Eur J Appl Physiol (2009) 105:357363
DOI 10.1007/s00421-008-0911-7
O R I G I N A L A R T I CL E
The eVects of beta-alanine supplementation and high-intensity
interval training on neuromuscular fatigue and muscle function
Abbie E. Smith Jordan R. Moon Kristina L. Kendall Jennifer L. Graef
Christopher M. Lockwood Ashley A. Walter Travis W. Beck Joel T. Cramer
JeVrey R. Stout
Accepted: 17 October 2008 / Published online: 7 November 2008
Springer-Verlag 2008
Abstract The purpose of this study was to determine the
eVects of beta-alanine supplementation and high-intensity
interval training (HIIT) on electromyographic fatigue
threshold (EMGFT) and eYciency of electrical activity
(EEA). A total of 46 men completed four, 2-min work
bouts on a cycle ergometer. Using bipolar surface elec-
trodes, the EMG amplitude was averaged and plotted over
the 2-min. The resulting slopes were used to calculate
EMGFT and EEA. Following initial testing, all participants
were randomly assigned to either placebo (PL; n = 18),
beta-alanine (BA; n = 18) or control groups (CON; n = 10).
Following randomization, participants engaged in 6 weeks
of HIIT training. SigniWcant improvements in EMGFT and
EEA resulted for both training groups. In conclusion, HIIT
appeared to be the primary stimulus eVecting EMGFT or
EEA, suggesting adaptations from HIIT may be more inXu-
ential than increasing skeletal muscle carnosine levels on
delaying fatigue in recreationally active men.
Keywords Nutritional supplements
Neuromuscular fatigue Muscle buVering capacity
Training
A. E. Smith J. R. Moon K. L. Kendall J. L. Graef
C. M. Lockwood J. R. Stout (&)
Metabolic and Body Composition Laboratory,
Department of Health and Exercise Science,
University of Oklahoma, 1401 Asp Ave HHC 104,
Norman, OK 73019, USA
e-mail: jrstout@ou.edu
A. A. Walter T. W. Beck J. T. Cramer
Biophysics Laboratory,
Department of Health and Exercise Science,
University of Oklahoma, Norman, OK 73019, USA
Introduction
The use of electromyography (EMG) as a tool for indenti-
fying neuromuscular fatigue has become increasingly more
popular as a method for characterizing changes in muscle
activity. In particular, Moritani et al. (1986, 1993) have
established a valuable relationship between an increase in
EMG amplitude over time as result of progressive recruit-
ment of additional motor units (MU) and/or an increase in
the Wring frequency of MUs that have already been
recruited. The speciWc physiological mechanism responsi-
ble for the increase in EMG amplitude seen during a fatigu-
ing task is unknown. However, three potential mechanisms
have been proposed; an accumulation of metabolic by-
products [lactate, hydrogen ions (H+), inorganic phosphate
(Pi), and ammonia], a depletion of stored energy substrates
[adenosine tri-phosphate (ATP), phosphocreatine (PCr),
and glycogen] and/or impaired muscle cation [potassium
(K+), sodium (Na+) and calcium (Ca2+)] regulation (McCla-
ren et al. 1989; McKenna 1992).
Based on this premise, Matsumoto et al. (1991) and
Moritani et al. (1993) developed an incremental cycle
ergometer test utilizing fatigue curves to identify the maxi-
mal power output at which an individual can maintain with-
out evidence of fatigue, known as the electromyographic
fatigue threshold (EMGFT). The EMGFT test is an adapta-
tion to deVries (1968b) original incremental cycle ergome-
ter test called the physical working capacity at fatigue
threshold (PWCFT), which utilizes the relationship between
EMG amplitude and fatigue during submaximal cycle erg-
ometry to identify the power output that corresponds to the
onset of neuromuscular fatigue (NMF). Similarly, imple-
menting an additional technique developed by deVries
(1968a) identiWed as eYciency of electrical activity (EEA),
uses a change in EMG amplitude that accompanies an
123
358
increase in power output, quantifying the functional state of
a muscle.
Enhancing an individuals ability to buVer H+ may delay
fatigue by improving the use of energy substrates and main-
taining the strength of muscular contraction. Although
recent Wndings question the role of accumulating Pi, adeno-
sine di-phosphate (ADP), and H+ on a decline in perfor-
mance (Pedersen et al. 2004; Westerblad et al. 1997), most
researchers agree that they all are contributing factors in
fatigue. In particular, low intracellular pH levels have been
suggested to aVect muscle Wber action potentials, and
thereby inducing NMF (Mortimer et al. 1970). Furthermore,
enhancing an individuals ability to buVer H+, through high-
intensity training and/or supplementation, may be an eVec-
tive tactic in delaying fatigue (Edge et al. 2006; Juel 2008).
Physiologically, when protons accumulate, the bicarbonate
(HCO3) buVering system assumes the primary role to
maintain homeostasis. However, it has recently been shown
that intramuscular carnosine (
-alanyl-L-histidine) may be
another eVective physiological buVer. Carnosine, a cytoplas-
mic di-peptide is synthesized in the muscle from its two con-
stituents, beta-alanine and histidine. Synthesis is limited,
however, by the availability of beta-alanine (Bakardjiev and
Bauer 1994; Dunnett et al. 1997; Harris et al. 2006). Eleva-
tion of intramuscular carnosine content via beta-alanine sup-
plementation has been shown to be eVective in delaying
fatigue (Derave et al. 2007; Stout et al. 2007) and increasing
time to exhaustion after only 28 days of supplementation
(Hill et al. 2007; Kim et al. 2007).
Several recent studies have suggested that muscle carno-
sine content may be an important variable to consider when
evaluating high-intensity performance (Derave et al. 2007;
Hill et al. 2007; Stout et al. 2007; Suzuki et al. 2004). As an
acute method for inducing fatigue, high-intensity interval
training (HIIT) is an exercise technique using a series of
repeated bouts of high-intensity intervals, interspersed with
short rest periods, with each subsequent trial resulting in
diminished stores of ATP, PCr and glycogenic substrates,
and a subsequent accumulation of metabolites [ADP, Pi, H+
and magnesium (Mg+)], each of which may contribute to
fatigue (Allen et al. 2008; Robergs et al. 2004). The acute
metabolic response is believed to be the driving force
behind the fundamental chronic adaptations reported with
the use of HIIT, leading to an enhanced ability to delay the
onset of acidosis (Weston et al. 1997).
An increasing amount of data supports the hypothesized
role of augmented carnosine levels, as a result of beta-ala-
nine supplementation, for an improvement in muscle buVer
capacity, and in turn, a delay in fatigue (Derave et al. 2007;
Hill et al. 2007; HoVman et al. 2007; Stout et al. 2007). To
date, however, there have been no studies investigating the
eVects of a fatigue inducing training protocol combined
with beta-alanine supplementation on measures of muscle
123
Eur J Appl Physiol (2009) 105:357363
function and fatigue. Thus, the purpose of this study was to
examine the eVects of beta-alanine supplementation in
combination with HIIT on neuromuscular fatigue as mea-
sured by EMGFT, and electrical eYciency activity of the
working muscle in recreationally trained males.
Methods
A total of 46 recreationally active (14 h/week) men
(mean SD, age: 22.2 3.3 years; height: 177.6 7.3 cm;
weight: 77.9 11.4 kg) volunteered to participate in this
investigation. Activity levels were assessed using a health
history questionnaire, detailing hours per week and types of
activity. This project was approved by the Universitys
Institutional Review Board and informed consent was
obtained from each participant prior to enrollment.
Supplementation
Using a randomized, double-blind, placebo-controlled pro-
tocol, participants were randomly assigned to either a pla-
cebo (PL: 16.5 g Xavored dextrose powder per packet;
n = 18),
-alanine (BA: 1.5 g
-alanine, 15 g Xavored dex-
trose powder per packet; n = 18) or control group (CON;
n = 10). Both treatments were pre-packaged to be identical
in taste and appearance and were dissolved in 812 oz. of
water. Each treatment group ingested one packet four times
per day for the Wrst 3 weeks (total of 6 g
-alanine/day). On
the 3 days that subjects visited the lab for training they con-
sumed two pre-mixed doses, one 30 min prior to-, and one
immediately after completing their training session. The
remaining two doses were taken that day, ad libitum. For
the remaining 4 days of the week, participants were asked
to mix and consume the four doses of supplements daily.
During the second 3-week training sessions, participants
supplemented in a similar manner for on- and oV-training
days for an additional 21 days at a dose of 3 g per day taken
in two, 16.5 g doses (1.5 g
-alanine, 15 g dextrose)
throughout the day.
Electromyography
Pre-gelled bipolar (2.54 cm center-to-center) surface elec-
trodes (AgAgCl, Quinton Quick Prep, Quinton Instru-
ments Co., Bothell, WA) were placed on the right thigh
over the lateral portion of the vastus lateralis muscle, midway
between the greater trochanter and the lateral condyle of the
femur (Matsumoto et al. 1991; Moritani et al. 1986). A sin-
gle reference electrode was placed over the spinous process
of the 7th cervical vertebrae. Interelectrode impedance was
kept below 2,000
by careful abrasion of the skin. The
raw EMG signals were pre-ampliWed (gain 1,000) using
Eur J Appl Physiol (2009) 105:357363
a diVerential ampliWer (EMG 100C, Biopac Systems, Inc.,
Santa Barbara, CA), sampled at 1,000 Hz and bandpass
Wltered from 10 to 500 Hz (zero-lag 8th order Butterworth
Wlter). All EMG amplitude values were stored on a personal
computer (Dell Inspiron 8200, Dell, Inc., Round Rock, TX)
and analyzed oV-line using custom written software (Lab-
VIEW v 7.1, National Instruments, Austin, TX).
Determination of EMGFT
The procedures for determination of EMGFT have been
described in detail in a previous report (deVries et al.
1982). BrieXy, the EMGFT was determined using the EMG
amplitude values from the vastus lateralis muscle while
cycling on an electronically braked cycle ergometer (Quin-
ton Corval 400) with the seat height adjusted at near full
extension of the legs while pedaling. After a 5-min warm-
up (50 W), participants performed four, 2-min incremen-
tally ascending workloads (75300 W) at a set cadence of
70 rpm. The initial workload was assigned individually
according to the corresponding workload at which ventila-
tory threshold (VT) was reached (measured during a graded
exercise test). Adequate rest was allotted between bouts to
allow for participants heart rate to drop to within 10 beats
of their resting heart rate. The rate of rise in EMG ampli-
tude values (EMG slope) from four fatiguing power outputs
were plotted over 120 s (Fig. 1a). EMG slope values for
each of the four power outputs were then plotted (Fig. 1b)
to determine the EMGFT. The line of best Wt was then
extrapolated to the y-axis and the power output at which the
y-intercept occurred was deWned as the EMGFT. Partici-
pants completed the EMGFT protocol two times prior-to the
training and supplementing intervention, one familiariza-
tion trial and one pre-testing trial.
Testretest reliability for the EMGFT protocol was deter-
mined by ten healthy male participants measured 2448 h
apart. The intraclass correlation coeYcient (ICC) was
0.933, which was similar to previously reported values
from this lab (ICC = 0.935) and higher than previously
reported by Pavlat et al. (1993) (ICC = 0.65). In addition,
there was no signiWcant diVerence between the mean
EMGFT values from the reliability testing (mean SEM;
pre: 166.1 14.6 vs. post: 154.8 15.6 W).
EYciency of electrical activity (EEA)
The EEA represents the functional state of a muscle and
coincides with the change in electrical activity that accom-
panies an increase in workload (DeVries 1968a). The EEA
technique has been previously described in detail by DeV-
ries (1968a). BrieXy, using bipolar surface electrodes
placed over the vastus lateralis of the right leg, EMG ampli-
tude was measured while participants pedaled for two
359
a
EMG (V)
0 10 20 30 40 50 60 70 80 90 100 110 120
Time (s)
b 400
350
Power Output (W)
300
250
200
EMGFT= 86.52W
150
100
50
0
0 1 2 3 4 5 6 7 8 9 10 11 12
Slope Coefficient ( Vs-1)
Fig. 1 a The graph describes the relationship between EMG ampli-
tude and time for the four power outputs used in the EMGFT test. The
greatest slope was a result from the highest power output. b The graph
depicts the relationship for the power outputs versus slope coeYcients
with the y-intercept deWned as the EMGFT
minutes at four discontinuous workbouts. EEA was deWned
as the average of the four slopes determined during the
respective workloads used to quantify the EMGFT. Mean slope
values were compared across pre- mid- and post-trials.
High-intensity interval training (HIIT)
Training was performed on an electronically braked cycle
ergometer (Corval 400, Groningen, The Netherlands) to
maintain testing speciWcity. Participants began the super-
vised training session within 24 days following testing.
Following the baseline-testing and group randomization,
participants began the Wrst of two, 3-week training periods.
Training followed a fractal periodized plan to allow for
adequate progression and to prevent overtraining (Brown
and Greenwood 2005). The training intensity began at 90%
of the maximum power output achieved during the baseline
VO2 peak test and progressed in an undulating manner,
reaching a maximum of 115% by the end of the second 3-
week training period. The Wrst 3-week training period con-
sisted of Wve sets of 2-min intervals with 1-min rest peri-
ods. The second 3-week session, which began after mid-
testing, followed a similar protocol modifying the progres-
sion by alternating the repetitions during weeks 6 and 7.
123
360 Eur J Appl Physiol (2009) 105:357363

Statistical analysis
A two-way repeated measures analysis of variance [group
(PL vs. BA vs. CON) time (pre vs. mid vs. post)] was
used to identify any group by time interaction. If a signiW-
cant interaction occurred, the statistical model was decom-
posed by examining the simple main eVects with separate
one-way repeated measures ANOVAs for each group and
one-way factorial ANOVAs for each time. If the result was
a simple main eVect, Tukey post hoc comparison were per-
formed among groups, while dependent-samples t tests
with Bonferroni corrections were performed across time. If
there was no interaction, the main eVects were analyzed by
collapsing across the non-interacting variables and ana-
lyzed in the same approach as described for the simple
main eVect. An alpha of P 0.05 was used to determine
statistical signiWcance. The analyses were performed using
SPSS v. 14.0 (SPSS Inc., Chicago, IL). All data are
reported as mean standard deviation (SD).
Results
Table 1 presents the mean and standard deviation values for
EMGFT and EEA values between groups.
EMGFT
A two-way ANOVA resulted in a signiWcant interaction
(P = 0.044) for group and time for pre- to mid-EMGFT
absolute values. Results for the simple time group inter-
actions demonstrated a signiWcant improvement from pre-
to mid-testing for both the PL (P = 0.001) and BA
(P = 0.001) (Table 1). In addition, there was a signiWcant
main eVect for time (P = 0.001) for pre- to post-testing
EMGFT values. Simple main eVect results indicated that
both treatment groups (PL and BA) demonstrated a signiW-
cant delay in neuromuscular fatigue (P = 0.016 and P = 0.001,
respectively). Although there were no signiWcant diVerences
for the absolute change in EMGFT between PL and BA
groups, the change in EMGFT from baseline were substan-
tial for both treatment groups at mid-testing(29.6 29.9 vs.
26.6 28.3 W for PL and BA) and little change at post-
testing (2.2 34.4 vs. 1.6 27.6 W, respectively). Fur-
thermore, individual response data demonstrated that 89 and
56% of the placebo group participants improved at mid-test
and post-test assessments, respectively. A total of 79 and
39% of the individuals in the BA group demonstrated
improvements at mid- and post-testing, respectively (Fig. 2).
EEA
Similar to the Wndings for EMGFT, the results for EEA dem-
onstrated a signiWcant interaction for pre- to mid-EEA
assessments (P = 0.001). Both treatment groups demon-
strated a signiWcant absolute change from pre- to mid (PL
and BA, P = 0.001) and from pre- to post-EEA (PL and BA
P = 0.001) with no change from mid- to post-testing assess-
ments. A signiWcant interaction was also reported for pre- to
post-EEA assessments (P = 0.015). Post hoc comparisons
demonstrated that mid-EEA values were signiWcantly less for
placebo compared to control (P = 0.016) with no diVerence
for the BA group. Furthermore, post-EEA values were sig-
niWcantly lower for both PL and BA compared to the control
group (P = 0.009 and P = 0.043, respectively), with no diVer-
ences between groups. Individuals in both the PL and BA
groups demonstrated similar increases in EEA at mid- (89%)
and post-EEA testing (44 and 50%, respectively).

Table 1 Mean SD values

Pre EMGFT Mid EMGFT Post EMGFT Pre EEA Mid EEA Post EEA
for pre-, mid- and post-EMGFT
EEA values
-Alanine 138.3 164.9* 166.59 1.350 0.593* 0.5549
n = 18 46.4 33.7 35.9 0.961 0.8.8 0.402
Placebo 124.5 154.1* 156.39 1.034 0.485* 0.3739
* SigniWcant diVerence from pre n = 18 36.0 40.6 53.2 0.709 0.490 0.430
to mid
Control 154.8 152.4 170.8 1.066 1.288 1.066
9 SigniWcant diVerence from
n = 10 49.2 58.6 58.0 1.045 1.169 0.879
prepost

Fig. 2 The change in EMGFT Beta-Alanine Placebo Control

from pre- to mid- and mid- to
EMGFT(% Change)

EMGFT(% Change)

EMGFT(% Change)

200 200
post-testing for each individual, 200
150 150 150
across all treatment groups 100
100 100
(beta-alanine, placebo 50
50
and control) 50
0
0
0 -50
-50
-100
-50 Baseline %Change %Change -100
MID POST Baseline %Change %Change
-100 Baseline %Change %Change
MID POST
MID POST

123
Eur J Appl Physiol (2009) 105:357363
Discussion
The present study is the Wrst to utilize a neuromuscular
fatigue threshold as a non-invasive way of evaluating phys-
iological adaptations that may occur following HIIT and
beta-alanine supplementation. The Wndings of this study
suggest that 3 weeks of HIIT may be suYcient for eliciting
a signiWcant increase in EMGFT, with only slightly greater
improvements resulting following 6 weeks of HIIT. In
addition, EEA improved signiWcantly following 3 and
6 weeks of HIIT in college-aged males. However, the addi-
tion of beta-alanine provided no additional improvements
in either EMGFT or EEA.
Twenty-eight days of beta-alanine supplementation has
previously demonstrated signiWcant improvements in neu-
romuscular fatigue, as measured by the physical working
capacity at fatigue threshold (PWCFT) in both men (14.5%
increase) (Stout et al. 2006) and women (12.6% increase)
(Stout et al. 2007). The delay in neuromuscular fatigue has
been attributed to an increase in muscle carnosine concen-
trations as a result of beta-alanine supplementation. It has
been suggested that augmenting muscle carnosine may
enhance intramuscular hydrogen ion (H+) buVering capac-
ity (Harris et al. 1990, 2006; Hill et al. 2007), calcium sen-
sitivity and excitationcontraction coupling (Batrukova and
Rubtsov 1997; Lamont and Miller 1992). Furthermore, pre-
vious research supports the use of beta-alanine supplemen-
tation, in combination with training, to augment
performance (Derave et al. 2007; Hill et al. 2007). Whereas
training alone has been unable to augment intramuscular
carnosine levels (Harris et al. 2007; Kim et al. 2007).
McClaren et al. (1989) have suggested that a decrease in
muscle pH, resulting from the accumulation of intramuscu-
lar H+ or an increase in intracellular and extracellular
ammonia, may be responsible for fatigue-induced increases
in motor unit recruitment and the corresponding increase in
EMG amplitude. In agreement, Taylor et al. (1997) also
found that, for incremental cycle ergometry, the accumula-
tion of plasma lactate and ammonia was associated with an
increase in EMG amplitude. Therefore, there is evidence to
suggest that a signiWcant reliance on anaerobic glycolysis
leads to an increase in EMG amplitude from the working
muscles as a result of changes in muscle and blood lactate
levels and the corresponding decrease in skeletal muscle
pH (Moritani et al. 1993; Taylor et al. 1997).
Moritani et al. (1993) speculate that the EMGFT may be
closely associated with a steady state of lactate metabolism
and H+ accumulation in the active muscle. The current
study utilized the EMGFT protocol as a means of identify-
ing intramuscular changes following HIIT and/or beta-ala-
nine supplementation. Although no other studies have
reportedly used the EMGFT to assess neuromuscular
changes following training, the EMGFT has been closely
361
related to the aerobicanaerobic transition phase of exercise
and the lactate and ventilatory thresholds (Maestu et al.
2006; Moritani et al. 1993). Similarly, high-intensity train-
ing studies utilizing brief recovery periods (50 s to 4 min)
have reported improvements in aerobic metabolism
(Harmer et al. 2000; Stathis et al. 1994), as well as
enhanced lactate/H+ clearance (Bishop et al. 2004; Harmer
et al. 2000; Pilegaard et al. 1999). Coupled with the
improved lactate/H+ transport, intense training has report-
edly enhanced lactate/H+ transport capacity in the sarco-
lemma (Pilegaard et al. 1999). Furthermore, studies
utilizing the same short (1 min) rest periods, as employed in
the current study; have reported signiWcant increases in
muscle buVering capacity of 1625% (Bishop et al. 2004;
Edge et al. 2006).
The EMGFT has been closely related to steady state lac-
tate metabolism (Moritani et al. 1993) and, thus, as sug-
gested from training, should reXect improvements in
lactate/H+ clearance and muscle buVering capacity. The
EMGFT is also unique in that it may be inXuenced by cen-
tral and/or peripheral manifestations of high-intensity
exercise. In agreement, signiWcant improvements in
EMGFT were evident following 3 and 6 weeks of HIIT in
the current study (Table 1). However, the addition of beta-
alanine did not elicit signiWcantly greater improvements
in EMGFT compared to training alone. These results may
be due to the sizeable reoccurring improvements in mus-
cle buVer capacity as a result of the high-intensity training
alone.
The EEA, has also been shown reXect the functional
state of a muscle, yet distinct in its ability to discount psy-
chological factors when determining muscular strength
(DeVries 1968a). Additionally, the EEA has shown sensi-
tivity to muscular hypertrophy and atrophy (DeVries
1968a). The current study demonstrated signiWcant
improvements in EEA after 3 and 6 weeks of HIIT
(Table 1). While there were no additional improvements
in EEA with the use of beta-alanine supplementation,
these Wndings are supported by the hypothesis that EEA
more closely represents a muscles ability to overpower a
given resistance than the capacity to maintain the resis-
tance for an extended period of time (Housh et al. 1991).
The use of beta-alanine would, in theory, improve a mus-
cles ability to maintain a given workload. Furthermore,
the degree of training intensity used in this protocol, may
account for the improvements in the functional capacity
of the leg muscles.
Conclusions
In summary, the EMGFT theoretically represents the highest
power output that can be sustained during cycle ergometry
123
362
for an extended period of time without signs of neuromus-
cular fatigue (Matsumoto et al. 1991). The primary Wndings
of this study suggest that HIIT may signiWcantly increase
EMGFT in college-aged men, and thereby increase the
power output that can be maintained on a cycle ergometer
for an extended period of time without exhaustion. In addi-
tion, the current study supports the use of HIIT to improve
EEA, ultimately reXecting an improvement in the physio-
logical functioning of the lower body muscle tissue. While
beta-alanine supplementation had no signiWcant inXuence
on EMGFT or EEA, the training protocol may have been a
superior stimulus in untrained men, minimizing any eVect
of increased carnosine levels. Future studies utilizing
trained participants or implementing a less demanding
training protocol may be important in assessing the role of
beta-alanine in muscle buVering.
Acknowledgments The authors would like to thank FSI Nutrition,
2132 South 156th Circle, Omaha, NE (www.fsinutrition.com) and
RunFast Promotions, 8790 Wendy Lane South, West Palm Beach FL,
33411(www.runfastpromotions.com) for supporting and funding this
research endeavor.
References
Allen DG, Lamb GD, Westerblad H (2008) Skeletal muscle fatigue:
cellular mechanisms. Physiol Rev 88:287332. doi:10.1152/
physrev.00015.2007
Bakardjiev A, Bauer K (1994) Transport of beta-alanine and biosyn-
thesis of carnosine by skeletal muscle cells in primary culture. Eur
J Biochem 225:617623. doi:10.1111/j.1432-1033.1994.00617.x
Batrukova MA, Rubtsov AM (1997) Histidine-containing dipeptides
as endogenous regulators of the activity of sarcoplasmic reticu-
lum Ca-release channels. Biochim Biophys Acta 1324:142150.
doi:10.1016/S0005-2736(96)00216-7
Bishop D, Edge J, Goodman C (2004) Muscle buVer capacity and aer-
obic Wtness are associated with repeated-sprint ability in women.
Eur J Appl Physiol 92:540547. doi:10.1007/s00421-004-1150-1
Brown L, Greenwood M (2005) Periodization essentials and innova-
tions in resistance training protocols. JSCR 27:8085
Derave W, Ozdemir MS, Harris RC, Pottier A, Reyngoudt H, Koppo
K, Wise JA, Achten E (2007) beta-Alanine supplementation aug-
ments muscle carnosine content and attenuates fatigue during re-
peated isokinetic contraction bouts in trained sprinters. J Appl
Physiol 103:17361743. doi:10.1152/japplphysiol.00397.2007
DeVries HA (1968a) EYciency of electrical activity as a physiolog-
ical measure of the functional state of muscle tissue. Am J Phys
Med 47:1022
DeVries HA (1968b) Method for evaluation of muscle fatigue and
endurance from electromyographic fatigue curves. Am J Phys
Med 47:125135
deVries HA, Moritani T, Nagata A, Magnussen K (1982) The relation
between critical power and neuromuscular fatigue as estimated
from electromyographic data. Ergonomics 25:783791
Dunnett M, Harris RC, Soliman MZ, Suwar AA (1997) Carnosine,
anserine and taurine contents in individual Wbres from the middle
gluteal muscle of the camel. Res Vet Sci 62:213216
Edge J, Bishop D, Goodman C (2006) The eVects of training inten-
sity on muscle buVer capacity in females. Eur J Appl Physiol
96:97105
123
Eur J Appl Physiol (2009) 105:357363
Harmer AR, McKenna MJ, Sutton JR, Snow RJ, Ruell PA, Booth J,
Thompson MW, Mackay NA, Stathis CG, Crameri RM, Carey
MF, Eager DM (2000) Skeletal muscle metabolic and ionic adap-
tations during intense exercise following sprint training in hu-
mans. J Appl Physiol 89:17931803
Harris RC, Marlin DJ, Dunnett M, Snow DH, Hultman E (1990) Mus-
cle buVering capacity and dipeptide content in the thoroughbred
horse, greyhound dog and man. Comp Biochem Physiol A
97:249251
Harris RC, Tallon MJ, Dunnett M, Boobis L, Coakley J, Kim HJ, Fal-
lowWeld JL, Hill CA, Sale C, Wise JA (2006) The absorption of
orally supplied beta-alanine and its eVect on muscle carnosine
synthesis in human vastus lateralis. Amino Acids 30:279289
Harris RC, Kendrick IP, Kim CK, Hyojeong K, Dang VH, Lam TQ,
Bui TT, Wise JA (2007) The eVect of physical training on the car-
nosine content of V Lateralis using a one-leg training model. Med
Sci Sports Exerc 39:S91
Hill CA, Harris RC, Kim HJ, Harris BD, Sale C, Boobis LH, Kim CK,
Wise JA (2007) InXuence of beta-alanine supplementation on
skeletal muscle carnosine concentrations and high intensity cy-
cling capacity. Amino Acids 32:225233
HoVman J, Ratamess N, Faigenbaum A, Ross R, Kang J, Stout J, Wise
JA (2007) Short-duration beta-alanine supplementation increases
training volume and reduces subjective feelings of fatigue in col-
lege football players. Nutr Res 28:3135
Housh TJ, Devries HA, Housh DJ, Tichy MW, Smyth KD, Tichy
AM (1991) The relationship between critical power and the
onset of blood lactate accumulation. J Sports Med Phys Fitness
31:3136
Juel C (2008) Regulation of pH in human skeletal muscle: adaptations
to physical activity. Acta Physiol (Oxf) 193:1724
Kim CK, Kim HJ, Lee YW, Harris RC, Sale C, Harris BD, Wise JA
(2007) Combined training and B-alanine supplementationmus-
cle carnosine synthesis, ventilatory threshold and exercise capac-
ity in cyclists. Med Sci Sports Exerc 39:S364
Lamont C, Miller DJ (1992) Calcium sensitizing action of carnosine
and other endogenous imidazoles in chemically skinned striated
muscle. J Physiol 454:421434
Maestu J, Cicchella A, Purge P, Ruosi S, Jurimae J, Jurimae T (2006)
Electromyographic and neuromuscular fatigue thresholds as con-
cepts of fatigue. J Strength Cond Res 20:824828
Matsumoto T, Ito K, Moritani T (1991) The relationship between
anaerobic threshold and electromyographic fatigue threshold in
college women. Eur J Appl Physiol Occup Physiol 63:15
McClaren DP, Gibson H, Parry-Billings M, Edwards RHT (1989) A
review of metabolic and physiological factors in fatigue. Exerc
Sport Sci Rev 17:2968
McKenna MJ (1992) The roles of ionic processes in muscular fatigue
during intense exercise. Sports Med 13:134145
Moritani T, Muro M, Nagata A (1986) Intramuscular and surface elec-
tromyogram changes during muscle fatigue. J Appl Physiol
60:11791185
Moritani T, Takaishi T, Matsumoto T (1993) Determination of maxi-
mal power output at neuromuscular fatigue threshold. J Appl
Physiol 74:17291734
Mortimer JT, Magnusson R, Petersen I (1970) Conduction velocity in
ischemic muscle: eVect on EMG frequency spectrum. Am J Phys-
iol 219:13241329
Pavlat DJ, Housh TJ, Johnson GO, Schmidt RJ, Eckerson JM (1993)
An examination of the electromyographic fatigue threshold test.
Eur J Appl Physiol Occup Physiol 67:305308
Pedersen TH, Nielsen OB, Lamb GD, Stephenson DG (2004) Intracel-
lular acidosis enhances the excitability of working muscle. Sci-
ence 305:11441147
Pilegaard H, Domino K, Noland T, Juel C, Hellsten Y, Halestrap AP,
Bangsbo J (1999) EVect of high-intensity exercise training on lac-
Eur J Appl Physiol (2009) 105:357363
tate/H+ transport capacity in human skeletal muscle. Am J Phys-
iol 276:E255E261
Robergs RA, Ghiasvand F, Parker D (2004) Biochemistry of exercise-
induced metabolic acidosis. Am J Physiol Regul Integr Comp
Physiol 287:R502R516
Stathis CG, Febbraio MA, Carey MF, Snow RJ (1994) InXuence of
sprint training on human skeletal muscle purine nucleotide metab-
olism. J Appl Physiol 76:18021809
Stout JR, Cramer JT, Mielke M, OKroy J, Torok DJ, Zoeller RF (2006)
EVects of twenty-eight days of beta-alanine and creatine monohy-
drate supplementation on the physical working capacity at neuro-
muscular fatigue threshold. J Strength Cond Res 20:928931
Stout JR, Cramer JT, Zoeller RF, Torok D, Costa P, HoVman JR, Har-
ris RC, OKroy J (2007) EVects of beta-alanine supplementation
on the onset of neuromuscular fatigue and ventilatory threshold in
women. Amino Acids 32:381386
363
Suzuki Y, Ito O, Takahashi H, Takamatsu K (2004) The eVect of sprint
training on skeletal muscle carnosine in humans. Int J Sport
Health Sci 2:105110
Taylor AD, Bronks R, Bryant AL (1997) The relationship between
electromyography and work intensity revisited: a brief review
with references to lacticacidosis and hyperammonia. Electro-
myogr Clin Neurophysiol 37:387398
Westerblad H, Bruton JD, Lannergren J (1997) The eVect of intracel-
lular pH on contractile function of intact, single Wbres of mouse
muscle declines with increasing temperature. J Physiol 500 (Pt
1):193204
Weston AR, Myburgh KH, Lindsay FH, Dennis SC, Noakes TD, Haw-
ley JA (1997) Skeletal muscle buVering capacity and endurance
performance after high-intensity interval training by well-trained
cyclists. Eur J Appl Physiol Occup Physiol 75:713
123