HÖGSKOLAN I GÄVLE
Institutionen för vårdvetenskap och sociologi
Enheten för medicinsk vetenskap
Institutionen för vårdvetenskap och sociologi
Enheten för medicinsk vetenskap
Sodium Bicarbonate ingestion increases pH in blood but does not
attenuate Exercise Induced Arterial Hypoxemia or enhance
performance
Jens Westergren
maj 2007
Handledare: Michail Tonkonogi, docent
Examinator: Gudmund Stintzing
Abstract
Introduction: The exact causes of Exercise Induced Arterial Hypoxemia (EIAH) are not yet
known. Earlier studies on the ergogenic effects of NaHCO3 have neglected to investigate the
occurrence of EIAH among their subject, something that could explain the conflicting results,
EIAH cannot be over looked since reportedly 50% of well trained athletes experience EIAH.
One possible ergogenic effect of NaHCO3 would be to attenuate EIAH through an increase in
blood pH in a subject. This has been shown previously by means of intravenous infusion
during maximal rowing.
Aim: The aim of the study was to examine the effect of oral intake of NaHCO3 on EIAH and
performance in trained cyclists.
Method: Seven male cyclists (age 23.7 (22-27) years, VO2peak 64 (60-72) ml min-1 (kg body
mass) -1 volunteered for the study. The subjects performed two maximal exercise tests to
exhaustion 48 hours apart in a counter balanced cross over double blind fashion. Subjects
received 0.3 g kg BW-1 CaCO3 and 0.3 g kg BW-1 NaHCO3 in the placebo and bicarbonate
trial respectively.
Free flowing arterialized capillary blood was sampled at rest and exhaustion and analyzed for
pH, O2 Saturation, pO2, pCO2, and blood lactate. Ventilatory variables were measured
continuously throughout the test V'O2, V’CO2, V'E, V'E/VO2, RER and HR. In addition pulse
oximetry was used to evaluate O2 saturation.
Results/Discussion: At rest pH and PCO2 was elevated (p<0.05) in the bicarbonate trial
compared to the placebo trial. At exhaustion in the bicarbonate trial pH, blood lactate, RER,
was significantly elevated (p<0.05) when compared to the placebo trial. O2 saturation from
blood samples at exhaustion in the bicarbonate trial showed a trend towards improving
(p=0.061). No difference was seen between the two trials in PO2, VO2peak, V'Emax, HRmax
or performance. During exercise, bicarbonate ingestion increased blood pH but did not
improve arterial saturation or performance. The increase in blood pH achieved by ingestion of
bicarbonate was not as large as the increase achieved by intravenous infusion in another
study. Even with the larger increase in blood pH in those studies, there was only a small
improvement in performance. One possible explanation for the performance improvement
with bicarbonate infusion in that study was a reduced ventilation that could effect respiratory
muscle work and thereby work capacity. The bicarbonate ingestion in the present study did
not reduce ventilation. This could possible be achieved with higher doses of NaHCO3, which
would most likely result in increased frequency of gastrointestinal distress among subjects.
Key words: EIAH, SaO2, Sodium Bicarbonate
ABSTRACT ........................................................................................................................................................... 2
INTRODUCTION................................................................................................................................................. 5
EXERCISE INDUCED ARTERIAL HYPOXEMIA (EIAH) ......................................................................................... 5
SODIUM BICARBONATE SUPPLEMENTATION ...................................................................................................... 6
AIM OF THE STUDY ............................................................................................................................................ 6
MATERIALS AND METHODS ......................................................................................................................... 6
SUBJECTS .......................................................................................................................................................... 6
EXPERIMENTAL PROTOCOL ................................................................................................................................ 7
DRUG ADMINISTRATION .................................................................................................................................... 7
BLOOD SAMPLING ............................................................................................................................................. 7
GAS MEASUREMENT .......................................................................................................................................... 8
PULSE OXIMETRY .............................................................................................................................................. 8
STATISTICAL ANALYSIS .................................................................................................................................... 9
RESULTS .............................................................................................................................................................. 9
EXERCISE PERFORMANCE .................................................................................................................................. 9
Fig. 1. Relative performance Wmax·kg bw-1 of each subject in each of the two trials. ............................. 9
VENTILATION AND HEART RATE ........................................................................................................................ 9
BLOOD-GAS VARIABLES .................................................................................................................................. 10
LACTATE AND PH ............................................................................................................................................ 10
Fig. 2. Mean blood lactate values at rest, at every workload and at five and ten minute recovery for
NaHCO3 and CaCO3 trials. ...................................................................................................................... 11
Fig. 3. Mean blood pH values at rest, at every workload and at five and ten minute recovery for NaHCO3
and CaCO3 trials. ..................................................................................................................................... 11
PULSE OXIMETRY ............................................................................................................................................ 11
DISCUSSION ...................................................................................................................................................... 12
EXERCISE PERFORMANCE ................................................................................................................................ 12
VENTILATION AND HEART RATE ...................................................................................................................... 12
BLOOD-GAS VARIABLES AND PULSE OXIMETRY............................................................................................... 12
LACTATE AND PH ............................................................................................................................................ 13
ACKNOWLEDGEMENTS ................................................................................................................................ 13
REFERENCES .................................................................................................................................................... 14
Abbreviations
VO2max
Maximal Oxygen Consumption
RER
Respiratory Exchange Ratio (VCO2/V’O2)
EIAH
Exercise Induced Arterial Hypoxemia, a lowering of the
oxyhaemoglobin saturation induced by exercise
V’O2
Oxygen Consumption
VCO2
Carbon Dioxide production
V’E
Minute Ventilation
V’E max
Maximal Minute Ventilation
HR
Heart Rate
HR max
Maximal Heart Rate
pO2
Partial Pressure of Oxygen
pCO2
Partial Pressure of Carbon Dioxide
NaHCO3
Sodium Bicarbonate
SaO2
Arterial Oxygen Saturation
INTRODUCTION
Exercise Induced Arterial Hypoxemia (EIAH)
Traditionally, arterial haemoglobin O2 saturation was thought to remain unchanged during
intense exercise, thereby suggesting that the pulmonary system was not a limiting factor in
determining maximum oxygen uptake in healthy individuals (25). However more recent
research has shown that exercise induced arterial hypoxemia (EIAH) is possible and that it is
present in approximately half of well trained endurance athletes but not in moderate or
untrained subjects during intense exercise (24). It has been showed that blood viscosity
increased to a greater extent in EIAH subjects during exercise, possible leading to vascular
shear stress (3). Whether this could impair the blood gas barrier required further study, a six
week polyunsaturated fatty acid diet improved EIAH in master athletes strengthening high
blood viscosity as a factor (23). Moderate hyperoxia has been shown to increase VO2 max and
aerobic power to a greater degree in EIAH subject than in non EIAH subjects (11) Triathletes
show no difference in the magnitude of EIAH between running and cycling modes of testing
(15). Sildenafil has been shown to decrease the reduction in VO2max during a six day
exposure to a altitude of 4350 m (27). Legrand et al. showed that increased O2 arterial
desaturation increased muscle deoxygenation (17)(16). Acute hypervolaemia improved
arterial oxygen pressure in subjects experiencing EIAH (29). Athletes who display reduced
arterial O2 saturation during intense exercise in normoxia are more susceptible to reduced
VO2max in mild hypoxia (5). Lately the existence of intrapulmonary arteriovenous shunts
have been put forward as a probably cause of EIAH (8).
It has been concluded that EIAH is now recognised to occur in a significant number of fit and
healthy individuals of both sexes and of varying ages, but the cause has yet to be determined,
even what organ system, directly or indirectly is responsible for this limitation (7).
The definitions of EIAH vary between researchers, but the most common definition is a
reduction of SaO2 by 4% from resting values. An arterial saturation below 90% is considered
severe exercise induced arterial hypoxemia.(16). There are some excellent review articles that
examine EIAH in depth (7, 21, 26).
Sodium Bicarbonate supplementation
The ergogenic effects of Sodium Bicarbonate (NaHCO3) are somewhat uncertain, since it has
only been proved ergogenic over shorter periods of intense exercise (1, 2, 10, 18, 19).
Unfortunatley earlier studies on the ergogenic effects of NaHCO3 have neglected to
investigate the occurrence of EIAH among their subject, something that could explain the
conflicting results. EIAH cannot be over looked since reportedly 50% of well trained athletes
experience EIAH. One possible ergogenic effect of NaHCO3 would be to attenuate EIAH
through an increase in blood pH. This has been shown previously by means of intravenous
infusion during maximal rowing (22). A possible reason for the conflicting results regarding
ergogenic effects of NaHCO3 could be because of subjects experiencing different severity of
arterial desaturation during maximal exercise.
Aim of the study
The aim of the study was to test the hypothesis that an oral intake of NaHCO3 would attenuate
EIAH and improve performance in trained male cyclists.
MATERIALS AND METHODS
Subjects
Seven male competitive cyclists [mean age 23.7 yr (range 22-27 yr), body weight 71.4 kg
(range 63-79 kg), height 181.3 cm (range 175-190 cm), maximal oxygen uptake (VO2max) 64
ml·kg-1·min-1 (range 60-72 ml· kg-1·min-1 ] were recruited from the local collegiate cycling
team and volunteered for the study. Male subjects were recruited because of their generally
higher aerobic capacity. Subjects were informed in detail of the experimental procedure and
gave their written informed consent. In the three weeks preceding the experiments all subjects
were healthy, injury free and none were taking any medication. The study was approved by
the Ethics Committee of Högskolan Dalarna University College and performed according to
the Declaration of Helsinki.
Experimental protocol
All subjects performed three trials, with the first being a screening trial, although identical to
the two following intervention trials. The two intervention trials were administered in a
counter-balanced, cross-over double-blinded fashion. All trials were separated by exactly 48
hours. The subjects performed a graded exercise test on a friction braked cycle ergometer
(Monark 839 E, Monark Exercise AB, Vansbro Sweden) starting at 100 w, with workloads
increasing by 50 w every four minutes until volatile exhaustion or when the subjects were
unable to keep cadence above 70 rpm. No verbal encouragement was given to the the
subjetcs, except constant information of workload and time checks. A rest period of 1 minute
intercepted each four minute work period, to allow for blood sampling without disturbing the
subject. Maximal power output (Wmax) of each trial was calculated as follows (12).
Wmax=Wf+(x/240)*50
Where Wf is the workload of the last completed increment and x is the number of seconds
completed during the last attempted increment. During every trial, a powerful fan was used to
cool the subject.
Drug Administration
Either 0.30 g· kg-1 bw of Sodium Bicarbonate pills (NaHCO3) or 0.33 g· kg-1 bw Calcium
Carbonate pills (CaCO3) was ingested prior to the second and third trial. The drugs(29)
divided into five servings, with one serving ingested every 20 minutes together with 0.2 litres
of water. The first serving was ingested 90 minutes prior to each exercise trial. The dosage of
0.3 g· kg-1 bw, the five servings and the total intake of 1 litre of water has been demonstrated
in earlier studies on NaHCO3 supplementation to be sufficient to provide ergogenic benefits
without causing severe side effects (1). The possible side effects from NaHCO3 are
gastrointestinal distress and nausea, but the risks for these side effects are minimised with the
current intake regimen.
Blood Sampling
Blood samples for the measurement of bicarbonate, O2 pressure, CO2 pressure, pH, and base
excess in arterialized capillary blood was obtained from a free flowing puncture(13, 28) of a
preheated fingertip on the non-dominant hand and collected in a 100 microlitre heparized tube
(Clinitubes D957G-70-100-100 µL, Radiometer, Copenhagen, Denmark). All blood samples
were stored horizontally and analysed within one minute of sampling (ABL 825 Flex,
Radiometer, Copenhagen, Denmark). In addition a 25 microlitre sodium heparinized tube (
Plastic capillaries 20 µL, EKF Diagnostics, Barleben, Germany) was used to collect a blood
sample for a separate analysis of lactate ( Biosen 5140, EKF Diagnostics, Barleben, Germany
(6).
Blood samples were obtained after 15 minutes of supine resting, at the end of each workload,
directly after termination of exercise and after five and ten minutes of recovery. During the
resting period prior to testing the subjects hand was placed in a warm water bath (~ 42ºC),
during ergometer cycling the lower arm and hand was covered by a heated pad. The fan used
to cool the subject also cooled the dominant hand with the pulsoximeter fingertip sensor, this
cooling was not desired since it could effect periphal circulation of the hand, and therefore
SaO2 measurement. To combat this the dominant hand was covered by a towel.
Gas measurement
A computerized metabolic system with a mixing chamber (Oxycon Pro, Erich Jaeger GmbH,
Hoechberg, Germany) (4, 9) was used to measure VO2, VCO2, V’E, RER and heart rate (HR).
HR was also measured with a portable heart rate monitor (Polar S810i, Kempele, Finland)
VO2, VCO2 and RER was sampled every ten seconds and averaged over the last minute of
every workload. HR was average over the last five seconds of each workload. The Oxycon
Pro was calibrated according to the instruction manual post and prior to all trials.
Pulse oximetry
Pulse oximetry (Datex-Ohmeda 3900, Louisville, USA) was monitored continuously
throughout both the 15 minute rest and the entire exercise test. The index finger of the
dominant hand was cleaned with alcohol and let to air dry before placing the sensor according
to the user manual. SaO2 data and signal strength data was averaged and stored in the device
every six seconds and later downloaded to a laptop computer. For resting values, the values of
the entire 15 minute period were averaged and for exercise values, the 10 lowest consecutive
values (representing 1 minute) of each workload were averaged, in the majority of cases these
values were also the final readings of each work load. Pulse oximetry to measure arterial
oxyhemoglobin saturation during exercise have previously been validated, fingertip sensor
placement being prefered to earlobe sensor placement (17) (20).
Statistical Analysis
Data are presented as Mean ± SD. Differences between means were tested for statistical
significance by using two-tail Student’s t-test. Statistical significance was set at the 95%
confidence limit (P<0.05).
RESULTS
Exercise performance
The performance measure of Wmax was 367± 26 W for the placebo trial and 368± 23 W for
the bicarbonate trial, with no significant difference between the trials. See figure 1.
7,0
6,0
Wmax (Watt)
5,0
4,0
CaCO3
NaHCO3
3,0
2,0
1,0
0,0
1
2
3
4
5
6
7
Subject #
Fig. 1. Relative performance Wmax·kg bw-1 of each subject in each of the two trials.
Ventilation and heart rate
The maximal ventilation for the placebo trial was 187± 22 l·min-1 and for the bicarbonate
trial 191±18 l·min-1, with no significant difference between the trials. Maximal heart rate was
195 ±9 bpm for the placebo trial and 194±10 bpm for the bicarbonate trial. Maximal oxygen
uptake was 4.7±0.4 and 4.7±0.3 l·min-1 for the placebo and bicarbonate trial respectively.
However RER at maximal exercise increased significantly from 1.21±0.02 to 1.24±0.03
(P<0.05).
Blood-gas variables
SaO2 as measured from blood samples decreased from 96.5± 0.8% at rest to 94.1± 1.8 % at
maximal exercise in the placebo trial and from 96.4± 1.3 % to 95.2± 1.6 % in the bicarbonate
trial, with no significant difference between trials. CO2 pressure at rest was higher in the
bicarbonate trial 5.71± 0.26 compared to 5.33± 0.16 kPa in the placebo trial to (P<0.05), but
there was no significant difference at maximal exercise with 4.11± 0.46 kPa in the placebo
trial and 4.25± 0.32 kPa in the bicarbonate trial. Oxygen pressure increased from 9.63±0.54
kPa at rest to 11.54± 0.59 kPa at maximal exercise in the placebo trial and from 9.12± 1.96
kPa to 11.56± 0.85 in the bicarbonate trial, with no significant difference between trials. One
potential source of errror in the measurement of O2 and CO2 pressure could be the heating of
the hand, during rest this was achieved using a warm water bath, and during exercise a
heating pad was used. Every ten minutes the heating pad was replaced with new one, freshly
heated in a microwave oven. This could induce differences in temperature of the hand thus
effecting peripheral circulation and pressure of O2 and CO2. The best solution to this problem
would be to use anaerobic arterial sampling of the radial artery, unfortunatley this procedure
involves greater risks for the subject and was therefore beyond the scope of the present study.
Another aspect of the preheated hand is that both the warm water bath and the heating pad
possibly exaberated the core temperature inrease experienced during exercise.
Lactate and pH
Resting blood lactate values were 1.04±.28 and 1.14± 0.13 mmol/l for the placebo and
bicarbonate trial respectively. Maximal lactate values increased significantly from 15.25±2.73
to 18.05± 2.48 mmol/l l for the placebo and bicarbonate trial respectively (P<0.05). Blood pH
was significantly elevated at both resting 7.489± 0.021 vs. 7.396± 0.045 and maximal
exercise 7.217± 0.074 vs. 7.143± 0.064 in the bicarbonate trial when compared with the
placebo trial (P<0.05).
20,00
18,00
14,00
12,00
10,00
CaCO3
NaHCO3
8,00
6,00
4,00
2,00
0,00
Rest
100
150
200
250
300
350
400
5 min
post
10 min
post
Power Output (Watt)
rkload and at five and ten minute
Fig. 2. Mean blood lactate values at rest, at every workload
recovery for NaHCO3 and CaCO3 trials.
7,550
7,500
7,450
7,400
pH
Blood Lactate (mmol/L)
16,00
7,350
CaCO3
NaHCO3
7,300
7,250
7,200
7,150
7,100
Rest
100 W
150 W
200 W
250 W
300 W
350 W
400 W
5 min
post
10 min
post
Power Output (Watt)
Fig. 3. Mean blood pH values at rest, at every workload and at five and ten minute
recovery for NaHCO3 and CaCO3 trials.
Pulse Oximetry
Resting arterial saturation as measured by pulse oximetry was 98.3± 1.3 and 98±1.6 % and
decreased significantly (P<0.05) to 90± 1.7 and 90.7±2.7 % at maximal exercise for the
placebo and bicarbonate trial respectively, but with no significant difference between the
trials. All subjects in the present study experienced a greater than 4% reduction in arterial
saturation and does thereby qualify as EIAH subjects.
DISCUSSION
Exercise performance
Since there was no difference in Wmax between the two trials this study does not suggest
sodium bicarbonate to be an ergogenic aid potent enough to increase performance during
incremental ergometer cycling exercise. The reason for this could be dependent on the dosage
of the bicarbonate supplementation, with earlier studies showing small improvements in
performance through intravenous infusion of bicarbonate (22). However, because of the
possible side effects of bicarbonate loading, a higher dosage could prove problematic (1). The
fact that neither heart rate nor ventilation was different between the trials, helps to explain the
absence of performance improvement in the NaHCO3 trial, since one of the possible
ergogenic mechanisms of NaHCO3 would be to induce hypoventilation and a lowering of the
metabolic cost of breathing.
Ventilation and heart rate
Conflicting with earlier studies, in the present study, hypoventilation was not induced by
NaHCO3 intake (22). The possible reason for this was probably the relatively small dose of
sodium bicarbonate. Nielsen et al, showed that by an intravenous infusion of ~50-60 ml·min-1
NaHCO3, the usual decrease of blood pH during maximal exercise was almost avoided and
arterial desaturation was only slightly attenuated (22). In the present study NaHCO3 ingestion
elevated pH when compared to the placebo trial, but to a much smaller degree than, this
would also explain the even smaller (~ 1%) and non significant increase of arterial saturation
in the present study.
Blood-gas variables and pulse oximetry
According to the arterial saturation measured from arterialized capillary blood only two
subjects experienced mild EIAH. This is problematic since the data from the pulse oximeter
suggests that all subjects experience mild to severe EIAH. In the case of the pulse oximeter
data the results are surprising since we would only expect roughly 50% of the subjects to
experience EIAH (24). This finding could possibly challenge the general notion that 50% of
well trained athletes suffer from EIAH, and suggest that in the sub group tested in the present
study the prevalence of EIAH is higher than previously reported. Because of the one litre of
water ingested together with the drugs, all subjects showed a one kilogram increase in body
weight in both intervention trials, one could argue that the extra intake of water caused the
possible side effect of hypervolemia and thus open the possibility of improved arterial oxygen
pressure (29). However since this was equally present in both intervention trials, it should
represent no problem. Another issue when measuring blood-gases is that measurement is
sensitive to temperature. However, in the present study blood-gases were measured by an
ABL 825 Flex analyzer, were measurements are not affected by small changes in temperature
due to the 37º C measuring chamber. One possible reason for the low SaO2 values could be
that the towel covering the dominant hand with the pulseoximeter sensor was not sufficient to
offset the cooling effects of the fan. However, since the signal values of the pulseoximeter
were acceptable, this is not a likely possibility.
Lactate and pH
Blood pH increased as a result of bicarbonate ingestion, both at rest and during maximal
exercise when compared to the placebo trial. Blood lactate values also increased in the
bicarbonate trial and both these results are supported by earlier findings.
However the increase in maximal lactate values of ~ 2.5 mmol·L-1 is of a much smaller
magnitude than the ~ 10 mmol·L-1 achieved by means of NaHCO3 intravenoues infusion
(22). There are several mechanisms that can explain the elevated blood lactate values, a
higher lactate output caused by a higher efflux of protons due to an increase in extracellular
bicarbonate, diffusion via bicarbonate-chloride exchange and via sodium-hydrogen exchange
(14).
CONCLUSION
The results of this study did not show any ergogenic effect of sodium bicarbonate ingestion,
however, further research on the topic is warranted to investigate if any ergogenic effect could
be dose related.
ACKNOWLEDGEMENTS
I would like to thank my mentor Michail Tonkonogi for his invaluable help with the
preparation of this manuscript. I also want to thank all the subjects who participated in the
study for their time and effort.
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