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Branched chain amino acids supplementation enhance exercise capacity and lipid oxidation during endurance exercise after muscle glycogen depletion


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It has been demonstrated that branched-chain amino acids (BCAA) transaminase activation occurs simultaneously with exercise-induced muscle glycogen reduction, suggesting that BCAA supplementation might play an energetic role in this condition. This study aimed to test whether BCAA supplementation enhances exercise capacity and lipid oxidation in glycogen-depleted subjects. Using a double-blind cross-over design, volunteers (N.=7) were randomly assigned to either the BCAA (300 mg . kg . day -1) or the placebo (maltodextrine) for 3 days. On the second day, subjects were submitted to an exercise-induced glycogen depletion protocol. They then performed an exhaustive exercise test on the third day, after which time to exhaustion, respiratory exchange ratio (RER), plasma glucose, free fatty acids (FFA), blood ketones and lactate were determined. BCAA supplementation promoted a greater resistance to fatigue when compared to the placebo (+17.2%). Moreover, subjects supplemented with BCAA showed reduced RER and higher plasma glucose levels during the exhaustive exercise test. In conclusion, BCAA supplementation increases resistance to fatigue and enhances lipid oxidation during exercise in glycogen-depleted subjects.
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Anno: 2011
Mese: March
Volume: 51
No: 1
Lavoro: 3005-JSM
titolo breve: Branched-chain amino acids supplementation
primo autore: GUALANO
pagine: 1-2
Branched-chain amino acids supplementation
enhances exercise capacity and lipid oxidation during
endurance exercise after muscle glycogen depletion
Acknowledgements.—The authors would like to thank Fundação de
Amparo à Pesquisa do Estado de São Paulo (FAPESP) and Conselho
Nacional de Desenvolvimento Cientíco e Tecnológico (CNPq) for -
nancial support.
Part of this work was presented at the 52nd Annual Meeting of the
American College of Sports Medicine, held in Nashville, TN, USA;
June 3, 2005.
*Both authors have contributed equally to this manuscript.
Received on December 1, 2009.
Accepted on December 10, 2010.
Corresponding author: B. Gualano, Av. Professor Mello Moraes 65,
Butantã 05508-900, São Paulo, SP, Brazil.
E-mail address:
1School of Physical Education and Sport
University of Sao Paulo, Sao Paulo, SP, Brazil
2Institute of Biology, University of Campinas
Campinas, SP, Brazil
Aim. It has been demonstrated that branched-chain amino
acids (BCAA) transaminase activation occurs simultaneously
with exercise-induced muscle glycogen reduction, suggesting
that BCAA supplementation might play an energetic role in
this condition. This study aimed to test whether BCAA sup-
plementation enhances exercise capacity and lipid oxidation
in glycogen-depleted subjects.
Methods. Using a double-blind cross-over design, volunteers
(N.=7) were randomly assigned to either the BCAA (300 mg
. kg . day -1) or the placebo (maltodextrine) for 3 days. On the
second day, subjects were submitted to an exercise-induced gly-
cogen depletion protocol. They then performed an exhaustive
exercise test on the third day, after which time to exhaustion,
respiratory exchange ratio (RER), plasma glucose, free fatty
acids (FFA), blood ketones and lactate were determined. BCAA
supplementation promoted a greater resistance to fatigue when
compared to the placebo (+17.2%). Moreover, subjects supple-
mented with BCAA showed reduced RER and higher plasma
glucose levels during the exhaustive exercise test.
Results. No signicant differences appeared in FFA, blood ke-
tones and lactate concentrations.
Conclusion. In conclusion, BCAA supplementation increases
resistance to fatigue and enhances lipid oxidation during ex-
ercise in glycogen-depleted subjects.
K : Amino acids, branched-chain - Exercise - Glyco-
gen - Citric acid cycle.
The tricarboxylic acid cycle (TCA) is the major
common pathway for the oxidation of carbohy-
drates, lipids and some amino acids. The TCA cy-
cle is regulated directly by accessible pools of its
two substrates oxaloacetate and acetyl-CoA, and its
product citrate,1, 2 suggesting that the continuous
production of oxaloacetate can theoretically deter-
mine oxidative metabolic rate.2 However, it is well
established that only muscle and liver glycogen lev-
els cannot support the great oxaloacetate demand
imposed by either fasting or prolonged physical ac-
tivity.2 Hence, one can expect that lipid oxidation
might be partially limited by carbohydrate availabil-
ity.3 Accordingly, muscle fatigue seems to coincide
with depleted glycogen content during prolonged
exercise. Thus it seems plausible to discuss that in
this case, fatigue is related to provision mediated
through a limited supply of substrate (i.e., oxaloa-
cetate) to the TCA cycle and/or limitations in the
TCA ux due to reduced TCA intermediates con-
centration,4 although the latter has been a matter of
intense debate, for details, see the excellent review
by Bowtell et al. 2007.1
The TCA cycle is characterized by a continuous
generation of its intermediates, which releases CO2
and other metabolites, such as citrate and glutamine.
During catabolic conditions (i.e., exhaustive exer-
cise or fasting), a constant loss of carbon skeletons
occurs, commonly referred as “cataplerosis”, which
need to be replenished by specic reactions aimed to
promote TCA expansion, namely “anaplerosis”. For
example, our group has demonstrated that oxaloac-
etate can be generated through aspartate, asparagine
and glutamate transamination.5, 6
Branched-chain amino acids (BCAA) which are
primarily oxidated in skeletal muscle, may contrib-
ute to energy metabolism during exercise as energy
sources and substrates to expand the pool of TCA
intermediates through anaplerosis reactions.7 Isoleu-
cine and valine may increase succinyl-CoA availa-
bility, possibly leading to an increase in oxaloacetate
concentration, which could hypothetically result in
a higher FFA oxidation, especially in a glycogen-
depleted condition (i.e., during fasting or prolonged
physical activity).
Also, it has been demonstrated that BCAA
transaminase activation occurs simultaneously with
exercise-induced muscle glycogen reduction.3, 8, 9 In
light of this, we hypothesized that glycogen deple-
tion might enhance the BCAA contribution to en-
ergy provision, thus delaying the onset of fatigue.
Therefore, the aim of this study was to test whether
BCAA supplementation improves exercise capacity
and FFA oxidation in glycogen-depleted subjects.
Materials and methods
Study population
Seven healthy and physically active male volun-
teers (age: 24±2 years, body mass index: 22.3±2.5
kg m-2, VO2peak: 47.2±3.9 ml kg-1 min-1) were select-
ed to participate in this study.
The study protocol was approved by the Universi-
ty’s Ethics Committee, and all eligible study subjects
gave written, informed consent before their partici-
Overall design
A double-blind cross-over design was used, in
which each subject completed two experimental
conditions randomly. At baseline, subjects under-
went maximal progressive treadmill exercise for
VO2max and anaerobic threshold determination (T1).
One week after T1, subjects were supplemented with
either BCAA (300 mg kg day -1) or placebo (mal-
todextrine, at the same dose) for three days. On the
second day of supplementation, subjects were sub-
mitted to an exercise-induced glycogen depletion
protocol (T2). On the following day, after a 10-hour
fast, subjects performed an exercise bout at 80% of
their anaerobic threshold until exhaustion (T3 or
T4). During this test, resistance to fatigue, respira-
tory exchange ratio (RER), plasma glucose, plasma
free-fatty acids (FFA) and blood ketones were deter-
mined. After a seven-day washout period, subjects
underwent the aforementioned protocol in a cross-
over fashion. Participants were instructed to main-
tain the same food intake pattern during the trials.
The experimental design is depicted in Figure 1.
VO2peak and anaerobic threshold determination (T1)
Subjects completed a graded, continuous exercise
test on a treadmill. The test commenced at 7 km/h
with incremental increases in speed (1.2 km/h ev-
ery 4 min with a 1 min interval for plasma deter-
minations) until voluntary exhaustion. Gas exchange
measurements (VO2, VCO2 , RER and VO2 peak de-
termination) were obtained continuously through-
out the test by a portable espirometer (K4®). Blood
lactate was analyzed every 4 minutes for anaerobic
threshold determination. Attainment of VO2max was
accepted when two of three criteria were met:
a plateau in VO2, a respiratory exchange ratio
(RER)> 1.1 and volitional exhaustion.
T1 S1 S2T2 T2T3 T4
0 3 13 14 154 5
Figure 1.—Experimental design. Subjects (N.=7) were supple-
mented with either BCAA or placebo (S1) for 3 days. On the sec-
ond day, they were submitted to a glycogen depletion protocol
(T2). Then, they performed an exhaustive exercise test on the 3rd
day (T3). After a 7-day washout period, subjects received BCAA
or placebo in a cross-over fashion (S2) and then repeated T2.
Thereafter, they performed other exhaustive exercise tests (T4).
For further details, see Overall Design. T1 = VO2 max test; T2 =
glycogen depletion protocol; T3 and T4 = exhaustive exercise
tests; S1 and S2 = BCAA or placebo supplementation.
Glycogen depletion protocol (T2)
On the second day of supplementation in both ex-
perimental conditions, subjects underwent an exer-
cise session aimed at glycogen depletion. This ses-
sion consisted of treadmill running for 45 minutes at
70% VO2 peak, followed by two 10-minute sprints at
90% VO2 peak, with a two-minute interval. After this
exercise the subjects remained fasted (~10 h) until
the experiment the next morning. Similar protocols
including continuous and interval exercise have been
reported to give a reduced muscle glycogen level the
following morning.10, 11
Exhaustive exercise tests (T3 and T4)
Subjects performed an exhaustive exercise test
which consisted of treadmill running at 80% of their
anaerobic threshold at a constant velocity (9.9±0.7
km/h) in glycogen depleted condition. Exhaustion
was determined when the subjects were not able to
maintain their initial speed or when test interruption
was requested. Blood samples were collected before
the test and every ve minutes for plasma glucose
and lactate determinations. Ketone bodies, FFA and
ammonia were measured immediately before and
after the test. RER was also determined at rest and
every ve minutes until exhaustion.
BCAA or placebo supplementation
As mentioned earlier, subjects received either en-
capsulated BCAA (300 mg . kg . day -1) or a placebo
(maltodextrine, at same dose) supplementation in a
randomized, cross-over, double-blind fashion. The
supplementation was given three days prior to T3
and T4, including on the days of tests. The BCAA
and placebo conditions were separated by a 7-day
washout period and for the rst trial (T3) 4 subjects
were randomly submitted to BCAA supplementation
and 3 subjects to placebo. For the second trial (T4),
the opposite distribution was adopted. Adherence to
the supplementation protocol was veried through
personal communication on a daily basis.
Plasma analysis
Blood samples were drawn and immediately cen-
trifuged at 4000 rpm for 15 minutes and stored at -20
°C until further analysis.
Plasma FFAs and ketones were analyzed using
commercial kits (Sigma®, SP, Brazil). Plasma glu-
cose and lactate were determined using automatic
lactimeter/glucosimeter (Yellow Spring 2300®, OH,
US). All analyses were performed in duplicate, and
the mean value was calculated.
Statistical analysis
SAS® proc Mixed Model was used to analyze re-
peated measures, and when applicable, Tukey Post
hoc was used for multiple comparisons. All data
is expressed as mean ± sd. The signicance level
adopted to reject the null hypothesis was P≤0.05.
According to daily personal communication, sub-
jects’ compliance to supplementation protocol was
Time (min)
BCAA Placebo
Figure 2.—Time to exhaustion (min) in maximal exercise (T3
and T4) after BCAA and placebo supplementation. The subjects’
performance was signicantly greater after BCAA supplementa-
tion when compared to placebo (*P=0.001). A) Mean ± SD; B)
individual data.
100%. Moreover, no reports were received of any
deleterious effects during the study.
BCAA supplementation promoted a greater time
to exhaustion (+17.2%) when compared to the pla-
cebo (Figure 2). It is important to highlight that all
the subjects showed greater exercise capacity after
BCAA supplementation (Figure 2B).
Moreover, a reduction in RER was observed after
10 (1 vs. 1.08) and 20 (0.96 vs. 1.07) minutes of the
exhaustive exercise test (P<0.05), and a trend toward
a lower RER at 30 minutes (0.95 vs. 1.1) (P=0.08)
was observed following BCAA supplementation
when compared to the placebo (Figure 3). The
pooled RER data during the exhaustive exercise re-
veal that, in fact, BCAA supplementation diminished
RER when compared to the placebo (0.97±0.02 vs.
1.05±0.03, P=0.002), suggesting a shift from carbo-
hydrate to lipid oxidation.
Plasma glucose levels were higher at 20, 25 and 30
minutes (P=0.02, P=0.03 and P=0.06, respectively)
after BCAA supplementation when compared to the
placebo. We observed the same trend when consider-
ing pooled glycemic data during exhaustive exercise
(3.5±0.08 vs. 3.1±0.2, P=0.001) (Figure 4).
There were no signicant differences in plasmatic
FFA (Figure 5), blood ketones (Figure 6) and lactate
Respiratory exchange ratio (RER)
Baseline 10 20 30
Time (min)
BCAA Placebo
Glycemia (mmol/L)
5 10 15 20 25 30
Time (min)
BCAA Placebo
Figure 3.—Respiratory exchange ratio (RER) after BCAA and placebo supplementation. A) BCAA led to a signicant reduced RER
after 10 and 20 minutes (*P=0.01) during an exhaustive exercise test (T3 and T4), suggesting an increase in lipid oxidation. Also, a
trend was noted toward an increase in RER after BCAA supplementation at 30 minutes (#P=0.08); B) pooled data only during exhaus-
tive exercise test (10 + 20 + 30 minutes) also indicated lower RER after BCAA supplementation compared to placebo (*P=0.002).
Figure 4.—Glycemic levels during exhaustive exercise test (T3 and T4) after BCAA and placebo supplementation. A) The subjects in
BCAA condition showed greater glucose concentration than in placebo trial at 20, 25 (*P=0.04) and 30 minutes (# trend P=0.06); B)
The pooled data throughout the exhaustive exercise test (5 + 10 + 15 + 20 + 25 + 30 minutes) also showed that BCAA supplementation
prevents the glycemic fall observed in placebo (*P=0.001). To convert mmol/L to mg/dL, multiply by 18.
(data not shown) concentrations between the BCAA
and placebo conditions.
The aim of the present study was to test whether
BCAA supplementation was able to improve exer-
cise capacity and FFA oxidation in glycogen-deplet-
ed subjects.
The main results of the present study demonstrate
that 3-day BCAA supplementation improved exer-
cise capacity, lipid oxidation and plasma glucose
levels during an exhaustive exercise in glycogen-
depleted subjects. On the other hand, BCAA sup-
plementation did not affect plasma ketones, plasma
FFA and lactate concentration.
TCA activity is regulated by the concentration of
its intermediates and by the balance between ana-
plerotic and cataplerotic reactions.1, 12 Theoretically,
during a lower carbohydrate availability condition
(i.e., prolonged fasting and/or glycogen depletion),
carbon skeletons provided by amino acids transami-
nation are the main substrates that replenish TCA
intermediates through anaplerotic reactions and he-
patic gluconeogenesis. However, the studies regard-
ing the contribution of supplementary amino acids
as an energy source during glycogen depletion are
contradictory. In fact, some authors indicate that
BCAA transamination during lower carbohydrate
availability might have zero effect on TCA interme-
diates concentration 13 or even stimulate cataplero-
sis, thus limiting oxidative activity.14, 15 These latter
authors hypothesized that, as a consequence of the
initial BCAA aminotransferase reaction, the oxida-
tion of BCAA places a carbon “drain” on the TCA
cycle, which may lead to a reduction in the muscle
concentration of 2-oxoglutarate or other TCAI. Ac-
cording to this theory, the BCAA-mediated drain of
2-oxoglutarate is normally counteracted by the re-
generation of this intermediate through the alanine
aminotransferase reaction, provided that sufcient
glycogen is available to sustain the rate of pyruvate
production. However, during conditions in which
glycogen availability becomes limited, and particu-
larly if the rate of BCAA oxidation is increased, it
was suggested that the concentrations of 2-oxoglu-
tarate and/or other TCA intermediates will decrease.
These authors have further proposed that this scenar-
io may lead to a “suboptimal concentration” of TCA
intermediates and impair oxidative energy provision
in skeletal muscle by reducing TCA ux. In contrast,
our group did not previously observe any changes in
the performance and TCA intermediates concentra-
tion of glycogen-depleted rats that were submitted
to intensive exercise, supplemented with BCAA or
isoleucine, leucine and valine alone (unpublished
data). Additionally, Wagenmakers theory has also
been refuted 13 demonstrating that BCAA ingestion,
FFA (mmol/L)
FFA (mmol/L)
Figure 5.—Free fatty acids (FFA) concentration immediately be-
fore and after the exhaustive exercise test, following BCAA and
placebo supplementation. No signicant differences were noted.
Figure 6.—Beta hydroxybutyrate concentration immediately be-
fore and after the exhaustive exercise test, following BCAA and
placebo supplementation. There were no signicant differences
between the trials.
during conditions of reduced glycogen availability,
did not affect the concentration of 2-oxoglutarate or
other TCA intermediates in human skeletal muscle
during exercise. However, it is worthwhile to high-
light that subjects were not completely glycogen-
depleted (~200 mmol/kg dry wt).13 In the present
study, we used a severe protocol in order to induce
glycogen depletion (see Glycogen Depletion Pro-
tocol) and despite the fact that we were not able to
assess glycogen muscle content, we may presume
the effectiveness of this maneuver based on previ-
ous studies, which used similar protocol.10, 11 There-
fore, whilst the extent of glycogen depletion could
not be directly determined, it is far unlikely that a
substantial glycogen diminution did not occur. Our
ndings also are in disagreement with hypothesis of
Wagenmakers et al.,15 since we observed a greater
resistance to fatigue as a consequence of BCAA sup-
plementation. Collectively, these studies suggest that
any potential drain of TCA during exercise is likely
to be small and to not signicantly impact the total
concentration of intermediates, even following rigor-
ous glycogen depletion.
It has been suggested that TCA ux is regulated
by the condensation of proper amounts of oxaloac-
etate and citrate.2 Thus, the continuous production
of oxaloacetate can be considered a key step in oxi-
dative metabolism. As glycogen concentration itself
cannot support the oxaloacetate demand imposed by
severe fasting and exhaustive exercise, FFA oxidation
becomes limited by carbohydrate availability.2, 3 As-
suming the veracity of this hypothesis, it was expected
that a possible BCAA supplementation-mediated aug-
mentation in oxaloacetate concentration would lead to
increased lipid oxidation. In spite of no changes in se-
rum FFA concentration, we observed with interest that
BCAA supplementation promoted a decreased RER
when compared to the placebo, suggesting increased
lipid oxidation. Considering again that TCA may be a
limiting factor for lipid oxidation by the skeletal mus-
cle during exhaustive exercise,2 our ndings suggest
that BCAA supplementation may contribute to this
process, possibly expanding TCA ux. Furthermore,
the reduced RER can also reveal a BCAA supplemen-
tation-induced glycogen-sparing effect, which might
explain the greater exercise capacity. In fact, we and
others 16 veried that BCAA supplementation pro-
motes a higher hepatic and muscle glycogen concen-
tration in fasting and after exercise. However, caution
should be exercised because we were not able to per-
form muscle biopsies; therefore, we cannot conclude
if TCA intermediates (i.e., oxaloacetate) and muscle
glycogen concentration are indeed affected by BCAA
supplementation as we previously hypothesized.
Alternatively, we cannot rule out the hypothesis
that the improved glycemia maintenance during ex-
ercise as a result of BCAA supplementation might
also have contributed to a better exercise capacity,
since even a slight reduction of glycemia seems to
be associated with fatigue. Importantly, our nd-
ings suggest that BCAA supplementation appears to
prevent the exercise-induced hypoglycemia, particu-
larly in glycogen depleted subjects. Opposing our
results, Tang 17 observed no plasma glucose changes
in swimmers supplemented with BCAA for 15 days
after a 25-minute crawl stroke session. Nonetheless,
it is important to highlight that these athletes were
not in a glycogen-depleted condition. Calders et
al.18 veried that rats receiving BCAA signicantly
improved their resistance to fatigue compared with
those receiving saline, but not with those supple-
mented with glucose. Furthermore, these authors ob-
served that when glucose is administered before ex-
ercise, the supplementary administration of BCAA
had no additional effect on performance. Overall,
these ndings corroborate the hypothesis that the ef-
fect of BCAA administration on performance could
be related to carbohydrate availability during exer-
In addition to the hypothesis that BCAA supple-
mentation could enhance lipid oxidation, we specu-
lated that, in glycogen-depleted subjects, this sup-
plement would inhibit or attenuate plasma ketones
production as a result of a greater TCA expansion.
However, no signicant differences were noted in
beta hydroxybutyrate concentration. Moreover, we
cannot prove the hypothesis that BCAA supplemen-
tation-induced RER reduction would occur in par-
allel to lactate concentration decreasing. In contrast
to our ndings, De Palo et al.19 found a decreased
lactate concentration in athletes supplemented with
BCAA for one month. The authors conclude that the
lower lactate level at the end of an intense muscular
exercise may reect an improvement of BCAA use,
due to the chronic supplementation with BCAA. Ap-
parently, the short-term supplementation used in our
study may partially explain this discrepancy. Thus,
blood ketones and lactate concentration did not pro-
vide evidence for explaining the higher exercise ca-
pacity after BCAA supplementation in the present
Of note, the reader should be aware that practical
application of the present ndings has some limita-
tions, since it seems unreasonable to give supple-
mentary amino acids instead carbohydrate to an in-
dividual in glycogen depleted state. In fact, one can
say that of more practical relevance are the previous
ndings that BCAA conferred no further benet to
exercise performance when subjects were also give
glucose prior to exercise. Perhaps most importantly,
however, is the fact that our experimental design al-
lowed us to obtain direct evidence that BCAA in-
gestion do not induce fatigue in glycogen depletion
state, contrasting the previous hypothesis by Wagen-
makers et al.14, 15 Additionally, even though our re-
sults are consistent in all of the subjects, our sample
is rather small, which warrants further investigation.
In summary, BCAA supplementation increases re-
sistance to fatigue and enhances lipid oxidation dur-
ing exercise in glycogen-depleted subjects. These
actions do not seem to be related to changes in plas-
ma FFA, lactate and blood ketones concentration.
Further studies should consider the use of a muscle
biopsy aimed to investigate the mechanisms under-
lying these ndings.
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... [7] indicated that the amino acids present in fish muscles are one of the most effective nutritional supplements in improving health performance, especially BCAA which is a part of the Essential amino acids and constitute 30-35% Which has an important role in building protein in the muscles as it works to reduce muscle damage and reduce pain after exercise and high physical exertion [8]. International studies have proven the important role of the amino acid leucine in building muscle protein, while isoleucine and valine work in energy production and regulation of sugar level in the A Ad dv va an nc ce es s i in n B Bi io or re es se ea ar rc ch h © 2022 Society of Education, India body [9]and also contribute to reducing fatigue during exercise by reducing serotonin production in the brain [10]. Some quantitative differences between the types of amino acids are related to a set of changes, especially changes in the genetic information specific to the same species and on the basis of muscle proteins that are manufactured by the body itself [11]. ...
... Nonessential amino acids are considered part of amino acids that the human body cannot manufacture, but rather are formed from essential amino acids from food or as a result of the process of breaking down proteins [27], as the results of the current study showed an increase in the concentration of non-essential amino acids. The main reason is in the white muscle fibers in the R1 region for both species of study is due to the high amount of protein, and since the non-essential amino acids result from the breakdown and decomposition of proteins, so the reason for its rise in this region is due to the functional role of white muscles, [28] referred to the functional role of white muscle fibers in producing fast and sudden movements that require high energy, while the value of the total concentration in red muscle fibers decreases as a result of the over powering of (BCAAs) [9]. ...
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The current study was conducted to calculate the concentrations of amino acids in two types of Mugilidae fish. They are Planiliza klunzingeri and P. subviridis in red and white muscle fibers for two regions ; The first region (R1) which is 2 cm away from the operculum and the second region (R2) that lise 2 cm near the caudal fin. The results recorded 16 amino acids , Essential amino acids(EAAs) having highest concentration in fish studied in white muscle fibers in the R1 region with a value of 4665.4 (43.9%) in P. subviridis, while the lowest value was at a concentration 1427.12 (56%) in P. klunzingeri. Branched chain amino acids (BCAAs) included (valine, isoleucine and lysine) recorded the highest value in the R2 region 1624.79 (35.4%) in P. subviridis and the lowest value in white muscle fibers in R2 with a total concentration of 182.31 (6.0%). As for the Non-essential amino acids (Non-EAAs), the highest value of 5974.41 (55.9%) was recorded in the white muscle fibers in the R1 region of P. klunzingeri and the lowest value by 1000.86 (41%) in the white muscle fibers in R2 in P. subviridis.
... According to another study, BCAA supplementation after a treadmill test did not provide any differences in the sensation of fatigue and plasma concentration of glucose, lactate, or ammonia [12]. In contrast, Gualano et al. (2011) demonstrated that BCAA supplementation increases exercise capacity and lipid oxidation [13]. The heterogeneity of the findings does not completely confirm the use of BCAAs as an ergogenic supplement for sports [14]. ...
... According to another study, BCAA supplementation after a treadmill test did not provide any differences in the sensation of fatigue and plasma concentration of glucose, lactate, or ammonia [12]. In contrast, Gualano et al. (2011) demonstrated that BCAA supplementation increases exercise capacity and lipid oxidation [13]. The heterogeneity of the findings does not completely confirm the use of BCAAs as an ergogenic supplement for sports [14]. ...
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Branched-chain amino acids (BCAAs) are one of the most controversial ergogenic aids in terms of effectiveness and safety. This study aimed to evaluate the quality and reliability of BCAA supplements related to English videos on YouTube and to synthesize with the sentiment-emotion analysis of comments on videos. The content analysis of the information on videos was evaluated with the use of DISCERN, Journal of American Medical Association (JAMA) benchmark criteria, and Global Quality Score (GQS). In addition, word cloud and sentiment and emotional analysis of comments in videos were performed with the R package. As a result, the mean ± standard error values of DISCERN, JAMA, and GQS scores of all videos were 29.27 ± 1.97, 1.95 ± 0.12, and 2.13 ± 0.17, respectively. It was found that advertisement-free videos have a significantly higher DISCERN and GQS score than advertisement-included videos (p < 0.05). A moderately significant positive correlation was determined between DISCERN score of video content and the positive sentiment of video comments (rs: 0.400, p = 0.002). In conclusion, it was determined that BCAA-related YouTube videos have mostly very poor quality in terms of content and that videos with higher quality may receive positive comments from viewers according to the DISCERN instrument.
... Furthermore, acute exercise stimulus has proven to activate branched-chain α-ketoacid dehydrogenase (BCKD) [13,14], which is the main regulator of BCAA oxidation. In line with our hypothesis, a growing number of both rodent and human studies suggest that BCAA-rich protein supplementation has beneficial effects on several healthand-fitness-related factors, such as body composition, exercise performance and muscle properties, as well as glucose and lipid metabolism [15][16][17][18][19][20][21][22]. On the other hand, BCAA deficiency has been shown to result in impaired growth and protein wasting, as well as changes in hormonal secretion and intracellular signaling [23,24]. ...
... This phenomenon, called "athlete's paradox", is thought to store and serve energy in the form of LDs for long-lasting exercise [30]. Some studies suggest that BCAA supplementation may further promote resistance to fatigue by increasing lipid oxidation during exercise [16]. ...
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Impaired lipid metabolism is a common risk factor underlying several metabolic diseases such as metabolic syndrome and type 2 diabetes. Branched-chain amino acids (BCAAs) that include valine, leucine and isoleucine have been proven to share a role in lipid metabolism and hence in maintaining metabolic health. We have previously introduced a hypothesis suggesting that BCAA degradation mechanistically connects to lipid oxidation and storage in skeletal muscle. To test our hypothesis, the present study examined the effects of BCAA deprivation and supplementation on lipid oxidation, lipogenesis and lipid droplet characteristics in murine C2C12 myotubes. In addition, the role of myotube contractions on cell metabolism was studied by utilizing in vitro skeletal-muscle- specific exercise-like electrical pulse stimulation (EPS). Our results showed that the deprivation of BCAAs decreased both lipid oxidation and lipogenesis in C2C12 myotubes. BCAA deprivation further diminished the number of lipid droplets in the EPS-treated myotubes. EPS decreased lipid oxidation especially when combined with high BCAA supplementation. Similar to BCAA deprivation, high BCAA supplementation also decreased lipid oxidation. The present results highlight the role of an adequate level of BCAAs in healthy lipid metabolism.
... Long-term or strenuous exercise can lead to a decrease in blood sugar, mainly because exercise stimulates the activity of glucose transporters on the muscle fiber cell membrane. However, it increases the glucose uptake of cells for glycolysis, and promotes glycolysis in the liver to increase the blood sugar concentration to provide energy [30]. In addition to BCAA, alanine can also be transported through the blood circulation to the liver, where gluconeogenesis is converted to glucose, which can then be transported through the blood circulation to the muscles for use [31]. ...
... Therefore, supplementation with SPSPE for four consecutive weeks can not only increase glycogen storage but also provide energy usage for exercise, thereby improving exercise endurance performance ( Figure 2). In addition, a previous study noted that subjects supplemented with 300 mg/kg BCAA for three consecutive days had significantly higher blood glucose concentrations after exercise and recovered 30 min post-exercise compared to the maltodextrin-supplemented placebo group's stability [30]. This seems to explain the results of our study. ...
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Silver perch (Bidyanus bidyanus) has many nutrition and health benefits, being a rich source of macro and micronutrients, phospholipids, polyunsaturated fatty acids, and a variety of essential minerals while having a high protein content. In addition to direct consumption, it is often made into a soup as an important nutritional supplement for strengthening the body and delaying fatigue. By extracting the essence, its quality can be controlled, and it is convenient to supplement. This study aimed to evaluate the effect of supplementation with Santé premium silver perch essence (SPSPE) on improving exercise performance and anti-fatigue. Fifty male institute of cancer research (ICR) mice were divided into five groups (n = 10/group): (1) vehicle (vehicle control or water only), (2) isocaloric (0.93 g casein/kg/mice/day), (3) SPSPE-1X (0.99 g/kg/mice/day), (4) SPSPE-2X (1.98 g/kg/mice/day), and (5) SPSPE-5X (4.95 g/kg/mice/day). A sample or an equal volume of liquid was fed orally for four consecutive weeks. Grip strength and swimming exhaustion tests were used as exercise performance assessments. After 10 and 90 min of unloaded swimming, biochemical parameters of fatigue were evaluated. We found that supplementation with SPSPE for four consecutive weeks could significantly improve mice’s grip strength, exercise endurance performance, and glycogen content (p < 0.05), and significantly reduced post-exercise fatigue biochemical parameters, such as lactate, blood ammonia (NH3), blood urea nitrogen (BUN) concentration, and muscle damage index creatine kinase (CK) activity (p < 0.05). In summary, supplementation with SPSPE for 4 weeks could effectively improve exercise performance, reduce sports fatigue, and accelerate fatigue recovery. In addition, it did not cause any physiological or histopathological damage.
... The knockdown of branched-chain aminotransferase (BCAT) gene that encodes the enzyme involved in BCAA catabolism resulted in increased plasma BCAAs, decreased adiposity and body weight, and increased energy expenditure in mice [37]. In addition, dietary BCAA restriction has been found to alter substrate utilization in Zucker fatty rats [38], and BCAA supplementation was shown to enhance lipid oxidation during exercise [39]. However, the effect of BCAA supplementation on RMR and substrate utilization during hypocaloric diet-induced weight loss intervention in overweight and obese adults has not been investigated. ...
... Further studies are required to examine the long-term effect of the BCAA-induced postprandial fat oxidation response on body fat composition. BCAA supplementation has been found to increase lipid oxidation during exercise in glycogen-depleted subjects [39]. Mourier et al. showed that a BCAA-supplemented hypocaloric diet produced the highest body fat loss in male wrestlers with a high level of exercise performance as compared to hypocaloric diets without BCAA supplementation, and it was postulated that the fat loss may be caused by specific hormonal adaptations induced by BCAA [32]. ...
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Background: Branched chain amino acids (BCAA) supplementation is reported to aid in lean mass preservation, which may in turn minimize the reduction in resting metabolic rate (RMR) during weight loss. Our study aimed to examine the effect of BCAA supplementation to a hypocaloric diet on RMR and substrate utilization during a weight loss intervention. Methods: A total of 111 Chinese subjects comprising 55 males and 56 females aged 21 to 45 years old with BMI between 25 and 36 kg/m2 were randomized into three hypocaloric diet groups: (1) standard-protein (14%) with placebo (CT), (2) standard-protein with BCAA, and (3) high-protein (27%) with placebo. Indirect calorimetry was used to measure RMR, carbohydrate, and fat oxidation before and after 16 weeks of dietary intervention. Results: RMR was reduced from 1600 ± 270 kcal/day to 1500 ± 264 kcal/day (p < 0.0005) after weight loss, but no significant differences in the change of RMR, respiratory quotient, and percentage of fat and carbohydrate oxidation were observed among the three diet groups. Subjects with BCAA supplementation had an increased postprandial fat (p = 0.021) and decreased postprandial carbohydrate (p = 0.044) oxidation responses compared to the CT group after dietary intervention. Conclusions: BCAA-supplemented standard-protein diet did not significantly attenuate reduction of RMR compared to standard-protein and high-protein diets. However, the postprandial fat oxidation response increased after BCAA-supplemented weight loss intervention.
... PS supplementation combined with BCAA could be more efficient than PS alone for promoting glycogen synthesis, anabolic state, antioxidant system, and recovery during HIIT. Studies reported that the BCAA administration can increase macronutrient influx due to the insulinotropic effect in order to attenuate cellular stress and catabolic process (Gualano et al., 2011;Rasmussen et al., 2000;Shimomura et al., 2010;Tsuda et al., 2020). However, it is not clear whether the catabolic state is reversed by anabolic hormones, suppressing cortisol, or both mechanisms. ...
Acute phosphatidylserine (PS) or branched-chain amino acids (BCAA) supplements alone may have an adrenocorticotropic hormone, cortisol suppressive effect and increase the testosterone/cortisol ratio, but the associated effect of these supplements during a period of high-intensity physical stress is not yet known. The study investigated the effects of chronic PS supplementation alone and combined with BCAA during high-intensity interval training (HIIT) on training volume tolerance, anabolic-catabolic balance and stress biomarkers in rats. Thirty-three rats were separated into: placebo (PLA, n=11), PS alone (n=11) and combined with BCAA (PSBCAA, n=11). Groups performed swimming sessions of HIIT (5 series × 1 min × 1 min recovery; external load equivalent to 13% of body mass) and nine recovery sessions of moderate-intensity training (30 min at 5% of body mass) alternately. One-way ANOVA was used to compare biochemical variables and two-way ANOVA was calculated to compare training volume. Training volume performed (TVP) was higher in first, fourth, fifth, sixth, and eighth HIIT sessions in the PS group in comparison to PLA (P<0.05). TVP was higher in the fourth session in PSBCAA compared to PLA. There were no differences in TVP during the sessions between PS and BCAA groups. Creatine kinase (CK) was lower in PSBCAA in comparison to PS alone (P=0.03) and PLA (P=0.04) after the experimental period. Testosterone concentration was enhanced in PSBCAA group compared to PLA (P=0.01); testosterone/corticosterone ratio was higher in PSBCAA compared to PS (P=0.05) and PLA (P=0.004) after protocol. PS combined with BCAA increases testosterone concentration and testosterone/corticosterone ratio, demonstrating an enhancement of anabolic state in trained rats.
... Cet effet peut s'expliquer par le fait que l'activité de la BCAT est diminuée par les BCAA, ce qui réduit leur catabolisme contrairement à la Leu (Campos-Ferraz et al. 2013). Le métabolisme des BCAA semble pouvoir être activé par des acides gras à chaîne longue via PPARγ et la promotion de l'oxydation des lipides dans les cellules musculaires afin de pourvoir aux besoins énergétiques de celles-ci durant l'effort une fois le glucose utilisé (Shimomura et al. 2004;Gualano et al. 2011), ce qui serait en accord avec les observations citées précédemment. Une intolérance au glucose a été démontrée chez les souris anx/anx par Lindfors et al. (Lindfors et al. 2015). ...
L’anorexie mentale est un trouble majeur du comportement alimentaire décrit dans le DSM-V affectant en majorité les femmes et se caractérisant principalement par une réduction sévère de l’apport calorique. Elle est fréquemment associée à des troubles anxiodépressifs, une hyperactivité physique ainsi qu’à des troubles fonctionnels digestifs (TFI). Bien que sa prévalence soit faible, il s’agit de la pathologie mentale avec le plus fort taux de mortalité et un risque de rechute très élevé. Le but de cette thèse était de vérifier l’efficacité d’une supplémentation orale en acides aminés tels que la glutamine (Gln) et les acides aminés branchés (BCAA) dans un modèle murin activity-based anorexia (ABA). Ce dernier possède des caractéristiques très proches de ce qui est observé en clinique comme une perte de poids importante, une hyperactivité physique et une augmentation du temps de vidange gastrique. Chez les souris ABA, une supplémentation orale de sept jours en Gln a permis de restaurer, dans le colon, la perméabilité paracellulaire, la synthèse protéique totale et le taux en ARNm codant pour la mucine-2. En revanche, aucun effet bénéfique n’a été trouvé pour les BCAA qui semblaient même diminuer la synthèse protéique colique totale. Le poids et la composition corporelle n’ont pas été affectés par la Gln ou les BCAA, peut-être en raison d’un apport calorique trop faible. Pour vérifier cette hypothèse, après induction de l’anorexie par le modèle ABA, nous avons choisi de combiner une renutrition progressive avec une supplémentation en Gln ou en BCAA. La renutrition a restauré partiellement le poids et la masse maigre des souris ABA avec un rebond de masse grasse mais la Gln n’a montré aucun effet supplémentaire. En revanche, les BCAA tendaient à augmenter légèrement le regain de masse grasse, et donc le poids, par rapport à la renutrition. Les animaux ABA renourris ont retrouvé une leptinémie normale, sans effet des supplémentations, alors que seule la Gln a restauré le taux en triglycérides plasmatiques. Les BCAA, quant à eux, tendaient à augmenter la glycémie et la cholestérolémie. Les effets bénéfiques de la Gln observés dans le colon dans l’étude précédente ont été confirmés. La Gln a montré des effets supérieurs à la renutrition seule sur la restauration de la synthèse protéique totale, via la phosphorylation de la p70S6kinase, et l’expression de protéines des jonctions serrées telles que la claudine-1 et l’occludine. En revanche, les BCAA semblaient atténuer, voire supprimer, les effets bénéfiques de la renutrition seule. La Gln paraît donc intéressante pour l’optimisation des produits de renutrition destinés aux personnes anorexiques et l’effet inhibiteur des BCAA devra être étudié pour en comprendre les mécanismes.
In many of the Asian countries, fish roe products are considered important condiments and are consumed not only as a source of dense nutrients but also as a sign of strong cultural customs from the time immemorial. Fish roes are consumed and enjoyed in fresh or processed forms (e.g., salted, fermented, canned, or smoked). The main principles of fish roe processing are the reduction of moisture content and the use of curing agents and spices to enhance shelf life, nutritional value and sensory attributes. Fish roe is rich in protein, contains all essential and nonessential amino acids and has tremendous bioactivities such as anticancer, antiinflammatory, antihypertensive, and immunomodulatory activities. The lipid fraction of fish roe contains a substantial amount of the health-beneficial long-chain ω-3 polyunsaturated fatty acids, for example, eicosapentaenoic acid (EPA, C20:5n3) and docosahexaenoic acid (DHA, C22:6n3). These essential fatty acids are effective in preventing atherosclerosis, maintaining favorable blood lipid profile, aiding in brain maturity, exerting antiinflammatory activity, and relieving rheumatoid arthritis. Also, there are some health-beneficial fatty acids such as linoleic acid, linolenic acid, arachidonic acid, palmitoleic acid, and oleic acid available in fish roe. Additionally, fish roe contains a substantial amount of essential trace elements, that is, K, S, P, Na, Mg, and Zn, which contribute to crucial biological functions and health benefits. However, fish roe and roe products are associated with several biological, chemical, and physical hazards if they are not handled and processed properly, which makes them unsafe for consumption. Therefore guidelines and processing recommendations have been streamlined to ensure that the roe and roe products are safe for public health.
Backgroud: Astragali Radix (AR) and Codonopsis Radix (CR) are widely used as the tonic herbal medicine with efficacy of tonifying qi in traditional Chinese medicine (TCM), which showed significant antifatigue activities. In this study, AR and CR were combined, with Jujubae Fructus (JF) further added to improve the taste, to afford the ACJ extracts in the ratio of 2:1:2. Results: The results showed that ACJ water extract exhibited antifatigue effect by the weight-loaded exhaustive swimming test in mice. The untargeted fecal metabolomic approach and 16S rRNA gene sequencing analysis showed that ACJ could improve exercise performance by regulating changes of gut metabolites and microbiota to alleviate fatigue. Four pathways were determined as the key pathways relating with its antifatigue effect, which included sphingolipid metabolism, glycerophospholipid metabolism, valine, leucine and isoleucine biosynthesis and D-arginine and D-ornithine metabolism. Correlation analysis showed the complex association among bacteria, metabolites and phenotypes. Conclusion: In conclusion, this study revealed new perspectives to study the antifatigue mechanism of ACJ extracts from the gut microbiota, which provided the basis for further functional food development. This article is protected by copyright. All rights reserved.
Context Acknowledging the importance of protein in the diet of athletes and nonathletes and its potential influence in the sports environment, isoleucine, leucine, and valine, also called branched-chain amino (BCAA) acids are being portrayed as a potential ergogenic supplement. Objective The aim of this systematic review was to review the existing evidence on the effects of BCAA supplementation on physical exercise. Data Sources Pubmed, Scopus, Cochrane Library and SciELO were searched from 2000 to May 2020. Study Selection Randomized controlled trials were eligible for inclusion if they measured the effect of BCAA supplementation on physical performance, muscle damage and body composition. Results Twelve studies were selected. Most of them included physically active individuals or untrained males. The intervention period was ranged from 1 day to 8 weeks, and mean BCAA dose was 19.5 g/day. After BCAA supplementation, no statistically significant difference was observed for most parameters (body composition, blood parameters and performance), only subjective muscle pain appeared lower with supplementation in some studies. Conclusion BCAA supplementation seems not improve performance and gain of strength and muscle mass.
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The tricarboxylic acid (TCA) cycle is the major final common pathway for oxidation of carbohydrates, lipids and some amino acids, which produces reducing equivalents in the form of nicotinamide adenine dinucleotide and flavin adenine dinucleotide that result in production of large amounts of adenosine triphosphate (ATP) via oxidative phosphorylation. Although regulated primarily by the products of ATP hydrolysis, in particular adenosine diphosphate, the rate of delivery of reducing equivalents to the electron transport chain is also a potential regulatory step of oxidative phosphorylation. The TCA cycle is responsible for the generation of ≈67% of all reducing equivalents per molecule of glucose, hence factors that influence TCA cycle flux will be of critical importance for oxidative phosphorylation. TCA cycle flux is dependent upon the supply of acetyl units, activation of the three non-equilibrium reactions within the TCA cycle, and it has been suggested that an increase in the total concentration of the TCA cycle intermediates (TCAi) is also necessary to augment and maintain TCA cycle flux during exercise. This article reviews the evidence of the functional importance of the TCAi pool size for oxidative metabolism in exercising human skeletal muscle. In parallel with increased oxidative metabolism and TCA cycle flux during exercise, there is an exercise intensity-dependent 4- to 5-fold increase in the concentration of the TCAi. TCAi concentration reaches a peak after 10–15 minutes of exercise, and thereafter tends to decline. This seems to support the suggestion that the concentration of TCAi may be of functional importance for oxidative phosphorylation. However, researchers have been able to induce dissociations between TCAi pool size and oxidative energy provision using a variety of nutritional, pharmacological and exercise interventions. Brief periods of endurance training (5 days or 7 weeks) have been found to result in reduced TCAi pool expansion at the start of exercise (same absolute work intensity) in parallel with either equivalent or increased oxidative energy provision. Cycloserine inhibits alanine aminotransferase, which catalyses the predominant anaplerotic reaction in exercising human muscle. When infused into contracting rat hindlimb muscle, TCAi pool expansion was reduced by 25% with no significant change in oxidative energy provision or power output. Glutamine supplementation has been shown to enhance TCAi pool expansion at the start of exercise with no increase in oxidative energy provision. In summary, there is a consistent dissociation between the extent of TCAi pool expansion at the onset of exercise and oxidative energy provision. At the other end of the spectrum, the parallel loss of TCAi, glycogen and adenine nucleotides and accumulation of inosine monophosphate during prolonged exercise has led to the suggestion that there is a link between muscle glycogen depletion, reduced TCA cycle flux and the development of fatigue. However, analysis of serial biopsies during prolonged exercise demonstrated dissociation between muscle TCAi content and both muscle glycogen content and muscle oxygen uptake. In addition, the delay in fatigue development achieved through increased carbohydrate availability does not attenuate TCAi reduction during prolonged exercise. Therefore, TCAi concentration in whole muscle homogenate does not seem to be of functional importance. However, TCAi content can currently only be measured in whole muscle homogenate rather than the mitochondrial subfraction where TCA cycle reactions occur. In addition, anaplerotic flux rather than TCAi content per se is likely to be of greater importance in determining TCA cycle flux, since TCAi content is probably merely reflective of anaplerotic substrate concentration. Methodological advances are required to allow researchers to address the questions of whether oxidative phosphorylation is limited by mitochondrial TCAi content and/or anaplerotic flux.
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Fatty acids are important fuels for muscle during moderate and prolonged exercise. The utilization of fatty acids by skeletal muscle depends on important key steps such as lipolysis in the adipose tissue, plasma fatty acids transport, and passage through plasma and mitochondrial membranes, b-oxidation, and finally oxidation through the Krebs cycle and respiratory chain activity. Acute exercise and exercise training induce adaptations that lead to an increase in fatty acid oxidation. As a result muscle glycogen is preserved. Nevertheless, diet manipulation and supplementation with lipolytic agents that raise fatty acids mobilization and oxidation during exercise failed to show beneficial results on exercise performance. The hypothesis that Krebs cycle is a limiting factor for fatty acid oxidation by the skeletal muscle during prolonged exercise is presented herein.
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Os ácidos graxos (AG) representam uma fonte importante de energia durante exercícios de intensidade leve ou moderada, e principalmente naqueles de duração prolongada. A utilização dos AG pelos músculos esqueléticos depende de passos importantes como a mobilização, transporte via corrente sangüínea, passagem pelas membranas plasmática e mitocôndrial, beta-oxidação e, finalmente, a oxidação no ciclo de Krebs e atividade da cadeia respiratória. O exercício agudo e o treinamento induzem adaptações que possibilitam maior aproveitamento dos AG como fonte de energia, ao mesmo tempo em que o glicogênio muscular é preservado. Contudo, as tentativas de manipulação da dieta e suplementação com agentes ativos para aumentar a mobilização e utilização dos AG durante o exercício não apresentam resultados conclusivos. Nesse trabalho, a hipótese de que o ciclo de Krebs é o fator limitante da utilização de ácidos graxos pelo tecido muscular no exercício prolongado é apresentada.
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Eight highly trained cyclists were studied during exercise after glycogen depletion (test A) and during carbohydrate (CHO) loading (test B). In test B subjects were able to complete 2 h of exercise at 70-75% maximal workload (Wmax), whereas the initial intensity of 70% Wmax had to be reduced to 50% in test A. Plasma ammonia increased more rapidly, and plasma alanine, glutamate, and glutamine were lower in test A. Exercise caused a 3.6-fold increase in the proportion of active branched-chain 2-oxoacid dehydrogenase (BC) complex in muscle in test A. No activation occurred in test B. There was an inverse correlation between the activity of the BC complex and the glycogen content of the postexercise biopsies. Exercise did not cause changes in the muscle content of ATP, ADP, AMP, IMP, hypoxanthine, and lactate. It is concluded that CHO loading abolishes increases in branched-chain amino acid (BCAA) oxidation during exercise and that part of the ammonia production during prolonged exercise originates from deamination of amino acids. The data appear to confirm the hypothesis (A.J. M. Wagenmakers, J.H. Coakley, and R.H.T. Edwards. Int. J. Sports Med. 11: S101-S113, 1990) that acceleration of the BCAA aminotransferase reaction may drain the tricarboxylic acid cycle and that glycogen is a carbon chain precursor of tricarboxylic acid cycle intermediates and glutamine.
This study evaluated the effect of aspartate (ASP) and asparagine (ASG) supplementation on fatigue determinants in Wistar rats exercised to exhaustion by swimming. Methods: The animals were tested for anaerobic threshold (AT) determination and then supplemented with 350 MM ASP + 400 mM ASG (.) day(-1) (AA group, n = 16) or 2 ml (.) day(-1) of distillated water (PLC group, n = 16) for 7 days. On the 7th day of supplementation, the animals were divided into 4 new groups and killed at rest (RAA, n = 8; RPLC, n = 8), or immediately after the swimming exercise to exhaustion (EAA, n = 8; EPLC, n = 8). Results: No significant differences were observed between amino, acids and placebo rest groups for muscle and liver glycogen, blood glucose, lactate, alanine, and glutamine concentrations. However, in the exhaustion groups, the EAA group showed higher exercise time (68.37 +/- 25.42 X 41.12 +/- 13.82 min, p < .05) and lower blood lactate concentration (8.57 +/- 1.92 x 11.28 +/- 2.61 mmol (.) L-1, p < .05) than the EPLC group. Moreover, the ASP+ASG supplementation decreased the rate of glycogen degradation of gastrocnemius (1.00 0.51 X 3.43 +/- 0.99 mug (.) 100 mg of tissue sample(-1) (.) min(-1)), extensor digitorius longus (5.70 +/- 2.35 x 8.11 +/- 3.97 mug (.) 100 mg of tissue sample(-1) (.) min(-1)) and liver (0.51 +/- 0.34 x 3.37 +/- 2.31 mug (.) 100 mg of tissue sample(-1) (.) min(-1)) for EAA. Conclusion: These results suggest that ASP+ASG supplementation may increase the contribution of oxidative metabolism in energy production and delay fatigue during exercise performed above the AT.
Patients with McArdle's disease (myo-phosphorylase deficiency) cannot use muscle glycogen as an energy source during exercise. They therefore are an ideal model to learn about the metabolic adaptations which develop during endurance exercise leading to glycogen depletion. This review summarizes the current knowledge of ammonia and amino acid metabolism in these patients and also adds several new data. During incremental exercise tests in patients with McArdle's disease, forearm venous plasma ammonia concentration rises to a value between 200 and 500µM. Femoral arteriovenous difference studies show that muscle produces the ammonia. The leg release of both ammonia and glutamine (in µmol/min) has been estimated to be five-to tenfold larger in one of these patients than in healthy individuals exercising at comparable relative work load. Patients with McArdle's disease have a larger uptake of branched-chain amino acids (BCAA) by exercising leg muscles and show a more rapid activation of the muscle branched-chain 2-oxo acid dehydrogenase complex, a key enzyme in the degradation of the BCAA. In general, supplements of BCAA taken before the exercise test lead to a deterioration of exercise performance and a higher increase in heart rate and plasma ammonia during exercise, whereas supplements of branched-chain 2-oxo acids improve exercise performance and lead to a smaller increase in heart rate and plasma ammonia. At constant power output, patients with McArdle's disease show a rapid increase in heart rate and exertion perceived in the exercising muscles, which peak within 10 min after the start of exercise and then fall again (“second wind”). Peak heart rate and peak exertion coincide with a peak in plasma ammonia. Ammonia production during exercise in these patients is estimated to exceed the reported breakdown of ATP to IMP and therefore most likely originates from the metabolism of amino acids. Deamination of amino acids via the reactions of the purine nucleotide cycle and gluta-mate dehydrogenase are possible pathways. Deamination of glutamine, released by muscle, by glutaminase present in the endothelial cells of the vascular system may also contribute to the ammonia production. The observations made in these patients have led to the hypothesis that excessive acceleration of the metabolism of BCAA drains 2-oxoglutarate in the primary aminotransferase reaction and thus reduces flux in the citric acid cycle and impedes aerobic oxidation of glucose and fatty acids. This draining effect is normally counteracted by the anaplerotic conversion of muscle glycogen to citric acid cycle intermediates, a reaction which is severely hampered in these patients due to the glycogen breakdown defect. Deamination of amino acids is required then to regenerate 2-oxoglutarate, but inevitably leads to ammonia generation. It is suggested that similar metabolic adaptations may occur in healthy individuals during prolonged exhaustive exercise leading to glycogen depletion.
1. An increased uptake of tryptophan in the brain may increase serotoninergic activity and recently has been suggested to be a cause of fatigue during prolonged exercise. The present study, therefore, investigates whether ingestion of tryptophan or the competing branched-chain amino acids (BCAAs) affect performance. Ten endurance-trained male athletes were studied during cycle exercise at 70-75% maximal power output, while ingesting, ad random and double-blind, drinks that contained 6% sucrose (control) or 6% sucrose supplemented with (1) tryptophan (3 g l-1), (2) a low dose of BCAA (6 g l-1) or (3) a high dose of BCAA (18 g l-1). 2. These treatments greatly increased the plasma concentration of the respective amino acids. Using the kinetic parameters of transport of human brain capillaries, BCAA supplements were estimated to reduce brain tryptophan uptake at exhaustion by 8-12%, while tryptophan ingestion caused a 7- to 20-fold increase. Exercise time to exhaustion was not different between treatments (122 +/- 3 min). 3. The data suggest that manipulation of tryptophan supply to the brain either has no additional effect upon serotoninergic activity during prolonged exhaustive exercise or that manipulation of serotoninergic activity functionally does not contribute to mechanisms of fatigue.
The present study examined the effect of diet supplementation of oxaloacetate precursors (aspartate and asparagine) and carnitine on muscle metabolism and exercise endurance. The results suggest that the diet supplementation increased the capacity of the muscle to utilize FFA and spare glycogen. Time to exhaustion was about 40% longer in the experimental group compared to the control, which received commercial diet only. These findings suggest that oxaloacetate may be important to determine the time to exhaustion during a prolonged and moderate exercise.
The mitochondrial pyruvate carboxylase catalyses the ATP-dependent carboxylation of pyruvate to oxaloacetate. Since pyruvate carboxylase generates oxaloacetate for Krebs cycle function, it is proposed that the enzyme activity may be enhanced by exercise. To investigate this proposition, pyruvate carboxylase activity was determined in the heart, soleus and gastrocnemius (white portion) muscles of sedentary and swimming-trained adult rats (1 hour per day, 5 days a week, during 5 weeks) under the following conditions: rest, one hour of exercise and exhaustion. The results show that the pyruvate carboxylase activity is increased during exercise in both the sedentary and trained groups of rats. The stimulatory mechanism is unknown but it is possibly related to the generation of pyruvate from the breakdown of glycogen and acetyl CoA during fatty acid oxidation.