Exercise-induced muscle damage is reduced in resistance-trained males by branched chain amino acids: a randomized, double-blind, placebo controlled study.

Abstract

BACKGROUND: It is well documented that exercise-induced muscle damage (EIMD) decreases muscle function and causes soreness and discomfort. Branched-chain amino acid (BCAA) supplementation has been shown to increase protein synthesis and decrease muscle protein breakdown, however, the effects of BCAAs on recovery from damaging resistance training are unclear. Therefore, the aim of this study was to examine the effects of a BCAA supplementation on markers of muscle damage elicited via a sport specific bout of damaging exercise in trained volunteers. METHODS: Twelve males (mean +/- SD age, 23 +/- 2 y; stature, 178.3 +/- 3.6 cm and body mass, 79.6 +/- 8.4 kg) were randomly assigned to a supplement (n = 6) or placebo (n = 6) group. The damaging exercise consisted of 100 consecutive drop-jumps. Creatine kinase (CK), maximal voluntary contraction (MVC), muscle soreness (DOMS), vertical jump (VJ), thigh circumference (TC) and calf circumference (CC) were measured as markers of muscle damage. All variables were measured immediately before the damaging exercise and at 24, 48, 72 and 96 h post-exercise. RESULTS: A significant time effect was seen for all variables. There were significant group effects showing a reduction in CK efflux and muscle soreness in the BCAA group compared to the placebo (P < 0.05). Furthermore, the recovery of MVC was greater in the BCAA group (P < 0.05). The VJ, TC and CC were not different between groups. CONCLUSION: The present study has shown that BCAA administered before and following damaging resistance exercise reduces indices of muscle damage and accelerates recovery in resistancetrained males. It seems likely that BCAA provided greater bioavailablity of substrate to improve protein synthesis and thereby the extent of secondary muscle damage associated with strenuous resistance exercise. Clinical Trial Registration Number: NCT01529281.

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RESEARCH ARTICLEOpen Access
Exercise-induced muscle damage is reduced in
resistance-trained males by branched chain
amino acids: a randomized, double-blind, placebo
controlled study
Glyn Howatson1,2*, Michael Hoad3, Stuart Goodall1, Jamie Tallent1, Phillip G Bell1and Duncan N French1
Abstract
Background: It is well documented that exercise-induced muscle damage (EIMD) decreases muscle function and
causes soreness and discomfort. Branched-chain amino acid (BCAA) supplementation has been shown to increase
protein synthesis and decrease muscle protein breakdown, however, the effects of BCAAs on recovery from
damaging resistance training are unclear. Therefore, the aim of this study was to examine the effects of a BCAA
supplementation on markers of muscle damage elicited via a sport specific bout of damaging exercise in trained
volunteers.
Methods: Twelve males (mean±SD age, 23±2 y; stature, 178.3±3.6 cm and body mass, 79.6±8.4 kg) were randomly
assigned to a supplement (n=6) or placebo (n=6) group. The damaging exercise consisted of 100 consecutive
drop-jumps. Creatine kinase (CK), maximal voluntary contraction (MVC), muscle soreness (DOMS), vertical jump (VJ),
thigh circumference (TC) and calf circumference (CC) were measured as markers of muscle damage. All variables were
measured immediately before the damaging exercise and at 24, 48, 72 and 96 h post-exercise.
Results: A significant time effect was seen for all variables. There were significant group effects showing a reduction in
CK efflux and muscle soreness in the BCAA group compared to the placebo (P<0.05). Furthermore, the recovery of
MVC was greater in the BCAA group (P<0.05). The VJ, TC and CC were not different between groups.
Conclusion: The present study has shown that BCAA administered before and following damaging resistance exercise
reduces indices of muscle damage and accelerates recovery in resistance-trained males. It seems likely that BCAA
provided greater bioavailablity of substrate to improve protein synthesis and thereby the extent of secondary muscle
damage associated with strenuous resistance exercise. Clinical Trial Registration Number: NCT01529281.
Keywords: Recovery, BCAA, Muscle damage, Resistance training
Background
Resistance exercise is a common mode of training and is
considered an integral part in the athletes’ training regimen.
Although many resistance exercises require both shortening
and lengthening contractions, it has been well documented
that exercise biased by lengthening contractions are a more
powerful stimulus for neuromuscular adaptation compared
to shortening contractions [1-3]. As a consequence, many
athletes will routinely incorporate this exercise modality in
order to maximise the potential adaptations from lengthen-
ing contractions. However, lengthening contractions, par-
ticularly when high forces are generated, precipitate
temporary exercise-induced muscle damage (EIMD) that
can last for several days after the initial bout [4]. This EIMD
manifests as a reduction in neuromuscular function,
reduced range of motion, increased muscle soreness, limb
swelling and the elevation of intramuscular proteins in
blood [4-6]. These signs and symptoms impair muscle func-
tion and inhibit the potential to engage in high intensity
* Correspondence: glyn.howatson@northumbria.ac.uk
1School of Life Sciences, Northumbria University, Newcastle upon Tyne, UK
2School of Environmental Sciences and Development, Northwest University,
Potchefstroom, South Africa
Full list of author information is available at the end of the article
© 2012 Howatson et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
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exercise on subsequent days, which is often required by ath-
letic populations.
In an attempt to reduce the negative effects of EIMD a
number of interventions have been explored; these include
cold water immersions [7], antioxidant supplementation
[8,9], ergogenic aids [5], non-steroidal anti-inflammatory
drugs [10] and nutritional interventions [11]. These exam-
ples have shown mixed success, however one nutritional
intervention, branched chain amino acids (BCAA), have
shown a reasonable degree of efficacy in reducing the effects
of EIMD; in the most part following strenuous endurance
exercise. BCAA are a group of essential amino acids that are
a key substrate for protein synthesis and recovery [12]. Fur-
thermore, BCAA conserve muscle mass in conditions char-
acterised by protein loss and catabolism [13] and a recent
review has proposed BCAA to provide a therapeutic effect
following damaging resistance exercise [14]. Indeed, studies
examining recovery from heavy endurance activity [15-18]
have shown evidence that BCAA are beneficial in reducing
muscle damage and accelerating the recovery process.
Whilst this positive evidence is encouraging, muscle
damage is far more prevalent following high intensity re-
sistance exercise, although few studies have examined the
efficacy of BCAA following damaging resistance exercise.
Nosaka et al. [19] showed that amino acid supplementation
(containing around 60% BCAA) was effective in reducing
muscle damage and soreness when consumed immediately
before and during the four recovery days that followed a
damaging bout of lengthening contractions. Additionally,
in a recent well-controlled example [20], muscle soreness
was reduced with BCAA; however, changes in blood indi-
ces or recovery of muscle function were absent. The afore-
mentioned studies [19,20] used untrained volunteers and
an isolated muscle group, which are not wholly representa-
tive of the stimulus often encountered by many athletic
populations who routinely use damaging lengthening-
biased resistance exercise as a training stimulus.
Shimomura et al. [21] examined BCAA supplementation
in untrained females and whilst these authors demonstrated
some efficacy in reducing indices of damage in the BCAA
group, the placebo control consumed carbohydrate, which
has been shown to facilitate protein uptake [12,22], thus
having a synergistic effect to any exogenous protein con-
sumed following the laboratory visit. Interestingly, and in
some support of this supposition, Stock et al. [23] showed
that in a mixed sex group of trained participants there were
no differences in damage indices between a carbohydrate
versus a carbohydrate+leucine supplement. This study con-
tradicts the general findings from other research, which
may partly be attributable to a methodological difference
such as providing leucine alone (and not leucine, isoleucine
and valine combined). Additionally, Sharp and Pearson [24]
recently examined BCAA supplementation during a resist-
ance training programme designed to induce over-reaching.
These authors showed some efficacy with BCAA supple-
mentation in resistance-trained individuals (with the excep-
tion of creatine kinase), however, the study was not
focussed on damaging exercise and/or recovery making the
findings somewhat disparate. Nevertheless, the current evi-
dence is promising and we therefore hypothesised the mag-
nitude of EIMD in resistance-trained individuals would be
lower with BCAA supplementation compared to a placebo
control. Consequently, the aim of this study was to investi-
gate the effect of BCAA supplementation on recovery from
a sport-specific damaging bout of resistance exercise in
trained volunteers.
Methods
Participants
Twelve trained males who were competitive national league
games players (rugby and football) and familiar with resist-
ance training volunteered to participate (mean±SD age,
23±2 y;stature,178.3±3.6
79.6±8.4 kg). Participants engaged in specific resistance ex-
ercise at least twice per week during the competitive season.
Following a health-screening questionnaire, all volunteers
provided written, informed consent. Participants were ran-
domly assigned to one of two groups, supplement or pla-
cebo, in a stratified (according to strength), double-blind
fashion (Figure 1). The sample size was based on previous
research examining supplementation and EIMD that had
shown a significant effect [21,25]. Prior to the start of data
collection all procedures were given institutional research
ethics approval and subsequently registered as a clinical trial
(ClinicalTrials.gov, www.clinicaltrials.gov, NCT01529281).
cm;andbodymass,
Experimental design
The supplementation protocol followed a randomised,
double-blind, placebo controlled design. The research was
Figure 1 Experimental design and a flow diagram of the
participants allocation to groups.
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based around a 12 day testing period. Participants consumed
either the BCAA supplement or a placebo for the duration
of the study, which included a 7 day ‘loading’ phase; on day
8 the damaging exercise was performed. The criterion mea-
sures creatine kinase (CK), muscle soreness (DOMS), max-
imum voluntary contraction (MVC), vertical jump (VJ) and
limb circumference were obtained pre-exercise and then at
24 h intervals up to 96 h post-exercise. Participants were in-
jury free and were asked to refrain from any physical activity
during the 12 day testing period and avoid taking anti-in-
flammatory medication, therapies and additional nutritional
supplements.
Supplementation protocol
Pre- and post-exercise supplementation lasted for a total
of 12 days; this was based on previous research showing
positive effects with BCAA supplementation on markers
of EIMD16. Participants ingested 10 g, twice per day
(morning and evening) of either BCAA or placebo (aspar-
tame based artificial sweetener). The BCAA supplement
(Myprotein, Cheshire, UK) contained a ratio of 2:1:1 leu-
cine, isoleucine and valine, respectively. The BCAA and
artificial sweetener were in powder form; each serving was
mixed with ~300 ml of water. Artificial sweetener rather
than a carbohydrate-based placebo was used to prevent a
rise in insulin that may have altered protein metabolism
[22]. The dosage of BCAA was based on the manufac-
turer’s recommendations and previous BCAA supplemen-
tationresearch [16,26]. Additionally,
overnight fast, participants ingested a further 20 g bolus,
1 h pre-exercise and immediately post-exercise. In accord-
ance with previous work [21], all participants were
strongly advised to maintain regular dietary habits and
avoid taking additional protein or any supplements for the
duration of the study. In an attempt to control for diet,
participants were asked to record food intake in the load-
ing phase of the trial and replicate this diet as closely as
possible following the damaging protocol.
following an
Damaging exercise protocol
Participants performed a total of 100 drop-jumps from a
height of 0.6 m. Upon landing, participants were encour-
aged to immediately jump vertically with maximal force.
Five sets of 20 drop-jumps were performed with a 10 s
interval between each jump and a 2 min rest between sets.
This protocol has been previously shown to cause signifi-
cant elevations in muscle damage indices [19,27,28].
Indices of muscle damage
Plasma CK was determined from an earlobe capillary
blood sample. The sample was analysed immediately
using an automated, dry slide photospectrometer (Reflo-
tron Plus, Bio Stat Ltd. Stockport, UK). The normal
reference ranges of plasma CK activity for this method
are 24–195 IU and the intra-sample CV was<3%.
Muscle soreness
Participants were asked to perform and hold a squat (90°
knee angle) whilst they rated their perceived muscle
soreness on a 200 mm visual analogue scale [5,27,29].
The scale consisted of a line from 0 mm (no pain) to
200 mm (unbearably painful).
Maximal voluntary contraction
Isometric MVC of the participants’ dominant knee
extensors was assessed using a strain gauge (MIE Med-
ical Research Ltd., Leeds, UK). Similarly to previous
work [5,11,27], participants were seated on a plinth
where the strain gauge was assembled. The strain gauge
was attached to the ankle, immediately above the malle-
oli. Each MVC was performed at a knee joint angle of
900. The joint angle was assessed prior to each repetition
with a goniometer (Bodycare Products, Warwickshire,
UK) at the lateral condyle of the femur. MVCs were per-
formed for 3 s with a 60 s rest between each repetition.
Each participant was familiarised with the test procedure
and received strong verbal encouragement for each at-
tempt. Three MVCs were recorded and the maximum
value was used for data analysis. To account for inter-
subject variability, MVC was expressed as a percentage
of pre-damage MVC.
Vertical jump performance
Vertical jump (VJ) performance was assessed using the
Vertec instrument (Sports Imports, Columbus Ohio).
Participants performed a counter movement jump in
which, on command from a standing position, they des-
cended rapidly (to approximately a 90° knee angle) and
performed a maximal vertical jump, tapping the device
with the dominant arm [30]. Each participant was famil-
iarised with the test procedure prior to the recorded
efforts and received strong verbal encouragement for
each attempt. Three attempts were made, each separated
by 60 s, and the highest value was used for data analysis.
Limb circumference
Mid-thigh and calf circumference was assessed as a
measure of limb swelling using an anthropometric tape
measure (Bodycare Products, Warwickshire, UK). Both
measures were obtained with the participant in a stand-
ing position. The calf measurement was made at the
widest part of the calf, whereas the mid-thigh measure
was determined as the mid-point between the inguinal
crease and superior aspect of the patella. Both sites were
marked with semi-permanent ink to ensure consistent
measurements between days [27].
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Data analysis
All data are expressed as means±SD. Detection of differ-
ences were determined using a 2-way, repeated measures
ANOVA (group, 2; time, 5). Significant interactions were
followed-up using LSD post-hoc, pair-wise comparisons.
Statistical significance was set at P≤0.05 prior to analyses.
Results
All dependent variables showed significant time effects (P
<0.05) demonstrating the protocol successfully induced
muscle damage. CK (Figure 2) showed a significant group
effect (F=7.0, P=0.024), where CK was significantly lower
in the BCAA group compared to placebo. Both BCAA and
placebo groups peaked at 24 h post-exercise (312 IU.L-1
and 398 IU.L-1, respectively), which equated to a 3 to 4-fold
increase above baseline. Muscle soreness (Figure 3) peaked
at 48 h post-exercise in both groups and showed a signifi-
cant group (F=21.3, P=0.001) and interaction (F=3.6.
P=0.037) effect. Post-hoc analysis showed that soreness was
significantly lower at 24 and 48 h post-exercise in BCAA
compared to control (P<0.05).
MVC (Figure 4) showed a significant group effect
(F=9.9, P=0.010) where the decrement in force was
lower and recovery of force was greatest in the BCAA
group. At 24 h post-exercise the BCAA and placebo
groups showed a peak decrement of 18 vs. 27% below
pre-exercise MVC, respectively. There were no group or
interaction effects for vertical jump performance or limb
girth at either the calf of thigh (Table 1).
Discussion
The initial aim of the present study was to examine the
effects of BCAA supplementation on indices of muscle
damage in resistance-trained volunteers. The principle
findings show BCAA can reduce the negative effects of
damaging exercise by attenuating CK efflux, reducing
residual muscle soreness and improving recovery of
muscle function to a greater extent than a placebo
control.
The protocol successfully induced muscle damage,
which was evident from the significant time effects for all
dependent variables. This supports the efficacy of the
protocol as a model to induce muscle damage in a sport
specific manner [27,28]. Additionally, the data presented
here support previous literature suggesting BCAA as an
effective intervention to reduce the negative effects of
damaging exercise [15-18] and more specifically from
damaging resistance exercise [14,20,21]. The novel infor-
mation offered by these data demonstrate that BCAA can
be used as an effective intervention to ameliorate the nega-
tive effects EIMD precipitated from a sport specific dam-
aging bout of resistance exercise in trained participants.
Creatine kinase, a surrogate index of muscle damage, is
more indicative of damage or gaps in the sarcolemma and
Figure 2 Plasma creatine kinase concentration before and up to
96 h after the damaging bout of exercise. * denotes a significant
group effect. Values are means±SD; N=12.
Figure 3 Delayed onset muscle soreness before and up to 96 h
after the damaging bout of exercise. * denotes a significant
group effect. Values are means±SD; N=12.
Figure 4 Maximal voluntary force before and up to 96 h after
the damaging bout of exercise. * denotes a significant group
effect. Values are means±SD; N=12.
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hence causing the cytosolic enzymes to ‘leak’ from the cell
in to the blood [20]. However, the cell membrane is likely
to have undergone some degree of lipolysis as a result of
an imbalance in calcium homeostasis [4], almost certainly
from the exercise insult. The damage literature often
shows a high degree of inter-subject variability in CK and
other cytosolic markers of EIMD, however, variability in
the current study was relatively small, partly attributable
to the trained status of the volunteers. The greater condi-
tioning of these participants has almost certainly led to a
repeated bout effect [31], whereby, a conditioning bout of
exercise (in this case prior training) leads to a decrease in
damage indices on subsequent bouts [4,31,32]. This is fur-
ther supported by the low CK response seen in both
groups following the exercise, when compared to the dam-
age responses seen in untrained volunteers [19,20]. Despite
this relative homogeneity, the CK response was less in the
BCAA group suggesting the membrane integrity was
maintained to greater extent than the placebo group. The
damage response is known to be bi-phasic in nature; a pri-
mary response caused by the mechanical stress of the ex-
ercise, followed by a secondary, transient inflammatory
response over the following hours and days [4]. The subse-
quent inflammatory response increases protein uptake ne-
cessary for use as an energy source and/or pathways
responsible for cell signaling and subsequent muscle re-
modeling [14,33]. Although we cannot definitively support
this postulate, it seems plausible that the greater bioavail-
ability provided by BCAA facilitated this response and
thereby decreased secondary damage to the muscle.
Our data concur with previous studies that show a peak
in soreness at 48 h post-exercise [27,32]. Furthermore, the
group effects support previous data [20,21,34] showing a
reduction in muscle soreness following a damaging bout of
exercise with BCAA supplementation. Although the mech-
anism surrounding muscle soreness following a damaging
bout of exercise is not well understood, it seems likely to
be related to inflammation, particularly to the connective
tissue elements [35] that sensitise nociceptors in muscle
and hence increase sensations of pain [36]. However, previ-
ous work [20] demonstrating a reduction in soreness fol-
lowing BCAA supplementation also measured the acute
inflammatory response (interleukin-6, a pro-inflammatory
cytokine) and showed no difference between the BCAA
and placebo groups. Jackman et al. [20] suggested that the
increase in food or feeding per se, particularly amino acids,
might be related to reductions in soreness. Although this
idea is somewhat speculative and has no supporting evi-
dence or proposed mechanism, we show similar trends in
our data, but it is not possible to support or refute this the-
ory. Based on the reductions in CK, it makes the expect-
ation tenable that the secondary damage phase is reduced
by the aforementioned uptake of BCAA for protein synthe-
sis, thus, limiting the extent of damage and hence reducing
the precipitation of soreness.
Whilst there was no difference in vertical jump per-
formance and limb girth, the most notable finding is that
reductions in MVC were attenuated and recovery of
MVC was accelerated following BCAA supplementation.
This study demonstrated an effect on function and is in
contrast to other work [20] that used untrained partici-
pants in a similar experimental design showing no bene-
fits in the recovery of force production with BCAA.
Interestingly, other studies [21,37] using non-resistance-
trained student populations have shown some benefit in
the recovery of muscle function. These data should be
treated with caution however, as both studies [21,37]
used a cross-over design which suffers the limitation of
the repeated bout effect (RBE). The RBE refers to a pro-
tective effect or attenuation of damage indices when the
exercise is repeated [4,31,32]. Although up to 11 weeks
was given between damaging bouts, the RBE has been
previously shown to accelerate the recovery of muscle
function for between 6 and 9 months following the initial
damaging bout [38].
It would seem that differences between our findings and
those of Jackman et al. [20] might lie largely with the par-
ticipant populations; Jackman et al. [20] chose untrained
participants, whereas the current study recruited resist-
ance-trained volunteers. This is evident in the group famil-
iar with resistance exercise at 72 h (> 90% recovery of
MVC) in comparison to the untrained population [20] that
were only ~60% recovered at the same time point. The
other obvious difference between the current investigation
and previous literature is the amount of BCAA adminis-
tered. Historically, previous literature [21,34] examining
Table 1 Vertical jump height, thigh and calf circumference before and up to 96 h after the damaging bout of exercise
Pre24 h
Vertical Jump (cm)BCAA
61.8±7.457.4±
48 h72 h96 h
7.9 58.2± 8.560.5±7.962.3±7.6
Placebo
65.3±5.260.3±3.361.5 ±4.163.3±4.264.1± 4.5
Thigh Circ. (mm) BCAA
55.7 ±6.256.8 ±5.657.1±5.7 55.8± 6.155.7±6.2
Placebo
57.9± 5.358.4 ± 5.158.3± 5.257.9± 5.357.9±5.3
Calf Circ. (mm)BCAA
38.1±1.838.6 ±1.538.8±1.638.2±1.838.1±1.8
Placebo
37.9±1.338.3±1.3 38.3±1.437.9 ±1.037.9±1.0
Values are means±SD; N=12.
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recovery from damaging resistance exercise has only used
a single bolus of ~5 g BCAA, finding small positive effects,
particularly on muscle soreness. Interestingly, Jackman
et al. [20] fed participants considerably more BCAA than
this previous work, consisting of 88 g in total over the test
period (with no loading phase), whereas the present study
gave 280 g total over the test period. Our supplementation
procedure included a 7 day loading phase (20 g per day)
and 20 g per day during the subsequent recovery phase.
Furthermore, we provided a 20 g dose immediately before
and after the bout of exercise, which is when the biggest
discrepancy in BCAA feeding occurred between studies.
Previous work [39] has shown that timing of a protein
based recovery strategy is important and immediately fol-
lowing a damaging bout of exercise can be most beneficial
in accelerating recovery. Whist Jackman et al. [20] did sup-
plement with BCAA after the damaging bout, there was a
delay of at least 1 h that may also account for the positive
effect found in the present study, which fed immediately
after the bout of damaging exercise. Previous work [40]
showed BCAA to rise in plasma within 15 min and peak
30 min after ingestion, which means the bioavailability of
BCAA post-exercise in our investigation was at least 1 h
earlier than that of Jackman et al. [20]; therefore, it seems
plausible thatearly feeding
increased the efficacy of the intervention. This is some-
what conjectural and would serve as an interesting ques-
tion for future research to ascertain the optimal strategy
for BCAA supplementation.
Regardless of whether the loading phase and timing of
the supplementation post-exercise was effective in in-
creasing the bioavailability of BCAA, there is still a stark
difference in the total supplementation volume (88 vs.
140 g). The larger quantity of BCAA we provided might
partly account for the difference between studies in dam-
age indices (MVC and CK). We based our supplementa-
tion regimen on previous work that showed a positive
effect [16,26] and propose that positive effects beyond at-
tenuation of muscle soreness (i.e., recovery of muscle
function) may need a more immediate bioavailability and
greater quantity of BCAA than those used previously.
There are two limitations from the study, which need to
be acknowledged. Firstly the lack of specific dietary control
might have led to discrepancies in caloric and, more specif-
ically, protein ingestion between the groups. Although we
attempted to control this by asking participants to record
food intake during the loading phase and replicate this fol-
lowing the damaging exercise, an approach that has been
previous used [11,21], there was no specific control between
groups. Conceivably discrepancies in protein intake can
affect the bioavailability of the substrate and hence affect
protein turnover and ultimately influence the outcome of
these data. The second limitation is that we used an artifi-
cial sweetener with little or no calorific value was used,
post-damagingexercise
which will certainly alter the energy balance by around
80 kcal/day, and may be problematic if the placebo group
were in energy deficit, but based on the food record sheets
this does not seem likely. Although the current investiga-
tion has a good degree of external validity, future research
might like to consider more rigorous dietary control mea-
sures such as; 1) asking participants to weigh food and ac-
curately log food intake; or 2) providing a pre-determined
menu for the participants to ensure no discrepancies be-
tween and within groups, although this still relies on par-
ticipant adherence outside the laboratory. Finally, 3)
although difficult to facilitate, participants could be housed
in an environment where dietary behavior can be imposed
and thereby strictly controlled.
In summary, these data offer novel information on the
application of BCAA supplementation. A 20 g/day supple-
mentation regimen administered 7 days prior to (with add-
itional 20 g immediately before and following the
damaging exercise) and for 4 days after a damaging bout of
eccentric biased exercise reduced soreness and the plasma
level of intramuscular enzymes. Most importantly, BCAA
attenuated reductions in muscle function and accelerated
recovery post-exercise in a resistance-trained population.
Competing interests
The authors declare that they have no competing interests.
Author details
1School of Life Sciences, Northumbria University, Newcastle upon Tyne, UK.
2School of Environmental Sciences and Development, Northwest University,
Potchefstroom, South Africa.3School of Sport Health and Applied Science, St
Mary’s University College, Twickenham, UK.
Authors’ contributions
GH, as the principal investigator, contributed to conception and design of
the experiment, data collection and analysis, data interpretation, manuscript
draft and the editorial process. MH, as a post-graduate student, was
responsible for conception, participant recruitment, data collection, initial
data analysis, interpretation and initial drafting of the manuscript. SG
contributed to data interpretation, data presentation and manuscript drafting
and editing. JT, PGB, DNF contributed to data analysis, data interpretation
and manuscript editing. All authors approved the final version of the
manuscript.
Received: 9 February 2012 Accepted: 8 May 2012
Published: 8 May 2012
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doi:10.1186/1550-2783-9-20
Cite this article as: Howatson et al.: Exercise-induced muscle damage is
reduced in resistance-trained males by branched chain amino acids: a
randomized, double-blind, placebo controlled study. Journal of the
International Society of Sports Nutrition 2012 9:20.
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