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Post Exercise Alcohol Ingestion Exacerbates Eccentric-Exercise Induced Losses in Performance


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The effect of acute alcohol intake on muscular performance in both the exercising and non-exercising legs in the days following strenuous eccentric exercise was investigated to ascertain whether an interaction between post-exercise alcohol use and muscle damage causes an increase in damage-related weakness. Ten healthy males performed 300 maximal eccentric contractions of the quadriceps muscles of one leg on an isokinetic dynamometer. They then consumed either a beverage containing 1 g of ethanol per kg bodyweight ethanol (as vodka and orange juice; ALC) or a non-alcoholic beverage (OJ). At least 2 weeks later they performed an equivalent bout of eccentric exercise on the contralateral leg after which they consumed the other beverage. Measurement of peak and average peak isokinetic (concentric and eccentric) and isometric torque produced by the quadriceps of both exercising and non-exercising legs was made before and 36 and 60 h post-exercise. Greatest decreases in exercising leg performance were observed at 36 h with losses of 28.7, 31.9 and 25.9% occurring for OJ average peak isometric, concentric, and eccentric torques, respectively. However, average peak torque loss was significantly greater in ALC with the same performance measures decreasing by 40.9, 42.8 and 44.8% (all p < 0.05). Performance of the non-exercising leg did not change significantly under either treatment. Therefore, consumption of moderate amounts of alcohol after damaging exercise magnifies the loss of force associated with strenuous eccentric exercise. This weakness appears to be due to an interaction between muscle damage and alcohol rather than the systemic effects of acute alcohol consumption.
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Post-exercise alcohol ingestion exacerbates eccentric-exercise
induced losses in performance
Matthew J. Barnes Toby Mu
Stephen R. Stannard
Accepted: 23 November 2009 / Published online: 11 December 2009
ÓSpringer-Verlag 2009
Abstract The effect of acute alcohol intake on muscular
performance in both the exercising and non-exercising legs
in the days following strenuous eccentric exercise was
investigated to ascertain whether an interaction between
post-exercise alcohol use and muscle damage causes an
increase in damage-related weakness. Ten healthy males
performed 300 maximal eccentric contractions of the quad-
riceps muscles of one leg on an isokinetic dynamometer.
They then consumed either a beverage containing 1 g of
ethanol per kg bodyweight ethanol (as vodka and orange
juice; ALC) or a non-alcoholic beverage (OJ). At least 2
weeks later they performed an equivalent bout of eccentric
exercise on the contralateral leg after which they consumed
the other beverage. Measurement of peak and average peak
isokinetic (concentric and eccentric) and isometric torque
produced by the quadriceps of both exercising and non-
exercising legs was made before and 36 and 60 h post-
exercise. Greatest decreases in exercising leg performance
were observed at 36 h with losses of 28.7, 31.9 and 25.9%
occurring for OJ average peak isometric, concentric, and
eccentric torques, respectively. However, average peak tor-
que loss was significantly greater in ALC with the same
performance measures decreasing by 40.9, 42.8 and 44.8%
(all p\0.05). Performance of the non-exercising leg did not
change significantly under either treatment. Therefore,
consumption of moderate amounts of alcohol after damaging
exercise magnifies the loss of force associated with strenuous
eccentric exercise. This weakness appears to be due to an
interaction between muscle damage and alcohol rather than
the systemic effects of acute alcohol consumption.
Keywords Ethanol Muscle strength Soft tissue injuries
The mechanisms and consequences of exercise-induced
muscle damage (EIMD) have received considerable sci-
entific attention over the past 20 years. Strenuous eccentric
muscle action is now known to cause micro-structural
damage resulting in delayed onset muscle soreness
(DOMS), inflammation and more importantly, impaired
muscle function which typically lasts for a number of days,
depending on the severity of the damage (Cleak and Eston,
1992; Proske and Morgan, 2001). Over this same period
EIMD has been employed as a model of soft tissue injury
where a number of modalities aimed at improving the rate
of recovery (e.g. cold water immersion therapy (Eston and
Peters 1999), non-steroidal anti-inflammatory medication
(Gulick et al. 1996), massage (Jo
¨nhagen et al. 2004) and
compression therapy (Kraemer et al. 2001)) have been
tested. This research has provided mixed and often
inconclusive results. Surprisingly, compared to these and
other recovery modalities, less attention has been afforded
to post-exercise behaviours that may simultaneously impair
the recovery process after EIMD.
One such behaviour is post-exercise alcohol use. While
the consumption of large amounts of alcohol by sports-
people, often after competition or training, is common
place (Nelson and Wechsler 2001; Snow and Munro 2006;
O’Brien et al. 2007) little is known about how this
behaviour effects recovery and subsequent performance in
Communicated by William Kraemer.
M. J. Barnes (&)T. Mu
¨ndel S. R. Stannard
Institute of Food, Nutrition, and Human Health,
Massey University, Private Bag 11-222,
Palmerston North, New Zealand
Eur J Appl Physiol (2010) 108:1009–1014
DOI 10.1007/s00421-009-1311-3
the days after exercise. We have recently shown that
moderate amounts of alcohol (1 g per kg of body weight)
consumed immediately after strenuous eccentric exercise
exacerbates the weakness normally seen in the days fol-
lowing such exercise (Barnes et al. 2009). This finding
suggests that athletes competing in sports involving stren-
uous eccentric muscular work or those suffering from soft
tissue injury should avoid alcohol consumption, at least
immediately after exercise or injury, if rapid recovery is
important. However, the design of this previous study did
not allow us to ascertain whether this alcohol-induced
weakness was due to delayed recovery from strenuous
eccentric exercise or whether alcohol alters the ability to
recruit and create tension in any muscle group in the 60-h
period after drinking.
Previous research (Poulsen et al. 2007) suggests that the
acute consumption of clinically relevant levels of alcohol
does not affect muscular performance in the days following
a drinking session. Further, indices of EIMD are unaffected
when alcohol is acutely consumed prior to a bout of
damaging exercise (Clarkson and Reichsman 1990). The
results of these studies suggest that our previous findings
are due to the alcohol affecting the recovery processes in
already damaged muscle, not systemically weakening all
skeletal muscles.
The purpose of this study, therefore, was to investigate
whether alcohol interacts with damaged skeletal muscle to
magnify the typical weakness associated with EIMD or
whether our previous findings are due to the systemic effects
of acute alcohol consumption, independent of EIMD.
The current study utilised a modified version of the pro-
tocol described by Barnes et al. (2009). Adapted from the
work of MacIntyre et al. (1996), this exercise protocol has
previously been shown to bring about significant levels of
muscle damage as characterised by decreased muscular
performance, DOMS and elevations in circulating creatine
kinase concentrations (MacIntyre et al. 1996; Barnes et al.
2009). Briefly, subjects performed 300 maximal eccentric
contractions of the quadriceps muscles of one leg on an
isokinetic dynamometer. They then consumed either an
alcoholic beverage or a non-alcoholic control beverage. At
least 2 weeks later they performed an equivalent bout of
eccentric exercise on the contralateral leg after which they
consumed the other beverage. Muscular performance of the
damaged (exercising) and non-damaged (non-exercising)
legs was measured prior to the damaging exercise bout and
at 36 and 60 h post-exercise.
Twelve males volunteered to participate in this study.
However, due to an obvious learning effect the results of
two subjects were excluded from statistical analysis, as
their strength was higher than pre-exercise values in the
days after the damaging protocol. Analysis was there-
fore carried out on the results of 10 subjects (age
23.5 ±5.1 years, body mass 76.9 ±12.9 kg). All subjects
were healthy and had at least 2 years of resistance training
experience at a recreational level (minimum twice per
week). The protocol was approved by the Massey Uni-
versity Human Ethics Committee and written consent was
obtained from each subject.
Familiarisation of the protocol was carried out at least 1
week before the first trial. Subjects were instructed to
abstain from alcohol consumption and any form of exercise
from 48 h before and until 60 h after the exercise bout.
Subjects were also instructed to abstain from practices that
could potentially improve or delay their recovery during
the 60 h post-exercise period. Subject’s diets were repli-
cated between trials by way of a food diary that was filled
out from the morning of the first trial until the last mea-
surements were taken at 60 h post-exercise. Utilising a
single cross-over design, treatment and leg were randomly
allocated in a counter-balanced fashion. This was done to
account for ordering and (leg) dominance effects.
Muscular performance
Four hours after consuming a standardised, solid meal
(3765 kJ; CHO 133 g, Fat 28 g, Protein 25 g) subjects
returned to the laboratory in the evening and warmed up on
a cycle ergometer (Monark, Varberg, Sweden) for five
minutes at 100 W. They were then seated on a Biodex
isokinetic dynamometer (Biodex Medical Systems, New
York, USA) and straps were fixed across the chest, hips and
active leg to isolate movement to the quadriceps. Knee
joint range of motion was set and recorded for use in
subsequent follow-up tests. Subjects then performed sepa-
rate sets of five maximal isometric, concentric and eccen-
tric contractions of the quadriceps muscles of both the
non-exercising and the exercising legs. Each set was sep-
arated by 2 min of passive recovery. Isometric tension was
measured at a knee angle of 758(1.31 rad). Concentric and
eccentric torques were measured at an angular velocity of
(0.52 rad s
). Absolute peak torque and average
peak torque over five contractions were recorded. Pre-
exercise muscular performance measures were made in the
early evening with subsequent follow-up measurements
made 36 and 60 h post-exercise. The time of day at which
subjects completed these measurements was standardised
between trials. Although time of day was different between
1010 Eur J Appl Physiol (2010) 108:1009–1014
measurements the lack of change in the performance of the
non-exercising leg illustrates that changes in circadian
rhythms did not affect force development capabilities in the
current study.
Exercise protocol
Subjects remained on the Biodex and completed 3 sets of
100 maximal eccentric contractions, over a 60°(1.05 rad)
range of motion at an angular velocity of 30°s
, using the
quadriceps muscles of one leg. Each set was separated by
5 min of passive recovery. Subjects were verbally encour-
aged to resist the downward action of the dynamometer arm
as hard as possible and had access to visual feedback of
their torque throughout the protocol to ensure continuous
maximal effort. Total work completed during the eccentric
exercise bouts was not significantly different between trial
one (34.9 ±11.5 kJ) and trial two (36.7 ±11.1 kJ)
(p =0.14) or between control (OJ) (35.2 ±11.5 kJ) and
alcohol (ALC) trials (36.5 ±11.5 kJ) (p=0.29).
Thirty minutes after completion of the exercise bout, and
having consumed a standardised meal immediately after
exercise (1532 kJ; CHO 50.4 g, fat 9.1 g, protein 7 g),
subjects began drinking a beverage containing either 1 g of
alcohol per kg of body weight as vodka (37.5% alcohol/
volume; Smirnoff, Australia) in orange juice (Frucor
Beverages, New Zealand) (ALC) or a control beverage of
orange juice alone (OJ). Equivalent to 8 ±2.8 standard
drinks, the mean volume of vodka consumed per subject
was 211.9 ±51.4 ml. In order to balance total energy
value (2794.5 ±476.1 kJ) and fluid volume (1638 ±
268 ml) between trials, subjects consumed a greater vol-
ume of orange juice in the OJ trial while in the ALC trial
they consumed an additional volume of water (751 ±
128 ml) along with the alcoholic beverage. An equal vol-
ume of beverage was consumed every 15 min over a total
time of 90 min. Once the required amount of beverage was
consumed participants were driven home and instructed to
go directly to bed.
For the second trial, the contralateral leg was exercised
and the other beverage was consumed using the same
protocol, as outlined above.
Statistical analysis
Data were analysed using the Statistical Program for Social
Sciences (SPSS) for Windows (version 15.0, SPSS Inc.,
Chicago, IL). A general linear-model three-way repeated-
measures ANOVA (treatment 9time 9leg) was used to
compare conditions over time for each performance
measure. This analysis provided main effects of time,
treatment and leg; thus treatment 9time, treatment 9leg,
time 9leg and treatment 9time 9leg interactions were
also investigated. If conditions differed significantly, post
hoc pairwise comparisons using Bonferroni adjustment
were performed to identify the differences between time
points within each treatment and leg. As no significant
change was seen in muscular performance of the non-
exercising leg (see Results section for details) and to allow
comparison between the results of the current study and our
previous findings (Barnes et al. 2009), exercising leg data
was analysed separately with two-way repeated-measures
ANOVA providing additional treatment 9time interac-
tions. As different legs were used for each trial, resulting in
significantly different pre-exercise values between treat-
ments, data was analysed as absolute change in torque
relative to pre-exercise values. Reported values are
means ±standard deviation (SD). Statistical significance
was set at the 95% level of confidence (P\0.05).
Completion of 300 eccentric muscular contractions of the
quadriceps resulted in significant decreases in isometric,
concentric and eccentric peak and average peak torque over
time in the exercising leg only (all P\0.001, Table 1). No
significant change in non-exercising leg performance was
observed at any time point under either treatment (all
P[0.2). Significant Treatment 9Time 9Leg interac-
tions were found for isometric (P=0.036) and eccentric
(P=0.02) peak torques as well as for isometric (P=
0.032), concentric (P=0.032) and eccentric (P=0.023)
average peak torques.
Analysis of the exercising leg data, independent of the
leg variable, found significant changes over time for all
performance measures (all P\0.001). Significant treat-
ment effects (all P\0.02) and treatment 9time interac-
tions (all P\0.05) were seen for all performance
measures except peak concentric torque (P=0.16 and
0.42, respectively). Greatest decreases in performance were
seen with ALC at 36 h while no significant change in
performance was observed between 36 and 60 h under
either treatment.
Repeated-measures ANOVA of trial one versus trial two
found no significant order effect for any of the muscular
performance measures (all P[0.15).
The aim of the present study was to investigate whether the
systemic effects of alcohol bring about muscular weakness
Eur J Appl Physiol (2010) 108:1009–1014 1011
in the days following alcohol consumption after strenuous
eccentric exercise or whether alcohol interacts with EIMD
to exacerbate the loss of muscular performance, as previ-
ously observed (Barnes et al. 2009).
Completion of 300 maximal eccentric contractions of
the quadriceps resulted in significant decreases in all per-
formance measures in the exercising leg only (Table 1). In
accordance with the results of Poulsen et al. (2007), our
data confirm that a moderate dose of alcohol has no affect
on muscular performance in the days following a drinking
episode provided the muscle has not been damaged as a
result of strenuous eccentric work. The results of our pre-
vious study (Barnes et al. 2009) are thus due to an inter-
action between post-exercise alcohol consumption, the
damaged muscle and/or the recovery processes initiated by
Confirming our previous observations, in the current
study significant differences in post-exercise muscle per-
formance between treatments were seen after 36 h. At this
time point, isometric and eccentric peak torques were 39
and 44% lower than pre-exercise measures, respectively,
with ALC compared to losses of 29 and 27% for the same
measures with OJ. Perhaps more important than a single all
out effort, the ability to generate force repeatedly was
greatly reduced, with losses in average peak torque of 41%
(isometric), 43% (concentric) and 45% (eccentric) with
ALC compared to 29, 32 and 26% with OJ, respectively.
Together with the results of our previous work (Barnes
et al. 2009), the current study reinforces the observation
that the consumption of moderate amounts of alcohol after
damaging exercise magnifies the loss in force production
capability typically associated with EIMD.
To date considerable effort has been made to identify
modalities that improve the rate of performance recovery
after strenuous eccentric exercise. The majority of this
research, however, has failed to conclusively show that
losses in performance can be minimised if a particular
modality is used during the post-exercise period (Cleak and
Eston 1992; Barnett 2006; Wilcock et al. 2006). An alter-
native, as suggested by Reilly and Ekblom (2005), is to
adhere to proper nutritional strategies including moderation
when drinking alcohol. Indeed, given our current and
previous findings, moderation of alcohol after strenuous,
damaging exercise is a sound advice if a timely return to
optimal performance is desired. However, whether mod-
eration alone is sufficient to avoid the negative effects of
Table 1 Absolute changes in torque (N-m) following strenuous eccentric exercise
Exercising leg Non-exercising leg
Pre 36 h 60 h Pre 36 h 60 h
Peak ISO
OJ 275.8 ±48.9 -78.8 ±38.7* -72.9 ±48.7* 286.0 ±51.2 -3.4 ±16.0 -0.1 ±19.6
ALC 295.6 ±49.8
-113.7 ±45.3*
-108.9 ±84.4* 289.6 ±62.6 -10.0 ±21.8 -3.0 ±42.7
Peak CON
OJ 227.8 ±50.3 -71.5 ±32.4* -57.9 ±22.8* 255.9 ±69.4 -11.5 ±26.0 -12.1 ±23.2
ALC 240.9 ±50.4 -88.3 ±44.4* -78.2 ±64.6* 238.3 ±45.3 -11.4 ±24.2 -3.5 ±37.7
Peak ECC
OJ 284.9 ±77.3 -77.1 ±59.3* -63.5 ±51.9* 311.0 ±81.7 -0.3 ±32.2 4.9 ±37.8
ALC 345.6 ±81.7
-150.2 ±58.8*
-133.2 ±88.2*
335.6 ±79.0 -22.6 ±47.7 -33.0 ±73.1
Average ISO
OJ 256.9 ±39.0 -73.8 ±41.5* -72.0 ±55.7* 271.3 ±40.1 -7.8 ±18.7 -1.5 ±22.1
ALC 281.1 ±37.7
-115.1 ±50.3*
-111.7 ±86.8*
271.3 ±54.1 -8.9 ±15.3 -3.7 ±43.7
Average CON
OJ 205.1 ±31.2 -65.6 ±32.7* -55.3 ±32.7* 230.7 ±50.2 -10.0 ±19.7 -9.9 ±32.8
ALC 226.8 ±37.9
-97.0 ±47.7*
-91.0 ±64.0*
222.7 ±36.2 -11.6 ±16.8 -9.4 ±40.5
Average ECC
OJ 266.9 ±76.9 -69.1 ±93.6
-63.6 ±47.4* 291.3 ±84.3 2.6 ±33.7 6.4 ±41.5
ALC 320.4 ±70.1
-143.5 ±68.6*
-127.8 ±91.6*
306.3 ±75.9 -8.6 ±37.1 -23.8 ±60.1
ISO isometric, CON concentric, ECC eccentric torque (N-m), OJ control, ALC alcohol treatment
Data presented as mean ±SD
Significant difference from pre-exercise value: *P\0.01,
Significant difference between trials:
No significant difference between 36 and 60 h values under either treatment
1012 Eur J Appl Physiol (2010) 108:1009–1014
alcohol on recovery after damaging exercise is currently
unclear as only one dose (1 g of alcohol per kg of body
weight) has been investigated. In fact, the dose used in the
current study is considerably lower than levels of alcohol
consumption frequently reported by sportspeople (Snow
and Munro 2006; O’Brien et al. 2005; O’Brien et al. 2007)
suggesting that alcohol use would have to be restricted to
an even greater extent if results such as those observed in
the present study are to be avoided. Further research is
warranted to investigate the dose effects of alcohol use in
the post-exercise period.
Although the mechanisms behind our findings are not
yet understood, previous research into acute alcohol use
suggests that a number of similarities may exist between
the separate effects of EIMD and acute alcohol consump-
tion on skeletal muscle. Alterations in excitation–contrac-
tion (E–C) coupling and central nervous system (CNS)
function have been proposed as contributors to the force
loss associated with EIMD (Deschenes et al. 2000; Carson
et al. 2002; Prasartwuth et al. 2005; Racinais et al. 2008;
Dartnall et al. 2009). Similarly, acute alcohol exposure has
been shown to negatively affect sarcoplasmic Ca
port, thus altering E–C coupling (Cofa
´n et al. 2000); while
alcohol acts on the CNS to impact axonal conductance and
neurotransmission leading to dose-dependent impairment
of psychomotor and cognitive skills. These actions con-
tribute to the popularity of alcohol as a recreational drug
(Valenzuela 1997; Reilly 2003). Finally, a well-coordi-
nated immune response is initiated by EIMD to facilitate
repair and recovery of damaged tissue (Tidball 2005). As
acute alcohol use has been shown to adversely affect
recovery from trauma/injury by altering the normal
inflammatory response (Szabo and Mandrekar 2009), our
results may be due to alcohol-related impairment of the
normal recovery processes. Whether any or all of these
factors combine to bring about the results observed in the
current study is worth further investigation.
When consumed after strenuous eccentric exercise, a
moderate dose of alcohol magnifies the temporary loss of
muscular performance associated with EIMD but does not
affect performance of the unexercised muscle. Alcohol thus
appears to exert its ergolytic effect by impairing the normal
recovery processes which occur following exercise-
induced microstructural damage, not by a systemic effect
on skeletal muscle innervation. This study provides evi-
dence that the management of alcohol use after strenuous
eccentric exercise is as important, if not more important,
than the use of popular recovery modalities if optimal
recovery of performance is desired. The mechanisms
behind our findings are yet to be fully elucidated.
Conflict of interest statement None.
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... The maximum score a study can receive is 32, with higher scores indicating better quality. The studies were then divided into groups and marked as 'high quality' (score [23][24][25][26][27][28][29][30][31][32], 'moderate quality' (score [19][20][21][22], 'lower quality' (score [16][17][18] or 'poor quality' (<14) (Supplementary File S1 and S2). Kendall Tau correlation coefficient statistical method was used to determine inter-rater reliability. ...
... The maximum score a study can receive is 32, with higher scores indicating better quality. The studies were then divided into groups and marked as 'high quality' (score [23][24][25][26][27][28][29][30][31][32], 'moderate quality' (score [19][20][21][22], 'lower quality' (score [16][17][18] or 'poor quality' (<14) (Supplementary file 1 and 2). Kendall Tau correlation coefficient statistical method was used to determine inter-rater reliability. ...
... Of the retrieved studies, 10 took into account at least one biological measure [9,[18][19][20][21][22][23][24][25][26], 11 took into account at least one physical measure [9,[18][19][20][21][22][23][24][25]27,28] and cognitive function only one [24]. ...
Full-text available
Background: The aim of this manuscript was to describe the effects of alcohol ingestion on recovery following resistance exercise. Methods: A literature search was performed using the following database: Web of Science, NLM Pubmed, and Scopus. Studies regarding alcohol consumption after resistance exercise evaluating recovery were considered for investigation. The main outcomes took into account biological, physical and cognitive measures. Multiple trained researchers independently screened eligible studies according to the eligibility criteria, extracted data and assessed risk of bias. Results: A total of 12 studies were considered eligible and included in the quantitative synthesis: 10 included at least one measure of biological function, 10 included at least one measure of physical function and one included measures of cognitive function. Conclusions: Alcohol consumption following resistance exercise doesn't seem to be a modulating factor for creatine kinase, heart rate, lactate, blood glucose, estradiol, sexual hormone binding globulin, leukocytes and cytokines, C-reactive protein and calcium. Force, power, muscular endurance, soreness and rate of perceived exertion are also unmodified following alcohol consumption during recovery. Cortisol levels seemed to be increased while testosterone, plasma amino acids, and rates of muscle protein synthesis decreased.
... Consuming alcohol after a resistance exercise session can interfere with at least some aspects of performance on subsequent days (2,3). For example, Barnes and colleagues found that when men consume a moderately high dose of alcohol after strenuous eccentric resistance exercise, strength recovery in the exercised muscle is delayed (2,3). ...
... Consuming alcohol after a resistance exercise session can interfere with at least some aspects of performance on subsequent days (2,3). For example, Barnes and colleagues found that when men consume a moderately high dose of alcohol after strenuous eccentric resistance exercise, strength recovery in the exercised muscle is delayed (2,3). Such alcohol consumption does not appear to affect strength in non-exercised muscle (3). ...
... For example, Barnes and colleagues found that when men consume a moderately high dose of alcohol after strenuous eccentric resistance exercise, strength recovery in the exercised muscle is delayed (2,3). Such alcohol consumption does not appear to affect strength in non-exercised muscle (3). However, the effect of alcohol appears to be dose-dependent, as a low dose of alcohol did not affect strength recovery after the same eccentric resistance exercise protocol (4). ...
The purpose of this study was to investigate the effect of alcohol consumed after heavy eccentric resistance exercise on measures of muscle power. After familiarization and an initial eccentric exercise bout to control for the "repeated-bout effect," ten recreationally resistance-trained men completed two identical heavy eccentric squat bouts (4 sets of 10 repetitions at 110% of concentric 1-repetition maximum) one week apart. Each exercise bout was followed by ingestion of a beverage containing either alcohol (1.09 g ethanol[BULLET OPERATOR]kg fat-free body mass) or no alcohol (placebo; volume of alcohol replaced with water). Vertical jump (VJ) peak power, VJ peak force, VJ jump height, change-of-direction ability (shuttle run), sprint acceleration (sprint test), and muscle soreness were measured before (PRE), 24 hrs after (24H), and 48 hrs after (48H) each eccentric exercise bout. Although the exercise bout resulted in significantly (p < 0.05) decreased VJ peak power at 24H, significantly decreased VJ jump height at 24H, and significantly increased muscle soreness at 24H and 48H, consuming alcohol after the exercise bout did not affect any of the performance outcome measures. When consumed after a non-novel heavy eccentric resistance exercise bout, alcohol did not affect soreness or recovery of muscular power. Practitioners can use this information to advise their athletes with regards to responsible alcohol use after non-novel exercise. Although short-term anaerobic performance does not appear compromised as a result of acute post-exercise alcohol ingestion, practitioners and athletes should be aware of potential long-term effects of such alcohol use.
... Crowell et al. (2019) (68) compared the effect of chronic and acute alcohol consumption on murine skeletal muscle mass and function. In this experimental model, acute alcohol administration (a single dose) did not impair skeletal muscle function, in contrast to what has been seen in humans (72). In turn, chronic ethanol administration to mice significantly decreased muscle contractility and shortened the time taken for muscles to become fatigued (68). ...
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Alcohol misuse has deleterious effects on personal health, family, societal units, and global economies. Moreover, alcohol misuse usually leads to several diseases and conditions, including alcoholism, which is a chronic condition and a form of addiction. Alcohol misuse, whether as acute intoxication or alcoholism, adversely affects skeletal, cardiac and/or smooth muscle contraction. Ethanol (ethyl alcohol) is the main effector of alcohol-induced dysregulation of muscle contractility, regardless of alcoholic beverage type or the ethanol metabolite (with acetaldehyde being a notable exception). Ethanol, however, is a simple and “promiscuous” ligand that affects many targets to mediate a single biological effect. In this review, we firstly summarize the processes of excitation-contraction coupling and calcium homeostasis which are critical for the regulation of contractility in all muscle types. Secondly, we present the effects of acute and chronic alcohol exposure on the contractility of skeletal, cardiac, and vascular/ nonvascular smooth muscles. Distinctions are made between in vivo and in vitro experiments, intoxicating vs. sub-intoxicating ethanol levels, and human subjects vs. animal models. The differential effects of alcohol on biological sexes are also examined. Lastly, we show that alcohol-mediated disruption of muscle contractility, involves a wide variety of molecular players, including contractile proteins, their regulatory factors, membrane ion channels and pumps, and several signaling molecules. Clear identification of these molecular players constitutes a first step for a rationale design of pharmacotherapeutics to prevent, ameliorate and/or reverse the negative effects of alcohol on muscle contractility.
... Furthermore, alcohol consumption following concurrent exercise may impair cellular homeostasis and trigger intramyocellular apoptosis, and subsequently inhibit postexercise rates of MPS (163) . Similarly, there is evidence that alcohol consumption inhibits MPS and up-regulates UPS and AMP-activated protein kinase (AMPK) phosphorylation during exercise recovery (164)(165)(166)(167)(168) and following muscle injury and immobilisation (169,170) . Accordingly, alcohol consumption may inhibit muscle adaptations to resistance training in population groups (i.e. ...
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This narrative review provides mechanistic insight into the biological link between smoking and/or chronic excess alcohol consumption, and increased risk of developing sarcopenia. Although the combination of excessive alcohol consumption and smoking is often associated with ectopic adipose deposition, this review is focused on the context of a reduced caloric intake (leading to energy deficit) that also may ensue due to either lifestyle habit. Smoking is a primary cause of periodontitis and chronic obstructive pulmonary disease that both induce swallowing difficulties, inhibit taste and mastication, and are associated with increased risk of muscle atrophy and mitochondrial dysfunction. Smoking may contribute to physical inactivity, energy deficit via reduced caloric intake, and increased systemic inflammation, all of which are factors known to suppress muscle protein synthesis (MPS) rates. Moreover, chronic excess alcohol consumption may result in gut microbiota dysbiosis and autophagy-induced hyperammonemia, initiating the upregulation of muscle protein breakdown and downregulation of MPS via activation of myostatin, AMPK, and REDD1, and deactivation of IGF-1. Future research is warranted to explore the link between oral healthcare management and personalized nutrition counseling in light of potential detrimental consequences of chronic smoking on musculoskeletal health outcomes in older adults. Experimental studies should investigate the impact of smoking and chronic excess alcohol consumption on the gut-brain axis, and explore biomarkers of smoking-induced oral disease progression. The implementation of behavioural change interventions and health policies regarding smoking and alcohol intake habits may mitigate the clinical and financial burden of sarcopenia on the healthcare system.
... In our study, neuromuscular evaluation was performed approximately 10 hours after the end of alcohol intake and after 7-8 hours of normal sleep (ALC 1 SLE condition). This time period between alcohol intake and neuromuscular testing in previous studies ranged from minutes (10) to days (5)(6)(7)23), making comparisons difficult. Another aspect that needs attention is the amount of alcohol intake in ours and in previous studies (0.5-1.5 g of alcohol per kg of body mass) when compared with "real-life events," when apparently higher doses of alcohol ingestion occur (4,23) compared with the doses used in laboratory tests. ...
The aim of this work was to perform a cross-over study to compare isolated and combined effects of alcohol intake and sleep deprivation on neuromuscular responses. Ten young and physically active male subjects were allocated to 4 conditions: (a) placebo intake + normal sleep (PLA + SLE); (b) alcohol intake + normal sleep (ALC + SLE); (c) placebo intake + sleep deprivation (PLA + SDP); and (d) alcohol intake + sleep deprivation (ALC + SDP). In each condition, volunteers ingested 1 g of alcohol per kg of body mass of alcoholic beer or nonalcoholic beer (placebo), followed by one night of normal sleep or sleep deprivation. In the next morning, neuromuscular performance (knee extensor isometric and concentric peak torque and time to task failure during the endurance test) and muscle activation were assessed. No differences were observed in the neuromuscular performance. We observed a significant reduction in quadriceps activation during the knee extensor isometric test in ALC + SDP compared with PLA + SLE (−20.8%; p = 0.02; d = 0.56). Our results demonstrated that acute alcohol intake and one night of sleep deprivation reduced quadriceps muscle activation without impact on neuromuscular performance.
... Additionally, it must not be ignored that consumption of alcohol may be associated with decreased duration and quality of sleep [42], which is another important factor in recovery. Further, alcohol is a diuretic and increases dehydration, which is highly important factor in overall metabolism and consequent recovery from injury [43][44][45]. Therefore, the fact that alcohol drinking is related to time-off in dancers who consume alcohol to a greater extent deserves particular attention. ...
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Professional ballet is a highly challenging art, but studies have rarely examined factors associated with injury status in ballet professionals. This study aimed to prospectively examine gender-specific correlates of injury occurrence and time-off from injury in professional ballet dancers over a one-year period. The participants were 99 professional ballet dancers (41 males and 58 females). Variables included: (i) predictors: sociodemographic data (age, educational status), ballet-related factors (i.e., experience in ballet, ballet status), cigarette smoking, alcohol drinking, and consumption of illicit drugs; and (ii) outcomes: injury occurrence and time-off from injury. Participants were questioned on predictors at the beginning of the season, while data on outcomes were collected continuously once per month over the study period. Dancers reported total of 196 injuries (1.9 injuries (95% CI: 1.6–2.3) per dancer in average), corresponding to 1.4 injuries per 1000 dance-hours (95% CI: 1.1–1.7). In females, cigarette smoking was a predictor of injury occurrence in females (OR: 4.33, 95% CI: 1.05–17.85). Alcohol drinking was a risk factor for absence from dance in females (OR: 1.29, 95% CI: 1.01–4.21) and males (OR: 1.21, 95% CI: 1.05–3.41). Less experienced dancers were more absent from dance as a result of injury than their more experienced peers (Mann-Whitney Z: 2.02, p < 0.04). Ballet dancers and their managers should be aware of the findings of this study to make informed decisions on their behavior (dancers) or to initiate specific programs aimed at the prevention of substance use and misuse in this profession (managers).
... Alcohol consumption to excess is known to affect muscle strength and function [24][25][26]. Alcohol intake following heavy exercise with assumed minor damage to muscle fibres does also slow down muscle recovery [27][28][29][30][31][32][33][34][35][36][37][38][39][40]. In the present study, the participants all had an alcohol intake below the recommended level. ...
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Background Lifestyle is expected to influence muscle strength. This study aimed at assessing a possible relationship between smoking, alcohol intake and physical activity, and muscle strength in a healthy Danish population aged 20–79 years. Population study based on data collected from The Copenhagen City Heart Study (CCHS) and measurements of Isokinetic muscle strength from a sub-study of randomly selected healthy participants from CCHS. Methods 126 women and 63 men were studied. All participants completed a questionnaire regarding their lifestyle, including physical activity, alcohol intake and smoking habits. Isokinetic muscle strength was measured over the upper extremities (UE), trunk, and lower extremities (LE). Multivariate analyses including all of the variables were carried out. Results The level of daily physical activity during leisure was positively correlated to muscle strength in the lower extremities (p = 0.03) for women, and lower extremities (p = 0.03) and trunk (p = 0.007) for men. Alcohol Intake was in general not correlated to muscle strength. No clear effect of smoking was seen on muscle strength. Conclusion Our results show that physical activity during leisure is associated with a positive effect on muscle strength in both sexes. When keeping alcohol intake within the recommended limits, alcohol does not seem to affect muscle strength negatively. No effect of smoking on muscle strength was found in our group of healthy subjects. The findings are of importance when considering recommendation on life style when wishing to keeping fit with age to be able to carry out daily activities.
Conference Paper
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Purpose: Bodybuilding becomes more visible and acceptable within mainstream society thanks to social media, which is promoting, and developing grooving interest in bodies, fit-ness and active lifestyle. However, this is concerning knowing that according to the latest world anti-doping agency report bodybuilding is one of two sports with the highest number of Anti-Doping Rule Violations (ADRVs) committed by athletes. This study aimed to evaluate doping attitudes and correlates of doping attitudes in top level body builders. Methods: Study included 26 competitive bodybuilders form Croatia. Variables were collect-ed by a previously validated Questionnaire of Substance Use (QSU). Statistical procedures included means and standard deviations (for parametric variables), frequencies and percent-ages (for ordinal and nominal variables). Spearman’s correlations were calculated to deter-mine associations between studied variables. Results: The most positive attitudes are found towards injectable anabolic steroids (mean ± standard deviation; 4.00 ± 1.52), followed by fat burners (3.73 ± 1.46), growth hormone (3.69 ± 1.64), and estrogen blockers (3.60 ± 1.22), oral anabolic steroids (3.58 ± 1.27). Sig-nificant correlation was identified between: (i) result achieved in bodybuilding (RBB) and alcohol consumption, (R= -0.57 p < 0.05) (ii) RBB and subjective knowledge on nutrition (R=0.66, p < 0.05), (iii) RBB and subjective knowledge on doping (R=0.72, p < 0.05). Conclusion: The lack of correlation between self-perceived competence and objectively eval-uated knowledge on nutrition is alarming due to the possible “anchoring effect”, accordingly even though objective knowledge is not correlated with attitudes towards doping substances, it is important to properly educate athletes who are in the misconception of their true knowl-edge.
Background: Skeletal muscle myopathy accompanying chronic alcohol misuse results in part from a decrease in protein synthesis typically observed in type II-rich muscles that leads to muscle weakness. However, there are a paucity of studies investigating whether the alcohol-induced weakness is intrinsic to the muscle or results primarily from the loss of muscle mass. The present study determines whether acute alcohol (ethanol) intoxication or chronic alcohol consumption decreases the intrinsic contractile function of muscle. Methods: Adult male mice were randomly assigned to the chronic alcohol group or given a binge dose of alcohol, and contractile characteristics of the extensor digitorum longus (EDL) determined in vitro. Results: The weight and physiological cross-sectional area (PCSA) of the EDL were decreased in alcohol-fed mice. Maximum twitch and tetanic tension were also reduced, and there was a downward shift of the absolute force-frequency curve in alcohol-fed mice. However, no alcohol-induced changes were noted when these contractile parameters were normalized for the lower PCSA. Alcohol-fed mice demonstrated greater fatigability, and alcohol-induced decreases in post-fatigue specific twitch and tetanic force were independent of a decreased PCSA. Furthermore, post-fatigue recovery of muscle force over time was reduced. While alcohol did not alter the content of high-energy phosphates or oxidative phosphorylation complexes I-V, it did reduce myosin heavy chain and troponin-T content. In contrast, contractile properties were not altered when examined 2 hours after binge alcohol. Conclusion: These data demonstrate chronic alcohol consumption decreases isometric and tetanic tension development due to a reduction in muscle CSA, whereas the increased fatigability observed was independent of muscle mass. As none of the functional changes were produced by acute alcohol, which produced higher blood alcohol levels than chronic ingestion, our data suggest defects in intrinsic muscle contractility require sustained intake and appear independent of defects in basal energy production.
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The review considers the basic principles of recovery after exercise in professional and amateur sports. Restoration of the body is the return of physical parameters to the initial values, increasing the adaptive capacity after performing physical work. Proper recovery after exercise helps avoid problems such as physical fatigue, lack of nutrient intake, injuries of various severity, dehydration, etc. A number of factors influence the human body during recovery: a balanced diet, adequate rest and sleep, psychological and emotional unloading, gymnastics, massage, contrast shower and others. Comprehensive rehabilitation programs in sports should include methods with proven effectiveness, take into account the individual characteristics of the athlete and the dominant form of physical activity, and consider the recovery period as an integral part of the entire training plan.
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The purpose of this study was to determine the effect of eccentric muscle damage on recruitment threshold force and repetitive discharge properties of low-threshold motor units. Ten subjects performed four tasks involving isometric contraction of elbow flexors while electromyographic (EMG) data were recorded from human biceps brachii and brachialis muscles. Tasks were 1) maximum voluntary contraction (MVC); 2) constant-force contraction at various submaximal targets; 3) motor unit recruitment threshold task; and 4) minimum motor unit discharge rate task. These tasks were performed on three separate days before, immediately after, and 24 h after eccentric exercise of elbow flexor muscles. MVC force declined (42%) immediately after exercise and remained depressed (29%) 24 h later, indicative of muscle damage. Mean motor unit recruitment threshold for biceps brachii was 8.4+/-4.2% MVC, (n=34) before eccentric exercise, and was reduced by 41% (5.0+/-3.0% MVC, n=34) immediately after and by 39% (5.2+/-2.5% MVC, n=34) 24 h after exercise. No significant changes in motor unit recruitment threshold were observed in the brachialis muscle. However, for the minimum tonic discharge rate task, motor units in both muscles discharged 11% faster (10.8+/-2.0 vs. 9.7+/-1.7 Hz) immediately after (n=29) exercise compared with that before (n=32). The minimum discharge rate variability was greater in brachialis muscle immediately after exercise (13.8+/-3.1%) compared with that before (11.9+/-3.1%) and 24 h after exercise (11.7+/-2.4%). No significant changes in minimum discharge rate variability were observed in the biceps brachii motor units after exercise. These results indicate that muscle damage from eccentric exercise alters motor unit recruitment thresholds for >or=24 h, but the effect is not the same in the different elbow flexor muscles.
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This study investigated the effects of acute moderate alcohol intake on muscular performance during recovery from eccentric exercise-induced muscle damage. Eleven healthy males performed 300 maximal eccentric contractions of the quadriceps muscles of one leg on an isokinetic dynamometer. They then consumed a beverage containing 1g/kg bodyweight ethanol (as vodka and orange juice) (ALC). On another occasion they performed an equivalent bout of eccentric exercise on the contralateral leg after which they consumed an isocaloric quantity of orange juice (OJ). Measurement of maximal isokinetic (concentric and eccentric) and isometric torque produced across the knee, plasma creatine kinase (CK) concentrations and muscle soreness were made before and at 36 and 60h following each exercise bout. All measures of muscle performance were significantly reduced at 36 and 60h post-exercise compared to pre-exercise measures (all p<0.05). The greatest decreases in peak strength were observed at 36h with losses of 12%, 28% and 19% occurring for OJ isometric, concentric, and eccentric contractions, respectively. However, peak strength loss was significantly greater in ALC with the same performance measures decreasing by 34%, 40% and 34%, respectively. Post-exercise plasma creatine kinase activity and ratings of muscle soreness were not different between conditions (both p>0.05). These results indicate that consumption of even moderate amounts of alcohol following eccentric-based exercise magnifies the normally observed losses in dynamic and static strength. Therefore, to minimise exercise related losses in muscle function and expedite recovery, participants in sports involving eccentric muscle work should avoid alcohol-containing beverages in the post-event period.
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High-intensity eccentric contractions induce performance decrements and delayed onset muscle soreness. The purpose of this investigation was to study the magnitude and time course of such decrements and their interrelationships in 26 young women of mean(s.d.) age 21.4(3.3) years. Subjects performed 70 maximal eccentric contractions of the elbow flexors on a pulley system, specially designed for the study. The non-exercised arm acted as the control. Measures of soreness, tenderness, swelling (SW), relaxed elbow joint angle (RANG) and isometric strength (STR) were taken before exercise, immediately after exercise (AE), analysis of variance and at 24-h intervals for 11 days. There were significant (P < 0.01, analysis of variance) changes in all factors. Peak effects were observed between 24 and 96 h AE. With the exception of STR, which remained lower (P < 0.01), all variables returned to baseline levels by day 11. A non-significant correlation between pain and STR indicated that pain was not a major factor in strength loss. Also, although no pain was evident, RANG was decreased immediately AE. There was no relationship between SW, RANG and pain. The prolonged nature of these symptoms indicates that repair to damaged soft tissue is a slow process. Strength loss is considered particularly important as it continues when protective pain and tenderness have disappeared. This has implications for the therapeutic management of patients with myopathologies and those receiving eccentric exercise for rehabilitation.
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The purposes of this study were to assess the presence of 99mTc-labeled white blood cells (WBC) in exercised muscle compared with nonexercised muscle over time and to determine the time course of delayed onset muscle soreness (DOMS) and eccentric torque in 10 female subjects. A pretest was followed by 300 eccentric repetitions of the right quadriceps. DOMS and eccentric torque were measured at 2, 4, 20, 24, 48, and 72 h postexercise. Eccentric torque was also tested at 0 h. Radionuclide images of both quadriceps were taken at 2, 4, 20, and 24 h postexercise. The presence of 99mTc-WBC in the exercised muscle was significantly greater (P < 0.001) than in the nonexercised muscle. Eccentric torque declined at 0 and 24 h postexercise. DOMS peaked at 24 h postexercise. The presence of 99mTc-WBC in the exercised muscle in the first 24 h suggests that acute inflammation occurs as a result of exercise-induced muscle injury. The bimodal pattern of eccentric torque supports the hypothesis that more than one mechanism is involved.
Evidence suggests that alcohol affects brain function by interacting with multiple neurotransmitter systems, thereby disrupting the delicate balance between inhibitory and excitatory neurotransmitters. Short-term alcohol exposure tilts this balance in favor of inhibitory influences. After long-term alcohol exposure, however, the brain attempts to compensate by tilting the balance back toward equilibrium. These neurological changes occur as the development of tolerance to alcohol's effects. When alcohol consumption is abruptly discontinued or reduced, these compensatory changes are no longer opposed by the presence of alcohol, thereby leading to the excitation of neurotransmitter systems and the development of alcohol withdrawal syndrome. Long-term alcohol intake also induces changes in many neurotransmitter systems that ultimately lead to the development of craving and alcohol-seeking behavior.
We studied an antiferromagnetic CrMnPt x [(Cr:Mn≂1:1) in atomic percent] film for an exchange‐biased layer, focusing especially on the relationships between the exchange coupling properties of the CrMnPt x (top)/Ni 81 Fe 19 (bottom) films and the character of its CrMnPt x film. The best Pt content to obtain a large exchange coupling of the CrMnPt x film was 5.0–8.0 at. %. Typically, the exchange coupled 50 nm CrMnPt 5-8 /40 nm Ni 81 Fe 19 films exhibited a relatively large exchange coupling field of ∼22 Oe and a high blocking temperature of ∼380 °C. Besides, the CrMnPt 5-8 film deposited on the Ni 81 Fe 19 film had a considerably high resistivity of ∼300–350 μΩ cm. These large exchange coupling and high resistivity values were obtained only when the α‐phase with a disordered bcc structure was stabilized in the CrMnPt x film by the underlying fcc Ni 81 Fe 19 film. The Pt within the CrMnPt x film might localize the Mn magnetic moment. As to why the CrMnPt x film having the Pt content of 5.0–8.0 at. % could give the Ni 81 Fe 19 film a large exchange coupling, this was attributed to the nearest neighbor Mn–Mn atomic distance within the CrMnPt 5-8 film being the same as the distance at which the Mn–Mn exchange interaction showed the maximum negative value. Furthermore, the decrease in size of the exchange coupling field and lowered blocking temperature for t CrMnPt ≪30 nm (t CrMnPt : CrMnPt x film thickness) were thought to originate from a decrease of antiferromagnetic CrMnPt x anisotropy with decreasing t CrMnPt . © 1996 American Institute of Physics.
Thesis (Ph. D.)--Temple University, 1995. Abstract. Includes bibliographical references (leaves 117-125).
Multiple line of clinical and experimental evidence demonstrates that both acute, moderate, and chronic, excessive alcohol use result in various abnormalities in the functions of the immune system. Medline and PubMed databases were used to identify published reports with particular interest in the period of 2000-2008 in the subject of alcohol use, infection, inflammation, innate, and adaptive immunity. This review article summarizes recent findings relevant to acute or chronic alcohol use-induced immunomodulation and its consequences on host defense against microbial pathogens and tissue injury. Studies with in vivo and in vitro alcohol administration are both discussed. The effects of alcohol on lung infections, trauma and burn injury, liver, pancreas, and cardiovascular diseases are evaluated with respect to the role of immune cells. Specific changes in innate immune response and abnormalities in adaptive immunity caused by alcohol intake are detailed. Altered inflammatory cell and adaptive immune responses after alcohol consumption result in increased incidence and poor outcome of infections and other organ-specific immune-mediated effects.
The effect of ethanol ingestion on exercise-induced muscle damage was examined. It has been reported that a reduced leakage of muscle proteins was found when alcohol was ingested prior to exercise. The results of that study were confounded by repeating the same exercise using the same muscle groups; the alcohol treatment was always given on the second exercise bout so that the reduced protein leakage may be due to a rapid training effect. The present study was designed to control for rapid training effect when examining the effects of ethanol ingestion on exercise-induced protein leakage from muscle. Also, this study examined the effect of acute ethanol ingestion on other indicators of muscle damage: force generation, muscle stiffness and muscle soreness. Ten women subjects performed two similar exercise regimens, one with each arm, separated by at least 10 days. Alcohol was ingested prior to exercising one arm and a nonalcoholic beverage ingested prior to exercising the contralateral arm. The exercises resulted in increased serum creatine kinase activity (p less than .05) and muscle pain (p less than .01), and decreased range of motion (p less than .01) and strength (p less than .01), indicating muscle damage. There was no significant difference between the alcohol and nonalcohol conditions for any criterion measure. It was concluded that acute ingestion of alcohol has no effect on several indicators of exercise-induced muscle damage.