The effects of sodium citrate on repeated maximal cycling bouts

Introduction
<strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on repeated maximal cycling bouts
M.J. Crowe* James Cook University, Townsville, Australia
“Fatigue during anaerobic performance is <strong>of</strong>ten the result <strong>of</strong> lactic acid build up and subsequent acidosis. Sodium bicarbonate is one <strong>of</strong> the
main buffers <strong>of</strong> acid in the body and it acts by neutralising protons to form carbon dioxide and water. Oral ingestion <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> is known
to increase blood bicarbonate levels and blood pH (Tiryaki & Atterbom, 1995; Potteiger et al., 1996; Ball & Maughan, 1997). However, the
possible ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on anaerobic performance remain equivocal.
In general, studies investigating doses <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> <strong>of</strong> less than 0.4 g/kg body weight have failed to show any ergogenic effect. A 0.3 g/kg
body weight dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> did not affect mean and peak power and total work in a 3 x 30 s Wingate anaerobic test (Parry-Billings &
MacLaren, 1986), repeated 45 s bouts <strong>of</strong> cycling (van Someren et al., 1998), cycle time to exhaustion at 100% VO 2 max (Ball & Maughan, 1997)
or 600 m run time (Tiryaki & Atterbom, 1995) compared to a placebo.
Although more positive evidence exists for <strong>sodium</strong> <strong>citrate</strong> as an ergogenic aid at or above doses <strong>of</strong> 0.4 g/kg body weight, there are still
contradictory findings. Isometric knee extensions were sustained for significantly longer after ingestion <strong>of</strong> 0.4 g/kg body weight <strong>sodium</strong> <strong>citrate</strong>
compared to a placebo (Hausswirth et al., 1995). Run time to exhaustion at 120% VO 2 peak was also significantly increased in comparison to a
placebo with 0.5 g/kg body weight <strong>sodium</strong> <strong>citrate</strong> (Linossier et al., 1997). Interestingly, two studies have shown elevated blood lactate levels
following intense exercise with 0.5 g/kg body weight <strong>sodium</strong> <strong>citrate</strong> in comparison to a placebo but no increase in performance (Ibanez et al.,
1995; Potteiger et al., 1996). Performance on five repeated 60 s cycling sprints was also unaffected by a 0.5 g/kg body weight dose <strong>of</strong> <strong>sodium</strong>
<strong>citrate</strong> compared to a placebo (Cox & Jenkins, 1994).
Timing <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> ingestion relative to commencement <strong>of</strong> exercise may be partly responsible for the lack <strong>of</strong> consistent findings with
higher doses <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong>. Potteiger et al. (1996) investigated the timing <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> absorption and reported that blood pH was
significantly increased 50 minutes after consumption <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> and that pH peaked at 100-120 minutes post-ingestion. A number <strong>of</strong>
studies utilising a dose <strong>of</strong> 0.4 g/kg body weight or greater have shown positive ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> with 90 or 120 minutes
between ingestion and exercise (Hausswirth et al., 1995; Linossier et al., 1997; McNaughton & Cedero, 1992). Ibanez et al. (1995) used a
three-hour absorption time which may have been too long as there were no reported ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> in this study. However,
Cox and Jenkins (1994) and Potteiger et al. (1996) also used 90 and 120-minute absorption times respectively and found no ergogenic <strong>effects</strong>
<strong>of</strong> <strong>sodium</strong> <strong>citrate</strong>. Thus, other factors must underlie the variable <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on anaerobic performance.
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<strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on repeated maximal cycling bouts
M.J. Crowe* James Cook University, Townsville, Australia
Duration <strong>of</strong> exercise may play a role in determining the effectiveness <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> as an ergogenic. McNaughton and Cedero (1992) found
a positive effect <strong>of</strong> 0.5 g/kg body weight <strong>sodium</strong> <strong>citrate</strong> on maximal cycling <strong>of</strong> 120 s and 240 s duration but no effect when exercise duration was
10 s or 30 s. <strong>The</strong>refore, exercise must be <strong>of</strong> sufficient duration to elicit a substantial lactic acid response.
Statement <strong>of</strong> the Problem
Equivocal evidence exists as to the potential ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on anaerobic performance. Doses <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> equal to or
greater than 0.4 g/kg body weight with an absorption time <strong>of</strong> 90-120 minutes and exercise duration longer than 30 s appear to enhance
anaerobic performance. <strong>The</strong>refore, this study aimed to investigate the <strong>effects</strong> <strong>of</strong> a 0.5 g/kg body weight dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on three
repeated 30 s maximal cycling bouts with an absorption time <strong>of</strong> 90 minutes. Under these conditions, it was expected that <strong>sodium</strong> <strong>citrate</strong> would
cause an increase in peak power, total work and blood lactate in comparison to a placebo.
Methods
<strong>The</strong> subjects in this study were 20 healthy students (12 male and 8 female). <strong>The</strong> mean (± SD) age <strong>of</strong> the subjects was 22.3 ± 3.8 years and
mean body weight was 75.5 ± 18.9 kg. Participation was on a volunteer basis with subjects providing informed consent after the procedures <strong>of</strong>
the study were explained. <strong>The</strong> study was approved by the James Cook University Ethics Committee.
<strong>The</strong> subjects first performed a familiarisation session where they were asked to warm up on a cycle ergometer (Repco) at a moderate pace for
3-5 minutes. <strong>The</strong> subjects then commenced a 3 x 30 s maximal cycle test with verbal encouragement from the experimenters and 30 s rest
periods between bouts. No measurements were taken during this session.
<strong>The</strong> subjects returned to the laboratory seven days after the familiarisation session to perform baseline testing. <strong>The</strong> protocol for baseline
testing was identical to that <strong>of</strong> the familiarisation session. Peak heart rate was recorded for each 30 s exercise bout using a heart rate monitor
(Polar Vantage). Peak power (watts/kg) and total work (joules/kg) were recorded using a Repco Supermonitor for each exercise bout. A finger
prick blood sample was taken at three and six minutes after completion <strong>of</strong> the third 30 s exercise bout to ascertain blood lactate levels using an
Acusport blood lactate tester. <strong>The</strong> highest blood lactate value from the three and six minute samples was used in the analysis. <strong>The</strong> subjects
were encouraged to continue cycling at a slow pace for several minutes to warm down after completion <strong>of</strong> the third 30 s exercise bout.
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<strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on repeated maximal cycling bouts
M.J. Crowe* James Cook University, Townsville, Australia
Seven days after baseline testing, the subjects returned to the laboratory and consumed either a 0.5 g/kg body weight dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong>
dissolved in a cordial drink (n=10, 7 males and 3 females) or a cordial–<strong>sodium</strong> chloride (0.045 g/kg) placebo (n=10, 5 males and 5 females).
Allocation <strong>of</strong> <strong>citrate</strong> or placebo was performed in a double-blind manner. A period <strong>of</strong> 90 minutes elapsed between consumption <strong>of</strong> the cordial
drink and retesting with the 3 x 30 s maximal cycle test. Testing was performed in an identical manner to the baseline testing.
Comparison <strong>of</strong> peak power, total work and peak blood lactate was made between the <strong>citrate</strong> and placebo groups and the baseline and retest
sessions using a two-way repeated measures ANOVA. Maximal heart rate was compared between all six 30 s exercise bouts using a one-way
ANOVA. Statistical significance was set at p 0.05). This indicates a consistent exercise effort from
the subjects on each <strong>of</strong> the three bouts at each testing session.
Oral ingestion <strong>of</strong> 0.5 g/kg body weight <strong>sodium</strong> <strong>citrate</strong> did not enhance performance on the repeated maximal cycling test. Neither peak power
nor total work was significantly higher in the <strong>sodium</strong> <strong>citrate</strong> group compared to the placebo group on any <strong>of</strong> the three exercise bouts (p > 0.05;
see Table 1). Furthermore, there was no increase in peak power or total work from baseline to retest for the subjects in the <strong>sodium</strong> <strong>citrate</strong> group
(p > 0.05; see Table 1). Similarly, the placebo group did not improve their peak power or total work from the baseline testing session to the
repeat testing session suggesting that there were no anaerobic adaptations between exercise sessions (p > 0.05; see Table 1).
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<strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on repeated maximal cycling bouts
M.J. Crowe* James Cook University, Townsville, Australia
repeat testing sessions for each 30 s exercise bout.
Peak Power (W/kg) Placebo Sodium Citrate
Baseline Testing
Bout 1 12.5 ± 2.0 13.2 ± 2.3
Repeat Testing
Total Work (j/kg)
Baseline Testing
Repeat Testing
Bout 2 8.3 ± 1.9 8.9 ± 1.5
Bout 3 6.5 ± 1.4 7.2 ± 1.7
Bout 1 12.2 ± 1.7 12.5 ± 2.8
Bout 2 8.0 ± 2.1 8.7 ± 2.0
Bout 3 7.0 ± 1.3 7.7 ± 2.0
Bout 1 270.1 ± 41.5 290.3 ± 45.4
Bout 2 169.9 ± 30.0 192.0 ± 42.4
Bout 3 134.9 ± 25.2 172.6 ± 47.3
Bout 1 271.7 ± 40.8 280.2 ± 57.4
Bout 2 167.6 ± 30.9 193.1 ± 44.0
Bout 3 143.0 ± 24.6 146.9 ± 59.1
Table 1. Mean peak power (W/kg) and total work (j/kg) for the <strong>sodium</strong> <strong>citrate</strong> and placebo groups
at the baseline and repeat testing sessions for each 30 s exercise bout.
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<strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on repeated maximal cycling bouts
Blood Lactate (mmol/l)
20
18
16
14
12
10
8
6
4
2
0
M.J. Crowe* James Cook University, Townsville, Australia
Baseline Repeat
Testing Session
Figure 1. Mean peak blood lactate concentrations (mmol/l) for all subjects at the baseline and repeat testing sessions.
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<strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on repeated maximal cycling bouts
M.J. Crowe* James Cook University, Townsville, Australia
<strong>The</strong>re was no effect <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> ingestion on the peak blood lactate concentration when compared to the placebo (p > 0.05). Furthermore,
there was no significant increase in peak blood lactate between baseline testing and repeat testing for the subjects in the <strong>sodium</strong> <strong>citrate</strong> group
(p > 0.05). However, when the <strong>sodium</strong> <strong>citrate</strong> and placebo subjects were grouped together, there was a significant increase in peak blood
lactate from 12.8 ± 3.0 mmol/l at the initial baseline testing session to 14.5 ± 3.5 mmol/l at the repeat testing session (p = 0.033; see Figure 1).
Sodium <strong>citrate</strong> is <strong>of</strong>ten used in preference to <strong>sodium</strong> bicarbonate because <strong>of</strong> a reported lower incidence <strong>of</strong> gastrointestinal discomfort (Linderman
& Fahey, 1991). It was therefore interesting to note that 6 <strong>of</strong> the 10 subjects who consumed <strong>sodium</strong> <strong>citrate</strong> in this study reported mild to
moderate diarrhoea. <strong>The</strong> <strong>sodium</strong> <strong>citrate</strong> was delivered to the subjects in 600 ml <strong>of</strong> cordial-flavoured water. It may be possible that this was
insufficient fluid to avoid the gastrointestinal upset experienced by the subjects.
Although the findings <strong>of</strong> this study are in contrast to those <strong>of</strong> Hausswirth et al. (1995) and Linossier et al. (1997) who reported an ergogenic
effect <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on short-term, intense exercise, they are consistent with the findings <strong>of</strong> Cox and Jenkins (1994), Ibanez et al. (1995) and
Potteiger et al. (1996) who found no ergogenic effect <strong>of</strong> 0.5 g/kg oral <strong>sodium</strong> <strong>citrate</strong> on short-term, intense exercise. In contrast to Potteiger
(1996) and Ibanez et al. (1995), however, is the fact that blood lactate levels were no higher as a result <strong>of</strong> taking <strong>sodium</strong> <strong>citrate</strong>. Sodium <strong>citrate</strong>
is known to alkalise the blood (Tiryaki & Atterbom, 1995; Potteiger et al., 1996; Ball & Maughan, 1997) facilitating a pH gradient to draw H + ions
and lactate from the muscle compartment into the blood. Sodium <strong>citrate</strong> does not alkalise the muscle compartment with a 90 minute absorption
time at a dose <strong>of</strong> 0.5 g/kg body weight (Linossier et al., 1997). Thus, it is unlikely that the muscle compartment would have been alkalised in this
study. Under these conditions, <strong>sodium</strong> <strong>citrate</strong> can only reduce muscle acidosis by drawing H + and lactate from the muscle cytosol into the
blood. However, this is unlikely to have happened here as higher blood lactate levels were not recorded with <strong>sodium</strong> <strong>citrate</strong>, nor were peak
power or total work elevated as would be expected with increased removal <strong>of</strong> H + from the muscle compartment. <strong>The</strong> subjects in this study were
reasonably anaerobically trained reaching average post-exercise blood lactate levels <strong>of</strong> 13.6 ± 3.3 mmol/l, concentrations that would be
correlated with a significant drop in pH (not measured here). Thus, if <strong>sodium</strong> <strong>citrate</strong> were an effective buffer able to augment the natural buffers
<strong>of</strong> the body, it would have been expected to show some effect here.
Conclusions
<strong>The</strong> results <strong>of</strong> this study showed that a 0.5 g/kg body weight dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> had no ergogenic effect on male and female subjects
performing three maximal 30 s cycling bouts compared to a placebo. Peak blood lactate concentrations were also unaffected by this dose <strong>of</strong>
<strong>sodium</strong> <strong>citrate</strong> under these conditions.
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References
<strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on repeated maximal cycling bouts
M.J. Crowe* James Cook University, Townsville, Australia
Ball, D. & Maughan, R. J. (1997) <strong>The</strong> effect <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> ingestion on the metabolic response to intense exercise following diet manipulation
in man. Exp. Physiol. 82(6): 1041-1056.
Cox, G. & Jenkins, D. G. (1994) <strong>The</strong> physiological and ventilatory responses to repeated 60 s sprints following <strong>sodium</strong> <strong>citrate</strong> ingestion. J.
Sports. Sci. 12(5): 469-475.
Hausswirth. C., Bigard, A. X., Lepers, R., Berthelot, M. & Guezennec, C. Y. (1995) Sodium <strong>citrate</strong> ingestion and muscle performance in acute
hypobaric hypoxia. Eur. J. Appl. Physiol. 71(4): 362-368.
Ibanez, J., Pullinen, T., Gorostiaga, E., Postigo, A. & Mero, A. (1995) Blood lactate and ammonia in short-term anaerobic work following
induced alkalosis. J. Sports Med. Phys. Fitness. 35(3): 187-193.
Linderman, J. K. & Fahey, T. D. (1991) Sodium bicarbonate ingestion and exercise performance: an update. Sports Med. 11: 71-77.
Linossier, M. T., Dormois, D., Bregere, P., Geyssant, A. & Denis, C. (1997) Effect <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on performance and metabolism <strong>of</strong> human
skeletal muscle during supramaximal cycling exercise. Eur. J. Appl. Physiol. 76(1): 48-54.
McNaughton, L. & Cedero, R. (1992). Sodium <strong>citrate</strong> ingestions and its <strong>effects</strong> on maximal anaerobic exercise <strong>of</strong> different durations. Eur. J.
Appl. Physiol. 64(1): 36-41.
Parry-Billings, M. & MacLaren, D. P. (1986) <strong>The</strong> effect <strong>of</strong> <strong>sodium</strong> bicarbonate and <strong>sodium</strong> <strong>citrate</strong> ingestion on anaerobic power during intermittent
exercise. Eur. J. Appl. Physiol. 55(5): 524-529.
Potteiger, J. A., Webster, M. J., Nickel, G. L., Haub, M. D. & Palmer, R. J. (1996) <strong>The</strong> <strong>effects</strong> <strong>of</strong> buffer ingestion on metabolic factors related to
distance running performance. Eur. J. Appl. Physiol. 72(4): 365-371.
Tiryaki, G. R. & Atterbom, H. A. (1995) <strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> bicarbonate and <strong>sodium</strong> <strong>citrate</strong> on 600 m running time <strong>of</strong> trained females. J.
Sports Med. Phys. Fitness. 35(3): 194-198.
van Someren, K., Fulcher, K., McCarthy, J., Moore, J., Horgan, G. & Langford, R. (1998) An investigation into the <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong>
ingestion on high-intensity exercise performance. Int. J. Sports Nutr. 8(4): 356-363.
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<strong>The</strong> <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on repeated maximal cycling bouts
M.J. Crowe*
James Cook University, Townsville, Australia
INTRODUCTION: Fatigue during anaerobic performance is <strong>of</strong>ten the result <strong>of</strong> lactic acid build up and subsequent
acidosis. Sodium bicarbonate is one <strong>of</strong> the main buffers <strong>of</strong> acid in the body and it acts by neutralising protons to form carbon
dioxide and water. Oral ingestion <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> is known to increase blood bicarbonate levels and blood pH (Tiryaki &
Atterbom, 1995; Potteiger et al., 1996; Ball & Maughan, 1997). However, the possible ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on
anaerobic performance remain equivocal.
In general, studies investigating doses <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> <strong>of</strong> less than 0.4 g/kg body weight have failed to show any
ergogenic effect. A 0.3 g/kg body weight dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> did not affect mean and peak power and total work in a 3 x
30 s Wingate anaerobic test (Parry-Billings & MacLaren, 1986), repeated 45 s bouts <strong>of</strong> cycling (van Someren et al., 1998),
cycle time to exhaustion at 100% VO2 max (Ball & Maughan, 1997) or 600 m run time (Tiryaki & Atterbom, 1995) compared to
a placebo.
Although more positive evidence exists for <strong>sodium</strong> <strong>citrate</strong> as an ergogenic aid at or above doses <strong>of</strong> 0.4 g/kg body weight,
there are still contradictory findings. Isometric knee extensions were sustained for significantly longer after ingestion <strong>of</strong> 0.4
g/kg body weight <strong>sodium</strong> <strong>citrate</strong> compared to a placebo (Hausswirth et al., 1995). Run time to exhaustion at 120% VO2 peak
was also significantly increased in comparison to a placebo with 0.5 g/kg body weight <strong>sodium</strong> <strong>citrate</strong> (Linossier et al., 1997).
Interestingly, two studies have shown elevated blood lactate levels following intense exercise with 0.5 g/kg body weight
<strong>sodium</strong> <strong>citrate</strong> in comparison to a placebo but no increase in performance (Ibanez et al., 1995; Potteiger et al., 1996).
Performance on five repeated 60 s cycling sprints was also unaffected by a 0.5 g/kg body weight dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong>
compared to a placebo (Cox & Jenkins, 1994).
Timing <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> ingestion relative to commencement <strong>of</strong> exercise may be partly responsible for the lack <strong>of</strong>
consistent findings with higher doses <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong>. Potteiger et al. (1996) investigated the timing <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong>
absorption and reported that blood pH was significantly increased 50 minutes after consumption <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> and that
pH peaked at 100-120 minutes post-ingestion. A number <strong>of</strong> studies utilising a dose <strong>of</strong> 0.4 g/kg body weight or greater have
shown positive ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> with 90 or 120 minutes between ingestion and exercise (Hausswirth et al.,
1995; Linossier et al., 1997; McNaughton & Cedero, 1992). Ibanez et al. (1995) used a three-hour absorption time which
may have been too long as there were no reported ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> in this study. However, Cox and
Jenkins (1994) and Potteiger et al. (1996) also used 90 and 120-minute absorption times respectively and found no
ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong>. Thus, other factors must underlie the variable <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on anaerobic
performance.
Duration <strong>of</strong> exercise may play a role in determining the effectiveness <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> as an ergogenic. McNaughton and
Cedero (1992) found a positive effect <strong>of</strong> 0.5 g/kg body weight <strong>sodium</strong> <strong>citrate</strong> on maximal cycling <strong>of</strong> 120 s and 240 s duration
but no effect when exercise duration was 10 s or 30 s. <strong>The</strong>refore, exercise must be <strong>of</strong> sufficient duration to elicit a substantial
lactic acid response.
STATEMENT OF THE PROBLEM: Equivocal evidence exists as to the potential ergogenic <strong>effects</strong> <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on
anaerobic performance. Doses <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> equal to or greater than 0.4 g/kg body weight with an absorption time <strong>of</strong> 90-
120 minutes and exercise duration longer than 30 s appear to enhance anaerobic performance. <strong>The</strong>refore, this study aimed
to investigate the <strong>effects</strong> <strong>of</strong> a 0.5 g/kg body weight dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on three repeated 30 s maximal cycling bouts with
an absorption time <strong>of</strong> 90 minutes. Under these conditions, it was expected that <strong>sodium</strong> <strong>citrate</strong> would cause an increase in
peak power, total work and blood lactate in comparison to a placebo.
METHODS: <strong>The</strong> subjects in this study were 20 healthy students (12 male and 8 female). <strong>The</strong> mean (± SD) age <strong>of</strong> the
subjects was 22.3 ± 3.8 years and mean body weight was 75.5 ± 18.9 kg. Participation was on a volunteer basis with
subjects providing informed consent after the procedures <strong>of</strong> the study were explained. <strong>The</strong> study was approved by the
James Cook University Ethics Committee.
<strong>The</strong> subjects first performed a familiarisation session where they were asked to warm up on a cycle ergometer (Repco)
at a moderate pace for 3-5 minutes. <strong>The</strong> subjects then commenced a 3 x 30 s maximal cycle test with verbal encouragement
from the experimenters and 30 s rest periods between bouts. No measurements were taken during this session.
<strong>The</strong> subjects returned to the laboratory seven days after the familiarisation session to perform baseline testing. <strong>The</strong>
protocol for baseline testing was identical to that <strong>of</strong> the familiarisation session. Peak heart rate was recorded for each 30 s
exercise bout using a heart rate monitor (Polar Vantage). Peak power (watts/kg) and total work (joules/kg) were recorded
using a Repco Supermonitor for each exercise bout. A finger prick blood sample was taken at three and six minutes after
completion <strong>of</strong> the third 30 s exercise bout to ascertain blood lactate levels using an Acusport blood lactate tester. <strong>The</strong> highest
blood lactate value from the three and six minute samples was used in the analysis. <strong>The</strong> subjects were encouraged to
continue cycling at a slow pace for several minutes to warm down after completion <strong>of</strong> the third 30 s exercise bout.
Seven days after baseline testing, the subjects returned to the laboratory and consumed either a 0.5 g/kg body weight
dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> dissolved in a cordial drink (n=10, 7 males and 3 females) or a cordial–<strong>sodium</strong> chloride (0.045 g/kg)
placebo (n=10, 5 males and 5 females). Allocation <strong>of</strong> <strong>citrate</strong> or placebo was performed in a double-blind manner. A period <strong>of</strong>

90 minutes elapsed between consumption <strong>of</strong> the cordial drink and retesting with the 3 x 30 s maximal cycle test. Testing was
performed in an identical manner to the baseline testing.
Comparison <strong>of</strong> peak power, total work and peak blood lactate was made between the <strong>citrate</strong> and placebo groups and the
baseline and retest sessions using a two-way repeated measures ANOVA. Maximal heart rate was compared between all
six 30 s exercise bouts using a one-way ANOVA. Statistical significance was set at p
0.05). This indicates a consistent exercise effort from the subjects on each <strong>of</strong> the three bouts at each testing session.
Oral ingestion <strong>of</strong> 0.5 g/kg body weight <strong>sodium</strong> <strong>citrate</strong> did not enhance performance on the repeated maximal cycling test.
Neither peak power nor total work was significantly higher in the <strong>sodium</strong> <strong>citrate</strong> group compared to the placebo group on any
<strong>of</strong> the three exercise bouts (p > 0.05; see Table 1). Furthermore, there was no increase in peak power or total work from
baseline to retest for the subjects in the <strong>sodium</strong> <strong>citrate</strong> group (p > 0.05; see Table 1). Similarly, the placebo group did not
improve their peak power or total work from the baseline testing session to the repeat testing session suggesting that there
were no anaerobic adaptations between exercise sessions (p > 0.05; see Table 1).
Table 1. Mean peak power (W/kg) and total work (j/kg) for the <strong>sodium</strong> <strong>citrate</strong> and placebo groups at the baseline and
repeat testing sessions for each 30 s exercise bout.
Peak Power (W/kg) Placebo Sodium Citrate
Baseline Testing
Bout 1 12.5 ± 2.0 13.2 ± 2.3
Repeat Testing
Total Work (j/kg)
Baseline Testing
Repeat Testing
Blood Lactate (mmol/l)
20
18
16
14
12
10
8
6
4
2
0
Bout 2 8.3 ± 1.9 8.9 ± 1.5
Bout 3 6.5 ± 1.4 7.2 ± 1.7
Bout 1 12.2 ± 1.7 12.5 ± 2.8
Bout 2 8.0 ± 2.1 8.7 ± 2.0
Bout 3 7.0 ± 1.3 7.7 ± 2.0
Bout 1 270.1 ± 41.5 290.3 ± 45.4
Bout 2 169.9 ± 30.0 192.0 ± 42.4
Bout 3 134.9 ± 25.2 172.6 ± 47.3
Bout 1 271.7 ± 40.8 280.2 ± 57.4
Bout 2 167.6 ± 30.9 193.1 ± 44.0
Bout 3 143.0 ± 24.6 146.9 ± 59.1
Baseline Repeat
Testing Session
Figure 1. Mean peak blood lactate concentrations (mmol/l) for all subjects at the baseline and repeat testing sessions.
<strong>The</strong>re was no effect <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> ingestion on the peak blood lactate concentration when compared to the placebo (p
> 0.05). Furthermore, there was no significant increase in peak blood lactate between baseline testing and repeat testing for
the subjects in the <strong>sodium</strong> <strong>citrate</strong> group (p > 0.05). However, when the <strong>sodium</strong> <strong>citrate</strong> and placebo subjects were grouped
together, there was a significant increase in peak blood lactate from 12.8 ± 3.0 mmol/l at the initial baseline testing session
to 14.5 ± 3.5 mmol/l at the repeat testing session (p = 0.033; see Figure 1).

Sodium <strong>citrate</strong> is <strong>of</strong>ten used in preference to <strong>sodium</strong> bicarbonate because <strong>of</strong> a reported lower incidence <strong>of</strong>
gastrointestinal discomfort (Linderman & Fahey, 1991). It was therefore interesting to note that 6 <strong>of</strong> the 10 subjects who
consumed <strong>sodium</strong> <strong>citrate</strong> in this study reported mild to moderate diarrhoea. <strong>The</strong> <strong>sodium</strong> <strong>citrate</strong> was delivered to the subjects
in 600 ml <strong>of</strong> cordial-flavoured water. It may be possible that this was insufficient fluid to avoid the gastrointestinal upset
experienced by the subjects.
Although the findings <strong>of</strong> this study are in contrast to those <strong>of</strong> Hausswirth et al. (1995) and Linossier et al. (1997) who
reported an ergogenic effect <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> on short-term, intense exercise, they are consistent with the findings <strong>of</strong> Cox
and Jenkins (1994), Ibanez et al. (1995) and Potteiger et al. (1996) who found no ergogenic effect <strong>of</strong> 0.5 g/kg oral <strong>sodium</strong>
<strong>citrate</strong> on short-term, intense exercise. In contrast to Potteiger (1996) and Ibanez et al. (1995), however, is the fact that
blood lactate levels were no higher as a result <strong>of</strong> taking <strong>sodium</strong> <strong>citrate</strong>. Sodium <strong>citrate</strong> is known to alkalise the blood (Tiryaki
& Atterbom, 1995; Potteiger et al., 1996; Ball & Maughan, 1997) facilitating a pH gradient to draw H + ions and lactate from
the muscle compartment into the blood. Sodium <strong>citrate</strong> does not alkalise the muscle compartment with a 90 minute
absorption time at a dose <strong>of</strong> 0.5 g/kg body weight (Linossier et al., 1997). Thus, it is unlikely that the muscle compartment
would have been alkalised in this study. Under these conditions, <strong>sodium</strong> <strong>citrate</strong> can only reduce muscle acidosis by drawing
H + and lactate from the muscle cytosol into the blood. However, this is unlikely to have happened here as higher blood
lactate levels were not recorded with <strong>sodium</strong> <strong>citrate</strong>, nor were peak power or total work elevated as would be expected with
increased removal <strong>of</strong> H + from the muscle compartment. <strong>The</strong> subjects in this study were reasonably anaerobically trained
reaching average post-exercise blood lactate levels <strong>of</strong> 13.6 ± 3.3 mmol/l, concentrations that would be correlated with a
significant drop in pH (not measured here). Thus, if <strong>sodium</strong> <strong>citrate</strong> were an effective buffer able to augment the natural
buffers <strong>of</strong> the body, it would have been expected to show some effect here.
CONCLUSIONS: <strong>The</strong> results <strong>of</strong> this study showed that a 0.5 g/kg body weight dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> had no ergogenic
effect on male and female subjects performing three maximal 30 s cycling bouts compared to a placebo. Peak blood lactate
concentrations were also unaffected by this dose <strong>of</strong> <strong>sodium</strong> <strong>citrate</strong> under these conditions.
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