J Appl Physiol 101: 918 –925, 2006.
First published April 20, 2006; doi:10.1152/japplphysiol.01534.2005.
Effects of chronic NaHCO3 ingestion during interval training on changes to
muscle buffer capacity, metabolism, and short-term endurance performance
Johann Edge, David Bishop, and Carmel Goodman
School of Human Movement and Exercise Science, The University of Western Australia, Perth, Australia
Submitted 6 December 2005; accepted in final form 8 March 2006
alkalosis; lactate threshold; time to fatigue
INTENSE MUSCLE CONTRACTIONS result in large ionic changes and
an increased nonmitochondrial ATP turnover, contributing to
the accumulation of hydrogen ions (H⫹). Whereas recent
findings indicate that the role of H⫹ accumulation during the
fatigue process of mammalian muscle fibers may be limited
(36), the accumulation of H⫹ has been shown to affect oxidative phosphorylation, enzyme activity, and ion regulation during some exercise tasks (i.e., repeated, intense muscle contractions) (18, 27, 41, 43). Both intra- and extracellular buffer
systems act to reduce the buildup of H⫹ and therefore aid in the
regulation of intracellular pH (pHi). An increased muscle
buffer capacity (␤m) after training may improve exercise
performance by preventing a large drop in pHi during intense
muscle contractions; however, little is known about the stimulus required to improve ␤m.
Despite the limited research, it appears that the intensity of
training is an important stimulus to increase ␤m. In support of
Address for reprint requests and other correspondence: D. Bishop, School of
Human Movement and Exercise Science, The Univ. of Western Australia,
Perth, Australia (e-mail: [email protected]).
918
this hypothesis, changes in ␤m were reported to be greater after
high-intensity training than moderate-intensity training
matched for total work (kJ) (16). Others have also shown a
greater ␤m in sprint-trained athletes and those participating in
high-intensity sports (rowing, team sports), than in marathon
runners and untrained subjects (17, 35). However, whereas
many reports have shown improvements in ␤m after intense
interval training (4, 45), some have not (21, 33). Typically,
training studies that have employed short rest periods (⬃1 min)
between high-intensity intervals [80 –150% peak O2 uptake
(V̇O2 peak)] have reported an improved ␤m (4, 16, 45), whereas
those employing longer rest intervals (3–10 min) (21, 33) have
not. Therefore, factors in addition to the intensity of exercise
training may be important to effect changes in ␤m. It has been
suggested that the accumulation of H⫹ within the skeletal
muscle may be an important stimulus for improving ␤m (16).
The accumulation of H⫹ within skeletal muscle during
exercise depends on both the production and removal of H⫹.
The production and removal rates of H⫹ are affected by the
muscle’s oxidative capacity, specific transport proteins, fiber
type, and the work-to-rest ratio employed during repeated
exercise bouts (28, 46, 47). The H⫹ efflux out of the muscle is
also reduced during extracellular acidosis and enhanced by an
elevated extracellular buffer concentration (25, 34, 43). The
ingestion of a buffering agent [i.e., sodium bicarbonate
(NaHCO3) or sodium citrate] ⬃90 –120 min before exercise
has subsequently been shown to reduce the accumulation of
H⫹ in skeletal muscle, interstitium, and blood during repeated,
intense muscle contractions (12, 39, 43). Although previously
used as an ergogenic aid, ingestion of a blood-buffering agent
provides a novel approach to alter the H⫹ accumulation during
training and to investigate the role of H⫹ accumulation as a
stimulus for changes in ␤m.
The main purpose of this study was to determine the effects
of chronic (3 times per week for 8 wk) ingestion of NaHCO3
before training on ␤m. Because of the possible ergogenic
effects of NaHCO3 ingestion, the experimental training groups
were matched for work (kJ) (supervised training program). We
also measured changes in muscle metabolism, time to fatigue
(TTF; at V̇O2 peak intensity), V̇O2 peak, and the lactate threshold
(LT). We hypothesized that ingestion of NaHCO3 and therefore a
reduction in H⫹ accumulation within the muscle and blood
during training would negatively affect improvements in ␤m.
METHODS
Sixteen female students (mean ⫾ SD: age 19 ⫾ 1 yr, mass 60 ⫾ 5
kg, V̇O2 peak 42.1 ⫾ 7.0 ml 䡠 kg⫺1 䡠 min⫺1), who were moderately
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Edge, Johann, David Bishop, and Carmel Goodman. Effects of
chronic NaHCO3 ingestion during interval training on changes to
muscle buffer capacity, metabolism, and short-term endurance performance. J Appl Physiol 101: 918 –925, 2006. First published April
20, 2006; doi:10.1152/japplphysiol.01534.2005.—This study determined the effects of altering the H⫹ concentration during interval
training, by ingesting NaHCO3 (Alk-T) or a placebo (Pla-T), on
changes in muscle buffer capacity (␤m), endurance performance, and
muscle metabolites. Pre- and posttraining peak O2 uptake (V̇O2 peak),
lactate threshold (LT), and time to fatigue at 100% pretraining
V̇O2 peak intensity were assessed in 16 recreationally active women.
Subjects were matched on the LT, were randomly placed into the
Alk-T (n ⫽ 8) or Pla-T (n ⫽ 8) groups, and performed 8 wk (3
days/wk) of six to twelve 2-min cycle intervals at 140 –170% of their
LT, ingesting NaHCO3 or a placebo before each training session
(work matched between groups). Both groups had improvements in
␤m (19 vs. 9%; P ⬍ 0.05) and V̇O2 peak (22 vs. 17%; P ⬍ 0.05) after
the training period, with no differences between groups. There was a
significant correlation between pretraining ␤m and percent change in
␤m (r ⫽ ⫺0.70, P ⬍ 0.05). There were greater improvements in both
the LT (26 vs. 15%; P ⫽ 0.05) and time to fatigue (164 vs. 123%; P ⫽
0.05) after Alk-T, compared with Pla-T. There were no changes to
pre- or postexercise ATP, phosphocreatine, creatine, and intracellular
lactate concentrations, or pHi after training. Our findings suggest that
training intensity, rather than the accumulation of H⫹ during training,
may be more important to improvements in ␤m. The group ingesting
NaHCO3 before each training session had larger improvements in the
LT and endurance performance, possibly because of a reduced metabolic acidosis during training and a greater improvement in muscle
oxidative capacity.
INTERVAL TRAINING AND MUSCLE BUFFER CAPACITY
J Appl Physiol • VOL
percent of V̇O2 peak (2). The subjects performed three training sessions
per week (Monday, Wednesday, Friday) for 8 consecutive weeks.
Group 1 ingested NaHCO3 (0.2 mg/kg body mass ⫻ 2) at 90 and 30
min before performing each high-intensity, interval training session
(Alk-T), whereas group 2 ingested a placebo [sodium chloride (NaCl);
0.1 mg/kg body mass ⫻ 2] at 90 and 30 min before performing each
high-intensity, interval training session (Pla-T). A similar NaHCO3
supplement protocol resulted in a sustained (⬃80 min of intermittent
exercise) increase in blood [HCO3] ([HCO3]b) without any gastrointestinal disturbances (5). Pilot work within our laboratory also showed
that there were large differences in blood pH (pHb) during interval
training when this protocol of NaCO3 ingestion was compared with a
placebo (Fig. 1).
All training sessions were completed on mechanically braked cycle
ergometers (818E, Monark, Stockholm, Sweden) and were preceded
by a 5-min warm-up at 50 W. Training followed a periodized plan so
as to simulate athletic training programs, allow progression, and
prevent overtraining. The training was performed at an intensity of
140% (weeks 1 and 2), 150% (weeks 3 and 4), 160% (week 5), and
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trained and involved in various club level sports (basketball, soccer,
netball, rowing, and hockey), volunteered to participate in this study.
Subjects were informed of the study requirements, benefits, and
risks before giving written, informed consent. Approval for the
study’s procedures was granted by the Institutional Research Ethics
Committee.
Experimental overview. All subjects completed a familiarization
trial of both the graded exercise test (GXT) and TTF test before
baseline testing. The GXT and TTF tests were then performed by each
subject before and after the training intervention. On the day of the
TTF test, a muscle biopsy was taken from the vastus lateralis muscle
at rest and immediately upon cessation of the exercise test. Posttraining tests were conducted in the same order as the pretraining tests. At
least 48 h separated each testing session, and pre- and posttraining
tests were conducted approximately at the same time of day (⫾2 h).
Subjects were asked to maintain their normal diet and prescribed
training program throughout the study. They were also required to
consume no food or beverages (other than water) 2 h before testing
and were asked not to consume alcohol or to perform vigorous
exercise in the 24 h before testing. Food diaries were given to each
subject to record food and fluid consumption 2 days before each test,
and subjects were asked to replicate this during posttraining testing.
After the pretraining testing, subjects were matched on their LT and
randomly assigned to one of the two high-intensity interval-training
groups [NaHCO3 ingestion (Alk-T) or placebo (Pla-T)].
GXT. Pre- and posttraining, the GXT was performed on an electronically braked cycle ergometer (Lode, Gronigen, The Netherlands)
and consisted of graded exercise steps (4-min stages), using an
intermittent protocol (1-min break between stages). The test commenced at 50 W, and thereafter intensity was increased by 25 W every
4 min until volitional exhaustion. The test was stopped when the
subject could no longer maintain the required power output (cycling
cadence dropped below 60 rpm). Strong verbal encouragement was
provided to each subject as they came to the end of the test. Capillary
blood samples were taken at rest and immediately after each 4-min
stage of the GXT. The LT was calculated by the modified Dmax
method (6). This is determined by the point on the polynomial
regression curve that yields the maximal perpendicular distance to the
straight line connecting the first increase in lactate concentration
above resting level and the final lactate point. V̇O2 peak was determined
as the highest 30-s rolling average during the GXT, and the power
output at which the pretraining V̇O2 peak occurred was accordingly
used in the TTF test. If a subject did not complete the 4-min stage in
which V̇O2 peak occurred, then the fraction of the stage that was
completed was added to the workload of the previous stage, and this
was subsequently used as the power at V̇O2 peak and used for the TTF
test (e.g., 200-W stage completed ⫹ 2 min completed at 225 W;
power at V̇O2 peak ⫽ 200 ⫹ 0.5 ⫻ 25 W).
TTF cycle test. Pre- and posttraining, each subject performed a
constant-load (⬃80 rpm) TTF test on an electronically braked cycle
ergometer. Subjects performed 4 min of unloaded cycling and then
cycled until exhaustion at their individually determined exercise
intensity (power output associated with pretraining V̇O2 peak). The
subject’s TTF was defined as the time when her cycling cadence
dropped below 60 rpm despite strong verbal encouragement. In our
laboratory, the coefficient of variation (CV) for TTF at 100% V̇O2 peak
is 5.5%.
Training intervention and NaHCO3 supplementation. Once in their
assigned groups, each pair of matched subjects was required to
complete the same amount of work (kJ) during a training session.
Therefore, both Alk-T and Pla-T groups exercised at the same training
intensity and completed the same training volume. All subjects commenced the supervised, progressive training program within 4 –7 days
of their final pretraining test. Training intensity was set as a percentage of LT, rather than V̇O2 peak, because metabolic and cardiovascular
stresses are similar when individuals of differing fitness levels exercise at a percent of LT but can vary significantly when training at a
919
⫺
Fig. 1. Blood pH (pHb; A), HCO3 ([HCO⫺
3 ]b; B), and lactate ([La ]b; C)
changes during training [8 ⫻ 2-min intervals at 140% lactate threshold (LT),
1-min rest] after the ingestion of NaHCO3 (Alk-T) or placebo (Pla-T) trials
(pilot work collected on 3 subjects; int ⫽ interval number, samples taken after
each interval). *Significantly different from the placebo trial (P ⬍ 0.05).
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920
INTERVAL TRAINING AND MUSCLE BUFFER CAPACITY
J Appl Physiol • VOL
final display as micromoles H⫹ per gram dry muscle per unit pH
(␮mol H⫹ 䡠 g muscle dry wt⫺1 䡠 pH⫺1) and determined as the subject’s
␤min-vitro. This technique measures the buffering potential of the
physiochemical buffers within the muscle, excluding bicarbonate,
which is removed during the freeze-drying process. In our laboratory,
the CV for ␤min-vitro is 5.4%. This CV was determined from muscle
samples taken 5 wk apart from recreationally active female students.
Muscle metabolites. Freeze-dried rest and postexercise muscle
samples (3.5– 6 mg) were enzymatically assayed for lactate, phosphocreatine, creatine, and ATP (22). Muscle metabolite concentrations
were adjusted to the individual highest TCr content, to account for
measurement errors arising from the variable inclusion of connective
tissue, fat, or blood in tissue samples.
Statistical analysis. All values are reported as means ⫾ SD, except
Figs. 1, 2, and 3 (⫾SE). Two-way ANOVA with repeated measures
for time were used to test for interaction and main effects for the
dependent variables measured (SPSS 10.0, Chicago, IL). When an
effect was found, least significant difference post hoc tests were
performed to determine where the difference occurred. When no
between-group differences were found, analysis was performed on the
combined Alk-T and Pla-T group results. Pearson’s correlation was
used to determine the relationship between pre ␤min-vitro and percent
change in ␤min-vitro. The alpha level for statistical significance was set
at 0.05.
RESULTS
Pilot data showed that NaHCO3 ingestion before training
resulted in an increase in pHb immediately before exercise, and
after four and eight 2-min intervals (Fig. 1A). NaHCO3 ingestion resulted in an elevated [HCO3]b immediately before exercise and after one, four, and eight 2-min intervals (Fig. 1B).
NaHCO3 ingestion also elevated [La⫺]b after eight 2-min
intervals (Fig. 1C). The mean heart rate during a typical
training session (immediately after eight 2-min exercise intervals) was 188 ⫾ 5 and 189 ⫾ 3 beats/min for the Alk-T and
Pla-T groups, respectively, with no difference between groups;
this was ⬃95% of maximal heart rate. After training, there
were no changes in body mass for either group (Table 1).
V̇O2 peak and LT during the GXT. After the training period,
there was an increase in V̇O2 peak (Alk-T 22%, Pla-T 17%; P ⬍
0.05), with no difference between groups (Table 1). Training
also improved the LT for both groups (Alk-T 26%, Pla-T 15%;
P ⬍ 0.05), with a greater improvement after Alk-T (P ⫽ 0.05,
Table 1). There was a reduction in the relative intensity of the
TTF test from pretraining (100% power at V̇O2 peak for both
Table 1. Body mass, V̇O2peak, and LT before
and after 8 wk of training
Variable
Body mass, kg
V̇O2peak, l/min
Power at V̇O2peak, W
LTDmax, W
LT as percent of TTF power
Group
Pretraining
Posttraining
Alk-T
Pla-T
Alk-T
Pla-T
Alk-T
Pla-T
Alk-T
Pla-T
Alk-T
Pla-T
64.7⫾10.5
59.0⫾6.7
2.41⫾0.38
2.34⫾0.34
172⫾27
169⫾25
109⫾21
112⫾19
63.1⫾5.5
66.3⫾5.3
63.3⫾9.6
59.5⫾7.4
2.86⫾0.23*
2.76⫾0.32*
203⫾26*
200⫾20*
137⫾20*†
130⫾21*
79.9⫾3.1*
77.4⫾9.2*
Values are means ⫾ SD. V̇O2peak, maximal O2 uptake; LT, lactate threshold;
TTF, time to fatigue; Alk-T, NaHCO3 training group; Pla-T, placebo training
group. *Significantly different from pretraining (P ⬍ 0.05); †Significantly
different from PLA-T (P ⫽ 0.05).
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170% (weeks 6, 7, and 8) of subjects’ individually determined power
at the pretraining LT. This equated to 91% (weeks 1 and 2), 97%
(weeks 3 and 4), 103% (week 5), and 110% (weeks 6, 7, and 8) of the
power at pretraining V̇O2 peak. There were no significant differences in
the percentage of V̇O2 peak that subjects trained at between groups.
Subjects completed six to nine 2-min intervals during weeks 1 and 2,
eight to ten 2-min intervals on weeks 3 and 4, nine to twelve 2-min
intervals on weeks 5 to 7, and six to nine 2-min intervals on week 8.
All subjects completed the same total number of intervals, with
training sessions periodized so that the training volume altered from
Monday to Friday. Each 2-min interval (80 rpm) was interspersed
with a 1-min recovery period. Progression was controlled by increasing the workload (by altering the resistance) and the number of
intervals performed in a training session. During the taper period (last
two training sessions before posttesting), supplementation with
NaHCO3 or placebo was stopped for both groups so that there was not
an elevated resting [HCO3]b or pHb during posttesting, which has
been reported after chronic NaHCO3 supplementation by healthy
subjects (31). No NaHCO3 was ingested during posttesting.
Gas analysis (GXT). During both the pre- and posttraining GXT
and TTF test, pulmonary gas exchange was determined breath by
breath for O2 and CO2 concentrations and ventilation by use of a
portable gas analysis system (K4b2, Cosmed, Rome, Italy). The gas
analyzers were calibrated immediately before and verified after each
test by using a certified gravimetric gas mixture (BOC Gases, Chatswood, Australia). The ventilometer was calibrated preexercise and
verified postexercise using a 3-liter syringe in accordance with the
manufacturer’s instructions. There were no significant differences
between pre- and posttest calibrations for any test.
Capillary blood sampling and analysis. A hyperemic ointment
(Finalgon, Boehringer Ingelheim) was applied to the earlobe 5–7 min
before initial blood sampling. Capillary (earlobe) blood samples (50
␮l) were taken at rest and immediately after each 4-min stage of the
GXT. Samples (100 ␮l) were also taken at rest, immediately and 3 and
5 min after the TTF test. Capillary blood lactate concentration
([La⫺]b), pH, and HCO3 were measured via a blood-gas analyzer
(ABL 625, Radiometer, Copenhagen, Denmark).
Muscle sampling and analysis. On the day of the TTF test, one
incision was made under local anesthesia (5 ml, 1% xylocaine) into
the vastus lateralis of each subject. The incision was used for the
pretest biopsy and then closed with a Steri-Strip and subsequently
used for the posttest biopsy. Pre- and posttest biopsy samples were
taken with the needle inserted at different angles, with manual suction
applied for both samples. The first muscle sample was taken (before
warm-up) during supine rest. The second muscle sample was taken
immediately after the cessation of the TTF, although the subject
remained on the cycle ergometer. Pre- and posttraining samples were
taken on opposite legs from approximately the same position. The
samples were then removed from the biopsy needle and stored at
⫺80°C until subsequent analysis. Freeze-dried muscle was then dissected free from visible blood, fat, and connective tissue.
␤min-vitro and pHi. All in vitro ␤m (␤min-vitro) results were determined on resting, preexercise muscle samples. Freeze-dried samples
(1.8 –2.3 mg) were homogenized on ice for 2 min in a solution
containing sodium fluoride (10 mM) at a dilution of 30 mg dry
muscle/ml of homogenizing solution (30). The muscle homogenate
was then placed in a circulating water bath at 37°C for 5 min before
and during the measurement of pH. The pH measurements were made
with a microelectrode (MI-415, Microelectrodes, Bedford, NH) connected to a pH meter (SA 520, Orion Research, Cambridge, MA).
After initial pH measurement, muscle homogenates (rest samples)
were adjusted to a pH of ⬃7.2 with a sodium hydroxide (0.02 M)
solution and then titrated to a pH of ⬃6.2 by the serial addition of 2
␮l of hydrochloric acid (10 mM) blind to the subject being analyzed.
From the fitted titration trend line, the number of moles of H⫹ (per g
of dry muscle) required to change the pH from 7.1 to 6.5 was
interpolated. This value was then normalized to the whole pH unit for
INTERVAL TRAINING AND MUSCLE BUFFER CAPACITY
921
Fig. 2. Muscle buffer capacity (in vitro) (␤min-vitro) (␮mol H⫹ 䡠 g muscle dry
wt⫺1 䡠 pH⫺1) before and after the training period for Alk-T and Pla-T (A) and
before and after the training period after separation into either the pretraining
high (pretraining ␤min-vitro ⬎ 160 ␮mol H⫹ 䡠 g muscle dry wt⫺1 䡠 pH⫺1) or low
(pretraining ␤min-vitro ⬍ 140 ␮mol H⫹ 䡠 g muscle dry wt⫺1 䡠 pH⫺1) ␤min-vitro
groups (B). Values are means ⫾ SE. *Significantly different from pretraining
(P ⬍ 0.05). †Significantly different from high ␤min-vitro (P ⬍ 0.05).
groups) to posttraining for both groups (Alk-T 84.5 ⫾ 4.6%,
Pla-T 83.9 ⫾ 4.8% power at V̇O2 peak; P ⬍ 0.05), with no
differences between them.
Performance during the TTF test. The mean power during
the constant-load TTF test (matched pre- and posttraining) was
160 ⫾ 10 and 165 ⫾ 10 W for the Alk-T and Pla-T groups,
respectively (P ⬎ 0.05). Both groups had improvements in
TTF (s) after the training period (Alk-T 164%, Pla-T 123%;
P ⬍ 0.05, Fig. 2). However, there was a greater improvement
after Alk-T than Pla-T (P ⫽ 0.05). Both groups had an increase
in V̇O2 at 1 min, 6 min, and the end of exercise during the TTF
test (P ⬍ 0.05; Table 2); however, there were no differences
between groups.
␤m and muscle/blood metabolites and pH during the TTF
test. There was an improvement in ␤m after training, with no
differences between groups (P ⬍ 0.05, Fig. 3A). There was a
correlation between pretraining ␤m and percent change in ␤m
after training (r ⫽ ⫺0.70; P ⬍ 0.05, Fig. 4). Because of this
relationship between pretraining ␤m and percent change in
␤m, we then placed subjects (from both groups) into either a
high [⬎160 (range: 160.3–223.2) ␮mol H⫹ 䡠g muscle dry
wt⫺1 䡠pH⫺1] or low [⬍140 (range: 81.2–138.9) ␮mol H⫹ 䡠g
muscle dry wt⫺1 䡠pH⫺1] pretraining ␤m group (on the basis of
previous research; Refs. 16, 17). There was an improvement in
␤m for the low-␤m group (31%, P ⬍ 0.05; Fig. 3B), with no
change for the high-␤m group (4%, P ⬎ 0.05). After the
training period, there were no differences compared with
pretraining in resting or postexercise muscle ATP, phosphocreatine, lactate, or pHi for either group (P ⬎ 0.05, Table 3).
After training, there were no differences from pretraining in
Table 2. V̇O2 during the TTF test before
and after 8 wk of training
Variable
1 min V̇O2, l/min
6 min V̇O2, l/min
End exercise V̇O2, l/min
Group
Pretraining
Posttraining
Alk-T
Pla-T
Alk-T
Pla-T
Alk-T
Pla-T
1.78⫾0.41
1.70⫾0.20
2.40⫾0.33
2.24⫾0.48
2.41⫾0.24
2.20⫾0.38
2.06⫾0.13*
2.05⫾0.26*
2.75⫾0.31*
2.77⫾0.41*
2.68⫾0.28*
2.64⫾0.39*
Values are mean ⫾ SD. V̇O2, O2 uptake. *Significantly different from
pretraining (P ⬍ 0.05).
J Appl Physiol • VOL
Fig. 4. Relationship between pretraining ␤min-vitro and change (%) in ␤min-vitro
from pre- to posttraining.
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Fig. 3. Time to fatigue during the constant-load exercise test (100% pretraining peak O2 uptake intensity). Values are means ⫾ SE. *Significantly different
from pretraining (P ⫽ 0.05). §Alk-T significantly different from Pla-T (P ⬍
0.05).
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INTERVAL TRAINING AND MUSCLE BUFFER CAPACITY
Table 3. Muscle ATP, PCr, Cr, [La⫺]i, and pHi at rest and immediately postexercise during
the TTF test, before and after 8 wk of training
Pretraining
Posttraining
Variable
Group
Preexercise
Postexercise
Preexercise
Postexercise
[ATP], mmol/kg dry wt
Alk-T
Pla-T
Alk-T
Pla-T
Alk-T
Pla-T
Alk-T
Pla-T
Alk-T
Pla-T
24.0⫾1.7
23.1⫾1.3
96.9⫾22.5
88.9⫾14.8
49.0⫾13.8
45.5⫾17.8
9.4⫾5.3
6.3⫾3.6
7.13⫾0.06
7.15⫾0.04
19.7⫾4.4†
18.2⫾5.3†
55.3⫾13.5†
55.8⫾15.3†
90.6⫾28.3†
78.6⫾25.4†
52.6⫾16.6†
47.9⫾17.5†
6.94⫾0.08†
6.89⫾0.12†
23.6⫾1.5
22.4⫾1.3
96.6⫾18.4
84.3⫾13.2
46.2⫾17.9
52.8⫾19.3
8.3⫾3.8
5.7⫾1.0
7.11⫾0.05
7.14⫾0.04
20.3⫾4.0†
19.5⫾4.0†
56.6⫾28.7†
61.6⫾17.1†
87.2⫾26.8†
73.1⫾27.0†
63.3⫾26.8†
49.5⫾21.4†
6.87⫾0.04†
6.94⫾0.05†
[PCr], mmol/kg dry wt
[Cr], mmol/kg dry wt
[La⫺]i, mmol/kg dry wt
pHi
Values are means ⫾ SD. There were no significant differences between groups pre- or posttraining. PCr, phosphocreatine; Cr, creatine; [La⫺]i, intracellular
lactate concentration; pHi, intracellular pH. †Significantly different from rest (P ⬍ 0.05).
DISCUSSION
The main purpose of this study was to determine the effects
of NaHCO3 ingestion during training on changes in ␤m.
Induced alkalosis (NaHCO3 ingestion) before training did not
affect training-induced improvements in ␤m. Therefore, in
contrast to our hypothesis, the present results indicate that H⫹
accumulation during training is not an important factor in
improving ␤m. The present study also identified a relationship
between pretraining ␤m and the percent change in ␤m after
training (Fig. 4). We have shown that chronically induced
alkalosis does affect some training adaptations. Although training intensity and volume were matched between groups, the
Alk-T group had greater improvements in the LT and shortterm endurance performance (TTF at pretraining V̇O2 peak intensity) than the Pla-T group. There was an increase in O2
uptake, no significant change in muscle metabolites at exhaustion, and a reduced accumulation of blood metabolites for both
groups after the training period.
Study design. Our experimental group was required to ingest
a large dose of NaHCO3 before each training session. Pilot
research (see Fig. 1A), along with the results of previous
reports (5, 39), has demonstrated that this NaHCO3-ingestion
protocol results in a large reduction in both rest and exercise
blood H⫹ concentration ([H⫹]). Furthermore, NaHCO3 ingestion decreases intracellular [H⫹] during intense continuous and
interval exercise [i.e., pHi at the end of four 1-min intervals at
100% V̇O2 max intensity was 6.86 for NaHCO3 and 6.72 for a
placebo group (12)] (34, 39). To ensure a significant H⫹
accumulation during each training session and differences in
H⫹ accumulation between our training groups, we employed a
very demanding training protocol and used a greater dose of
NaHCO3 than employed by others (0.40 vs. 0.30 – 0.15 g/kg
body mass). Therefore, although we were unable to take blood
samples and muscle biopsies before and after training sessions,
we are confident that there were differences in blood [H⫹]
and intracellular [H⫹] between the Alk-T and Pla-T groups
during training.
␤m and training. The similar improvements in ␤m by both
groups (Fig. 2A) suggest that the ingestion of NaHCO3, and so
altering the likely accumulation of H⫹ during training, did not
Table 4. pHb, [La⫺]b, and [HCO3⫺]b at rest and immediately postexercise during
the TTF test, before and after 8 wk training
Pretraining
Variable
pHb
[La⫺]b, mmol/l
[HCO3⫺]b, mmol/l
Rest
Post 0
Post 3
Post 5
Rest
Post 0
Post 3
Post 5
Rest
Post 0
Post 3
Post 5
min
min
min
min
min
min
Posttraining
Alk-T
Pla-T
Alk-T
Pla-T
7.425⫾.027
7.179⫾.072†
7.161⫾.027†
7.162⫾.028†
1.1⫾0.4
18.9⫾5.0†
19.4⫾4.5†
16.3⫾2.4†
22.9⫾2.7
11.6⫾2.1†
9.7⫾1.3†
10.0⫾1.8†
7.443⫾.021
7.179⫾.066†
7.152⫾.080†
7.140⫾.079†
1.1⫾0.3
18.9⫾2.9†
19.8⫾3.8†
17.9⫾3.5†
24.2⫾3.2
11.4⫾2.0†
9.6⫾1.4†
9.4⫾1.8†
7.426⫾.053
7.178⫾.067†
7.180⫾.070†*
7.185⫾.055†*
1.1⫾0.5
15.6⫾4.2†*
14.6⫾3.5†*
13.6⫾3.6†*
23.0⫾2.4
10.6⫾1.7†
10.7⫾2.4†
11.0⫾2.4†
7.424⫾.031
7.168⫾.063†
7.197⫾.054†*
7.217⫾.074†*
1.2⫾0.5
16.7⫾1.6†*
15.6⫾2.0†*
14.8⫾2.9†*
24.4⫾1.9
10.1⫾1.4†
10.7⫾1.5†
11.3⫾2.4†
Values are means ⫾ SD. There were no significant differences between groups pre- or posttraining. pHb, blood pH; [La⫺]b, blood lactate concentration;
[HCO3⫺]b, blood bicarbonate ion concentration. *Significantly different from pretraining at the same time point (P ⬍ 0.05). †Significantly different from rest
(P ⬍ 0.05).
J Appl Physiol • VOL
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any of the resting blood variables; however, both groups
recorded smaller changes in postexercise [La⫺]b and pHb, with
no difference between groups (Table 4).
INTERVAL TRAINING AND MUSCLE BUFFER CAPACITY
J Appl Physiol • VOL
for Alk-T than the Pla-T group (26 vs. 15%, respectively; P ⫽
0.05). The LT is a good indicator of the aerobic capacity of the
working muscles, in particular O2 utilization within the muscle
(11, 26, 44). Those with a greater LT also have an elevated
muscle respiratory capacity and aerobic enzyme activity, despite similar V̇O2 peak values (23, 26). Although a relationship
between muscle oxidative capacity and V̇O2 peak has also been
reported, the association is smaller than that with the LT (3,
23), and it seems that V̇O2 peak is primarily determined by O2
delivery rather than O2 utilization within the muscle (24).
Therefore, the greater LT, but not V̇O2 peak, after Alk-T than
Pla-T may be indicative of a greater improvement in oxidative
capacity within their trained muscle.
To date, we have not found any reports identifying the
effects of chronic NaHCO3 ingestion before training on
changes in the LT, aerobic fitness, or oxidative capacity of the
muscle. However, although mild acidosis may benefit O2
unloading within the muscle during exercise (19, 20, 27), there
is an acute, detrimental effect of a large drop in pHi on
mitochondrial phosphorylation and cellular respiration (38).
Furthermore, an exhaustive interval training session negatively
affects some mitochondrial enzymes (10). Therefore, a smaller
drop in pHb and pHi (after NaHCO3 ingestion) during regular,
intense interval training may result in a reduced impact on
mitochondrial function and may, therefore, promote improved
mitochondrial adaptations.
Chronic NaHCO3 provides a protective effect against the
detrimental metabolic consequences of chronic metabolic acidosis in patients (8 –10, 13) and may act similarly during the
acidosis that occurs during repeated intense exercise. High
levels of acute and chronic acidosis negatively affect skeletal
muscle protein synthesis, amino acid oxidation, and insulin
sensitivity in rats and humans (1, 10, 29, 32, 40). In contrast,
correction of acidosis with NaHCO3 supplementation increases
skeletal muscle protein synthesis and insulin sensitivity and
reduces the content of enzymes involved in the ubiquitinproteasome pathway (43). Although no training studies to date
have used NaHCO3 supplementation and measured protein
synthesis, in a study employing exercise training (strenuous
treadmill training, 5–7 days/wk ⫻ 11 wk) and chronic
NaHCO3 ingestion (0.05 mg/kg each day), bone mineral content and density were both positively affected in rats supplemented with NaHCO3, compared with a training-only group (7,
37). Acute alkalosis also improves K⫹ regulation during intense exercise, possibly via a positive effect on transport
proteins (11, 14). Therefore, the greater endurance performance after NaHCO3 supplementation in the present study
may be due to greater changes in intracellular levels of proteins
involved in ion regulation and/or mitochondrial respiration,
and, if so, this may also be associated with the greater improvement in TTF.
TTF. Similar to others that have employed intense training
with subjects who are not highly endurance trained (11, 14),
there were large improvements (⬎100%) in TTF. However, a
novel finding was that there were greater improvements in TTF
after Alk-T than Pla-T (164 vs. 123%, respectively). This may
be associated with the elevated LT in the Alk-T group.
Changes in time to exhaustion after intense interval training are
associated with improvements in the LT (r ⫽ 0.71– 0.84, P ⬍
0.05) and in some circumstances may be better predictors of
training-induced changes to endurance performance than
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affect changes in ␤m. Therefore, the present results indicate
that H⫹ accumulation during training is not an important factor
in improving ␤m. In support of this, an increase in ␤m
occurred after training (⬃80% power at V̇O2 max by welltrained cyclists) (45) that does not result in large changes to
pHi (pHi, 7.09 to 7.01) (42). Therefore, training intensity,
rather than changes in intracellular [H⫹], may be the most
important stimulus to improve the intracellular buffers that
affect ␤m (i.e., protein and carnosine content).
As a result of the intense training (heart rate ⬃95% of
maximum), it is impossible to exclude the possibility that the
similar improvements in ␤m between the two groups were due
to an increase in intracellular [H⫹] beyond some “threshold
level” resulting in increases in ␤m in both groups. pHi is not
significantly altered during the early portion of intense exercise
(1–5 min) after induced alkalosis, but rather during the latter
half of an exercise bout or interval training session (12, 16, 34,
43). This suggests that there may have been a similar H⫹
accumulation within the muscle during the initial interval
bouts, which could have contributed to the similar training
adaptations between our two groups. However, in the present
study, there does not seem to have been an additive effect of
accumulating more H⫹ during the interval training on improvements in ␤m.
Although we did report improvements in ␤m, these changes
were varied within the groups and were less than reported after
a shorter (5-wk) training period (mean 9 –19 vs. 25%; Refs. 17,
35). These differences between studies are not likely to be due
to general subject characteristics, because subjects were similar
in age (⬃19 vs. 20 yr), sex (all women), and aerobic fitness
(⬃42 vs. 44 ml䡠kg⫺1 䡠min⫺1). Furthermore, the same training
program (2-min intervals with 1-min rest) and mode of exercise (cycling) were employed. However, the mean pretraining
␤m was ⬃20% greater in the present study than in the previous
report (⬃154 vs. 123 ␮mol H⫹ 䡠g muscle dry mass⫺1 䡠pH⫺1),
possibly because of differing sports participation and training
status (competitive club vs. recreational athletes) (33, 37). The
results from the present study show an association between
pretraining ␤m and percent improvement in ␤m (Fig. 4). This
indicates that there may be a reduced improvement in ␤m after
training in those that already have a well-developed ␤m. On
the basis of these findings, we performed further analysis,
separating subjects into a high-␤m and a low-␤m group. The
subsequent findings revealed that the low-␤m group had similar changes in ␤m to our previous report (31 vs. 25%, Fig. 2B),
whereas the improvement was much smaller for the high-␤m
group (4%). This may also explain why some studies have not
reported changes in ␤m after training (30, 33). However, care
must be taken when comparing different studies, because
muscle preparation methods (dilution ratios and wet or dry
muscle) affect ␤m values (11, 26).
Enhanced V̇O2 peak and LT after training. Both Alk-T and
Pla-T had improvements in V̇O2 peak and power at V̇O2 peak after
training, with no differences between groups. The increases in
power at V̇O2 peak resulted in a large reduction of the relative
intensity of the TTF test from 100% of pretraining V̇O2 peak
intensity to 84.5% (Alk-T) and 83.9% (Pla-T) of the power at
the posttraining V̇O2 peak. The changes in V̇O2 peak and relative
intensity during the TTF test were similar for both groups and
do not seem to explain the differences in TTF between the two
groups. However, there were greater improvements in the LT
923
924
INTERVAL TRAINING AND MUSCLE BUFFER CAPACITY
ACKNOWLEDGMENTS
The authors thank the volunteers for time and dedication during this
challenging project. The technical assistance of Dr. Rob Duffield is gratefully
acknowledged.
J. Edge is currently at the Institute of Food, Nutrition and Human Health,
Massey University, Palmerston North, New Zealand.
GRANTS
This study was supported by a University of Western Australia Research
Grant.
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