Bicarbonate and Citrate

Chapter 29
Bicarbonate and Citrate
LARS R . M C NA U G HTO N
Introduction
The ability to resist fatigue is an important aspect
of many types of sporting activity, whether it be
short-term, high-intensity anaerobic type work,
or longer, high-intensity endurance activity. Athletes who fatigue early do not perform as well as
those who fatigue more slowly, so, in order
to maximize performance, it is important that
fatigue is minimized wherever possible.
Fatigue is generally defined as the failure to
maintain an expected or required force or power
output (Edwards 1981). The causes of fatigue are
multifaceted (see Green 1990 and Hultman et al.
1990 for reviews) and can be roughly divided
into either physiological or psychological. In the
physiological realm, fatigue can be described as
either central or peripheral (Green et al. 1987). In
the latter case, there is a myriad of factors
which can interact to decrease power output and
hinder performance. During high-intensity work
of short duration, potential contributors to
fatigue could be related to muscle energy production (for example, a decline in muscle adenosine triphosphate, ATP) or they could be related
to impaired electrochemical events of muscle
contraction/relaxation production. Alternatively, fatigue could be related to the accumulation of metabolites — for example lactate,
hydrogen ions and ammonia. During prolonged
submaximal effort, energy substrate depletion
is generally regarded as the major cause of
fatigue, but a number of other factors such as
hyperthermia, dehydration and oxygen trans-
port problems may also contribute in differing
amounts.
Athletes and their coaches have always sought
ways to improve performance and overcome the
fatigue process. In doing so, they have targeted
a number of different areas, including training
methodology, nutritional practices, medical
interventions and the use of both legal and
illegal drugs — for a review of ergogenic aids, see
Chapter 26. With a ‘win at all costs’ mentality,
many athletes have ingested substances which
are claimed to have an ergogenic effect by overcoming the fatigue process. Over the last decade
or so, the use of sodium bicarbonate and sodium
citrate have become popular to offset fatigue
during short-term, high-intensity exercise. It is
claimed that these substances improve performance by buffering the acids which are produced during exercise.
The aim of this chapter is to discuss the current
knowledge with respect to metabolic acidosis
during both short-term, high-intensity and
endurance exercise and the effects of sodium
bicarbonate and sodium citrate ingestion on
these types of performance.
Basics of acid–base balance
Substances that release H+ when they dissociate
in solution are called acids, whereas substances
that accept H+ ions and form hydroxide ions
(OH-) are called bases. In the body there must be a
balance between the formation of hydrogen ions
and the removal of hydrogen ions for homeosta-
393
394
nutrition and exercise
Table 29.1 Approximate relationship between [H+]
and pH.
[H+] (nmol · l-1)
Acidic
H+
1
pH
Gastric fluid
2
20
30
40
50
60
70
7.7
7.5
7.4
7.3
7.2
7.15
Lemon juice
3
4
5
Tomatoes
Coffee
6
sis to be maintained. When this is not the case,
and the number of H+ ions increases, the pH
of the blood (which is normally around 7.4)
decreases to lower levels (7.0 or lower) (Table
29.1). Muscle pH is normally at 7.0 and decreases
to 6.8 or lower (Robergs & Roberts 1997). The pH
of a given substance is the negative logarithm of
the hydrogen ion concentration (-log [H+]). Since
it is logarithmic, a unit increase of 1.0 means a
tenfold increase in the number of H+ ions. Basic
solutions have few H+ ions and acids have plentiful amounts of H+ ions. Distilled water is considered a neutral substance at a pH of 7.0 (25 °C).
The pH scale is shown in Fig. 29.1 and was
initially devised by the Danish chemist Soren
Sorensen. Body fluids differ in their pH level,
with gastric fluids being an acidic 1.0 and arterial
and venous blood being slightly basic at c. 7.45.
During normal activity, the blood and extracellular fluid remain at a pH of approximately 7.4, a
slightly alkalotic state. When the number of H+
ions increases, such as during intense exercise,
the blood pH drops to below 7.0 (muscle pH is
even lower), and a state of acidosis exists. As
metabolism is highly H+ ion sensitive, the regulation of alkalosis and acidosis is extremely important. Figure 29.2 shows the relationship between
pH and [H+] with the extreme physiological
realms.
The body has three basic mechanisms for
adjusting and regulating acid–base balance and
which minimize changes within the body. First,
there are the chemical buffers which adjust [H+]
within seconds. Secondly, pulmonary ventilation
excretes H+ through the reaction
7
Urine
Distilled water
8
Egg white
9
10
Milk of magnesia
11
Alkaline
12
Cleaning ammonia
13
Caustic soda
14
OH–
Fig. 29.1 The pH scale with some typical examples.
H+ + HCO3- ´ H2CO3 ´ H2O + CO2
adjusting [H+] within minutes. Finally, the
kidneys excrete [H+] as fixed acid and work on a
long-term basis to maintain acid–base balance.
We are concerned with the bicarbonate buffer
system (Vick 1984).
The body’s chemical buffer, and more specifically the bicarbonate buffer, consists of a weak
acid (carbonic acid) and the salt of that acid
(sodium bicarbonate), often termed a conjugate
acid–base pair. Discussion of blood pH regulation has generally focused on the role of bicarbonate, since it can accept a proton to form
carbonic acid in the following equation:
HCO3- + H+ ´ H2CO3
When metabolism produces an acid such as lactic
acid, which is much stronger than carbonic acid,
a proton is liberated, binds with bicarbonate and
bicarbonate and citrate
395
1 x 10–7
N
o
r
m
a
l
Acidosis
[H+] (mol.l–1)
8 x 10–8
Alkalosis
6 x 10–8
4 x 10–8
2 x 10–8
Fig. 29.2 The relationship
between [H+] and pH within the
extreme physiological range.
7.0
forms sodium lactate and carbonic acid. Eventually this forms added carbon dioxide and water.
Effects of sodium bicarbonate and
citrate on performance
High-intensity exercise can be maintained for
only short periods of time (Parry-Billings &
MacLaren 1986). Energy for this type of activity
comes predominantly from the anaerobic
glycolysis system. In this process, energy is provided in the absence of oxygen as shown in the
following equation:
Glycogen + 3 ADP + 3 Pi ´ 3 ATP + 2 lactic acid
+ 2H2O
The energy for the muscle contractions then
comes from the ATP molecules which are produced. The above equation indicates that the
breakdown of glucose anaerobically results in
the formation of lactic acid, which dissociates
almost immediately at a normal physiological
pH to a lactate anion and a proton [H+] (Brooks
1985), which in turn would decrease intramuscular pH (Fletcher & Hopkins 1907; Hermansen &
Osnes 1972; Osnes & Hermansen 1972; Sahlin
et al. 1978) if the H+ was not buffered. High rates
7.1
7.2
7.3
7.4
7.5
7.6
7.7
7.8
pH
of glycolysis decreases pH even further, which
eventually shuts down the contractile process
(Fuchs et al. 1970; Donaldson & Hermansen 1978;
Bryant-Chase & Kushmerick 1988). Force generation in isolated muscle (Mainwood &
Cechetto 1980) has also been shown to be pH sensitive. More specifically, the myofibrillar protein
troponin does not bind as efficiently to calcium
when pH decreases, and this impairs the formation of the actomyosin complex (Fuchs et al.
1970). This reaction is reversible, so that when
pH is reversed, bringing it towards a normal
level, recovery of force generation takes place
(Bryant-Chase & Kushmerick 1988). Changes in
pH have also been shown to have an effect on
energy production (Hill & Lupton 1923; Hill
1955; Krebs 1964). When muscle intracellular
pH reaches 6.3, the process of glycolysis is inhibited by an impairment of the activity of the glycolytic enzyme phosphofructokinase (Trivedi &
Danforth 1966). In order to reduce or delay
these fatigue-producing processes, the ingestion
of sodium bicarbonate has been used both experimentally and practically.
Research into acid–base balance during exercise commenced many decades ago. Dennig et al.
(1931) used acid salts to make runners more
396
nutrition and exercise
acidic and established that this regimen made
them less able to use oxygen efficiently. In turn,
this led the researchers to infer that induced alkalosis could have an opposite effect. Dill et al.
(1932) demonstrated that runners could have a
1% decrease in running times when alkalotic.
While it has been shown previously the muscle
cell membranes are impervious to HCO3- (Katz
et al. 1984; Costill et al. 1988), an increase in
extracellular HCO3- increases the pH gradient
between the intracellular and extracellular environment. The effect of this increased pH gradient
is to facilitate the efflux of intracellular lactate
and H+, thus reducing the fall in intracellular pH
(Katz et al. 1984; Costill et al. 1988). Both lactate
and H+ have been shown to follow a favourable
pH gradient (Roth & Brooks 1990). The time
course for the production of lactate has been
shown to vary from 5 s (Pernow & Wahren 1968;
Saltin et al. 1971; Jacobs et al. 1983) to several
minutes (Wilkes et al. 1983). In an early, wellconducted study, Osnes and Hermansen (1972)
measured postexercise blood lactate levels in
subjects who ran distances from 100 to 5000 m.
Lactate concentrations increased with increasing
distance up to 1500 m, after which there was no
further increase: pH and blood bicarbonate concentrations were lowest after the 1500-m run.
This would seem to suggest that acid–base
balance shifts occur most dramatically after exercise lasting 4–5 min. It is reasonable to assume,
therefore, that if sodium bicarbonate were to be
effective as an ergogenic aid, it would be so over
a similar time span, since these time periods are
dependent upon high rates of energy production
from anaerobic glycolysis.
There has been some suggestion that the mechanisms whereby sodium bicabonate loading is
effective lie not with the bicarbonate ion but are
possibly due to the sodium load (Saltin 1964;
Kozak-Collins et al. 1994). Sodium could change
intravascular volume, which in turn could alter
performance. Kozak-Collins et al. (1994) tested
this hypothesis with the ingestion of either
NaHCO3 or NaCl, which both provided equimolar amounts of sodium given prior to repeated
bouts of 1-min exercise. Performance was not
enhanced in either condition but haematocrit
measures suggested that intravascular fluid
status remained similar. pH was significantly
raised in the bicarbonate trial when compared
with that in the NaCl trial. Further studies are
required to determine whether intravascular volume is responsible for the increased
performance.
A greater understanding of acid–base balance
during rest and exercise can be gained by reading
Jackson (1990), Jones (1990), Lindinger and
Heigenhauser (1990) and Heigenhauser et al.
(1990).
The work of Jervell (1928), Dennig et al. (1931)
and Dill et al. (1932) was, by and large, forgotten
by the coaching and scientific communities. The
modern era of the study of acid–base balance
during exercise performance essentially began in
the 1970s, with publication of the work of Jones et
al. (1977). These workers studied five men who
acted as their own controls, through treatments
consisting of either a placebo (calcium carbonate), 0.3 g ammonium chloride (acidic) per kilogram of body mass, or sodium bicarbonate in
the same dosage. All doses were taken after an
overnight fast and over a 3-h time period. The
exercise consisted of cycle ergometry utilizing
three different protocols: 20 min at both 33% and
66% of previously determined maximum oxygen
.
uptake (Vo2max.), followed by exercise to exhaus.
tion at 95% Vo2max., without rest in between. Time
.
to exhaustion at the 95% Vo2max. power output
level was approximately 4 min for the control
condition. In the bicarbonate treatment, exhaustion time was approximately twice that of the
control, whilst in the acidic condition, it was
about half the control time. Blood lactate concentration in the bicarbonate treatment was significantly greater (P < 0.01) than the control at both
the 66% power output level and at exhaustion. In
the ammonium chloride condition, blood lactate
levels were significantly lower in these two work
periods. Blood pH was consistently higher in
the bicarbonate treatment group and lower in
the ammonium chloride treatment than in the
bicarbonate and citrate
control during the dosing phase and throughout
the exercise. At the start of the final exercise
phase, pH in the bicarbonate treatment group
was about 7.41, while the control was 7.34 and
the acidic treatment was 7.19. At exhaustion, the
pH was 7.34, 7.26 and 7.14, respectively.
A number of studies in the early 1980s suggested that ingestion of sodium bicarbonate
could be effective in performance enhancement.
Wilkes et al. (1983), conducting a field type study,
examined six well-trained competitive 800-m
runners and compared the effects of sodium
bicarbonate, placebo (calcium carbonate) and
control treatments. The substances were both
given over a 2-h period in a dose of 300 mg · kg-1
body mass and water was taken ad libitum
(average intake was 504 ml). Each subject completed their normal 30-min warm-up prior to the
race. Each runner completed all three protocols,
thus acting as his own control. In the bicarbonate
condition, runners were 2.9 s faster, on average,
than in the control condition (P < 0.05), while the
control and placebo results were not significantly
different. Control, placebo and bicarbonate mean
times (min : s) were, respectively, 2 : 05.8, 2 : 05.1
and 2 : 02.9. While not particularly fast, the
difference between control and bicarbonate
(2.9 s) might mean the difference between first
and last place within a race.
In work from our own laboratory, Goldfinch et
al. (1988) saw improvements in 400-m race performance due to ingestion of sodium bicarbonate
in six competitive, trained runners. The experimental design was similar to that of Wilkes et al.
(1983), but with a major difference: the bicarbonate dose was 400 mg · kg-1 body mass. This was
done deliberately in order to eliminate ambiguities around dose size. The control, the calcium
carbonate placebo or the experimental treatment
were given over a 1-h period in a low-energy
drink to try to disguise the taste. Each of the subjects ran as part of a two-man competitive race to
simulate, as closely as possible, real competition.
The mean time of the bicarbonate ingestion
group was 56.94 s, and was significantly better by
1.25 s (P < 0.005) than the control and placebo,
397
which were not different from each other. The
time difference was equivalent to approximately
a 10-m distance at the finish, again enough to
warrant a first or last place finish.
A number of studies have also shown
NaHCO3 loading to be ineffective in delaying
fatigue or improving performance. Katz et al.
(1984) exercised eight trained men at 125% of
.
their predetermined Vo2max. in either a bicarbonate or control condition. Bicarbonate was given
in a dose of 200 mg · kg-1 body mass, while the
placebo consisted of NaCl. No significant difference between the two conditions was noticed. In
the bicarbonate condition, subjects cycled for
100.6 s, while with the placebo, the time to
exhaustion was 98.6 s. These results are of interest, since even though pH and base excess (which
is the measure of extra base above normal, principally bicarbonate ions) after correction for
haemoglobin content (Guyton & Hall 1981) were
significantly elevated following ingestion of
sodium bicarbonate, no improvement in performance was seen. In other words, the bicarbonate
increased the amount of buffer available to the
body, but this was not used. The pH values seen
after exercise in this experiment were lower in
the control condition, possibly suggesting the
subjects could have worked harder in the experimental condition, thus utilizing the extra buffer
available. In another study from the same laboratory, Horswill and colleagues (1988) found no
difference in performance when subjects performed four bouts of intense, 2-min sprint exercise. Again, the levels of blood bicarbonate were
significantly elevated in two of the conditions
tested prior to the performance tests, as was
pH, but again this increased buffering capacity
did not result in improved performance by the
subjects.
A number of practical problems have arisen in
the study of sodium bicarbonate loading due to
the nature of the experimental paradigms used.
That is, there is no single method employed by
researchers in order to detect any benefit. While
this is a natural process in research, from a practical sporting point of view it is a hindrance, as ath-
398
nutrition and exercise
letes are unable to make concrete choices about,
for example, how much sodium bicarbonate/
citrate should be used or over what time periods
it is effective.
Several authors (Wijnen et al. 1984; McKenzie
et al. 1986; Parry-Billings & MacLaren 1986) have
used a research paradigm involving multiple
exercise bouts interspersed with rest/recovery.
The exercise periods have varied, but have been
between 30 and 60 s with rest/recovery periods
from 60 s (Wijnen et al. 1984; McKenzie et al. 1986)
to 6 min (Parry-Billings & MacLaren 1986). The
results of this work have generally been inconclusive. Wijnen et al. (1984) infused bicarbonate
intravenously in one of two doses (180 or 360 mg·
kg-1 body mass) while subjects rode a cycle
ergometer for 60 s with a rest period of 60 s, and
repeated this a further three times. Both dosages
of NaHCO3 significantly raised pH (P < 0.01)
above the control condition in a manner which
was dependent upon the dosage. However, as
has been shown in some studies previously, the
increased pH did not lead to an increase in performance in all subjects. McKenzie et al. (1986)
used a protocol similar to that of Wijnen et al.
(1984), but used dosages of either 150 or 300 mg ·
kg-1 body mass. Blood pH and blood bicarbonate
levels increased in both experimental conditions
when compared with the control treatment.
When time to fatigue and the amount of work
done were compared, the two experimental conditions both increased these parameters but with
no difference between the two dose levels. In
another interval type paradigm, Parry-Billings
and MacLaren (1986) again found that a dose of
300 mg · kg-1 body mass had no effect on 30 s of
exercise when interspersed with 6-min recovery
periods. Again, this was despite an increase in
blood bicarbonate levels of approximately
8 mmol · l-1 above control levels.
Bicarbonate dose and exercise
Various studies have suggested, either directly or
indirectly, that there is a minimum level of
sodium bicarbonate ingestion needed to improve
performance. Katz et al. (1984) found no differ-
ences in performance time on a cycle ergometer
.
test at 125% Vo2max. after subjects ingested 200 mg
NaHCO3 · kg-1 body mass despite significant (P <
0.001) rises in pH prior to exercise. Blood
bicarbonate and base excess also significantly
increased and the hydrogen ion to lactate ratio
(nmol/mmol) was significantly lower in the
experimental trial than in the control trial, all of
which suggest that buffering was available but
for some reason was not effective. Horswill et al.
(1988) also found no improvement in exercise
performance with dosages between 100 and
200 mg · kg-1. In this interesting experiment, the
authors (Horswill et al. 1988) had subjects undertake four 2-min sprint tests after they had consumed either a placebo or one of three doses
of sodium bicarbonate (100, 150 or 200 mg · kg-1).
Pretest plasma bicarbonate levels were not different, nor were they different between the
placebo and 100 mg · kg-1 groups 1 h after the
test, but they were significantly increased in
the 150 and 200 mg · kg-1 conditions. Even
though plasma bicarbonate levels increased with
the latter dosages, subjects were still unable to
use the increased buffer capacity given by the
NaHCO3.
In a study from our laboratory (McNaughton
1992a), we attempted to extend the work of
Horswill et al. (1988) to determine which dosage
was most efficacious. We also decided to use an
exercise bout of 60 s, since previous experience
had led us to believe this would elicit high blood
lactate levels and low levels of blood pH. Each of
the subjects undertook a total of seven tests: one
control, one placebo and one of five doses of
NaHCO3 (100, 200, 300, 400 and 500 mg · kg-1)
(Fig. 29.3). These were undertaken in a random
fashion, after the control test, which was always
first. The ingestion of sodium bicarbonate as a
dose of 100 mg · kg-1 did not increase blood bicarbonate levels, in agreement with the work of
Horswill et al. (1988). Larger doses had the effect
of significantly increasing the levels of blood
bicarbonate.
Unlike Horswill et al. (1988), this author found
a significant increase in performance with a dose
of 200 mg · kg-1 and this improvement increased
bicarbonate and citrate
399
Blood bicarbonate (mM)
40
30
20
10
0
Control
Placebo
100
200
300
Level of bicarbonate ingestion (mg)
400
500
Fig. 29.3 Bicarbonate levels in the blood after the ingestion of different levels of sodium bicarbonate, before and
after exercise. 䊏, before exercise, , after ingestion; , after exercise. From McNaughton (1992a).
in a linear fashion with increasing dosage.
Improvements in performance, however, did not
follow the increasing levels of blood bicarbonate,
with the highest amount of work being performed after a dosage of 300 mg · kg-1, although
there were no significant differences between
300, 400 or 500 mg · kg-1.
In another approach to answering the question
of sodium bicarbonate and performance, Kindermann et al. (1977) intravenously induced
metabolic alkalosis by infusing an 8.4% sodium
bicarbonate solution until the arterial pH
reached 7.5. They then had subjects exercise by
running 400 m, but found no difference in performance when they compared them with performance in a control run. Similarly, Wijnen et al.
(1984) found no differences in the fifth bout of an
interval exercise regimen on a bicycle ergometer
when NaHCO3 was administered intravenously
in a dosage of 180 mg · kg-1. Again, this was
despite finding a significant increase in pH in the
30 min prior to the exercise test. In a second stage
of this study (Wijnen et al. 1984), the authors used
a higher dosage and found that a greater number
(80%) of their subjects performed significantly
better than in the control trial.
Exercise time
A further question to be asked is, ‘Over what
time period is sodium bicarbonate effective?’
The plethora of research papers examining the
ergogenic benefits of NaHCO3 have used time
periods ranging from 30 s (McCartney et al. 1983)
to 6 min (McNaughton & Cedaro 1991a).
McCartney and colleagues (1983) had six
subjects perform 30 cycle ergometer tests in a
control, an alkalosis and two acidotic trials, one
caused by ammonium chloride ingestion and a
respiratory acidosis trial caused by inhalation of
a 5% CO2 mixture. There were small, but not
significant, differences in the amount of work
accomplished by the subjects. In the alkalotic
trial, the work accomplished was 101% of
control, suggesting a difference of 0.3 s (over a
30-s trial), not statistically different, but certainly
practically so!
We (McNaughton et al. 1991) investigated the
effects of bicarbonate loading on anaerobic work
and maximal power output during exercise of
60 s duration. The dosage of NaHCO3 used was
400 mg · kg-1 body mass with a control and
placebo trial which were randomly assigned to
400
nutrition and exercise
each of the eight subjects. The work output
increased significantly (P < 0.01) in the experimental condition when compared with the
control or placebo condition (9940, 9263 and 9288
J, respectively). In the NaHCO3 trial, pretest
blood bicarbonate levels increased significantly
above either the resting or control/placebo
pretest levels. An interesting finding in this study
was that the peak power, as measured in watts,
achieved by the subjects, also increased significantly (P < 0.05) in the experimental condition
when compared with that in the control or
placebo conditions.
In order to examine more closely the time
periods over which sodium bicarbonate can be
used as an ergogenic aid, McNaughton (1992b)
studied four different time periods (10, 30, 120
and 240 s) with a dosage of 300 mg · kg-1 body
mass. Subjects ingested sodium bicarbonate or a
placebo and undertook a control test. There were
eight male subjects in each time group, and each
subject undertook three test sessions. As is usual
with a dosage of this size (300 mg · kg-1), the
blood bicarbonate levels were increased in the
experimental trial when compared with those in
either the control or placebo trials. This was also
true for the base excess and pH measurements.
However, the work and power data collected
during the cycle ergometer tests over the four
time periods were only significantly different in
the latter two time periods (120 and 240 s), even
though the blood lactate levels in both the 10and 30-s trial were significantly higher after exercise than the pre-exercise levels.
This work is in agreement with several other
studies suggesting that NaHCO3 loading is
not effective for short-term anaerobic work
(McCartney et al. 1983; Katz et al. 1984) but that it
is effective for longer-term work (Wilkes et al.
1983; McKenzie et al. 1986; Goldfinch et al. 1988).
McNaughton and Cedaro (1991) found the same
dosage of sodium bicarbonate to be effective in
rowing performance of 6 min duration using elite
rowers.
Sodium citrate
A number of authors (Simmons & Hardt 1973;
Parry-Billings & MacLaren 1986; McNaughton
1990; McNaughton & Cedaro 1991b) have used
sodium citrate as an alkalizing agent rather than
sodium bicarbonate. The results of work from
our laboratory (McNaughton 1990) would
suggest that sodium citrate is an effective
ergogenic substance when given in dosages
between 300 and 500 mg · kg-1 body mass, with
anaerobic capacity increasing in a linear fashion
in relation to these doses (McNaughton 1990). In
relation to duration of exercise, the high dosage
of sodium citrate appears to be effective in time
periods of between 2 and 4 min (McNaughton &
Cedaro 1991b). Sodium citrate does not appear to
be an effective ergogen when used with shortterm (30 s) maximal exercise (Parry-Billings &
MacLaren 1986; McNaughton & Cedaro 1991b).
A recent article (Potteiger et al. 1996) has also suggested that large doses (500 mg · kg-1 body mass)
of sodium citrate may improve 30-km cycling
performance. These competitive cyclists completed the placebo 30-km trial in 3562.3 ± 108.5 s,
while in the citrate trial they completed the same
distance in 3459.6 ± 97.4 s. More work needs to be
undertaken to determine if this regimen can be
applied to other endurance activities.
Some subjects have reported short-term gastrointestinal distress as a side-effect of sodium
bicarbonate/citrate use (Wilkes et al. 1983;
Goldfinch et al. 1988; McNaughton & Cedaro
1991b). Other possible side-effects have been
noted including gastric rupture (Downs &
Stonebridge 1989; Reynolds 1989), muscle
spasms and cardiac arrhythmias (Reynolds 1989;
Heigenhauser & Jones 1991).
Although detection of sodium bicarbonate and
citrate is difficult, several authors (Wilkes et al.
1983; Gledhill 1984; McKenzie 1988) have suggested it is possible to detect, and therefore
control, using existing procedures (urine sample,
post-exercise). The work of McKenzie (1988) is
most detailed, with subjects providing a postexercise urine sample. Of the 65 subjects, no subjects who had ingested NaHCO3 had a urinary
bicarbonate and citrate
pH of less than 6.8, whereas in the placebo group,
none was greater than a pH of 7.0. McKenzie
(1988) suggested using a pH of 7.0 as a baseline,
which would have captured 92% of the subjects
using NaHCO3 in his study. Even though this
was the case in the McKenzie (1988) study, other
factors, such as vomiting, a high-carbohydrate
diet (results in metabolic alkalosis) (Greenhaff et
al. 1987a, 1987b, 1988a, 1988b), a high-protein
diet (results in metabolic acidosis; Maughan &
Greenhaff 1991), a vegetarian diet and a low
glomerular filtration rate (Kiil 1990), can change
the alkalinity of the urine which normally ranges
from 4.5 to 8.2, thus giving a false positive result
(for a review, see Charney & Feldman 1989). It
would be virtually impossible to detect confidently those who had used a buffering agent to
improve performance.
Conclusion
Several reviews on the use of substances to
induce metabolic alkalosis in order to improve
short-term maximal performance have been
written (Gledhill 1984; Heigenhauser & Jones
1991; Linderman & Fahey 1991; Maughan &
Greenhaff 1991; Williams 1992; McNaughton et
al. 1993; Linderman & Gosselink 1994). Although
no firm conclusions can be drawn from the
plethora of research conducted, there does
appear to be some general agreement on a
number of factors. Firstly, both sodium bicarbonate and sodium citrate are effective buffering
agents. Second, there is a minimum level of
NaHCO3 or sodium citrate ingestion below
which no improvement in performance takes
place and this is approximately 200 mg · kg-1
body mass; the optimum dosage would appear
to be only slightly higher, at 300 mg · kg-1 body
mass. Dosages higher than 300 mg · kg body mass
do not appear to have any greater benefit to performance. Higher dosages of sodium citrate may
be more effective than sodium bicarbonate, but
this has not yet been confirmed. Thirdly, these
buffering agents have no effect on performance
of less than 30 s but do enhance performance
between 1 and 10 min. Finally, these substances
401
may be effective in enhancing high-intensity
endurance performance but more work needs to
be conducted.
Practical implications
Many substances used by athletes to improve
performance have been banned by such bodies
as the International Olympic Committee (IOC).
Presently, no ban exists for the use of sodium
bicarbonate or sodium citrate and they are hard
to detect. However, their use may be considered
a violation of the IOC Doping Rule which states,
at least in part, that athletes shall not use any
physiological substance taken in an attempt to
artificially enhance performance. An athlete may
attempt to legitimize the use of these substances,
however, by likening it to the use of carbohydrate loading. If athletes decide to use these
buffering agents, then they should do so for
short-term, high-intensity exercise only and
should use dosages of approximately 300 mg ·
kg-1 body mass dose. The substances should be
taken in or with fluid, preferably water, and in
large quantities (0.5 l or greater). Subjects should
be made familiar with possible side-effects prior
to usage.
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