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A low dose of alcohol does not impact skeletal muscle performance after exercise-induced muscle damage

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Moderate, acute alcohol consumption after eccentric exercise has been shown to magnify the muscular weakness that is typically associated with exercise-induced muscle damage (EIMD). As it is not known whether this effect is dose-dependent, the aim of this study was to investigate the effect of a low dose of alcohol on EIMD-related losses in muscular performance. 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 0.5 g of alcohol per kg bodyweight (as vodka and orange juice) or an isocaloric, isovolumetric non-alcoholic 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. Measurement of peak and average peak isokinetic (concentric and eccentric) and isometric torque produced by the quadriceps was made before and 36 and 60 h post-exercise. Significant decreases in all measures of muscular performance were observed over time under both conditions (all P < 0.05); however, no difference between treatments was evident at any of the measured time points (all P > 0.05). Therefore, consumption of a low dose of alcohol after damaging exercise appears to have no effect on the loss of force associated with strenuous eccentric exercise.
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SHORT COMMUNICATION
A low dose of alcohol does not impact skeletal muscle performance
after exercise-induced muscle damage
Matthew J. Barnes Toby Mu
¨ndel
Stephen R. Stannard
Accepted: 13 September 2010 / Published online: 28 September 2010
ÓSpringer-Verlag 2010
Abstract Moderate, acute alcohol consumption after
eccentric exercise has been shown to magnify the muscular
weakness that is typically associated with exercise-induced
muscle damage (EIMD). As it is not known whether this
effect is dose-dependent, the aim of this study was to
investigate the effect of a low dose of alcohol on EIMD-
related losses in muscular performance. Ten healthy males
performed 300 maximal eccentric contractions of the
quadriceps muscles of one leg on an isokinetic dyna-
mometer. They then consumed either a beverage contain-
ing 0.5 g of alcohol per kg bodyweight (as vodka and
orange juice) or an isocaloric, isovolumetric non-alcoholic
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. Mea-
surement of peak and average peak isokinetic (concentric
and eccentric) and isometric torque produced by the
quadriceps was made before and 36 and 60 h post-exercise.
Significant decreases in all measures of muscular perfor-
mance were observed over time under both conditions (all
P\0.05); however, no difference between treatments was
evident at any of the measured time points (all P[0.05).
Therefore, consumption of a low dose of alcohol after
damaging exercise appears to have no effect on the loss of
force associated with strenuous eccentric exercise.
Keywords Ethanol Muscle strength Soft tissue injuries
Introduction
The consumption of large amounts of alcohol by sports-
people, particularly those involved in team sports, after
competition and/or training is common place. This popu-
lation is further reported as consuming such hazardous
levels of alcohol more frequently than the general popu-
lation (Maughan 2006; O’Brien et al. 2007; Quarrie et al.
1996; Snow and Munro 2006). As with the non-sporting
population, these drinking patterns are associated with
increased risk-taking behaviours which often result in
alcohol-related injury (Cherpitel 1993; Nelson and
Wechsler 2001). For sportspeople, however, acute alcohol
use, particularly after strenuous exercise, provides another
risk through the influence alcohol can have on processes
involved in recovery and adaptation.
The physical nature of many team sports engenders a
high incidence of exercise-induced muscle damage (EIMD)
and soft tissue injury due to repeated rapid deceleration,
changes in direction, and collisions with other players and/
or the ground (LaStayo et al. 2003). Although both EIMD
and alcohol consumption are common in many sports, very
little is known about how the two interact to affect recovery
(of performance) in the days after the injurious event.
When alcohol’s ingestion is quickly followed by trauma/
injury, alcohol is known to increase the chance of infection
and medical complication resulting in delayed recovery
through alterations in the trauma-induced inflammatory
response (Szabo and Mandrekar 2009). However, this
combination of pre-exercise alcohol use and soft tissue
injury (as EIMD), investigated by Clarkson and Reichsman
(1990), found that a moderate dose of alcohol (0.8 g per kg
bodyweight) had no effect on recovery of performance in the
days after a damaging bout of exercise when compared to a
non-alcoholic beverage.
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
e-mail: M.Barnes@massey.ac.nz
123
Eur J Appl Physiol (2011) 111:725–729
DOI 10.1007/s00421-010-1655-8
Perhaps more relevant to the practices of sportspeople is
how the consumption of alcohol after strenuous damaging
exercise impacts muscular performance and recovery. We
recently investigated this scenario.Barnes et al. (2010a,b)
found that a moderate dose of alcohol (1 g per kg body-
weight) consumed after strenuous eccentric exercise
interacts with EIMD to magnify the force loss typically
associated with such exercise.
As well as having an exacerbating effect on EIMD-related
losses in force, a dose of 0.92 g of alcohol per kg bodyweight
has been shown to negatively influence the ability to rehy-
drate after dehydrating exercise (Shirreffs and Maughan
1997), while a dose of 1.5 g per kg bodyweight impairs
glycogen repletion after prolonged exercise if energy from
alcohol replaces energy from carbohydrate in the post-
exercise diet (Burke et al. 2003). Alterations in the post-
resistance exercise hormone response have been observed
after a dose of 0.83 g alcohol per kg bodyweight including a
prolonged elevation in cortisol (Koziris et al. 2000) and
elevated free testosterone (Vingren et al. 2003), the latter
potentially due to an effect of alcohol on the androgen
receptor. Both are thought to negatively affect adaptation to
resistance exercise (Vingren et al. 2003) and could partly
explain our previous findings (Barnes et al. 2010a,b).
These deleterious effects of post-exercise alcohol con-
sumption provide evidence that the use of alcohol after
strenuous exercise should be managed carefully; however,
more information is required if recommendations on
appropriate alcohol use during the post-event period are to
be made. The aim of this study, therefore, was to add to this
limited knowledge base by investigating whether a low
dose of alcohol interacts with damaged skeletal muscle to
magnify the typical weakness associated with EIMD as
previously observed with a moderate dose of alcohol.
Methods
The current study utilised a protocol previously described
(Barnes et al. 2010b). Briefly, this required each subject to
perform 300 maximal eccentric contractions of the quad-
riceps muscles of one leg on an isokinetic dynamometer.
They then consumed either an alcoholic beverage, equiv-
alent to 35 g of alcohol for a 70-kg person, or an isocaloric,
isovolumetric amount of 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
was measured prior to the damaging exercise bout and at
36 and 60 h post-exercise.
This ‘one-legged’ exercise model allows the subject to
act as their own control, therefore ensuring that the only
difference between treatments is the leg used, i.e. dominant
versus non-dominant. The design also negates any residual
effects in the muscle from the previous trial, such as the
well-known repeated bout effect (McHugh 2003). A limi-
tation of this model, however, is that only a single dose of
alcohol is able to be compared to the control beverage.
Subjects
Ten males (age 20.8 ±1.6 years, body mass 83.9 ±
12.9 kg) volunteered to participate in this study. All sub-
jects were healthy and regularly (minimum twice per week)
participated in recreational-level resistance training. The
protocol was approved by the Massey University Human
Ethics Committee, and written consent was obtained from
each subject.
Familiarisation 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 experimental bouts. Subjects were also
instructed to abstain from practices that could potentially
improve or worsen their recovery, for example the use of
anti-inflammatory medication, massage, stretching and
cryotherapy, during the 60-h post-exercise period. Subjects
recorded their diet from the morning of the first trial until
60 h post-exercise and were instructed to replicate this for
the second trial. Utilising a single cross-over design, treat-
ment and leg (dominant vs. non-dominant) order were
randomly allocated in a counter-balanced fashion.
Muscular performance
Four hours after consuming a standardised, solid meal
(3,700 kJ; CHO 50.1%, Fat 27.1%, Protein 11.7%), subjects
presented at the laboratory in the evening and warmed up on
a cycle ergometer (Monark, Varberg, Sweden) for 5 min at
100 W. Subjects then performed separate sets of five maxi-
mal isometric (ISO), concentric (CON) and eccentric (ECC)
contractions of the quadriceps muscles of one leg on a Bio-
dex
Ò
isokinetic dynamometer (Biodex Medical Systems,
New York, USA). Knee joint range of motion was recorded
for use in subsequent follow-up tests. Each set was separated
by 2 min of passive recovery. Isometric tension was mea-
sured at a knee angle of 75°(1.31 rad). Concentric and
eccentric torque was measured at an angular velocity of
30°s
-1
(0.52 rad s
-1
). Absolute peak and average peak
torque over five contractions were recorded. Muscular per-
formance was measured again at 36 and 60 h post-exercise.
Exercise protocol
Immediately after muscular performance was measured,
subjects completed three sets of 100 maximal eccentric
contractions, over a 60°(1.05 rad) range of motion at an
726 Eur J Appl Physiol (2011) 111:725–729
123
angular velocity of 30°s
-1
, using the quadriceps muscles of
the tested leg. Each set was separated by 5 min of passive
recovery.
Treatment
Immediately after the completion of the exercise protocol,
subjects consumed a standardised meal immediately after
exercise (1,468 kJ; CHO 51.1%, Fat 12.9%, Protein 28.2%).
Thirty minutes later subjects began drinking a beverage
containing either 0.5 g of alcohol per kg of bodyweight 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). The mean vol-
ume of vodka consumed per subject was 112.8 ±17.4 ml;
this was diluted in 714 ±109.9 ml of orange juice and
consumed in six equal volumes every 15 min over a total
time of 90 min. Total energy value (2,043.5 ±314.3 kJ)
and fluid volume (1,285.2 ±197.7 ml) were balanced
between trials. To achieve this, an additional volume of
water (458.4 ±70.4 ml) was consumed along with the
alcoholic beverage. Thirty minutes after the consumption of
the alcoholic beverage, blood alcohol concentration (BAC)
was estimated from breath alcohol content using a Digitech
fuel cell alcohol tester (Electus Distributions PTY, Ltd,
NSW, Australia). Subjects were then driven home and
required to go directly to bed. For the second trial, the con-
tralateral leg was exercised, and the other beverage was
consumed using the same protocol as outlined above.
Statistical analyses
Data were analysed using the Statistical Program for Social
Sciences (SPSS) for Windows (version 15.0, SPSS Inc.,
Chicago, IL.). A general linear-model repeated-measures
ANOVA (treatment 9time) was used to compare condi-
tions over time for each performance measure. Similarly,
repeated-measures ANOVA (trial 1 vs. trial 2) was carried
out to identify possible order effects for each performance
measure. If significant differences were found, post-hoc
pairwise comparisons were made using Bonferroni adjust-
ment to further investigate changes in performance over
time within each condition. As different legs were used for
each trial, resulting in significantly different pre-exercise
values between treatments, data were analysed as absolute
change in torque (N m) (Table 1) as well as percentage
change from pre-exercise values. Reported values are
mean ±SD. Statistical significance was set at P\0.05.
Results
Completion of 300 eccentric muscular contractions of the
quadriceps resulted in significant decreases in isometric
(P=0.004) and concentric (P=0.005) peak torque and
isometric (P=0.02), concentric (P=0.007) and eccen-
tric (P=0.004) average peak torque over time under both
treatments (Table 1). At 36 h ISO OJ was 12.3%
(P=0.05) and ALC 11.1% lower than pre-values while at
60 h ISO was not significantly lower than pre-values for OJ
(4.1%) or ALC (5.2%). Similarly, CON OJ and ALC
decreased by 21% (P=0.009) and 16.4% (P=0.017) at
36 h, respectively, before improving to be down by 12.2
and 11.7% at 60 h. Smaller decrements were seen for ECC
OJ (4.2%) at 36 h compared to 14.2% (P=0.032) for
ECC ALC at the same time point. These values had
improved at 60 h so that ECC OJ was 6.1% higher than
pre-values while ALC was still 6.1% lower than pre-values.
Similar decrements were seen for average peak torque
measures. No significant treatment or treatment 9time
effect was evident for any of these performance measures
(all P[0.2). Repeated-measures ANOVA of trial one
versus trial two found no significant order effect for any of
the muscular performance measures (all P[0.1). Total
work completed during the eccentric exercise bouts was
not significantly different between trial one (37.9 ±5.5 kJ)
and trial two (38.8 ±6 kJ) (P=0.7) or between OJ
(39.3 ±6.6 kJ) and ALC trials (37.6 ±4.6 kJ) (P=0.3).
Table 1 Changes in torque (N m) over time following strenuous
eccentric exercise
Pre 36 h 60 h
Peak ISO
OJ 301.4 ±48.9 -40.1 ±44.0* -17.1 ±45.2
ALC 284.2 ±49.8 -37.5 ±45.3 -19.1 ±59.1
Peak CON
OJ 265.1 ±50.3 -54.9 ±47.1* -35.3 ±41.4
ALC 249.5 ±50.4 -42.8 ±38.8* -31.5 ±41.4
Peak ECC
OJ 336.5 ±77.3 -20.6 ±89.6 15.9 ±66.0
ALC 330.9 ±81.7 -49.4 ±51.9* -20.4 ±55.4
Average ISO
OJ 269.7 ±39.0 -33.2 ±35.9* -15.4 ±45.2
ALC 264.4 ±37.7 -35.3 ±45.1 -18.8 ±54.7
Average CON
OJ 239.5 ±31.2 -46.1 ±42.8* -30.2 ±36.3
ALC 236.1 ±37.9 -51.7 ±45.2* -34.4 ±42.1
Average ECC
OJ 308.4 ±76.9 -51.4 ±76.0 17.4 ±77.3
ALC 310.3 ±70.1 -54.7 ±46.1* -24.8 ±51.6
Data presented as mean ±SD
ISO isometric, CON concentric, ECC eccentric torque (N m),
OJ control, ALC alcohol treatment
*P\0.05, significant difference from pre-exercise value
P\0.05, significant difference from preceding value
Eur J Appl Physiol (2011) 111:725–729 727
123
Average BAC concentration after the consumption of
0.5 g alcohol per kg bodyweight was 0.011 ±0.0013 g/dL
(2.42 ±0.29 mmol/L).
Discussion
The aim of the present study was to investigate whether a
low dose of alcohol (0.5 g per kg bodyweight) consumed
after strenuous eccentric exercise exacerbates EIMD-rela-
ted decrements in muscular performance in young, resis-
tance-trained males as previously observed with a dose of
1 g per kg bodyweight (Barnes et al. 2010a,b). As observed
in our previous work, the completion of 300 maximal
eccentric contractions of the quadriceps resulted in signifi-
cant decreases in all performance measures, except peak
eccentric torque, in the days following the exercise bout
(Table 1). Unlike our previous results (Barnes et al. 2010a,
b), however, the dose of alcohol used in the current study
did not increase the magnitude of this decrement.
Although the mechanisms behind our previous findings
are still unclear, similar volumes of alcohol to those con-
sumed in the current study have been shown to inhibit
neutrophil function (Patel et al. 1996) and whole muscle
action potential responses to nerve stimulation (Pagala
et al. 1995), while volumes slightly higher than this are
known to alter the immune response to a bacterial chal-
lenge (Szabo 1998). Comparable doses to those used in our
previous work have been found to decrease calcium tran-
sients (Nicolas et al. 1998) as well as negatively impacting
the regulation of a number of chemokines (Szabo et al.
1999). Separately, a humoral effect, importantly on the
androgens, has also been previously described (Vingren
et al. 2003). The inflammatory response to EIMD is well
documented (Proske and Morgan 2001) as is the potential
effect; this damage has on excitation–contraction (E-C)
coupling (Warren et al. 2001), processes that rely heavily
on the factors discussed above. We may therefore speculate
that acute alcohol use could alter the EIMD-related
inflammatory response while further suppressing the E-C
coupling process to magnify force loss and delay recovery
as previously observed with a dose of 1 g alcohol per kg
bodyweight. However, further investigation is required to
define the mechanisms behind the interaction between
acute alcohol use and EIMD.
The aim of this series of studies was to experimentally
investigate the effects of alcohol on EIMD-related losses in
force in a well-controlled manner so that any potential
confounding factors were minimised and any effects
clearly isolated. However, the findings of these studies are
limited in their application to a relatively homogenous
group of subjects, and how other populations might be
affected is not yet understood. The population investigated
to date, young recreationally trained males, is representa-
tive of the sporting demographic most often reported as
binging on alcohol after competition (Nelson and Wechsler
2001; O’Brien et al. 2007). However, this fact should not
limit future research to this group at the expense of other
populations, for example females participating in team
sports also report regularly consuming alcohol at hazardous
levels (Ford 2007; O’Brien et al. 2005; Quarrie et al. 1996).
Further, the protocol utilised has been used extensively
to investigate the physiological effects and mechanisms of
EIMD (Beaton et al. 2002;Jo
¨nhagen et al. 2004; Paulsen
et al. 2005); however, future research should investigate
more ecologically valid measures of performance such as
sports specific measures of power, endurance and speed
thus providing the wider sporting community with results
directly applicable to a sports setting.
Together, the findings of the present study and the
results of our previous work (Barnes et al. 2010a,b)
indicate that an acute dose of alcohol of 1 g, but not 0.5 g,
per kg bodyweight, when consumed after strenuous
eccentric exercise, negatively impacts the magnitude of
force loss associated with EIMD. Until more information is
available on how different doses of alcohol impact EIMD-
related decrements in force we tentatively make the rec-
ommendation that if alcohol is to be consumed in the hours
after damaging/injurious exercise then the dose of alcohol
consumed should be kept at or below 0.5 g per kg body-
weight to ensure force loss is minimised. Collectively, the
research carried out on the effects of acute alcohol use after
strenuous exercise has shown only negative outcomes at a
range of doses higher than that used in the current study but
significantly lower than the volumes regularly reported as
being consumed by sportspeople (Nelson and Wechsler
2001; O’Brien et al. 2005). The management of alcohol
after sporting events should therefore be given greater
attention than may currently be the case if recovery is to
occur at an optimal rate.
Conclusion
When consumed after strenuous damaging exercise, a low
dose (0.5 g per kg bodyweight) of alcohol had no impact
on the EIMD-related losses in muscular performance.
Conflict of interest The authors declare that they have no conflict
of interest.
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Background: High-intensity interval training (HIIT) is an effective approach to improve physical fitness, but consuming beer, which is a regular practice in many physically active individuals, may interfere with these effects. The purposes of this study were to investigate the effects of a 10-week (2 days/week) HIIT program on cardiorespiratory fitness, muscle strength and power parameters, and also to assess the possible influence on them of a moderate consumption of beer (at least from Monday to Friday) or its alcohol equivalent. Methods: Young (24 ± 6 years old) healthy adults (n = 73, 35 females) were allocated to five groups. Four groups participated in the HIIT intervention program while the fifth group was a control Non-Training group (n = 15). Participants in the training groups chose whether they preferred receiving alcohol or alcohol-free beverages. Those choosing alcohol were randomized to either beer or ethanol intake: (i) T-Beer group (alcohol beer, 5.4%; n = 13) or (ii) T-Ethanol (sparkling water with vodka, 5.4%; n = 14). Those choosing alcohol-free intake were randomized to (iii) T-Water group (sparkling water, 0.0%; n = 16), or (iv) T-0.0Beer group (alcohol-free beer, 0.0%; n = 15). Men ingested 330 ml of the beverage at lunch and 330 ml at dinner; women ingested 330 ml at dinner. Before and after the intervention, maximal oxygen uptake in absolute and relative terms (VO2max.), maximal heart rate, total test duration, hand grip strength and four types of vertical jumps were measured. Results: HIIT induced significant improvements in absolute and relative values of VO2max, and total test duration (all p < 0.05) in all the training groups; also, clinical improvements were found in hand grip strength. These positive effects were not influenced by the regular intake of beer or alcohol. No changes in the vertical jumps occurred in any of the groups. Conclusions: A moderate beer or alcohol intake does not mitigate the positive effect of a 10-week HIIT on physical fitness in young healthy adults. Trial registration: ClinicalTrials.gov ID: NCT03660579. Registered 20 September 2018. Retrospectively registered.
... This study also focused on the effect on neuromuscular performance, suggesting that the alcohol-induced decrease in voluntary force has a neural, central, component besides the peripheral muscle damage. Interestingly, another study performed by the same research group revealed that a lower dose of alcohol (0.5 g/kg of body mass) did not affect skeletal muscle recovery from vigorous eccentric exercise (64). So then, these studies suggested that the effects of alcohol consumption on skeletal muscle recovery after exercise in men seem to depend on the ingested doses and probably the blood alcohol concentrations reached. ...
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Background: Chronic alcohol misuse is associated with alcoholic myopathy, characterized by skeletal muscle weakness and atrophy. Moreover, there is evidence that sports-related people seem to exhibit a greater prevalence of problematic alcohol consumption, especially binge drinking (BD), which might not cause alcoholic myopathy but can negatively impact muscle function and amateur and professional athletic performance. Objective: To review the literature concerning the effects of alcohol consumption on skeletal muscle function and structure that can affect muscle performance. Methodology: We examined the currently available literature (PubMed, Google Scholars) to develop a narrative review summarizing the knowledge about the effects of alcohol on skeletal muscle function and exercise performance, obtained from studies in human beings and animal models for problematic alcohol consumption. Results: Exercise- and sport-based studies indicate that alcohol consumption can negatively affect muscle recovery after vigorous exercise, especially in men, while women seem less affected. Clinical studies and pre-clinical laboratory research have led to the knowledge of some of the mechanisms involved in alcohol-related muscle dysfunction, including an imbalance between anabolic and catabolic pathways, reduced regeneration, increased inflammation and fibrosis, and deficiencies in energetic balance and mitochondrial function. These pathological features can appear not only under chronic alcohol misuse but also in other alcohol consumption patterns. Conclusions: Most laboratory-based studies use chronic or acute alcohol exposure, while episodic BD, the most common drinking pattern in amateur and professional athletes, is underrepresented. Nevertheless, alcohol consumption negatively affects skeletal muscle health through different mechanisms, which collectively might contribute to reduced sports performance.
... 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. ...
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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.
... 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). Furthermore, when women consumed a moderately high dose of alcohol after the same eccentric exercise protocol, strength recovery in the exercised muscle was not different from when a placebo (no alcohol) beverage was consumed (20,21), suggesting that post-exercise alcohol consumption affects women and men differently. ...
Article
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.
... The lesser dose (0.88 g) was chosen because it accounted for the reduced proportional lean mass of females. We have previously observed a dose effect of post exercise alcohol in males where 0.5 g/kg was not ergolytic (Barnes et al., 2011) so perhaps 0.88 g/kg was an insufficient dosage to produce an ergolytic effect in females. There is also the increased possibility of type 2 error as dosage declines, if indeed a true dosage effect is present. ...
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This study was designed to investigate the effects of alcohol consumption on recovery of muscle force when consumed immediately post-exercise in young females. Eight young women completed 300 maximal eccentric actions of the quadriceps femoris muscle on an isokinetic dynamometer on two occasions in a randomized, cross-over design after which an alcoholic beverage (0.88g ethanol/kg body weight) or an iso-caloric placebo was consumed. Maximal isokinetic (concentric and eccentric) torque and isometric tension produced across the knee were measured in both the exercised and control leg pre-damage, 36h-post, and 60h-post damage. Venous blood creatine kinase (CK) activity and muscle soreness ratings were taken prior to damage and once per day to 60h-post damage. Significant differences were observed between the exercised and control leg for maximal concentric, and eccentric torque and isometric tension (p<0.05). A near significant treatment*time interaction was observed for isometric tension (p=0.077), but not for concentric or eccentric torque. No main effects of treatment (alcohol) or interactions with time*leg or leg*treatment were observed. Perceived muscle soreness, during box stepping and squatting showed significant time effects (p<0.05), and CK activity did not significantly change. Our results indicate that the consumption of 0.88g ethanol/kg body weight following eccentric exercise-induced muscle damage does not affect recovery in the days following damage in females.
... CPET allows us to evaluate both the physical performance and, indirectly, the biochemical production of energy that is likely influenced by ethanol concentration. [2][3][4][5][6] Additionally, the impact of acute alcohol abuse on cardiac function, evaluated by echocardiography and brain natriuretic peptide (BNP) dosage, is unknown. 7 Furthermore, considering that alcohol is usually taken to reduce stress, it is interesting to explore whether there is any objective indicator justifying this theory or if this is merely an unproven excuse to drink alcohol. ...
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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.
Chapter
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The mechanisms that account for the strength loss after contraction-induced muscle injury remain controversial. We present data showing that (1) most of the early strength loss results from a failure of excitation-contraction coupling and (2) a slow loss of contractile protein in the days after injury prolongs the recovery time. Keywords: strength, damage, calcium, contractile protein, sarcoplasmic reticulum, plasmalemma
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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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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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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.
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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.
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The present study was undertaken to evaluate the acute effects of ethanol on responses of the rat heart and skeletal muscles both in vivo and in vitro. In the anesthetized rat, intravenous infusion of ethanol at 0.1-0.5 g/kg body weight (33-167 mM) decreased the breathing rate by 8-83%, heart rate by 4-52%, and QRS amplitude by 5-27%, and increased the P-R interval by 1-49%. In the anterior tibialis muscle subjected to repetitive nerve stimulation at 100 Hz for 0.5 sec, ethanol at 0.1 g/kg increased the amplitude of the muscle action potential (AP) by 7%, whereas at 0.5 g/kg it decreased the muscle AP by 32%. The nerve-evoked tetanic tension was reduced by 7-34% at 0.1-0.5 g/kg ethanol. In the isolated rat heart, perfusion of ethanol at 0.1-3.0% (22-651 mM) decreased the heart rate by 8-48% and QRS amplitude by 10-39%, and increased the P-R interval by 5-61%. Left ventricular pressure was increased by 10% at 0.1% ethanol, and decreased by 80% at 3.0% ethanol. In the isolated rat phrenic nerve-diaphragm muscle preparation subjected to repetitive nerve stimulation at 100 Hz for 0.5 sec, 0.1-3.0% ethanol decreased the amplitude of the nerve AP by 5-89%, nerve-evoked muscle AP by 2-96%, and peak tetanic tension by 1-87%. On repetitive direct muscle stimulation at 100 Hz for 0.5 sec, 0.1-3.0% ethanol decreased the amplitude of the muscle-evoked muscle AP by 8-65%, and muscle-evoked tetanic tension by 2-65%. These studies indicate that ethanol causes smaller reduction in responses of the heart and skeletal muscles at clinical concentrations, but marked reduction in these responses at higher concentrations due to direct action on excitability of these tissues. At higher concentrations, ethanol causes greater reduction in excitability of the skeletal muscle than of the heart.