Friedman’s and two way repeated measures ANOVA’s

compared to multiple t-tests increases type two errors each time an ANOVA was conducted.

Parametric data is said to be more powerful than non parametric data However, it may not

always be a better representation of the data (Field, 2010). Further to this, having had larger

sample numbers the data may have possibly have been parametric allowing less error to be

induced.

5. Conclusion:

Discrepancies in the reported study can partially be attributed to methodological differences

and failure to control confounding variables, diet, alcohol intake and stress. These stated

reasons have an effect on caffeine’s absorption. Due to such a small sample the power within

the study was reduced and therefore no significant interaction was found between any of the

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independent variables. It is therefore difficult to draw a representative conclusion of any

comparisons between treatment and history. Therefore, it is suggested that this study may

serve as a pilot study and be useful in the conduction of further research into these topic areas

with greater sample sizes and further control within the methods. Previous studies have not

investigated the time course of the treatment of a substantial period of time, therefore, the

effects of caffeine may need to be investigated into a period of time over 60 minutes utilising

a randomised double blind placebo controlled design.

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