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Beta-Alanine supplementation reduces acidosis but not oxygen uptake response during high-intensity cycling exercise


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The oral ingestion of beta-alanine, the rate-limiting precursor in carnosine synthesis, has been shown to elevate the muscle carnosine content. Carnosine is thought to act as a physiologically relevant pH buffer during exercise but direct evidence is lacking. Acidosis has been hypothesised to influence oxygen uptake kinetics during high-intensity exercise. The present study aimed to investigate whether oral beta-alanine supplementation could reduce acidosis during high-intensity cycling and thereby affect oxygen uptake kinetics. 14 male physical education students participated in this placebo-controlled, double-blind study. Subjects were supplemented orally for 4 weeks with 4.8 g/day placebo or beta-alanine. Before and after supplementation, subjects performed a 6-min cycling exercise bout at an intensity of 50% of the difference between ventilatory threshold (VT) and VO(2peak). Capillary blood samples were taken for determination of pH, lactate, bicarbonate and base excess, and pulmonary oxygen uptake kinetics were determined with a bi-exponential model fitted to the averaged breath-by-breath data of three repetitions. Exercise-induced acidosis was significantly reduced following beta-alanine supplementation compared to placebo, without affecting blood lactate and bicarbonate concentrations. The time delay of the fast component (Td(1)) of the oxygen uptake kinetics was significantly reduced following beta-alanine supplementation compared to placebo, although this did not reduce oxygen deficit. The parameters of the slow component did not differ between groups. These results indicate that chronic beta-alanine supplementation, which presumably increased muscle carnosine content, can attenuate the fall in blood pH during high-intensity exercise. This may contribute to the ergogenic effect of the supplement found in some exercise modes.
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b-Alanine supplementation reduces acidosis but not oxygen
uptake response during high-intensity cycling exercise
Audrey Baguet Katrien Koppo Andries Pottier
Wim Derave
Accepted: 22 September 2009 / Published online: 16 October 2009
ÓSpringer-Verlag 2009
Abstract The oral ingestion of b-alanine, the rate-limit-
ing precursor in carnosine synthesis, has been shown to
elevate the muscle carnosine content. Carnosine is thought
to act as a physiologically relevant pH buffer during
exercise but direct evidence is lacking. Acidosis has been
hypothesised to influence oxygen uptake kinetics during
high-intensity exercise. The present study aimed to inves-
tigate whether oral b-alanine supplementation could reduce
acidosis during high-intensity cycling and thereby affect
oxygen uptake kinetics. 14 male physical education stu-
dents participated in this placebo-controlled, double-blind
study. Subjects were supplemented orally for 4 weeks with
4.8 g/day placebo or b-alanine. Before and after supple-
mentation, subjects performed a 6-min cycling exercise
bout at an intensity of 50% of the difference between
ventilatory threshold (VT) and _
VO2peak. Capillary blood
samples were taken for determination of pH, lactate,
bicarbonate and base excess, and pulmonary oxygen uptake
kinetics were determined with a bi-exponential model fitted
to the averaged breath-by-breath data of three repetitions.
Exercise-induced acidosis was significantly reduced fol-
lowing b-alanine supplementation compared to placebo,
without affecting blood lactate and bicarbonate concen-
trations. The time delay of the fast component (Td
) of the
oxygen uptake kinetics was significantly reduced following
b-alanine supplementation compared to placebo, although
this did not reduce oxygen deficit. The parameters of
the slow component did not differ between groups. These
results indicate that chronic b-alanine supplementation,
which presumably increased muscle carnosine content, can
attenuate the fall in blood pH during high-intensity exer-
cise. This may contribute to the ergogenic effect of the
supplement found in some exercise modes.
Keywords Ergogenic supplements
High-intensity cycling Acidosis _
Maintaining acid–base balance is a major challenge during
high-intensity exercise, when large amounts of protons are
produced and released as a consequence of the anaerobic
energy delivery in the active musculature (Hultman and
Sahlin 1980). A significant portion of the contraction-
induced protons are rapidly transported out of the active
myocytes and buffered by the circulating buffers, such as
bicarbonate. In addition to the various sarcolemmal ion
transporters that can promote this proton efflux (Juel 1998),
several intramyocellular pH buffers are available as a first-
line defence against exercise-induced acidosis (Parkhouse
and McKenzie 1984). These include free inorganic phos-
phate, creatine phosphate and the histidine residues in both
proteins and in histidine-containing dipeptides (HCD). In
humans, the HCD are exclusively represented by carnosine
(b-alanyl-L-histidine) (Quinn et al. 1992). The relative
importance and quantitative contribution to total buffering
capacity of these skeletal muscle buffering constituents has
been a subject of discussion. Carnosine is likely not the
most important buffer in absolute terms, with a relative
contribution estimated to be approximately 8–15% in
human muscle (Hill et al. 2007; Parkhouse et al. 1985).
However, the molecule draws our special attention because
Communicated by Susan Ward.
A. Baguet K. Koppo A. Pottier W. Derave (&)
Department of Movement and Sports Sciences,
Ghent University, Watersportlaan 2, 9000 Ghent, Belgium
Eur J Appl Physiol (2010) 108:495–503
DOI 10.1007/s00421-009-1225-0
of two reasons: (1) its imidazole group has an optimal pKa
value of 6.83 (Bate Smith 1938), knowing that intramyo-
cellular pH at rest is 7.0–7.1 and can drop during high-
intensity contractions to values as low as 6.3–6.5, and (2)
because of the flexibility of its myoplasmic concentration.
Recent studies (Harris et al. 2006; Hill et al. 2007; Derave
et al. 2007) have shown that oral supplementation with
b-alanine, the rate-limiting precursor of the dipeptide
synthesis, can elevate muscle carnosine content by 40–80%,
depending on the dose (usually between 3.2 and 6.4 g/day)
and duration (4–10 weeks). Noneof the other skeletal muscle
buffer pools is nearly as expansible.
Carnosine is a pleiotropic molecule, with pH buffering
capacity in muscle as only one of several possible other
physiological functions (Begum et al. 2005). Carnosine can
act as metal chelator, an anti-oxidant and an antiglycation
agent. In skeletal muscle, where the majority of the body’s
carnosine is found, carnosine can act as a Ca
for the sarcomeres (Dutka and Lamb 2004; Lamont and
Miller 1992) and by this mechanism possibly protect
against fatigue (Rubtsov 2001). Additionally, exercise-
induced oxidative stress is involved in contractile muscle
fatigue (Powers and Jackson 2008) and can supposedly be
antagonised by the antioxidative effects of carnosine
(Kohen et al. 1988). Several lines of evidence suggest that
carnosine is ergogenic. b-Alanine supplementation resulted
in performance enhancement in some exercise modes, such
as a single high-intensity exercise bout (Hill et al. 2007;
Stout et al. 2007), in sprint exercise at the end of an
endurance cycling race (Van Thienen et al. 2009) and in
repeated maximal contraction bouts (Derave et al. 2007). In
vitro work on isolated frog muscles has shown that addition
of carnosine to the incubation medium can potently an-
tagonise contractile fatigue (Severin et al. 1953; Boldyrev
and Petukhov 1978). It remains to be established by which
mechanism these ergogenic effects are established. An
improved pH buffer capacity certainly is a candidate,
because alternative ways to improve the buffer capacity
(albeit in blood instead of muscle) by acute oral bicar-
bonate ingestion have shown to improve performance in
exercise modes of similar duration and intensity, i.e. single
or repeated maximal exercise bouts of 30 s to 7 min of
duration (Linderman and Gosselink 1994). A first aim of
the current study was to explore the potential of carnosine
to attenuate exercise-induced acidosis in high-intensity
exercise of fixed intensity and duration.
The low blood pH resulting from anaerobic work is
thought to affect the oxygen uptake ( _
VO2) kinetics of high-
intensity exercise. In the transition from rest to exercise at
an intensity above the ventilatory threshold (VT) three
phases can be distinguished: (1) a short cardio-dynamic
phase (15–25 s), (2) a fast component (2–3 min) charac-
terised by an exponential rise in _
VO2and (3) a slow
component where _
VO2shows a slow but gradual increase
towards a steady-state or peak oxygen uptake ( _
Several studies have shown that pre-exercise alkalosis,
either elicited by hyperventilation (Hayashi et al. 1999;
Ward et al. 1983) or by bicarbonate ingestion (Kolkhorst
et al. 2004), slows the fast component of _
VO2, probably by
inducing a leftward shift of the oxygen–haemoglobin dis-
sociation curve and reducing the O
delivery to the work-
ing muscles. However, others (Berger et al. 2006) did not
observe an effect of pre-exercise metabolic alkalosis on
VO2kinetics, and even others (Zoladz et al. 2005) found a
speeding of the fast component.
With regard to the nature of the slow component of _
kinetics, i.e. why _
VO2/W values are higher above than
below the VT, several physiological mechanisms have
been investigated, such as elevation in body and/or muscle
temperature, cardiac and ventilatory muscle work, auxil-
iary muscle work, recruitment of fast-twitch fibres and
metabolic factors (reviewed in Gaesser and Poole 1996;
Zoladz and Korzeniewski 2001). A possible candidate for
the latter is the acidosis, because a slow component only
occurs at exercise intensities above VT, i.e. where lactate
accumulation occurs. In order to investigate this more
causally, several interventions with enhancement or atten-
uation of exercise-induced acidosis have been performed.
Zoladz et al. (1998) observed that the magnitude of the
slow component is increased following acute pre-exercise
acidification induced by ingestion of ammonium chloride.
The effects of pre-exercise alkalinisation by oral sodium
bicarbonate ingestion are more equivocal. Some authors
found a significant reduction of the slow component
(Kolkhorst et al. 2004; Berger et al. 2006), whereas several
others observed no effect of bicarbonate (Heck et al. 1998;
Santalla et al. 2003; Zoladz et al. 1997).
The purpose of the present study was to explore whether
4 weeks of b-alanine supplementation can attenuate exer-
cise-induced acidosis during a fixed 6-min exercise bout at
an intensity calculated as 50% of the difference between
VT and _
VO2peak. In order to investigate the effect of the
possibly suppressed acidosis on the fast and slow compo-
nent of _
VO2kinetics, the exercise bout was repeated three
times in each condition on separate days, allowing optimal
bi-exponential modelling of breath-by-breath data.
Fourteen male physical education students volunteered to
participate in this study. All subjects were physically
active, but not involved in sports competition or organised
training. The subjects’ age, weight, height and maximal
496 Eur J Appl Physiol (2010) 108:495–503
oxygen uptake were 21.9 ±1.5 years, 74.9 ±8.3 kg,
1.80 ±0.05 m and 55.5 ±3.6 mL/(kg min) for placebo
and 21.1 ±0.7 years, 71.8 ±8.8 kg, 1.78 ±0.07 m and
57.1 ±4.7 mL/(kg min) for b-alanine group, respectively
(NS). Subjects reported that they did not take any other oral
supplement during the study nor had taken nutritional
supplements in the 3 months prior to the study. Subjects
were asked to abstain from exercise 24 h before each test
and to maintain their normal physical activity during the
study. During this study they did not participate in regular
or organised training. The subjects gave their informed
consent and the study was approved by the local Ethics
Committee (Ghent University Hospital, Belgium).
Experimental protocol
The subjects of this placebo-controlled, double-blind study,
were randomised, based on their ( _
VO2peak) and blood pH at
the end of a 6-min cycling exercise at a power output
equivalent to 50% of the difference between VT and
VO2peak (50% D) into a control and experimental group.
They were supplemented for 4 weeks with either placebo
(maltodextrine) or b-alanine (Carnosyn
, National
Alternatives International, San Marcos, USA). Supple-
ments were provided in capsules of 400 mg and were
administered each day as six divided doses, with at least
2 h in between ingestions. Daily doses consisted of 2.4 g/
day during the first 2 days, 3.6 g/day during the subsequent
2 days, and from then on 4.8 g/day until the end of the
supplementation. In a recent study on a similar study
population, we have shown that this supplementation
schedule leads to significant elevations in the carnosine
content of both slow-twitch and fast-twitch muscle types
(Baguet et al. 2009). Each subject performed a maximal
ramp exercise test on an electromagnetically braked cycle
ergometer (Lode, Excalibur sport; Groningen, The Neth-
erlands) to determine _
VO2peak and ventilatory threshold
(VT). Pedalling frequency was kept between 75 and
80 rpm. After a warm-up of 3 min at 50 W, the work load
was increased by 30 W/min to the point the subjects failed
to continue to pedal at 75 rpm. The gas exchange threshold
(GET) was determined as the point at which there was the
beginning of a systematic increase in _
VO2, but not in
VCO2, by two independent experienced researchers.
For all subjects, work rates equivalent to 50% Dwere
There were two test periods (Pre and Post) with 4 weeks
of supplementation with b-alanine or placebo in between.
Each test period lasted 1 week and included on Monday,
Wednesday and Friday a 6-min cycle exercise bout at a
power output equivalent to 50% D. The 50% Dtest was
preceded by 3 min of baseline pedalling at 10 W and was
followed by 4 min of unloaded pedalling. The exercise test
sessions were conducted at the same time of the day for
each subject to account for any possible circadian rhythm
Before and during the exercise bouts, _
VO2was measured
continuously on a breath-by-breath basis by means of a
computerised O
analyser-flowmeter combination
(Jaeger Oxycon Pro, Germany). Prior to each exercise
test, the gas analysers (an O
-analyser with functioning
based on the differential-paramagnetic principle and an
infrared CO
-analyser) were calibrated and the volume
calibration (‘triple V’ transducer) was conducted. Capil-
lary blood samples (150 lL) were taken from a hype-
raemic ear lobe in order to determine blood gas analysis
(GEM, Premier
3000, Instrumentation Laboratory) at
rest (following warm-up), after 3 min cycling at 50% D,
after 6 min cycling at 50% Dand after 4 min recovery.
The blood samples were taken in two of the three tests
per condition (Wednesday and Friday) and the data of the
two samples were averaged. In the blood samples pH
and lactate were measured and bicarbonate and base
excess were calculated (base excess =(1 -0.014[Hb]) 9
]-24 ?(1.43[Hb] ?7.7) (pH -7.4))). In sub-
jects where blood lactate exceeded 15 mmol/L during
exercise, Lactate Pro strips (Arkray Inc, Kyoto, Japan)
were used for blood lactate determination.
The breath-by-breath _
VO2data from each test were initially
examined to exclude errant breaths caused by coughing,
swallowing, sighing, etc., and those values exceeding local
mean by more than 4 standard deviations were deleted. The
breath-by-breath _
VO2data from each test were subsequently
linearly interpolated to give 1 s-values. For each subject and
each condition, the three identical repetitions were time-
aligned to the start of exercise, superimposed, and ensemble
averaged to reduce the breath-to-breath noise and enhance the
underlying physiological response characteristics. The base-
line _
VO2was defined as the average _
VO2measured during
baseline pedalling between 150 and 30 s before the start of the
50% Dbout. The initial cardiodynamic component was
ignored by eliminating the first 20 s of data after the onset of
exercise. Subsequently, each averaged response was descri-
bed using a bi-exponentialmodel with the following equation:
VO2tðÞ¼ _
VO2baseline þA11etTd1ðÞ
This model includes amplitudes (A), time constants (s)
and delay times (Td) for the _
VO2fast (subscript 1) and the
Eur J Appl Physiol (2010) 108:495–503 497
VO2slow (subscript 2) component which were determined
using a non linear least-square algorithm. Because the
asymptotic value A
may represent a higher value than that
actually reached at the end of the exercise, the value of the
VO2slow exponential term at the end of exercise was
defined as A
The O
deficit was computed by integrating the differ-
ence between the _
VO2requirement for the exercise
(assumed to be represented by the average _
VO2during the
last 30 s of exercise) and the actual measured _
A292 repeated measures analysis of variance (RM
ANOVA) was used to evaluate pH, lactate, bicarbonate,
base excess, _
VO2kinetic parameters (A, sand Td), _
ventilation ( _
VE) and CO
output ( _
VCO2) with ‘group’
(placebo vs. b-alanine) as between-subjects factor and
‘time’ (Pre and Post) as a within-subjects factor (SPSS
statistical software, SPSS Inc, Chicago, USA). Values are
presented as mean ±SD and significance was assumed at
Blood gas analysis
Table 1shows an overview of the blood gas analysis param-
eters. Blood pH at rest was approximately 7.41–7.42 and was
not affected by supplementation. The cycling exercise at an
intensity of 50% Delicited a marked acidosis towards values
around 7.20 at the sixth minute. There was no significant
interaction effect of the absolute pH values at 6 min of exer-
cise (Ex6), but Fig. 1shows that the pH difference between
baseline and Ex6 (i.e. the exercise-induced acidosis) is sig-
nificantly different between b-alanine and placebo group over
the time (interaction effect; p=0.031). As a result of
4 weeks’ supplementation the DpH from baseline to the end of
high-intensity cycling decreased with 0.015 units in the
b-alanine group and increased with 0.012 pH units in the
placebo group. Blood lactate increased to values of
*13 mmol/L at the end of exercise and slightly declined at
4 min into recovery. Bicarbonate and base excess markedly
decreased during high-intensity exercise. None of these
parameters (lactate, bicarbonate and base excess) showed a
significant group effect or interaction.
Pulmonary gas exchange
Figure 2shows a typical graph of the _
VO2before (Pre) and
after (Post) b-alanine and placebo supplementation. As
shown in Table 2, the _
VO2profile contains a clear slow
component (A
0)of*500 mL, as can be expected for
exercise intensities above the VT. For both groups there
were no significant differences (p[0.05) in _
throughout exercise prior to or after supplementation. As
shown in Table 3the _
VE was *22 L/min after warm up
and increased fivefold throughout the 6-min intensive
cycling, with no differences between both groups. For both
groups the _
VCO2was *750 mL/min after warm-up and
increased to *4,100 mL/min after a 6-min cycling exer-
cise at 50% Dbefore and after supplementation. Also for
VCO2there were no significant differences between
b-alanine and placebo (Table 3).
Table 1 Capillary pH, lactate, bicarbonate and base excess before (Pre) and after (Post) supplementation with b-alanine or placebo at rest, after
3 min exercise (Ex3), after 6 min exercise (Ex6) and 4 min into recovery (R4)
b-Alanine Placebo
Rest Ex3 Ex6 R4 Rest Ex3 Ex6 R4
Pre 7.419 ±0.009 7.284 ±0.042 7.214 ±0.058 7.251 ±0.057 7.425 ±0.026 7.270 ±0.039 7.203 ±0.062 7.229 ±0.067
Post 7.411 ±0.016 7.274 ±0.032 7.221 ±0.054 7.251 ±0.048 7.411 ±0.024 7.244 ±0.046 7.177 ±0.070 7.216 ±0.059
Lactate (mmol/L)
Pre 1.16 ±0.62 9.89 ±1.90 13.41 ±2.16 11.31 ±2.87 1.01 ±0.38 10.26 ±2.06 13.64 ±1.07 11.89 ±2.09
Post 1.36 ±0.66 10.69 ±1.97 13.82 ±2.13 12.24 ±2.63 1.06 ±0.35 10.16 ±1.78 13.91 ±0.98 11.97 ±1.80
Bicarbonate (mmol/L)
Pre 26.55 ±1.27 20.39 ±2.03 15.37 ±2.30 15.71 ±2.72 26.49 ±2.29 20.62 ±2.72 15.85 ±2.49 15.44 ±3.11
Post 26.21 ±1.02 19.99 ±2.07 15.74 ±2.57 15.58 ±2.50 26.76 ±1.91 20.69 ±1.83 16.36 ±2.54 15.43 ±2.98
Base excess (mmol/L)
Pre 1.82 ±1.15 -6.19 ±2.29 -11.72 ±3.05 -10.59 ±3.41 1.91 ±2.41 -6.31 ±2.84 -11.63 ±3.30 -11.31 ±3.98
Post 1.39 ±1.06 -6.71 ±2.20 -11.29 ±3.17 -10.66 ±3.06 1.84 ±2.06 -6.89 ±2.27 -11.84 ±3.46 -11.64 ±3.69
Data are mean ±SD of 7 subjects per group
498 Eur J Appl Physiol (2010) 108:495–503
VO2kinetic parameters
In the fast component of the _
VO2kinetics, a significant
interaction (p=0.007) in the time delay (Td
) was observed,
which resulted from both a decrease over time (-2.2 s post
vs. pre) in the b-alanine group and an increase (?3.9 s) in the
placebo group. The time constant (tau
), however, tended to
display an opposite pattern (p=0.088 for the interaction
effect), i.e. a slowing in the b-alanine group (?1.2 s) and a
speeding (-4.8 s) in the placebo group. Therefore, the oxy-
gen deficit, which is influenced by both the Td
and tau
not affected by either intervention (p=0.937). The ampli-
tude of the slow component (A
0) was not affected by
b-alanine supplementation. For the time constant (tau
time delay (Td
) of the slow component, there was a tendency
for an interaction effect (p=0.082 and p=0.068, respec-
tively) (Table 2).
The primary goal of the present study was to investigate the
role of muscle carnosine in the acid–base balance during
high-intensity exercise. According to the current working
hypothesis, an increased intramyocellular content of car-
nosine would attenuate the drop in intracellular pH during
high-intensity contractions. The smaller transsarcolemmal
concentration gradient of [H
] decreases the acid efflux
from the active muscle cells and results in less pronounced
circulating acidosis. Evidence for this hypothesis is now
presented in the current results. A 6-min exercise bout at a
fixed intensity above the VT (50% of the difference
between VT and _
VO2peak) in healthy male subjects resulted
in a decline in capillary blood pH from *7.4 to *7.2, yet
this acidosis, when expressed as the difference between
baseline and end-exercise, but not in absolute values, was
less pronounced after subjects were supplemented with
b-alanine for 4 weeks compared to placebo. Post-supple-
mentation, the exercise-induced acidosis was 19% smaller
in the b-alanine group compared to the placebo group
(Fig. 1). Although we did not measure the carnosine con-
centration, our two previous studies demonstrated that all
subjects had increased muscle carnosine content in 4–5
weeks of b-alanine supplementation (4–6 g/day) (Baguet
et al. 2009; Derave et al. 2007). This suggests that the
difference between groups is related to the presumable
elevation in muscle carnosine content (Harris et al. 2006;
Baguet et al. 2009). This supports the earlier suggestion of
Hill et al. (2007) that the physicochemical buffer property
of the dipeptide probably in part underlies the ergogenic
potential of b-alanine supplementation. However, it does
not exclude the additional contribution of other factors.
Traditionally, the importance of carnosine as a physi-
cochemical buffer in human skeletal muscle has been
largely ignored, because various calculations and mea-
surements have designated its relative contribution to only
8–15% of total buffer capacity (Hill et al. 2007; Parkhouse
et al. 1985; Hultman and Sahlin 1980). Indeed, in various
other vertebrates the HCD contribute more in both absolute
and relative terms (Abe 2000). In the middle gluteal muscle
of the thoroughbred horse, for example, the carnosine
concentration is 6.7-fold higher than in human vastus
lateralis, increasing its relative contribution to total buffer
capacity to 30.6% (Harris et al. 1990; Sewell et al. 1992).
The significant reduction in exercise-induced acidosis,
observed in the present study following b-alanine supple-
mentation (and a presumable increase in muscle carnosine
content of 40–50%), illustrates that the importance of
carnosine as a pH buffer should not be dismissed. The
cause for the discrepancy between its calculated small
importance and its observed physiological larger impor-
tance remains to be established. Part of the explanation
may be found in the fact that most changes in contracting
muscle occur in the narrow range of pH around the value of
6.8, where carnosine exerts its maximal effect, leading to
an underestimation of carnosine’s relative contribution.
In the present study the circulating bicarbonate and
lactate concentrations were not different between condi-
tions, which allows for the following interpretations. Given
the identical lactate levels, the lower degree of acidosis
evident in the b-alanine supplemented group, is not
caused by a lower anaerobic component of total energy
delivery. Hence, smaller acidosis genuinely represents
better buffering capacity, and not smaller acid production.
The identical bicarbonate levels suggest that the enhanced
intracellular buffering capacity (by b-alanine-induced
carnosine loading) is not compensated by sparing of
Fig. 1 DpH from baseline to the end (6 min) of high-intensity
cycling before and after 4 weeks’ supplementation of b-alanine or
placebo. Data are mean ±SD of seven subjects per group. *Signif-
icant interaction effect (p=0.03)
Eur J Appl Physiol (2010) 108:495–503 499
extracellular buffering capacity (mainly bicarbonate).
Carnosine has been implicated as an activator of carbonic
anhydrase activity (Temperini et al. 2005), but since in the
current study neither the circulating bicarbonate level and
pCO2, nor the pulmonary CO
output differed between
groups, it seems unlikely that b-alanine supplementation
attenuated acidosis through carbonic anhydrase activity.
Thus, the buffering actions of circulating bicarbonate and
intracellular carnosine are additive in order to better protect
the ‘milieu interieur’ against the homeostatic perturbation
of (extreme) acidosis. This is somewhat different from the
effects observed by Suzuki et al. (2006) during repeated
sprint exercise after subjects were acutely supplemented
with a 1.5 g carnosine/anserine or placebo mixture. In
that study, the enhanced circulating buffering capacity
by dipeptide supplementation was compensated by a
decreased utilisation (sparing) of bicarbonate (Suzuki et al.
2006). Therefore, acute dipeptide supplementation enhan-
ces the relative contribution of non-bicarbonate buffering
with only little effect on total blood buffer capacity. The
emerging conclusion of the latter and the current study is
that carnosine and bicarbonate can work as additive in
Fig. 2 Pulmonary oxygen
uptake before (Pre) and after
(Post) placebo (a) and b-alanine
(b) supplementation in a
representative subject
500 Eur J Appl Physiol (2010) 108:495–503
physicochemical buffering, provided they are located in
different compartments, i.e. carnosine intracellularly and
bicarbonate in the circulation.
An additional goal of the current study was to explore
the role of acidosis in the _
VO2kinetics during high-
intensity exercise. The Td
of the fast component was
significantly shorter following b-alanine compared to pla-
cebo supplementation, which suggests faster kinetics. The
physiological significance of this finding, however, is
probably limited because the effect was not sufficient to
alter the calculated oxygen deficit. The latter is probably
due to the fact that the time constant (tau
) changed, albeit
not significantly (p=0.088), in the direction of slower
kinetics (larger tau) following b-alanine supplementation.
Taken together, the effect of reduced exercise-induced
acidosis following b-alanine supplementation on the fast
component of the _
VO2kinetics is very limited. This is in
agreement with the recent study by Berger et al. (2006) that
reported no alteration in the fast component following
induced metabolic alkalosis. The fact that other studies did
find a significantly faster (shorter tau
, Zoladz et al. 2005)
or slower (longer tau
, Kolkhorst et al. 2004) kinetics
following metabolic alkalosis, may be caused by the
shortcoming that kinetic modelling was based on only one
repetition per condition, rather than several like transitions
in the current study and that of Berger et al. (2006).
As outlined in the introduction, some but not all studies
that have experimentally altered pre-exercise blood pH
(alkalinisation or acidification) support a role for proton
accumulation in the slow component of _
VO2. In the study by
Berger et al. (2006), the appearance of the slow component
(TD) is significantly delayed and the absolute _
baseline at the end of exercise was significantly reduced
following sodium bicarbonate ingestion. In the current study,
the absolute end-exercise _
VO2and A
0were not different
between conditions. Therefore, the present study does not
support a role for acidosis in the physiological basis of the
slow component. At first sight, our results appear to be in
contradiction with the study from Berger et al. (2006)and
others (Kolkhorst et al. 2004;Forbesetal.2005). However,
the magnitude of experimental alteration of pH is less pro-
nounced in the current study compared with the latter studies.
Furthermore, the experimental intervention is essentially
different in nature. In the bicarbonate supplementation
studies, the resting pH is substantially elevated beyond values
that lie within the physiological variation range. In the
present study, however, the chronic b-alanine supplementa-
tion has no direct effect on resting blood pH, but the enhanced
buffer capacity suppresses the acidosis that results from high-
intensity work. Thus, although the absolute pH cannot be
excluded as a contributing factor, the magnitude of the
decline in pH during exercise is not a factor involved in the
slow component of _
It can be concluded from the current data that chronic
b-alanine supplementation can reduce acidosis during
Table 2 _
VO2kinetic parameters: amplitude, tau and time delay of
the fast and slow components before (Pre) and after (Post) b-alanine
or placebo supplementation
b-Alanine Placebo Interaction effect
(mL/min), fast component
Pre 2,350 ±442 2,365 ±298 p=0.113
Post 2,462 ±670 2,311 ±259
(s), fast component
Pre 21.0 ±4.3 25.7 ±9.8 p=0.088
Post 24.2 ±6.8 20.9 ±4.9
(s), fast component
Pre 14.7 ±1.9 11.5 ±3.9 p=0.007
Post 12.5 ±3.1 15.4 ±1.4
0(mL/min), slow component
Pre 601 ±198 632 ±103 p=0.194
Post 508 ±167 684 ±136
(s), slow component
Pre 179 ±97 241 ±121 p=0.082
Post 119 ±48 318 ±207
(s), slow component
Pre 107 ±30 116 ±30 p=0.068
Post 131 ±42 98 ±34
deficit (L)
Pre 3.01 ±0.34 3.43 ±0.80 p=0.937
Post 3.06 ±0.53 3.47 ±0.69
Data are shown as mean ±SD
Table 3 Absolute oxygen uptake ( _
VO2), ventilation ( _
VE) and CO
output ( _
VCO2) after warm-up at 10 W (0 min) and after 6 min
intensive cycling at 50% Dbefore (Pre) and after (Post) supplemen-
tation with b-alanine or placebo
b-alanine Placebo
0 min 6 min 0 min 6 min
Pre 1,030 ±225 3,713 ±887 978 ±248 3,831 ±364
Post 937 ±128 3,844 ±702 972 ±226 3,876 ±410
VE (L/min)
Pre 23.6 ±3.4 111.7 ±39.6 22.4 ±3.5 106.1 ±23.3
Post 21.3 ±2.8 113.9 ±37.7 20.9 ±3.4 101.5 ±20.9
Pre 808 ±102 4,090 ±815 781 ±86 4,256 ±551
Post 742 ±66 4,138 ±766 745 ±103 4,189 ±455
Data are shown as mean ±SD. There were no significant differences
Eur J Appl Physiol (2010) 108:495–503 501
high-intensity exercise. This indicates that carnosine may
act as a physiologically meaningful physicochemical buffer
in human skeletal muscle and may provide at least a part of
the explanation for the ergogenic effect of the b-alanine
supplement found in some exercise modes. Additionally,
these data do not support an important role for acidosis in
the oxygen deficit or in the origin of the slow component of
VO2kinetics during high-intensity exercise.
Acknowledgments This study was financially supported by grants
from the Research Foundation—Flanders (FWO and
G.0046.09). Audrey Baguet is a recipient of a PhD-scholarship from
the Research Foundation—Flanders (FWO). We thank Dr. John Wise
and Natural Alternatives International (San Marcos, CA) for gener-
ously providing the b-alanine (CarnoSyn) and placebo supplements.
We thank Peter Van Mossevelde and Tim Decleir for their practical
contributions and Dr. Jacques Bouckaert for his valuable advice. The
experiments of this manuscript comply with the current laws of
Conflict of interest statement The authors declare that they have
no conflict of interest.
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... It is widely distributed in various tissues of the body, including the nervous tissue. It is has been reported that L-carnosine possesses a proton buffering effect [12] and acted as an antioxidant via scavenging of free radicals and singlet oxygen and chelating with heavy metals [11,13]. ...
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Background: Inflammation is known to underlie the pathogenesis in neuropathic pain. This study investigated the anti-inflammatory and neuroprotective mechanisms involved in antinociceptive effects of co-administration of acetaminophen and L-carnosine in chronic constriction injury (CCI)-induced peripheral neuropathy in male Wistar rats. Methods: Fifty-six male Wistar rats were randomly divided into seven experimental groups (n = 8) treated with normal saline/acetaminophen/acetaminophen + L-carnosine. CCI was used to induce neuropathic pain in rats. Hyperalgesia and allodynia were assessed using hotplate and von Frey tests, respectively. Investigation of spinal proinflammatory cytokines and antioxidant system were carried out after twenty-one days of treatment. Results: The results showed that the co-administration of acetaminophen and L-carnosine significantly (P < 0.001) increased the paw withdrawal threshold to thermal and mechanical stimuli in ligated rats compared to the ligated naïve group. There was a significant (P < 0.001) decrease in the levels of nuclear factor kappa light chain enhancer B cell inhibitor, calcium ion, interleukin-1-beta, and tumour necrotic factor-alpha in the spinal cord of the group coadministered with acetaminophen and L-carnosine compared to the ligated control group. Co-administration with acetaminophen and L-carnosine increased the antioxidant enzymatic activities and reduced the lipid peroxidation in the spinal cord. Conclusions: Co-administration of acetaminophen and L-carnosine has anti-inflammatory effects as a mechanism that mediate its antinociceptive effects in CCI-induced peripheral neuropathy in Wistar rat.
... In terms of buffering capacity, the ability of Carnosine to buffer protons is generally attributed to the nitrogen atoms in the imidazole ring. There is some data that suggests that when subjects supplemented with Beta-Alanine, a precursor for Carnosine synthesis, intramuscular Carnosine levels rose and helped prevent decreases in pH in exercising muscle, which may play a role in decreasing fatigue during training (2). However, intramuscular regulation of carnosine levels is dependent on relevant transporter and enzymatic activity, and may be influenced by dietary and hormonal factors (3), gender (4), muscle fiber type (5), and other factors. ...
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Anaerobic exercise is short-burst, high-intensity activity that exceeds the body's demand for oxygen and requires quick, readily available energy (sugar) that is stored in the skeletal muscle. This is known as anaerobic metabolism. During this process, lactic acid is produced faster than it can be metabolized. This study determined the effects of a topical carnosine-based gel (LactiGo) on blood lactate (HLa) production and anaerobic exercise performance variables during a 25sec. maximal sprint against a resistive force. Healthy and recreationally active men (n=10; ±SD; age=21.5±1.7 yrs, height=1.82±0.13 m, weight=82.6±11.4 kg) and women (n=10; age=19.8±1.0 yrs, height=1.71±0.05 m, weight=62.6±7.4 kg) performed the anaerobic maximal intensity resistive sprint protocol with the topical gel (LactiGo) and with placebo. Blood samples collected were analyzed with a Lactate Plus handheld blood lactate analyzer. Paired samples t-tests on performance measures (Gel vs. Placebo), and 3-way repeated measures ANOVAs (sex x condition x time) were performed on mean values for each subject. Follow-up analyses for ANOVA models were performed using paired samples t-tests with Bonferroni corrections. The level of significance was set at (p≤0.05). Comparisons indicated no sprint performance differences. However, the topical carnosine-based gel increased blood lactate accumulation following the 25 sec resistive sprint. The performance measures indicated no differences between condition (Gel vs. Placebo), however, the lactate indicated a 3-way interaction (p<0.01). Lactate measurements were significantly greater for the Post vs. Baseline (p<0.01) and Post vs. Pre (p<0.01).
... Second, carnosine also acts as a pH buffer and is estimated to be responsible for 4-9% of intramuscular buffer capacity (16). Hence, carnosine is able to delay the onset of muscle acidosis during high-intensity exercise (17). ...
Background: Oxidative/carbonyl stress is elevated in lower-limb muscles of patients with Chronic Obstructive Pulmonary Disease (COPD). Carnosine is a skeletal muscle antioxidant particularly present in fast-twitch fibers. Aims: To compare muscle carnosine, oxidative/carbonyl stress, antioxidants and fiber characteristics between patients with COPD and healthy controls (HCs), and between patients after stratification for airflow limitation (mild/moderate vs. severe/very-severe). To investigate correlates of carnosine in patients with COPD. Methods: A vastus lateralis muscle biopsy was obtained from 40 patients with stable COPD and 20 age/sex matched HCs. Carnosine, oxidative/carbonyl stress, antioxidants, fiber characteristics, quadriceps strength and endurance (QE), VO2peak (incremental cycle test) and physical activity (PA) were determined. Results: Patients with COPD had a similar carnosine concentration (4.16 mmol/kg wet weight (WW) (SD 1.93)) to HCs (4.64 mmol/kgWW (SD 1.71)) and significantly higher percentage of fast-twitch fibers and lower QE, VO2peak and PA vs. HCs. Patients with severe/very-severe COPD had a 30% lower carnosine concentration (3.24 mmol/kgWW (SD 1.79); n=15) vs. patients with mild/moderate COPD (4.71 mmol/kgWW (SD 1.83); n=25; P=0.02) and significantly lower VO2peak and PA vs. patients with mild/moderate COPD. Carnosine correlated significantly with QE (rs=0.427), VO2peak (rs=0.334), PA (rs=0.379) and lung function parameters in patients with COPD. Conclusion: Despite having the highest proportion of fast-twitch fibers, patients with severe/very-severe COPD displayed a 30% lower muscle carnosine concentration compared to patients with mild/moderate COPD. As no oxidative/carbonyl stress markers, nor antioxidants were affected, the observed carnosine deficiency is thought to be a possible first sign of muscle redox balance abnormalities.
... capillary density, mitochondrial content and oxidative enzyme activity) is likely the most important factor influencing the recovery time course (i.e. encompassing metabolite removal, PCr resynthesis and restoration of cytosolic pH) following maximal fatiguing efforts [187,199,201,202], although muscle carnosine content also predicts the rate of recovery of W' following hard exercise [199], presumably via an enhanced intramyocellular buffering capacity [203]. Muscle oxidative capacity tends to be lower in fast versus slow fibres [83,204], and accordingly, the rate of recovery in these fibres is slower [143]. ...
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Maximal muscular power production is of fundamental importance to human functional capacity and feats of performance. Here, we present a synthesis of literature pertaining to physiological systems that limit maximal muscular power during cyclic actions characteristic of locomotor behaviours, and how they adapt to training. Maximal, cyclic muscular power is known to be the main determinant of sprint cycling performance, and therefore we present this synthesis in the context of sprint cycling. Cyclical power is interactively constrained by force-velocity properties (i.e. maximum force and maximum shortening velocity), activation-relaxation kinetics and muscle coordination across the continuum of cycle frequencies, with the relative influence of each factor being frequency dependent. Muscle cross-sectional area and fibre composition appear to be the most prominent properties influencing maximal muscular power and the power-frequency relationship. Due to the role of muscle fibre composition in determining maximum shortening velocity and activation-relaxation kinetics, it remains unclear how improvable these properties are with training. Increases in maximal muscular power may therefore arise primarily from improvements in maximum force production and neuromuscular coordination via appropriate training. Because maximal efforts may need to be sustained for~15-60 s within sprint cycling competition, the ability to attenuate fatigue-related power loss is also critical to performance. Within this context, the fatigued state is characterised by impairments in force-velocity properties and activation-relaxation kinetics. A suppression and leftward shift of the power-frequency relationship is subsequently observed. It is not clear if rates of power loss can be improved with training, even in the presence adaptations associated with fatigue-resistance. Increasing maximum power may be most efficacious for improving sustained power during brief maximal efforts, although the inclusion of sprint interval training likely remains beneficial. Therefore, evidence from sprint cycling indicates that brief maximal muscular power production under cyclical conditions can be readily improved via appropriate training, with direct implications for sprint cycling as well as other athletic and health-related pursuits. Maximal muscle power production under cyclical conditions is interactively constrained by force-velocity properties, activation-relaxation kinetics and muscle coordination across the continuum of possible movement frequencies. Fatigue alters the power-frequency relationship, with a higher degree of power loss at higher movement frequencies. Maximal muscular power production can be readily increased with appropriate strength and power training; it remains less clear if rates of power loss during brief maximal sustained efforts can be improved with training.
... Carnosine contribution to pH homeostasis is allowed by such mobility [74]. When the amount of carnosine in skeletal muscle is increased by nutritional intervention, the level of blood acidosis during high-intensity exercise is reduced in humans [75]. ...
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Carnosine is a dipeptide synthesized in the body from β-alanine and L-histidine. It is found in high concentrations in the brain, muscle, and gastrointestinal tissues of humans and is present in all vertebrates. Carnosine has a number of beneficial antioxidant properties. For example, carnosine scavenges reactive oxygen species (ROS) as well as alpha-beta unsaturated aldehydes created by peroxidation of fatty acid cell membranes during oxidative stress. Carnosine can oppose glycation, and it can chelate divalent metal ions. Carnosine alleviates diabetic nephropathy by protecting podocyte and mesangial cells, and can slow down aging. Its component, the amino acid beta-alanine, is particularly interesting as a dietary supplement for athletes because it increases muscle carnosine, and improves effectiveness of exercise and stimulation and contraction in muscles. Carnosine is widely used among athletes in the form of supplements, but rarely in the population of cardiovascular or diabetic patients. Much less is known, if any, about its potential use in enriched food. In the present review, we aimed to provide recent knowledge on carnosine properties and distribution, its metabolism (synthesis and degradation), and analytical methods for carnosine determination, since one of the difficulties is the measurement of carnosine concentration in human samples. Furthermore, the potential mechanisms of carnosine’s biological effects in musculature, metabolism and on immunomodulation are discussed. Finally, this review provides a section on carnosine supplementation in the form of functional food and potential health benefits and up to the present, neglected clinical use of carnosine.
... In simulated taekwondo combats, the contribution of aerobic, anaerobic phosphagen, and glycolytic energy systems is 66 %, 30 %, and 4 %, respectively, with a probable shift towards anaerobic energy sources during real tournaments [40,41]. Our results are in agreement with the study by Baguet et al. [42] that found no effect on V O 2peak after βA supplementation in physically active males. It also seems that high-intensity interval training (HIIT) better supports aerobic capacity gains than moderate-intensity exercise. ...
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Background This study aimed to investigate the effect of multi-ingredient intra- (BA) versus extra- (ALK) cellular buffering factor supplementation, combined with the customary intake of branched-chain amino acids (BCAA) and creatine malate (TCM), on body composition, exercise variables, and biochemical and hematological parameters in 9 elite taekwondo athletes. Methods Eight-week randomized double-blind crossover BA (5.0 g·day ⁻¹ of β-alanine) versus ALK (0.07 g·kg FFM ⁻¹ ·day ⁻¹ of sodium bicarbonate) supplementation combined with BCAA (0.2 g·kg FFM ⁻¹ ·day ⁻¹ ) and TCM (0.05 g·kg FFM ⁻¹ ·day ⁻¹ ) during a standard 8-week taekwondo training period was implemented. In the course of the experiment, body composition (dual X-ray absorptiometry), aerobic capacity (ergospirometric measurements during an incremental treadmill test until exhaustion), and exercise blood biomarkers concentrations were measured. Data were analyzed using repeated measures within-between interaction analysis of variance with the inclusion of experimental supplementation order. Results The maximum post-exercise blood ammonia concentration decreased in both groups after supplementation (from 80.3 ± 10.6 to 72.4 ± 10.2 µmol∙L ⁻¹ , p = 0.013 in BA; from 81.4 ± 8.7 to 74.2 ± 8.9 µmol∙L ⁻¹ , p = 0.027 in ALK), indicating reduced exercise-related adenosine triphosphate degradation. However, no differences were found in body composition, aerobic capacity, blood lactate concentration, and hematological parameters after neither BA (combined with BCAA and TCM) nor ALK (combined with BCAA and TCM) supplementation. Conclusions In highly trained taekwondo athletes, neither extra- nor intracellular buffering enhancement resulting from BA and ALK supplementation, combined with BCAA and TCM treatment, affects body mass and composition, maximum oxygen uptake, and hematological indices, even though certain advantageous metabolic adaptations can be observed.
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Ergogenic nutritional supplements are a type of sports food. Sodium bicarbonate and b-alanine are two of the most popular and legally permitted ergogenic dietary supplements. These two chemicals have a comparable ergogenic effect because they help to neutralize hydrogen cations created during anaerobic glycolysis during exercise. The hydrogen ions will exit the trained muscles faster if the extracellular regulatory capacity of the organism is increased by strengthening the stores of bicarbonate ions. And before the acidification within the muscle cells becomes a limiting factor of athletic performance, more hydrogen ions and lactic acid will be produced. The goal of this review is to go over the two most common dietary supplements, sodium bicarbonate and b-alanine, that have been shown to improve athletic performance by neutralizing hydrogen cations created during anaerobic glycolysis during exercise. Sodium bicarbonate and b-alanine are legal ergogenic aids that are inexpensive and simple to make, and they have been used by athletes for decades. The extracellular mechanism of "neutralization" of hydrogen ions that build in the exercised muscle is aided by sodium bicarbonate consumption, which increases bicarbonate concentrations in the blood. The ideal dose is between 0.3 and 0.5 grams per kilogram of body weight, and it should be consumed 150-180 minutes before exercise to minimize or lessen gastrointestinal problems. B-alanine supplementation can also improve anaerobic exercise performance, with a more apparent effect in trials lasting 1 to 4 minutes at high intensity, whereas its ergogenic effect appears to be minimal to moderate in exercises lasting up to 25 minutes. Furthermore, it improves the volume of resistance training; yet, increasing strength has no added advantage. Carnosine reserves in muscle are greatly increased after 4 weeks of administration (4-6 gr/day), operating as an intramuscular mechanism for controlling H+ concentration. Furthermore, a loading dose of 4-6 grams per day in doses of 2 grams or fewer is necessary for a least of 2 weeks, with a larger benefit after 4 weeks. Paraesthesia is the sole negative effect at the prescribed levels (tingling). Article visualizations: </p
PurposeThe objective of this study was to investigate the effect of 4 weeks of strength training with beta-alanine supplementation on anaerobic power and carnosine level in boxer players.Methods Eighteen male boxer players participated in this study, randomly divided into two homogeneous groups (strength training + beta-alanine and strength training + placebo groups). The study design was double-blind, parallel, and placebo-controlled. An anaerobic Wingate test was performed by athletes before and after the intervention period (4 weeks). Participants received 0.3 g/kg of body mass of the supplement (maltodextrin or beta-alanine) per day during the intervention. Participants were also evaluated for anaerobic power, serum level of carnosine, and blood lactate before and after 4 weeks.ResultsAverage power in both groups was significantly increased compared with pre-intervention, but fatigue index was significantly decreased only after beta-alanine supplementation; however, there were no significant differences with either average power or fatigue index between the beta-alanine and placebo groups. There was no significant difference in the interaction between the groups and time, as well as no significant difference between groups for lactic acid. Carnosine level in both groups was significantly increased compared with pre-intervention. When changes in serum carnosine for the two groups were examined, statistical analysis showed a significant difference between the beta-alanine and placebo groups.Conclusion Four weeks of strength training accompanied by beta-alanine supplementation had a likely beneficial effect on boxer players' anaerobic performance and carnosine level.
Hintergrund und Ziele: Jucken ist ein häufiges klinisches Symptom, welches insbesondere in dessen chronischer Form von den betroffenen Patienten als äußerst quälend beschrieben wird. Die zugrundeliegenden Mechanismen des chronischen nicht Histamin-vermittelten Pruritus sind weitestgehend ungeklärt. In den letzten Jahren wurden deshalb viele Experimente auf zellulärer Ebene und am Tier durchgeführt, wobei zahlreiche neue Mediatoren und deren Rezeptoren identifiziert werden konnten. Aktuell ist jedoch noch nicht geklärt, inwieweit diese Ergebnisse auf den Menschen übertragbar sind. Eine Gruppe von Erkrankungen, bei denen die Patienten oft an chronischem Pruritus leiden, sind cholestatische Lebererkrankungen. Aufgrund mangelnder Informationen über den Entstehungsmechanismus dieses Symptoms existiert bisher noch keine kausale Therapie. In der Vergangenheit wurden verschiedene Theorien diskutiert, die erklären könnten, wie es zur Empfindung Jucken kommt und wie diese von der Empfindung Schmerz zu unterscheiden ist. Ein Erklärungsansatz ist die „labeled-line theory“ von MÜLLER (1837), die besagt, dass für jede Sinnesmodalität – also auch für Jucken – ein separater neuronaler Weg existiert. Im Gegensatz dazu behauptet die „spatial contrast theory of pain and itch“, dass die Empfindung Jucken durch einen starken Kontrast von aktivierten und nicht aktivierten Nozizeptoren zustande kommt (Namer und Reeh 2013). Vor diesem Hintergrund untersuchten wir zunächst die „spatial contrast theory of pain and itch“ genauer. Hierfür testeten wir an verschiedenen Pruritogenen, ob die Applikationsarten Injektion und fokale Applikation unterschiedliche Juck- und Schmerzempfindungen hervorrufen. Ebenfalls wurden diese Experimente für potenzielle Pruritogene des cholestatischen Pruritus wie Lysophosphatidsäure (LPA) und verschiedene Gallensalze analysiert. Zusätzlich wurde bei Patienten mit cholestatischer Lebererkrankung untersucht, ob eine veränderte Erregbarkeit der Nervenfasern das Jucken verursachen könnte. Material und Methoden: Diese Arbeit kann in drei Versuchsteile unterteilt werden: Bei allen drei Versuchsteilen wurden die Reize an der volaren Seite des Unterarms gesetzt. Nach der Applikation wurden Juck- und Schmerzratings anhand einer numerischen Ratingskala (NRS) alle 10 Sekunden über 7 Minuten abgefragt. Die Substanzen wurden zum einen fokal mithilfe winziger Härchen einer tropischen Bohne (Mucuna pruriens) und zum anderen großflächig mit einer Injektion in die Haut eingebracht. Bei allen drei Versuchsteilen wurde die Größe des Axonreflex-Erythems, das durch den jeweiligen Reiz ausgelöst wurde, mithilfe des Laserdoppler-Imagings (LDI) bestimmt. Im ersten Teil wurde an insgesamt 19 gesunden Probanden getestet, inwieweit die unter-schiedliche Applikationsart (fokale Applikation versus Injektion) die Juck- bzw. Schmerzempfindung beeinflusst. Als Testsubstanzen wurden die Pruritogene β-Alanin, BAM8-22, Chloroquin und Cowhage verwendet. Der zweite Teil der Dissertation beschäftigte sich mit der Empfindung gesunder Probanden bei der Injektion und fokalen Applikation verschiedener Gallensalze bzw. Gallensalz-Kombinationen. An insgesamt 19 Probanden wurden folgende Substanzen ausgetestet: Desoxycholat (DC), Glykodesoxycholat (GDC), Ursodesoxycholat (UDC), Glykochenodesoxycholat (GCDC), Gallensalzpool aus DC, UDC und GDC, Kombination aus dem Gallensalzpool und LPA, LPA, dem semi-synthetischen farnesoid X receptor (FXR)-Agonisten INT-747 sowie dem semi-synthetischen TGR5-Agonisten INT-777. Im dritten Teil wurde an insgesamt 24 Patienten mit cholestatischer Lebererkrankung (davon 12 mit Pruritus und 12 ohne Pruritus) die Empfindung von verschiedenen Gallensalzen und elektrischer Stimulation mit Sinus- und Halbsinus-Strompulsen untersucht. Es wurde ein Gallensalzpool (aus DC, GDC und UDC), INT-747 und INT-777 appliziert. Anschließend wurde abgefragt, inwieweit verschiedene Sinus- und Halbsinus-Strompulse Schmerz bzw. Jucken auslösen. Statistische Signifikanzen wurden mithilfe des Programms STATISTICA © ermittelt. Ergebnisse: Zusammenfassend wurden in dieser Studie folgende Ergebnisse erzielt. Die psychophysikalische Testung verschiedener Pruritogene (β-Alanin, BAM8-22, Chloroquin, Cowhage) an gesunden Probanden zeigte mit Ausnahme von β Alanin, dass die intradermale Injektion dieser Substanzen sowohl Schmerz als auch Jucken verursacht. Bei der fokalen Applikation hingegen dominierte sehr deutlich das Jucken gegenüber dem Schmerz. Die natürlichen Gallensalze DC, GDC sowie UDC lösten bei gesunden Testpersonen sowohl nach Injektion als auch nach fokaler Applikation leichtes Jucken aus, wohingegen nach der Applikation des Gallensalzes GCDC keine Empfindung beobachtet werden konnte. Die Injektion der minimal modifizierten Gallensalze INT 747 sowie INT 777 verursachte mehr Schmerz und weniger Jucken. Die fokale Applikation der INTs verursachte hingegen leichtes Jucken. Die psychophysikalische Testung verschiedener Gallensalze/Gallensalz-Kombinationen sowie Halbsinus-/Sinus-Strompulse bei cholestatischen Patienten zeigte bei Patienten mit Pruritus mehr Jucken als bei den Patienten ohne Pruritus. Dies konnte sowohl bei der Injektion des Gallensalzpools (aus DC, GDC und UDC) wie auch bei der fokalen Applikation von INT-747 und INT-777 und bei der elektrischen Reizung mit Halbsinus- und Sinus-Strompulsen verschiedener Intensitäten beobachtet werden. Diskussion: Dass die „spatial contrast theory of pain and itch“ ein vielversprechender Ansatz für die Entstehung der Empfindung Jucken ist, bekräftigen die Ergebnisse der von uns durchgeführten Psychophysik-Studie. Vorwiegend Jucken wurde empfunden, wenn die Testsubstanzen (BAM8-22, Chloroquin, Cowhage) fokal über Spicules in die Haut appliziert wurden, wodurch nur vereinzelte Nozizeptoren aktiviert werden. Schmerz hingegen wurde gespürt, wenn die Substanz viele nebeneinanderliegende Nozizeptoren gleichmäßig aktiviert – wie es bei der intradermalen Injektion der Fall war. Lediglich β-Alanin erzeugte unabhängig von der Applikationsart hauptsächlich Jucken. Dies kann ebenfalls mit der „spatial contrast theory of pain and itch“ erklärt werden: Erstens wird der MrgprD, der Rezeptor von β-Alanin, lediglich auf einer sehr kleinen Untergruppe aller DRGs exprimiert (Dong et al. 2001) und zweitens wird nur die Hälfte von den MrgprD-positiven Nervenfasern von β-Alanin aktiviert (Liu et al. 2012). Dass die Gallensalze an der Entstehung des cholestatischen Pruritus beteiligt sind, wurde bereits öfter diskutiert. In unserer Psychophysik-Studie verursachten jedoch nicht alle Gallen-salze gleichermaßen Jucken. Lediglich DC, GDC sowie UDC – bekannte MrgprX4-Agonisten („unpublished“ Daten von Katharina Wolf, AG Kremer) – erzeugten nach deren Applikation Jucken. GCDC, das den MrgprX4 nicht aktiviert, löste hingegen keine juckende Empfindung aus. Das lässt vermuten, dass der MrgprX4 eine entscheidende Rolle in der Vermittlung des cholestatischen Pruritus spielt. Die psychophysikalische Testung verschiedener chemischer und elektrischer Reize bei Patienten, die an einer cholestatischen Erkrankung leiden, zeigte, dass Patienten mit chronischem Pruritus nach Applikation der Reize mehr Jucken spürten verglichen mit Patienten ohne chronischen Pruritus. Das lässt vermuten, dass die Patienten mit Pruritus eine veränderte Empfindung aufweisen. Ursächlich kann sein, dass diese Patienten über erhöhte Konzentrationen bestimmter Substanzen, welche Prurizeptoren aktivieren, verfügen. Es könnten aber auch veränderte Nervenfasern oder ein Nervenfaserverlust zu dieser veränderten Empfindung führen.
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We tested whether the leftward shift of the oxygen dissociation curve of hemoglobin with hyperpnea delays the oxygen uptake ((V) over dotO(2)) response to the onset of exercise. Six male subjects performed cycle ergometer exercise at a work rate corresponding to 80% of the ventilatory threshold (VT) (V)over dotO(2) of each individual after 3 min of 20-W cycling under eupnea [control (Con) trial]. A hyperpnea procedure (minute ventilation = 60 l/min) was undertaken for 2 min before and during 80% VT exercise in hypocapnia (Hypo) and normocapnia (Normo) trials. In the Normo trial, the inspired CO2 fraction was 3% to prevent hypocapnia. The subjects completed two repetitions of each trial. To determine the kinetic variables of (V) over dotO(2) and heart rate (HR) at the onset of exercise, a nonlinear least-squares fitting was applied to the data averaged from two repetitions by a monoexponential model. The end-tidal CO2 partial pressure before the onset of exercise was significantly lower in the Hypo trial than in the Con and Normo trials (22 +/- 1 vs. 38 +/- 3 and 36 +/- 1 mmHg, respectively, P < 0.05). The time constant of (V) over dotO(2) and HR was significantly longer in the Normo trial (28 +/- 7 and 39 +/- 18 s, respectively) than in the Con trial (21 +/- 7, 34 +/- 16 s, respectively, P < 0.05). The (V) over dotO(2) time constant of the Hypo trial (37 +/- 12 s) was significantly longer than that of the Normo trial, although no significant difference in the HR time constant was seen (Hypo, 41 +/- 28 s). These findings suggested that respiratory alkalosis delayed the kinetics of oxygen diffusion in active muscle as a result of the left;ward shift of the oxygen dissociation curve of hemoglobin. This supports an. important role for hemoglobin-O-2 off loading in setting the (V) over barO(2) kinetics at exercise onset.
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Muscle carnosine synthesis is limited by the availability of β-alanine. Thirteen male subjects were supplemented with β-alanine (CarnoSyn™) for 4 wks, 8 of these for 10 wks. A biopsy of the vastus lateralis was obtained from 6 of the 8 at 0, 4 and 10 wks. Subjects undertook a cycle capacity test to determine total work done (TWD) at 110% (CCT110%) of their maximum power (Wmax). Twelve matched subjects received a placebo. Eleven of these completed the CCT110% at 0 and 4 wks, and 8, 10 wks. Muscle biopsies were obtained from 5 of the 8 and one additional subject. Muscle carnosine was significantly increased by +58.8% and +80.1% after 4 and 10 wks β-alanine supplementation. Carnosine, initially 1.71 times higher in type IIa fibres, increased equally in both type I and IIa fibres. No increase was seen in control subjects. Taurine was unchanged by 10 wks of supplementation. 4 wks β-alanine supplementation resulted in a significant increase in TWD (+13.0%); with a further +3.2% increase at 10 wks. TWD was unchanged at 4 and 10 wks in the control subjects. The increase in TWD with supplementation followed the increase in muscle carnosine.
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Carnosine (beta-alanyl-L-histidine) is present in high concentrations in human skeletal muscles. The oral ingestion of beta-alanine, the rate-limiting precursor in carnosine synthesis, has been shown to elevate the muscle carnosine content both in trained and untrained humans. Little human data exist about the dynamics of the muscle carnosine content, its metabolic regulation, and its dependence on muscle fiber type. The present study aimed to investigate in three skeletal muscle types the supplementation-induced amplitude of carnosine synthesis and its subsequent elimination on cessation of supplementation (washout). Fifteen untrained males participated in a placebo-controlled double-blind study. They were supplemented for 5-6 wk with either 4.8 g/day beta-alanine or placebo. Muscle carnosine was quantified in soleus, tibialis anterior, and medial head of the gastrocnemius by proton magnetic resonance spectroscopy (MRS), before and after supplementation and 3 and 9 wk into washout. The beta-alanine supplementation significantly increased the carnosine content in soleus by 39%, in tibialis by 27%, and in gastrocnemius by 23% and declined post-supplementation at a rate of 2-4%/wk. Average muscle carnosine remained increased compared with baseline at 3 wk of washout (only one-third of the supplementation-induced increase had disappeared) and returned to baseline values within 9 wk at group level. Following subdivision into high responders (+55%) and low responders (+15%), washout period was 15 and 6 wk, respectively. In the placebo group, carnosine remained relatively constant with variation coefficients of 9-15% over a 3-mo period. It can be concluded that carnosine is a stable compound in human skeletal muscle, confirming the absence of carnosinase in myocytes. The present study shows that washout periods for crossover designs in supplementation studies for muscle metabolites may sometimes require months rather than weeks.
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The first suggestion that physical exercise results in free radical-mediated damage to tissues appeared in 1978, and the past three decades have resulted in a large growth of knowledge regarding exercise and oxidative stress. Although the sources of oxidant production during exercise continue to be debated, it is now well established that both resting and contracting skeletal muscles produce reactive oxygen species and reactive nitrogen species. Importantly, intense and prolonged exercise can result in oxidative damage to both proteins and lipids in the contracting myocytes. Furthermore, oxidants can modulate a number of cell signaling pathways and regulate the expression of multiple genes in eukaryotic cells. This oxidant-mediated change in gene expression involves changes at transcriptional, mRNA stability, and signal transduction levels. Furthermore, numerous products associated with oxidant-modulated genes have been identified and include antioxidant enzymes, stress proteins, DNA repair proteins, and mitochondrial electron transport proteins. Interestingly, low and physiological levels of reactive oxygen species are required for normal force production in skeletal muscle, but high levels of reactive oxygen species promote contractile dysfunction resulting in muscle weakness and fatigue. Ongoing research continues to probe the mechanisms by which oxidants influence skeletal muscle contractile properties and to explore interventions capable of protecting muscle from oxidant-mediated dysfunction.
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1. The imidazole-containing compounds carnosine and homocarnosine, endogenous to skeletal and cardiac muscle, have been tested for effect on the contractile behaviour of chemically skinned (saponin or Triton X-100) skeletal and cardiac muscle. 2. Carnosine, at millimolar concentrations which are near physiological for many skeletal fibres, and in a concentration-dependent fashion, shifts the curve relating [Ca2+] to steady-state tension to lower [Ca2+] in both skeletal (frog but not crab) and cardiac (rat) muscle preparations. 3. Of other imidazoles endogenous to heart, homocarnosine is somewhat more effective, while N-acetyl L-histidine is much less so. 4. The maximum level of Ca(2+)-activated force is increased significantly by homocarnosine in cardiac trabeculae. 5. We propose that the cellular imidazoles related to carnosine are natural 'Ca2+ sensitizers' in striated muscle. Alterations in their levels as a result of disease or training, and between different fibre types, may contribute to differences in contractile performance of the intact tissues.
Purpose: Sodium bicarbonate was used to investigate the effect of blood pH on VO2 kinetics during heavy exercise. Methods: On separate days, 10 active subjects performed two 6-min cycling bouts (208 +/- 12 W) at 25 W above their ventilatory threshold. Each subject ingested 0.3 g(.)kg(-1) of sodium bicarbonate with similar to 1 L of water or water alone 1 h before exercise. VO2 kinetics were examined by means of a three-component mono-exponential model. Results: Bicarbonate ingestion caused a significant increase in the preexercise blood pH (7.512 +/- 0.009 vs 7.425 +/- 0.007; P < 0.001). In the bicarbonate trial, the time constant for the rapid component (27.9 +/- 3.5 s) was slower than the control trial (20.8 +/- 2.4 s; P = 0.017). The higher blood pH after bicarbonate ingestion would have diminished local blood flow and caused a leftward shift of the oxygen-hemoglobin dissociation curve both of which would slow oxygen delivery to working muscle. In addition, bicarbonate ingestion diminished the amplitude of the slow component 29% (463 +/- 43 vs 649 +/- 53 mL(.)min(-1); P = 0.040). The primary cause of the slow component during heavy exercise is fatigue of working fibers and an accompanying increase of motor unit recruitment. Elevated plasma bicarbonate concentration is reported to stimulate the efflux of H+ from muscle fibers and to increase intramuscular pH. Conclusions: ne slower time constant during the rapid component suggested that oxygen delivery is a limiting factor of VO2 kinetics during the onset of heavy exercise. Also, these results imply that bicarbonate ingestion diminished fatigue in working fibers during the slow component.
1. Muscle fibre fatigue is accompanied by characteristic changes in the parameters of a single isometric tension. The initial stage (early period) of the active state is prolonged, whereas the rate of tension development and maximal tension developed by the muscle is decreased.2. Carnosine prevents the development of fatigue, thereby preserving maximal isometric tension and the rate of its development as compared to the control.3. The effect of carnosine prevents the prolongation of early events of the active state relevant to the development of excitation, and does not change with certainty the duration of the tD−tH period, which corresponds to the formation of actomyosine.4. The carnosine effect observed provides for a more rapid rate of the contraction cycle as compared to the control.5. The authors suggest that the effect of carnosine on the parameters of the active state may be accounted for by its specific activation of the muscle tissue ionic pumps.
We examined the effects of sodium bicarbonate ingestion on the VO2 slow component during constant-load exercise. Twelve physically active males performed two 30-min cycling trials at an intensity above the lactate threshold. Subjects ingested either sodium bicarbonate (BIC) or placebo (PLC) in a randomized, counterbalanced order. Arterialized capillary blood samples were analyzed for pH, bicarbonate concentration ([HCO3-]), and lactate concentration ([La]). Expired gas samples were analyzed for oxygen consumption (VO2). The VO2 slow component was defined as the change in VO2 from Minutes 3 and 4 to Minutes 28 and 29. Values for pH and [HCO3-] were significantly higher for BIC compared to PLC. There was no significant difference in [La] between conditions. For both conditions there was a significant time effect for VO2 during exercise; however, no significant difference was observed between BIC and PLC. While extracellular acid-base measures were altered during the BIC trial, sodium bicarbonate ingestion did not attenuate the VO2 slow component during constant-load exercise.
Recent research has shown that chronic dietary beta-alanine (betaALA) supplementation increases muscle carnosine content, which is associated with better performance in short (1-2 min) maximal exercise. Success in endurance competitions often depends on a final sprint. However, whether betaALA can be ergogenic in sprint performance at the end of an endurance competition is at present unknown. Therefore, we investigated the effect of 8-wk betaALA administration in moderately to well-trained cyclists on sprint performance at the end of a simulated endurance cycling race. A double-blind study was performed, which consisted of two experimental test sessions interspersed by an 8-wk betaALA (2-4 g.d; n = 9) or matched placebo (PL; n = 8) supplementation period. In the pretesting and the posttesting, subjects performed a 10-min time trial and a 30-s isokinetic sprint (100 rpm) after a 110-min simulated cycling race. Capillary blood samples were collected for determination of blood lactate concentration and pH. Mean power output during the time trial was approximately 300 W and was similar between PL and betaALA during either the pretesting or the posttesting. However, compared with PL, during the final sprint after the time trial, betaALA on average increased peak power output by 11.4% (95% confidence interval = +7.8 to +14.9%, P = 0.0001), whereas mean power output increased by 5.0% (95% confidence interval = +2.0 to +8.1%, P = 0.005). Blood lactate and pH values were similar between groups at any time. Oral betaALA supplementation can significantly enhance sprint performance at the end of an exhaustive endurance exercise bout.