The Effect of Caffeine Ingestion on
Exercise Performance
Table of Contents
Key Points 4
Introduction 5
1. Caffeine: Cellular Mechanisms of Action 9
1.1. Muscle Caleium 9
1.2. Cellular cAMP Levels 10
1.3. Adenosine Receptor Antagonism 10
1.4. Caffeine and Cellular Actions: Conclusions 12
2. Other Effects of Caffeine: Catecholamines and Acetylcholine 13
3. Effect of Caffeine on Muscle 4
3.1. Direct Effects of Caffeine on Muscle 4
3.2. Effects of Caffeine on Muscle Metabolism 4
4. Caffeine and Exercise Performance: Studies Review 7
4.1. Methodological Considerations 7
4.2. Short Term, High Intensity Exercise 18
4.3. Graded Incremental Exercise 20
4.4, Prolonged Endurance Exercise 23
5. Caffeine’s Ergogenic Mechanisms of Action 30
5.1. Short Term, High Intensity Exercise 30
5.2. Graded Incremental Exercise 32
5.3. Prolonged Endurance Exercise 32
5.4, Caffeine’s Mechanisms of Action: Conclusions 35
6. Summary 36
7. References ee KEY POINTS
1. Recent, well-controlled studies have established that moderate doses of caffeine
ingested 1 hour prior to exercise, enhance the performance of certain types of
endurance exercise in the laboratory. Moderate caffeine doses produce urinary
caffeine levels well below the allowable limit, as determined by the International
Olympic Committee (I2ug/ml). The results are specific to well-trained elite or
recreational athletes. It is not known if these findings will improve performance in
competitions because controlled field studies of the effects of caffeine are lacking.
2. The mechanisms responsible for improved exercise endurance in prolonged exercise
remain elusive. A metabolic mechanism appears to contribute early in exercise, when
caffeine ingestion increases plasma free-fatty acid concentratipns and muscle
triglycerides use and spares muscle glycogen. However, it is not clear if increased fat
oxidation causes the glycogen sparing in muscle. Increases in plasma epinephrine
concentrations usually occur following caffeine ingestion, but are npt essential for the
accompanying metabolic changes. When studying caffeine effects in the human it is
difficult to identify the primary source of the "stimulus" because caffeine usually
increases epinephrine secretion and is also rapidly metabolized in the liver to three
dimethylxanthines (paraxanthine, theophylline andtheobromine). The
dimethylxanthines can remain in the circulation longer than cafffine and may be
metabolic signals in their own right.
3. Caffeine appears to enhance performance during short-term, intense cycling lasting
~5 min in the laboratory and in simulated 1500 m race time. However, positive
ergogenic effects of caffeine are much less frequent during sprint exercise lasting less
than 90 seconds and in graded incremental exercise tests lasting 8-20 min.
4, Potential mechanisms for improving performance during intense qxercise lasting 5-
20 min include direct effects of caffeine on the central nervoys system and/or
excitation-contraction coupling and increased anaerobic energy pravision in skeletal
muscle. Introduction
Caffeine (1,3,7-trimethylxanthine, see figure 1 - The structure of caffeine), one of
the most widely consumed drugs in the world and the most commonly used drug in North
America (8, 46), is found in coffee, tea, cocoa, soft drinks, and various other foods (8, 51,
61). Coffee consumption is increasing mainly in the middle-aged and older population
whereas soft drink consumption has increased by 14% in the younger population (43).
Caffeine is also common in several over-the-counter medications, often even in simple
aspirin compounds, The caffeine contents of some common produets arg listed in table 1.
Much of the popularity of beverages containing caffeine is because of the general
belief that caffeine improves both mental and physical performance. The notion that
caffeine is an ergogenic aid has led to widespread use of the drug by ajhletes engaged in
many sports, The possibility that caffeine or methylxanthines could improve performance
during sports events and prolonged effort aroused great interest and was the basis for
numerous studies. However, this hypothesis remains extremely controversial,
undoubtedly because of lack of standardization among the varius experimental
procedures (31, 43, 58). Furthermore, this type of study is complicates] by the fact that
caffeine effects vary with corpulence of the individual, the type, intensity and duration of
the given exercise, the dose of caffeine used, habituation to methylxpnthines and with
environmental conditions during exercise (31, 58). While it is common to equate caffeine
with coffee, it should be noted that rarely is coffee the vehicle of administration in
research studies. Therefore, it may be misleading to equate the two because cofice
contains hundreds of additional chemicals (34)
Tn 1990, Wileox (58) concluded that few well-controlled studies had examined the
effects of caffeine on endurance performance and that the results were inconsistent. Since
1990, the research examining calleine and exercise performance increased and
demonstrated the ergogenic effect of caffeine during prolonged endurance exercise (35,
44), In addition, investigations (11, 39, 42) examining the effects of caffeine on exercise
performance during sprinting (<90 s) intense exercise of short (~5 min) and long
uration (~20 min) have appeared. There has been general improvement in the quality of
the investigations because researchers have attempted to control several factors that may
confound the caffeine results. Three factors relate to the nature of the experimental
design, ic., the exercise modality, the power output, and the caffeine dose, whereas four
others relate to the status of the subjects prior to the experiment, ie., nutritional status,
training status, previous caffeine use, and individual variability. An additional factor is
the ability to reliably measure exercise performance. This reliability ig greater in highly
trained subjects than itis in the less well trained (58).
Caffeine is a central nervous system stimulant, and its effects are similar to those
noted previously for amphetamines, tough weaker (43, 51). The short-term consumption
of caffeine may result in increased urination (34, 46), gastrointestinal distress, (Igemors,
decreased sleep, and anxiety symptoms in certain individuals (46). The long term
Consumption of caffeine at less than 5 cupsiday does not appear to increase the risk of
cancer, cardiovascular disease, peptic ulcer disease or cardiac arrhythmia’s (46). Caffeine also has profound effects on metabolic processes. Caffeine stimulates heart
function (15), blood circulation, and release of epinephrine (adrenaline) from the adrenal
gland (1, 3). Epinephrine, also a stimulant, augments these effects and also, in
conjunction with caffeine, stimulates a wide variety of tissues. Together they potentiate
muscle contraction, raise the level of muscle and glycogen breakdown, increase release of
FEA from adipose tissue (1, 15), and increase use of muscle triglycerides (TMTG). These
varied physiological responses are mediated by the action of caffeine, or epinephrine, to
enhance appropriate intracellular funetions in specific cells.
This review provides findings relative to the cellular actions of caffeine and the
effect of caffeine ingestion on various types of work performance (i.e, short term, high
intensity exercise; graded incremental exercise; and prolonged endurance exercise). In
addition, after reviewing findings of work performance studies using caffeine, we try to
define the main ergogenic mechanism/s of action by which caffeine gnhances exercise
performance. Table 1 Caffeine Contents Of Some Common Products
__Caffeine (mg) _
Substance
Standard dose Prolamine
Standard dose Dexatrim, Dietac
Standard dose No Doz, Vivarin
6 oz automatic drip coffee
6 oz automatic perk coffee
6 07 hot tea (strong)
6 oz iced tea
6 oz instant coffee
12. oz cola beverages
12 oz Mountain Dew
12.02 Mello Yellow
8 07 chocolate milk
2 oz chocolate candy
1 oz baking chocolate
280
Sie 200 tie
100-200
181
125
65-107
70-75,
54.75
32-65,
45
“Recommended caffeine intake is less then 250 mg per day.
“The doping limit of the International Olympic Committee is 12.g/ml Cyetic AMP.
Figure 1 - The structure of caffeine, Caffeine and the other xanthines and purine-
based compounds consist of two heterocyclic rings containing various numbers of
methyl groups. Note the similarity in the structure of caffeine to adenosine and
cyclic AMP. 1. Caffeine: Cellular Mechanisms of Action
The understanding of the potential ergogenic effects of caffeine requires the
knowledge of its mechanisms of action at the cellular level. Three principal cellular
mechanisms (see figure 2) have been proposed to explain its possible ergogenic effect
during exercise: (1) elevated affinity of the myofilaments for calcium (Ca™) and/or
increased Ca"* release from the sarcoplasmic reticulum in skeletal myscle; (2) cellular
actions caused by accumulation of cyclie-3?5"-adenosine monophosphate (cAMP) in
various tissues including skeletal muscle and adipocytes; and (3} cellular actions
mediated by competitive inhibition of adenosine receptors in the central nervous system
and in somatic cells. A brief summary of each of these potential mechaypisms follows.
1.1.Muscle Calcium
While the debate continues on the effects of caffeine on in vivo muscular
strength, it is well established that large doses of caffeine increase the force of
muscular contractions in isolated (in vitro) skeletal muscle (16, 43, 51). There are 3
mechanisms that may account for this observation. First, caffeine could result in a
greater Ca” release from the sarcoplasmic reticulum in skeletal muscle (16, 43. 51).
Secondly, caffeine might increase the sensitivity of the myofilaments for Ca‘,
Thirdly, caffeine ingestion may result in both an increases in the release of Ca’! from
the sarcoplasmic reticulum and increase myofilaments Ca’' sensitivity. Indeed,
evidence exits that caffeine can influence both sarcoplasmic reticulum Ca‘* release
and the sensitivity of the myofibrils for Ca'*, For example, exposure to caffeine has
been shown to increase sarcoplasmic reticulum release of Ca‘ in both skinned fibers
and in in vitro muscle preparations exposed to caffeine at 500 mol/L concentrations.
Further, caffeine promotes a grater twitch tension development at a given submaximal
Ca™ concentration. This finding as been interpreted as a grpater myofibrillar
sensitivity to Ca’" in the presence of caffeine. Therefor, given the above findings, it
seems likely that the increased tension development in muscle expgsed to high doses
of caffeine is because of both an increase in the release of Ca‘ from the sarcoplasmic
reticulum and an increase in myofibrillar Ca“ sensitivity.
‘A minimal concentration of 250 iM of caffeine seems necessary to produce
detectable effects on calcium shifts. The circulating plasma concentrations of caffeine
afler ingestion of cofiee is usually less then 100 y M/L. toxie effects are observed with
concentration of this methylxanthine above 200 iM/L, and lethal intoxication’s are
‘observed with blood concentrations higher then 500 ,M/L. Thus, the mechanism
responsible for the pharmacological effects of caffeine are probably activated by
concentrations lower then 100 4M. given this conditions, it is unlikely that
mobilization of intracellular calcium represents an essential mechanism of caffeine
action in vivo. 1.2.Cellular cAMP Levels
Caffeine as been shown to increase cellular levels of cAMP, thus promoting
lipolysis by activation of hormone sensitive lipases. Increased lipolysis results in an
increased availability of free fatty acids as substrate for contrapting muscle. An
increased dependence on five fatty acids during exercise and a sparing of muscle
glycogen could theoretically improve performance during prolonged events.
By what physiological mechanism does caffeine increase cAMP levels in cells?
‘Theoretically, calleine could increase cAMP by increasing blood levels of
catecholamines or by an inhibition of the enzyme phosphodiesterase. Consumption of
caffeine by caffeine-naive subjects (ie. subject who have not developed a tolerance to
caffeine) results in increased levels of plasma catecholamine, Catecholamines
increase cellular cAMP levels by binding to B-receptors on cell merpbranes activating
the enzyme adenylate cyclase; active adenylate cyclase then catalyses the formation
‘of cAMP from adenosine triphosphate (ATP). Phosphodiesterpse enzymatically
degrades cAMP into the nonnative compound 3°, 5° AMP; therefor, inhibition of
phosphodiesterase increases the biological half-life of cAMP. It js well established
that high concentrations of caffeine (ie. >1000 mol/L) greatly reduce
phosphodiesterase activity
1.3.Adenosine Receptor Antagonism
‘There is growing evidence that many of the physiological effects of caffeine are
because of antagonism of adenosine receptors in both brain tissue and peripheral cells
(16, 43, 46, 51). Caffeine and other methylxanthines derivatives competitively inhibit
the binding of adenosine receptor ligands. In brain tissue, metabolically stable
adenosine analogues binding to adenosine receptors results in behavioral depression.
Conversely, caffeine antagonizes the behavioral depressant effects of adenosine
analogues, shifting their dose-response curve to the right in a manner consistent with
a competitive interaction at the receptor level. Indeed, it is generally agreed that
caffeine-mediated behavioral stimulation is because of inhibition of brain adenosine
receptors,
In addition to central nervous system effects, caffeine can also act on peripheral
adenosine receptors (A;) on adipocytes suppresses lipolysis by inhibition of adenylate
cyclase activity. Recent evidence demonstrates a reduction in triglycerides content in
adipocytes of caffeine treated rats. This observation can be interpreted as in vivo
evidence that caffeine ingestion promotes an increase in free fatty acids by
antagonizing adenosine-mediated inhibition of lipolysis. db ———aeryiare yaiase
:
ar
oe
Figure 2 — Three models for the caffeine mechanis1 (a) methylxanthines (MX)
cause increased mobilization of caleium (Ca™ ) from endoplas reticulum (ER)
and other vesicles. The Ca” triggers various cellular events. (b) MX inhibits
phosphodiesterase, causing an elevation in cAMP and greater cellular actions of t
second messenger. (c) MX binds to adenosine receptors (AI and A2) to inhibit
adenosine’s effect on GI and Gs proteins. 1.1.Caffeine and cellular Actions: conclusions
From the above discussion, it is clear that caffeine could influence physical
performance by 1 of 3 mechanisms. Which of these 3 mechanisms is the most
important in producing a biological effect during exercise? At present, a definitive
answer is not possible. However, there is growing evidence that adenosine receptor
inhibition is one of the most important, if not the most important, mechanisms to
explain the physiological effects of caffeine at nontoxic plasma concentrations of the
drug. This conclusion is based on critical examination of the dose-response
relationship of caffeine for producing the desired biochemical effect. For example,
consumption of 200 to 350 mg of caffeine in adults generally results in plasma
concentrations of ess then 50 ymoV/L. Toxic effects are observed at plasma
concentration of 200 tM/L, and plasma concentration of 500 uM/L Are considered to
be fatal. Caffeine is a potent adenosine receptor antagonist in plasmg concentration as
Jow as 40 MIL as this dose as been shown to inhibit 50% of the ayailable adenosine
receptors in adipocytes in vitro. In contrast, 50% inhibition of phosphodiesterase
activity (in vitro) requires caffeine concentrations of = 1000 wM/L. further, most
investigations demonstrating a caffeine-induced increase in sarcoplasmic reticulum
Ca‘ release have used in vitro caffeine concentrations in the 500 ta 750 4M/L range.
Therefore, on the basis of the above data, many of the biological effects of low to
moderate plasma concentrations of caffeine must be mediated by inhibition of
adenosine receptors. Research continues on this fascinating topic.
R 2. Other Effects of Caffeine: Catecholamines and Acetylcholine
Caffeine, which is a well-known stimulant of the central nervous system, increases
motoneurons recruitment as well as the frequency of potentials of the motor end plate
through release of acetylcholine. Caffeine at doses of 7 to 35 mg/kg also facilitates the
effect of acetylcholine and of acetylcholinesterase inhibitors, but only transiently.
Cafléine increases production of plasma catecholamines during and at the end of
exereise. Action of catecholamines is essential because it allows the body to adapt to the
stress created by physical exercise. In fact, catecholamines participate in a number of
critical process, including glycogenolysis, uptake of ghicose, gluconeogenesis, lipolysis
of muscle and adipose tissue, muscle contractility, intropic and chronotropic responses of
the heart, and circulatory adjustments. However, results of studies on plasma
catecholamine changes are somewhat contradictory. Only one study reports an increase in
plasma concentration of dopamine and noradrenaline after 60 min of exercise (43). At 90
tin after effort, other authors found no change in plasma levels of adrenaline and
noradrenaline, whereas in two other studies, plasma adrenaline is selectively increased
during non-intense and prolonged exercise without warm-up and after high doses of
caffeine (9 mg/kg) with no change in noradrenaline levels (35). 3. Effect of Caffeine on Muscle
3.1.Direct Effects of Caffe
Caffeine potentiates the tension of isolated muscle contraction by direct
stimulation and of nerve-muscle preparations by indirect stimulation, both at rest and
after fatigue. Sensitivity to caffeine is not the same for all muscles. Muscles, which
contain a majority of type I fibers, are much more sensitive to the effect of caffeine
then muscles which contain a majority of type II fibers (Figure 3 describes the
possible role of caffeine in the regulation of muscle action).
e on Muscle
3.2.Effects of Caffeine on Muscle Metabolism
Metabolic modifications of muscle vary with the type of exercise. Thus, during
brief and intense effort, mainly anaerobic metabolism is involved. During prolonged
effort, anaerobic glycolysis is involved first since it is needed for cardiovascular
adaptation. After about 2 minutes of exercise, aerobic glycolysis takes place in the
muscle, During intense and relatively long exercise, both metabolisms, aerobic and
anaerobic, are associated. Intense muscle exercise induces an increase in glycolytic
‘lux which results in an increase in lactic acid production and a decrease in pH, which
has been postulated to partly account for the onset of musele fatigue.
Fatty acids are used actively by the muscle during exercise, which results in
sparing of glycogen, Improvement in performance after absorption of caffeine,
observed in prolonged exercise involving aerobic metabolism has been attributed to
stimulation of lipolysis. Hydrolysis of triglycerides of adipose tissue increases blood
concentrations of free fatty acids (18, 25). However, some studies do not demonstrate
an increase in plasma concentration of free fatty acids after ingestion of caffeine (48).
The effect of caffeine on potential storing of muscle glycogen has been the focus
of many studies. Caffeine, fructose and glucose, either alone or combined, have a
marked effect on storing of muscle glycogen during cycling exercise (24). Similarly,
caffeine and suctose stimulate endurance to comparable degrees but have no
synergistic effect on performance. According to recent studies, ingestion of caffeine
‘one hour before exercise decreases muscle glycogen utilization about 55% during the
first 15 minutes of effort compared to subjects receiving placebo. The glycogen thus
saved becomes available for the following phases of exercise, delaying onset of
exhaustion. This mechanism is important, because depletion of muscle glycogen
could be to a great extent responsible for the fatigue observed during tests of
‘endurance (25). Furthermore, increased utilization of intra muscular triglycerides
and/or extramuscular fatty acids after ingestion of caffeine could inhibit glycogen
breakdown, especially by modifying muscle contractions of acetyl-coenzyme A and
citrate. However, increased plasma concentration of free fatty acids induced by
caffeine is not always accompanied by a modification of substrate utilization by the
muscle. Circulating concentration of free fatty acids is the product of both hepatic
release and amount taken up by all other tissues that can vary widely with
‘experimental conditions. Lastly, at high altitude, caffeine increases endurance by a
“4 mechanism other then that of mobilization of fatty acids, since it does not induce an
increase in plasma concentration of camitine; the mechanism involved is still
unknown.
During anaerobic exercise, caffeine seems to increase the production of lactate
by the muscle, regardless of the degree of training of the subjects (2, 11). This
phenomenon could reflect caffeine-induced potentiation of muscle glycogenolysis
and/or increase in release of lactate that does not necessarily reflect a stimulation of
lactate formation (12). Depletion of muscle glycogen during exercise is greater in
type 1 then in type If fibers, the later acting only intermittently in continues
contraction. The sparing of glycogen due to caffeine could apply more to type I fibers
by increasing their energy reserves. Thus, it is possible that the effects of caffeine
‘vary as a funetion of the type of fibers contained in the muscles that are called upon
ina given sport activity.
‘Some authors suggest that only well-trained athletes can draw benefit from use of
caffeine (11, 12). Highly trained athletes already posses, becquse of intensive
training, a stimulated lipolytic activity and an increase in the size and density of their
mitochondria (25). Also, in rats trained with endurance exercise, caffeine does not
modify plasma concentration of free fatty acids nor utilization of glycogen from
muscle or liver.
Recently, caffeine has been shown (o increase the levels of excess post-exercise
oxygen consumption in untrained female subjects both during ang after 90 min of
exercise (18). Therfore, the caffeine-induced increase in metabglic rate of these
‘women may have a beneficial effect for obese subjects or those whp are on a weight
Joss program, since caffeine intake enhances oxygen and energy gonsumption for a
Jong time afler exercise, However, there seems to be no signifigant advantage in
ingesting large (10 mg/kg) rather then small (5 mg/kg) doses of caffeine (18).
15 CAFFEINE
emp
greonae nen
wonton 12 wemsincor 9
ire 3 — Possible role of caffeine in the regulation of muscle action. These include
both direct and indirect mechanisms (clockwise from the left): alternations of
neuron threshold (1), stimulation of neurotransmitter release (2), alteration of
sarcolemma threshold (3), alteration of membrane activity related to calcium
storage (4), inhibition of adenosine binding (5), and phosphodiesterase activity (6),
ulation of catecholamine release (7), that, in turn, increases cAMP activity. The
ivates protein kinases that turn on glycogenolysis (10), lipolysis (11), and
, caffeine may inhibit glycogenolysis (8), increase blood
glucose levels (9), and induce FFA mobilization from adipose tissue (12). 4. Caffeine and Exercise Performance: Studies Review
1. Methodological Considerations
There are a number of factors that need to be considered in determining the
validity and reliability of studies of the effect of caffeine on performance. It makes
little sense to explore the results of studies using animals to examine the ergogenic
potential of caffeine for the question of dose equivalents and biological species
differences are always present. Several other factors to consider in the evaluation of
the ergogenic effect of caffeine include exercise type and intensity, training status of
the study participants and pre-exercise feedings.
From a critical evaluation standpoint, a number of factors are necessary
requisites for generalisability to an athletic population and to establish validity and
reliability due to individual variation amongst study participants. First, it is necessary
that the study population be athletic and the extrapolation from study to ‘the field”
should best be made under sport specific conditions (ic. cycling Vs running). In
addition, the testing variable upon which ergogenic potential is determined should
either be a true measure of performance (i.e. open-ended test to exhaustion (35), test
for a given time but with maximal power output measured (38), or a field test (4). The
general rules for a research study to minimize bias in an investigation of the effects of
fa drug upon a variable (performance) are as follows: sample size large enough to
avoid a type II error (at Ieast 5 study participants in a controlled rescarch study),
randomized, counterbalanced design and double-blinded administration (placebo
controlled). A factor that has been overlooked is that of gender, which is important
due to findings of a facilitated free fatty acid utilization by female’s vs. males during
endurance exercise (46). The impact of gender upon ergogenic potential of caffeine
has not yet been explored, but should be considered in future research.
‘A final factor to consider is the caffeine intake status of the study participants, for
it has been demonstrated that tolerance develops to several of the effects of caffeine
with habitual consumption (3). Development of tolerance to caffeine induced
increases in heart rate and blood pressure has been demonstrated to occur within 4
days of regular caffeine consumption. However, from limited studies data (3, 15, 35,
37, 40, 52, 53), it does not appear that habitual consumption of caffeine has
Significant effect upon variables that may be ergogenic to endurance exercise
performance (3). It also does not appear to alter the ergogenic effect of high doses of
caffeine (9 mg/kg) upon endurance running or cycling performance (35). A study
with a large group of individuals who are reselected based upon a wide range caffeine
intake status would be required to definitely determine whether a habitual caffeine
intake alters its ergogenic potential.
” 4.2.Short Term, High Intensity Exercise
Discrepancies exist between the findings of studies that have examined the in
vivo effects of caffeine on short term, high intensity work and those examining
isolated (in vivo or in situ) muscle performance. Studies utilizing isolated muscle
have consistently shown caffeine to enhance muscle force production, while the
majority of human studies have shown caffeine to have no effect on short term, high
intensity exercise performance. Recent studies (2, 12, 17, 59) do not support previous
reports that caffeine does not increase in vivo strength and power (11, 60). Collomp
and associates have performed a series of studies showing that caffeine ingestion can
increase maximal anaerobic power in a protocol in which brief cycle sprints (6 s) are
performed against increasing resistance (2) and also can increase the swimming
velocity in trained athletes during 100-m freestyle repeats (12). Simpilarly, Wiles and
associates (59) report that caffeine ingestion results in decreased timpe to run 1,500 m
and increases the speed of the “finishing burst”. Table 2 summarjzes those studies
that have examined short-term exercise. Table 2 - Summary Of Key Results From Studies Of Caffeine And Short Term
Intense Exercise
Study
Collomp et al. 1990
Collomp et al. 1991
Anselme et al. 1992
Collomp et al. 1992
Wiles et al. 1992
Test conditions
+
+
.
100% VOzmax
250 mg caffeine
Cycle ergometer 30-s
Wingate test
5 mg/kg caffeine an
hour before testing
Cycle ergometer
maximal anaerobic
power
‘A6-s cycle sprint
250 mg caffeine 30
min before testing
2X 100-m freestyle
swim
20 min rest
250mg caffeine
Simulated 1,500-m
runs on treadmill
3 g coffee (=150-200
mg caffeine) an hour
before testing
Subjects
7
3 Males and 3
females active in
sports 2-3
hours/week
#10 Males and 4
females active in
sports for an
average of 3.5
hours/week
* 7 trained
swimmers
(4 females&3 males)
* 7untrained
swimmers
(5 females&2 males)
¢ 18 Trained males
ae
Endurance T 9%
(nonsignificant)
No improvement
in maximal
anaerobic
capacity, power
and power
decrease
@ Increase in
catecholamine
and blood lactate
levels
# 7% Increase in
power
4 Increase in blood
lactate levels
* Trained-2% and
4% respectively,
greater velocity
in first and
second 100-m
+ Untrained-no
change
4 4.2: faster run
+ 0.6 km/hr faster
in final min
(finishing burst’)
19 4.3.Graded Incremental Exercise
Studies, examining the effects of caffeine on short term incremental exercise
performance, are limited. A number of studies suggest that caffeine has no effect on
short term incremental exercise performance (5, 15, 16, 30). On the other hand, one
study suggests that 10 mg/kg dose of caffeine, three hours prior to an incremental
work test will allow caffeine naive, recreational subjects to work for a longer period
of time and, therefore, to produce more work (28).
Two studies have examined the effects of caffeine tolerance during graded
incremental exercise (15, 30). First, Dodd and associates (1991) found that 5 mg/kg
dose of caffeine increased resting values for heart rate, VO2 and ventilation while
Gastin and associates (1990) found no difference in these variables. It may be that the
fitness level of the subjects caused these disparate findings since Dodd et al. (1991)
used subjects of average fitness levels while Gastin et al. (1990) used highly trained
subjects. Although Dodd et al. (1991) administered caffeine to subjects 1 hour before
the exercise and Gastin et al. (1990) administered caffeine to subjects 3.5 hours
before the exercise, both studies concluded that caffeine had no effect on time to
exhaustion, VO2 wax or the lactate threshold. Thus, the direct findings of these studies
indicate that the caffeine tolerance of the subjects does not effect pgrformance during
exercise to moderate intensity and duration. In addition, a comparison of findings
between the 2 studies suggests that the timing of dosage in relation to the exercise
bout does not effect performance.
However, one study suggests that caffeine improves performance during graded
incremental exercise (28). A high dose of caffeine (10 mg/kg) was administered to
moderately fit, caffeine-naive subjects at 1 and 3 hours before eyercise testing. In
addition to an increase in time to exhaustion, the study reported q right shift in the
lactate threshold. Table 3 summarizes those studies that have pxamined graded
incremental exercise.
20 Table 3 - Summary Of Key Results From Studies Of Caffeine And Graded
Incremental Exercise
Study Test conditions
Flinnetal. 1990 #
+
+
Gastin et al. 1990
.
Berry et al. (1991)
Dodd et al. 1991 ¢
.
Incremental VO2max
cycle ergometer
Anaerobic threshold
1omg/kg of caffeine 3
hours before testing
Incremental VOzmax
treadmill running
Anaerobic threshold
5 mg/kg of caffeine
3.5 hours before
testing
Incremental VOzmax
treadmill running
Anaerobic threshold
‘Tme/kg of caffeine
citrate 45 min before
testing
Incremental VOzmax
cycle ergometer
Anaerobic threshold
3 mg/kg or S mg/kg of
caffeine an hour
before testing
Subjects
+
.
.
9 Male
recreational
cyclist
caffeine
consumption less
then 2543
mg/day
8 Moderately
‘rained male
runners
Non-users of
caffeine
10 Males engaged
in regular aerobic
exercise
Non-users of
caffeine
17 Moderately
trained males
8 subjects with
caffeine
consumption
above 300
mg/day
9 subjects with
caffeine
consumption 25
mg/day or less
Findings
+
.
+
Increased time to
exhaustion
Right shift in the
lactate threshold
Lowered RER
between 250 and
450 watts
workload
No effect on
VOzmax
No effect on
anaerobic
threshold
Lower RPE
ratings in caffeine
trial
No effect on
VOzmax
No effect on
anaerobic
threshold
No effect on
VOsmax
No effect on
anaerobic
threshold
2 Btime to
Exhaustion
Work completed
(kilojoutes)
Work competed)
acebo Caffeine
Control
Figure 4 — Effect Of Caffeine On Time To Exhaustion And Total Work
(mean values). Data from Flinn et al. (1990),
* Significantly different from either the control or placebo measures (P<0.01).
;
i 3 ear wanes
aoe
1
i |
ae . Tike
Figure 5 — Effect Of Caffeine On Lactate Threshold (mean values). Data from Flinn
et al. (1990).
* Significantly different from either the control or placebo measures (P<0.01).
2 3.1.Prolonged Endurance Exercise
Unlike short term, high intensity exercise, in prolonged endurance exercise
aerobic metabolism is the main metabolic pathway. During prolonged effort,
anaerobic glycolysis is involved first since it is needed for cardiovascular adaptation.
‘After about 2 minutes of exercise, aerobic glycolysis takes place in the muscle.
During intense and relatively long exercise, both metabolisms, aerobic and anaerobic,
are associated. Intense muscle exercise induces an increase in glycolytic flux which
results in an increase in lactic acid production and a decrease in pH, which has been
postulated to partly account for the onset of muscle fatigue
During endurance exercise, fat is a major substrate, and muscle glycogen
depletion could be a limiting factor of performance. Therefore, if caffeine ingestion
can alter substrate turnover, itis likely to have a major effect on endurance exercise
performance. Fatty acids are used actively by the muscle during exercise, which
results in sparing of glycogen. Improvement in performance after absorption of
caffeine, observed in prolonged exercise involving aerobic metabolism has been
attributed to stimulation of lipolysis (10, 13, 15, 24, 25, 38, 45).
A now classic study in the late 1970s provoked much research activity in the area
of the ergogenic potential of caffeine by reporting a 20% prolongation in the time to
fatigue following 330 mg of caffeine (approximately 5 mg/kg) vs. decaffeinated
caffeine during cycling at 80% VOz mx (13). A well controlled study in 1982
examined the effects of caffeine (6 mg/kg) vs. placebo (double blind) administered to
elite Nordic skiers during races at low (300m above sea level /20 km/n=14) and high
(2900m above sea level /23 knv/n=13) altitude. The pre-exercise diet and caffeine
intake were controlled, and the data was carefully normalized to account for
differences in snow conditions, revealing a significant improvement in performance
time for the low (p<0.05) and high (p<0.001) altitude tests of 1.7% and 3.2%
respectively (about 1 and 2 minutes respectively) (4).
One of the best designed and controlled study reported to date investigating the
effects of caffeine on performance was by Graham and Spriet (35). These
investigators used a randomized/double-blind protocol to examine the effects of a
fairly high caffeine dose (9 mg/kg) upon the performance of 7 elite athletes (mean
VOz max = 73 mV/kg/min) during both cycling and running to exhaustion at
approximately 85% VO? mx. They found improvements in running and cycling time
that averaged 44% and 51%, respectively, to exhaustion in all study participants. This
study demonstrated quite dramatically the ergogenic potential of caffeine 9 mg/kg on
endurance exercise performance, and provided evidence that the mode of exercise
(ie. cycling vs. running) was not important in determining the ergogenic potential of
caffeine. In all of the above studies, the first dose of caffeine was administered 60
minutes prior 10 exercise, Table 4 summarizes those studies that have examined
graded incremental exercise prolonged endurance exercise,
2B BLOOD LACTATE
ME
i
i
[ya ]mrieete] atop auvetnon aE
fas msica =
te 08 moka aan rm
ie 4
in
Figure 6 — Effect Of Caffeine On Blood Concentration Of Lactate, Glucose, FFA,
‘And Glycerol. (Mean values). Data From Graham And Spriet. (1995).
4 Table 4, - Summary Of Key Results From Studies Of Caffeine And Prolonged
Endurance Exercise
Study Test conditions
Costill et al. 1978 Cycle ergometer at
80% VO2 mx tO
exhaustion:
Iyetal, 1979
Essig et al. 1980
330 mg of caffeine 60
min before testing
Cycle ergometer at
75% VO2 max/120
min
Treadmill running at
80% VO2 max to
exhaustion
250 mg of caffeine 60
min before testing
‘An additional 250 mg
of caffeine fed at 15
min intervals over the
first 90 min of
exercise
30 min on a cycle
ergometer at 65%-
75% VO2 max
5 mg/kg of caffeine 1
hour before testing
Subjects
4 Unknown
% Trained cyclists 7
males and 2
females
# 7 Active males
Findings
.
.
20%
prolongation in
the time to
fatigue (96 min
vs. 75 min
wieatteine)
TIFFAI
Increased work
production by
TA%
RPE unchanged
31% elevation in
fat oxidation
during last 70
min of caffeine
trial
No change in
‘CHO utilization
42% Decrease in
muscle glycogen
utilization
IMTG use was
150% greater in
caffeine trial
RER shifted from
CHO towards fat
metabolism
as Table 4 - Summary Of Key Results From Studies Of Caffeine And Prolonged
Endurance Exercise
Study
Ericson et al. 1989
French et al. 1991
Graham & Spriet 1991
Test conditions
+ 90min of eycle
ergometer at 65%-
70% VO mx
+S mgikg of caffeine
1 hour before testing
4 45 Min of treadmill
running at 75%
VO2 max
# After the first 45
rin speed was
increased by 2 mph
till exhaustion
#10 mg/kg of caffeine
immediately prior to
testing
Cycle ergometer and
treadmill run at 85%
VO2 mx tO
exhaustion
+ 9 mg/kg of caffeine
60 min before
testing
*
Subjects
4 4 Male and one
female highly
trained
competitive
cyclist
6 Male trained
munners
(participated in at
least 2 marathon
races)
Non habitual
users of caffeine
(caffeine
ingestion <20
mg/day)
well-trained
distance runners
6 males and 1
female
+ Users and non
users of caffeine:
© 2 Habitual users
of caffeine (450-
720 mg/day)
© 2 Habitual users
of caffeine (120-
150 mg/day)
= 3 non-users (<29
mg/day)
Findings
© 30% Decrease in
muscle glycogen
utilization
@ Lower RER for
caffeine trial
during final 60
min
4 No significant
differences in
VOz, and in RPE
© ‘Significant
increase in the
distance run
during the period
to exhaustion
(post 45 min) in
the caffeine trial
Running time to
exhaustion
increased 69%
Cycling time to
exhaustion
increased 66%
+ All subjects
increased their
running &
cycling time to
exhaustion
6 Table 4c - Summary Of Key Results From Studies Of Caffeine And Prolonged
Endurance Exercise
Study Test conditions
Titlow et al. 1991 ¢ 60 min of treadmill
running at 60%
VO2 mx
200 mg of caffeine
60 min before.
testing
Spriet et al. 1992 © Cycle ergometer
80% VO2 mx to
exhaustion
+ 9 mg/kg of caffeine
60 min before
testing
Van Soeren et al. 1993 ¢ Cycle ergometer
50% VO2 mn/60 min
+ 250 mg of caffeine
60 min before
testing
+ Smg/kg of caffeine
‘60 min before
testing
Wemple et al. (1994). Cycle ergometer
60% VOr mad 180
min
+ 25 mg/dl of caffeine
ina solution with a
mi/kg 60 min
before testing
Subjects
* 5 Males
involved in
moderate
exercise
programs
Recreational
cyclists 7 males
and one female
* 14 Males, not
engaged in
regular physical
activity:
* 7 Habitual users
of caffeine (400-
750 mg/day)
© TNon-users
(0-20 mg/day)
+6
Findings
.
20%
prolongation in
the time to
fatigue
55% Decrease in
muscle glycogen
utilization in
first 15 min
27%
prolongation in
‘the time to
fatigue (96 min
vs. 75 min)
No effect on
metabolism
In non-users
caffeine
increased plasma
epinephrine
concentrations
during exercise
Cycling
performance was
unaffected by
caffeine
‘No significant
difference in
plasma
catecholamine
concentration
7 4800
4800
4100
Distance (meters)
Distance Run To Exaustion
14,920m
44,222
Control
Placebo
Caffeine
Figure 7 ~ Effect Of Caffeine On Distance Run During The Period To Exhaustion
(mean values). Data from French et al. (1991).
* Significantly different from either the contro! or placebo measures (P<0.05).
28 RUNING
se teem 133%
é
:
g |
i eS
CAFFEINE
é
g
z
2
a 2
CYCLING
Figure 8 - Individual performance times (in minutes) of subjects running and
cycling to exhaustion after placebo or caffeine ingestion (mean values). Subjects 4
and 6 were caffeine users (450-720 mg/day), subjects 1, 2, and 7 were light users
(120-150 mg/day), and subjects 3 and 5 were nonusers (<20 mg/day). Data from
Graham and Spriet. (1991).
2» ms of Action
4. Caffeine’s Ergogenic Mecha
§.1.Short Term, High Intensity Exercise
Short term, high intensity activities last only seconds or a few minutes. During
brief and intense effort, mainly anaerobic metabolism is involved, fat metabolism is,
very minor fuel and muscle glycogen is not a limiting factor of performance.
Therefore, the metabolic explanation cannot pertain to short-term exercise. Metabolic
shifts may occur, but obviously additional actions must take place, which may act in
concert with the metabolic shifts
Caffeine is a drug that can enter every tissue of the body and thus can have
multiple effects. Under this circumstances it appears that caffeine must be acting
either directly on the muscle to enhance eross-bridge formation or acting on the
central nervous system, In the latter regard, the drug could influence motor
recruitment and/or the perception of fatigue
‘One needs to bear in mind that normally excitation/contraction coupling drives
metabolism, not vice versa, Thus we need to consider whether or not caffeine could
alter some aspect of the contraction process. It has been repeatedly demonstrated in
isolated sarcoplasmic reticulum, cardiac muscle, and skeletal muscle that caffeine
causes translocation of Ca” through plasma and sarcoplasmic reticular membranes
(Figure 2). This lowers the threshold potential for excitation and extends the active
period of contraction, The sensitivity of muscle to caffeine depends on the sarcomere
length (43). Thus, the increased force of contraction in muscle triggered by high
‘concentration of caffeine is probably related to both the increase in the release of
calcium from the sarcoplasmic reticulum and the increase in myofibrils sensitivity to
calcium. Ca" sensitivity is also greater in slow vs. fast twitch muscle fibers, which
may help to explain the force potentiation of caffeine.
An increase in cross-bridge formation would increase ATP demands and
stimulate metabolism including glycolysis, and an increase in intracellular Ca"
should stimulate glycogenolysis (6, 31). This could account for the increased power
‘output and high blood lactate results with intense exercise (2, 11, 12).
Caffeine and/or epinephrine may stimulate the Na‘/K” ATPase (41), resulting in
a more stable intracellular environment that would be more optimal for tension
development. These possible influences, together with the finding that performance is
enhanced when glycogen is not limiting (Table 2), means we must consider
alternatives to the common theory of altered carbohydrate metabolism following
caffeine ingestion (31),
30 ‘A. second theory focuses on caffeine inhibiting cAMP yhosphodiesterase,
elevating cAMP (Figure 2b). At physiological concentrations, methylxanthines are
very weak inhibitors of phosphodiesterase and do not elevate tissue cAMP, As a
result, this mechanism is not likely to enhance short-term, high intensity exercise
performance (31)
thas also been demonstrated that caffeine facilitates neuromuscular transmission
and increases neuronal excitability by reducing the threshold of motor neuron firing
and/or by reducing the adenosine inhibition of firing (60). This could result in
increased motor unit recruitment and altered pattems of substrate utilization in the
active muscle fibers (51).
Caffeine may also play an ergogenic role in exercise performance by alt
neural perception of effort and/or fatigue (ie. by lowering the perception of effort
and/or fatigue) (10, 13, 26). The perception of fatigue is a multifactorial process that
is influenced by numerous variables. Given the ‘black box’ of the central nervous
system it has been very difficult to objectively quantitate variables such as the
perception of fatigue. A reduced perception of fatigue at a given exercise intensity
may either arise from a reduction in inputs into the system, or an increased threshold
of detection, Semiquantitation of this may be obtained using a scale such as the Borg
Rating of Perceived Exertion (RPE) Scale, Reduced input could arise from a
reduction in afferent information to the CNS from the periphery if caffeine potentate
force at a submaximal frequency (46). Imespective of the mechanism involved,
caffeine as been shown to decrease the RPE in some (10, 13, 26) put not all studies
(48) of endurance exercise, In one study there was no difference in RPE for caffeine
ys. placebo in spite of significant increases in power output for the caffeine trial (38),
suggesting an ergogenic benefit.
In summary, there are very few studies upon which to conclude what is the
ergogenic mechanism of action that enhances short-term, high intensity exercise,
following caffeine ingestion. Furthermore, there is a great controversy regarding
caffeine, whether it is a true ergogenic aid. There is even greater confusion regarding
the ergogenic effect of caffeine on short-term, high intensity exercise. Many studies
have not demonstrated a performance enhancement following caffeine ingestion.
Indeed, data from studies are available to defend or refute its enhancement of short-
term, high intensity exercise.
Based on the data above, it seems that caffeine has multiple effects on muscle
action and muscle metabolism. It is likely that the increased power output in muscle
exposed to high doses of caffeine is because of both an increase in the release of Ca”
from the sarcoplasmic reticulum and an increase in myofibrils Ca” sensitivity, In
addition, through the stimulation of the Na'/K” ATPase activity, and the increased
neuronal excitability, there is increased motor unit recruitment, leading to a more
optimal tension development, resulting in a greater force production. Caffeine may
also lower the neural perception of effort and/or fatigue at a given exercise intensity,
but there are very few studies upon which to conclude whether or not caffeine alters
the perception of fatigue. Clearly, further study is necessary to determine which of the
above mechanisms has the greatest effect on short-term, high intensity exercise.
31 §5.2.Graded Incremental Exercise
Findings, from the studies of Dodd and associates (1991) and Gastin and
associates (1990), indicate that the caffeine tolerance of the subjects does not effect
performance during exercise to moderate intensity and duration. In addition, a
comparison of findings between the 2 studies suggests that the timing of dosage in
relation to the exercise bout does not effect performance. It would seem, therefore,
that the most likely explanation of the findings of Flinn and associates (1990), is that
the high dosage of caffeine may have resulted in improved exercise performance.
One possible explanation for the findings of Flinn et al, (1990) could be the
timing of caffeine ingestion prior to exercise, which could effects substrate turnover.
Based on their findings, one can suggest that caffeine needs to be taken between three
to four hours pre-exercise, (at least for incremental exercise) in order to allow FFA
levels to reach their peak, rather then one hour pre-exercise which only allows
caffeine levels to reach their peak (28). Furthermore, small doses of caffeine
(
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