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Journal of
Functional Morphology
and Kinesiology
Review
The Effects of Alcohol Consumption on Recovery
Following Resistance Exercise: A Systematic Review
Nemanja Laki´cevi´c
Sport and Exercise Research Unit, Department of Psychological, Pedagogical and Educational Sciences,
University of Palermo, 90144 Palermo, Italy; nemanja.lakicevic@unipa.it; Tel.: +39-3515881179
Received: 14 May 2019; Accepted: 21 June 2019; Published: 26 June 2019
Abstract:
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.
Keywords: strength; training; muscle mass; muscle function; performance
1. Introduction
Resistance exercise (RE) is a commonly practiced modality of physical exercise used by both
amateurs and elite athletes [
1
]. RE is a type of exercise that has gained a lot of interest over the
past two decades, specifically for its role in improving athletic performance by developing muscular
strength, power and speed, hypertrophy, local muscular endurance, motor performance, balance,
and coordination [
2
]. While non-athletes use it to simply develop muscular physique, professional
athletes engage in RE to enhance their athletic capabilities in various sports [
3
]. Variables such as
exercise intensity, exercise frequency, load, number of sets and repetitions, rest periods and training
volume can be manipulated in order to maximize RE induced effects in terms of muscle hypertrophy
and strength [
4
]. Physiological and psychological constraints leading to a reduction in physical or
mental performance can be classified as fatigue which is a phenomenon that has protective role in
human physiology [
5
]. Exercise is a potent stimulus with respect to altering homeostatic variables
which triggers adaptive reactions that counter the metabolic changes and repair the structural damage
caused by the previous training session [
5
]. The stressful effects of RE can temporarily impair athlete’s
performance [
6
]. Therefore, the speed and quality of recovery are absolutely essential for the high
performance athlete and, if done correctly, optimal recovery can lead to numerous benefits training and
upcoming competition [
7
]. The main purpose of recovery is to restore physiological and psychological
processes, so that the person engaging in vigorous exercise can repeat training sessions at an appropriate
J. Funct. Morphol. Kinesiol. 2019,4, 41; doi:10.3390/jfmk4030041 www.mdpi.com/journal/jfmk
J. Funct. Morphol. Kinesiol. 2019,4, 41 2 of 17
level [
7
]. It is also typically dependent on the nature of the exercise performed and any other outside
stressors that the athlete may be exposed to [7].
Certainly, one of the unnecessary stressors during recovery phase is alcohol (ALC) consumption [
8
,
9
]. Worldwide, alcohol is the most commonly used psychoactive drug; it is estimated that each adult
person consumes, on average, about 4.3 L of pure alcohol per year [
10
]. In the current era, consumption
of alcohol is increasing exponentially in Western society [
11
–
13
] and it is common knowledge that
alcohol can permeate virtually every organ and tissue in the body, resulting in tissue injury and
organ dysfunction [
14
]. Alcohol consumption results in hormonal disturbances that can disrupt the
physiological ability to maintain homeostasis and eventually can lead to various disorders, such as
cardiovascular diseases, reproductive deficits, immune dysfunction, certain cancers, bone disease, and
psychological and behavioral disorders [
14
]. In terms of post exercise recovery, acute alcohol ingestion
reduces muscle protein synthesis in a dose-and time-dependent manner, after the cessation of exercise
stimulus [
8
]. Alcohol does this mainly by suppressing the phosphorylation and activation of the mTOR
pathways, the crucial kinase cascade regulating translation initiation [
8
,
15
]. Concomitantly, alcohol
increases the expression of muscle specific enzymes that are up regulated by conditions that promote
skeletal muscle atrophy [8,16].
Emerging research provides new insights into the effect of alcohol consumption on post-exercise
muscle recovery but more research is needed to determine how this relationship exists and establish the
physiological mechanisms governing this response. Therefore, the aim of this review is to understand
the effects of alcohol consumption during recovery, on muscle function, following RE.
2. Materials and Methods
Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement has
been used to structure this manuscript.
2.1. Inclusion and Exclusion Criteria
Studies that meet the following criteria will be included or excluded in this systematic review.
2.2. Eligibility Criteria
When it comes to eligibility criteria, only articles written in English language and published in
peer-reviewed journals have been considered during the search. There was no limit on publication date
when it comes to article eligibility. Different formats of publications such as reviews, meta-analysis,
abstracts, citations, scientific conference abstracts, opinion pieces, books, book reviews, statements,
letters, editorials, non-peer reviewed journal articles and commentaries have been excluded. With
respect to intervention, publications were included only if they used a specific measure of performance
or biomarker, that considered recovery following RE and alcohol intoxication. Articles exploring
recovery after endurance type of training have been eliminated.
2.3. Participants
All the analyzed participants were adults to whom an ALC intervention was administered
following a bout of RE. Children were not considered for analysis. There was no limitation when
it comes to age, gender, number of participants, and duration of intervention or follow up period.
Furthermore, there was no limitation when it comes to training status.
2.4. Interventions
The interventions described in the eligibility criteria will be included in this review. The
interventions aimed to understand the effects of ALC on biological, physical and cognitive measures
following RE. According to the nature of the review different methodological approaches which
evaluate similar outcomes will be considered.
J. Funct. Morphol. Kinesiol. 2019,4, 41 3 of 17
2.5. Comparators
Comparators will be control groups (people not consuming ALC [NO-ALC]) if present or
if cross-over designs will be adopted the intervention groups will act as controls after each
wash-out period.
2.6. Outcomes
The primary outcome will be to understand the effects of ALC compared to the NO-ALC
intervention. Such findings will be applied to all the biological, physical and cognitive
measures retrieved.
2.7. Search Strategy
We used EndNote v. 8.1 software (Clarivate Analytics, Jersey, UK) for the article search. The
papers have been collected through PubMed (NLM), Web of Science (TS), and Scopus using the string:
((“alcohol” AND “exercise*” and “recovery*”; “ethanol” AND “exercise” AND “recovery”; “alcohol*”
AND “resistance training” AND “recovery”; “ethanol” AND “resistance training*” AND “recovery”;
“alcohol*” AND “strength*” AND “recovery”; “ethanol” AND “strength” AND “recovery”; “alcohol*”
AND “training” AND “recovery”; “ethanol” and “training” and “recovery”)).
2.8. Selection of Study Objects
The article screening was carried out in a three-step process: title reading, abstract reading and
full text reading, respectively. If any disagreements were noticed between the two investigators, a
third one considered the current process independently and discussed the decision with the other
investigators. Furthermore, investigators were not blinded to the manuscripts, study title, authors, or
associated institutions during the selection process. Both qualitative and quantitative articles were
included in the review. The screening processes have been summarized via PRISMA flow diagram
(Figure 1).
2.9. Risk of Bias
Risk of bias for the included studies was assessed through Downs and Black checklist [
17
]. This
tool is useful when evaluating the quality of original research articles in order to synthesize evidence
for public health purposes. This checklist contains 27 ‘yes’-or-’no’ questions over five different domains.
It offers both an overall score for study quality and a numeric score out of a possible 32 points. The
five domains contain questions about study quality, external validity, study bias, confounding and
selection bias, and power of the study.
Two independent researchers have completed the Downs and Black checklist of all included
articles to determine the quality of each study. 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 23–32), ‘moderate quality’ (score 19–22), ‘lower quality’ (score 16–18) or ‘poor quality’
(<14) (Supplementary File S1 and S2). Kendall Tau correlation coefficient statistical method was used
to determine inter-rater reliability. We used R statistical software (Bell Laboratories, Murray Hill, NJ,
USA) version 3.6 to perform this analysis. Quality of evidence was determined by the study design
and by Downs and Black score.
J. Funct. Morphol. Kinesiol. 2019,4, 41 4 of 17
J.Funct.Morphol.Kinesiol.2019,4,xFORPEERREVIEW4of19
Figure1.PrismaFlowDiagram
2.9.RiskofBias
RiskofbiasfortheincludedstudieswasassessedthroughDownsandBlackchecklist[17].This
toolisusefulwhenevaluatingthequalityoforiginalresearcharticlesinordertosynthesizeevidence
forpublichealthpurposes.Thischecklistcontains27‘yes’‐or‐ʹno’questionsoverfivedifferent
domains.Itoffersbothanoverallscoreforstudyqualityandanumericscoreoutofapossible32
points.Thefivedomainscontainquestionsaboutstudyquality,externalvalidity,studybias,
confoundingandselectionbias,andpowerofthestudy.
TwoindependentresearchershavecompletedtheDownsandBlackchecklistofallincluded
articlestodeterminethequalityofeachstudy.Themaximumscoreastudycanreceiveis32,with
higherscoresindicatingbetterquality.Thestudieswerethendividedintogroupsandmarkedas
‘highquality’(score23–32),‘moderatequality’(score19–22),‘lowerquality’(score16–18)or‘poor
quality’(<14)(Supplementaryfile1and2).KendallTaucorrelationcoefficientstatisticalmethodwas
usedtodetermineinter‐raterreliability.WeusedRstatisticalsoftware(BellLaboratories,Murray
Hill,NJ,USA)version3.6toperformthisanalysis.Qualityofevidencewasdeterminedbythestudy
designandbyDownsandBlackscore.
2.10.DataSynthesis
ThecriticalinformationacquiredfromtheincludedarticleswasextractedintoMicrosoftExcel
forMacintosh,version14.0(MicrosoftCorp,Redmond,WA,USA)spreadsheet.Themostimportant
characteristicsofthestudies,asauthornameandpublicationyear,samplesize,aim,alcoholdose,
howthiswasmixedandadministered,thestudymeasures,theREprotocoladopted,thestudy
designandtheoutcomeshavebeendelineatedinthetableswhilecertainspecificsaboutthe
particularstudyweredescribedinanarrativemanner.
Figure 1. Prisma Flow Diagram
2.10. Data Synthesis
The critical information acquired from the included articles was extracted into Microsoft Excel
for Macintosh, version 14.0 (Microsoft Corp, Redmond, WA, USA) spreadsheet. The most important
characteristics of the studies, as author name and publication year, sample size, aim, alcohol dose, how
this was mixed and administered, the study measures, the RE protocol adopted, the study design and
the outcomes have been delineated in the tables while certain specifics about the particular study were
described in a narrative manner.
3. Results
From a preliminary title and abstract search, a total number of 471 studies have been identified
in the three screened databases. After the application of inclusion criteria on each article’s title and
abstract, 63 records were considered eligible. Duplicates were removed leaving 24 studies for full text
screening. After full text screening, two additional studies from the relevant bibliography have been
added. Of the 24 studies analyzed, 10 were included for the final synthesis. Therefore a total number
of 12 studies were included in the qualitative synthesis of this review article. The process of article
inclusion has been synthesized in Figure 1. Risk of bias assessment was finalized through Downs
and Black checklist for all included studies (Supplementary File S1 and S2). The mean score was 19
(range =12–28). After performing the inter-rater reliability test via Kendall Tau analysis we detected
the score of 0.46 which can be classified as moderate but significant (p-value 0.026). As previously
stated, after comprehensive screening, files were split into different quality categories in accordance to
predetermined quality criteria (Supplementary File S1 and S2).
J. Funct. Morphol. Kinesiol. 2019,4, 41 5 of 17
In order to evaluate the effects of alcohol consumption on recovery following RE, the results
have been summarized into three categories: (1) biological and (2) physical measures and (3)
cognitive function.
Of the retrieved studies, 10 took into account at least one biological measure [
9
,
18
–
26
], 11 took
into account at least one physical measure [9,18–25,27,28] and cognitive function only one [24].
The retrieved biological measures include creatine kinase (CK) [
18
–
25
], heart rate [
19
,
26
],
lactate [19,26]
, blood glucose [
9
], urine measures [
24
], cortisol [
19
,
21
,
24
,
26
], testosterone [
19
,
21
,
24
,
26
],
estradiol [
26
], sexual hormone binding globulin (SHBG) [
21
,
26
], leukocytes and cytokines [
19
,
21
,
22
],
C-reactive protein (CRP) [
24
], plasma amino acids [
9
], intracellular signaling proteins and rates
of muscle protein synthesis (MPS) [
9
] and calcium (Ca
2+
) [
25
]. The physical measures include
force [
18
,
20
–
25
,
27
,
28
], power [
19
,
21
,
24
,
28
], muscular endurance [
25
], soreness [
18
,
20
,
22
,
23
,
28
] and rate
of perceived exertion (RPE) [
19
,
24
,
26
]. The cognitive measures included a modified version of the
STROOP test which evaluated time and accuracy of each response for congruent and incongruent
stimuli. The alcohol dose provided to the participants in the included studies ranged between 0.6g/kg
to 1.5g/kg. As defined by Kalinowski and Humphreys [29] a standard drink equals to 10 g of alcohol.
Therefore, the alcohol dose provided to the participants, if we consider a man of 70kg, equals to 42 to
105 g of alcohol (4.2 to 10.5 standard drinks), which corresponds to 3 bottles of beer of 330 mL at 5%
alcohol or a 370mL bottle of spirit at 37.5% alcohol, respectively. All the included studies adopted a
cross-over research design. A summary of the retrieved studies is shown in Table 1.
3.1. Biological Measures
3.1.1. Creatine Kinase
Eight studies included CK measurement [
18
–
25
]. All the retrieved studies showed that CK
increases following each RE protocol in both ALC and NO-ALC conditions showing a time interaction
with RE. However, when analysing interaction with the different conditions, no differences were shown
between the ALC and NO-ALC condition for none of the retrieved studies. Clarkson et al. [
20
], have
also correlated peak CK activity from the ALC and the NO-ALC condition and found a high correlation
coefficient (r=0.95), whereas Paulsen et al. [
25
] have also stratified the findings for man and women
finding again no differences between the two groups neither for time or treatment assessment. Such
results, as also highlighted by each author of the included studies, demonstrate that ALC cannot be
considered as a modulating factor for CK following RE and that the increases of CK are the result of
muscle damage following the exercise bouts.
3.1.2. Heart Rate
Two studies included measures of heart rate [
19
,
26
]. In both studies heart rate increased
following the exercise intervention, however no difference was shown between the ALC and the
NO-ALC condition.
3.1.3. Lactate
Two studies included measures of lactate [
19
,
26
]. In both studies lactate increased following the
exercise intervention, however no difference was shown between the ALC and the NO-ALC condition.
3.1.4. Blood glucose
Only Parr et al. [
9
] evaluated the concentration of blood glucose. It has to be noted that Parr
administered a concentration of alcohol in conjunction with either CHO or PRO. The results highlight
a significant time and treatment interaction. Blood glucose concentration increased 0.5 and 4.5 h post
intervention in the ALC-CHO group but not in the ALC-PRO or NO-ALC groups. Such findings
demonstrate that blood glucose is affected by CHO but not ALC during recovery after RE.
J. Funct. Morphol. Kinesiol. 2019,4, 41 6 of 17
Table 1. Descriptive characteristics of the retrieved studies.
Author [Ref]
(Year)
nAim Alcohol
(dose)
Mix Administration
Time
Measures Resistance Training Comparator Outcomes (Compared to
Comparator)
Barnes et al.
[27] (2010)
12 Evaluate if ALC interacts
with damaged muscles.
1g/kg 37.5%
ALC/volume;
Smirnoff
Vodka in
orange juice
(ratio 3.2:1)
A beverage was
consumed every 15
min over a total time
of 90 min.
-Strength.
-Peak and averaged
torque.
300 maximal eccentric
contractions of the
quadriceps muscles
of one lower limb at
an angular speed of
30◦/s.
Cross-Over No differences in acute
performance measures.
Decreased performance was seen
after 36h following ingestion.
Barnes et al.
[18] (2010)
11 To compare the effects of
post-exercise ALC
ingestion with that of an
isocaloricnon-ALC
beverage on changes in
muscle performance.
1g/kg 37.5%
ALC/volume;
Smirnoff
Vodka in
orange juice
(ratio 3.2:1).
A beverage was
consumed every 15
min over a total time
of 90 min.
-Soreness
-Peak and averaged
torque
-CK
300 maximal eccentric
contractions of the
quadriceps muscles
of one lower limb at
an angular speed of
30◦/s.
Cross-Over Peak concentric, eccentric were
lower in the ALC group.
No differences in CK and
soreness
Barnes et al.
[19] (2012)
10 To investigate the effects
of post-game ALC
consumption
on whole-body,
sport-specific
performance.
1g/kg 37.5%
ALC/volume;
Smirnoff
Vodka in
orange juice
(ratio 3.2:1).
A beverage was
consumed every 15
min over a total time
of 90 min.
-HR
-Lactate
-RPE
-CMJ
-HPO
-CK
-Cortisol and
Testosterone
-Leukocytes
BURST Protocol
(intense 20-m shuttle
run with 180◦turns)
Cross-Over HR and Lactate showed no
difference. RPE varied
significantly.
Differences in CMJ but not in
HPO were present.
No differences in the leukocyte
count. CK was higher in the
ALC group only after 48h.
Testosterone did not show any
differences. Cortisol was higher
in the ALC group after 36h.
Clarkson et al.
[20] (1990)
10 Assess the effect of acute
ALC ingestion on muscle
indicators.
0.8g/kg Vodka 40%
with orange
juice (ratio 1:1)
Single dose. -CK
-Soreness
-Isometric strength
50 repetitions at a
lat-pulley.
Cross-Over. No difference in CK.
No difference in soreness.
No difference in strength.
Haugvad et al.
[21] (2014)
9 Investigate the effects of
ethanol on recovery of
muscle function after RT.
-Low dose 0.6
or 0.7 g/kg
-High dose 1.2
or 1.4 g/kg
40%
ethanol/volume,
Absolut
vodka diluted
with 200-mL
sugar-free
lemonade(raspberry
flavour) and
water to a
total of 1.5 L
The beverage
was consumed in
about 90 min.
-MVC
-Power
-Cortisol and
Testosterone
-SHBG
-CK
-Leukocytes.
Squats, lower limb
presses, and bilateral
knee extensions were
performed in 4 sets
with a load of 8RM
with 2 min rest.
Cross-Over MVC was decreased after the
ALC trial 12h training. MVC
normalized in both groups after
24h. No difference in Jump
performance; Cortisol was
higher at 12 at 24h in the high
dose group. Neither testosterone
or SHBG were influenced by
ALC. Free testosterone was
lower in the high dose group at
12 and 24h. No differences in the
CK for any group. No
differences in leukocytes.
J. Funct. Morphol. Kinesiol. 2019,4, 41 7 of 17
Table 1. Cont.
Author [Ref]
(Year)
nAim Alcohol
(dose)
Mix Administration
Time
Measures Resistance Training Comparator Outcomes (Compared to
Comparator)
Levitt et al.
[22] (2017)
13 The effect of acute ALC
consumption on
muscular recovery
process.
1.09 g/kg The ALC was
diluted to 15%
v/vin an
artificially
sweetened
beverage.
The beverage volume
was split into 10 equal
portions; one portion
was administered
each minute over a
10min ingestion
period.
-TNF-α
-Il-1β
-Il-6
-Il-8
-Il-10
-Soreness
-Isometric, concentric
and eccentric torque
-CK
300 maximal
single-lower limb
eccentric leg
extensions.
Cross-Over No difference in soreness.
No difference in strength.
No difference in CK.
No difference in any cytokine.
Levitt et al.
[28] (2018)
10 To investigate the effect
of ALC consumed after
heavy eccentric
resistance exercise on
measures of muscle
power.
1.09 g/kg Smirnoff40%
ALC Vodka
diluted to 15%
v/vin an
artificially
sweetened
beverage.
The beverage was
split into 10 equal
portions and one
portion consumed
every 3 min during
the 30-min beverage
ingestion period.
-Soreness
-Peak power
-Peak force
-Jump height
4 sets of 10 repetitions
at 110% of concentric
1RM; 3 min passive
rest in between sets
Cross-Over No differences were found in
peak power nor peak force or
jump height.
No differences were found in
soreness measures.
McLeay et al.
[23] (2017)
8 To investigate the effects
of ALC consumption on
recovery of muscle force.
0.88 g/kg 37.5%
ALC/volume;
Smirnoff
Vodka in
orange juice
Six drinks were
consumed every 15
min over 1.5 hr.
-CK
-Soreness
-Isometric, concentric
and eccentric torque.
300 maximal
single-lower limb
eccentric leg
extensions through a
60◦ROM at an
angular speed of
30◦/s.
Cross-Over No difference in isometric,
concentric and eccentric torque.
No difference in CK.
No difference in muscle soreness.
Murphy et al.
[24] (2013)
9 To evaluate the effects of
ALC ingestion on
lower-body strength and
power
and physiological and
cognitive recovery
1g/kg 37.5%
ALC/volume;
Smirnoff
Vodka in
orange juice
(ratio 3.2:1).
An equal volume of
beverage was
consumed every 20
min over a total time
of 150 min
-RPE
-CMJ
-MVC
-Urine
-CK
-CRP
- Cortisol and
Testosterone
-Cognitive function
Rugby match Cross-Over No difference in RPE.
No differences in CMJ and MVC.
No difference in CK and CRP.
No difference in testosterone.
Large effect size for cortisol
increase after 16h in the ALC
group.
Larger urine volume after night
in the ALC group.
Decreased cognitive function
was observed in the ALC group.
J. Funct. Morphol. Kinesiol. 2019,4, 41 8 of 17
Table 1. Cont.
Author [Ref]
(Year)
nAim Alcohol
(dose)
Mix Administration
Time
Measures Resistance Training Comparator Outcomes (Compared to
Comparator)
Parr et al. [9]
(2014)
8 Evaluate the effect of
ALC intake on rates of
myofibrillar protein
synthesis following
strenuous exercise
-1.5g/kg with
CHO
-1.5g/kg with
PRO
Vodka and
Orange juice
(ratio 1:4)
6 equal volumes were
consumed during a 3
h period.
-Biopsy
-Blood glucose
-Plasma AA
concentration
-Intracellular
signalling proteins
-8 ×5 at ,80% of 1RM
-10 ×30 s high
intensity intervals at
110% of PPO; 3 min
rest between sets
Cross-Over Blood ALC was higher in the
CHO compared to the PRO
group after 6 and 8h after
consumption. Blood Glucose
was higher in the ALC-CHO
group after 5h.AA (EEA and
BCAA) were lower in the ALC
groups compared to the no ALC
group.mTOR phosphorylation
was higher in the no ALC group
at 2 and 8h post exercise.
p70S6Kphosphorylation was
higher in the no ALC and the
ALC-PRO group at 8h post
exercise. Muscle protein
synthesis was greater in the No
ALC group than the ALC-PRO,
which was greater than the
ALC-CHO group.
Poulsen et al.
[25] (2007)
19 Evaluate acute ALC
intoxication on skeletal
muscle function
1.5 g/L
ALC 96% with
orange juice
(ratio 1:4)
5 doses with intervals
of 1h each.
-CK
-Ca2+
-Strength
-Endurance
MVC Isokinetic
endurance and
isometric knee
extensors (30
extensions at a
velocity of 180◦/s)
Cross-Over No differences in strength and
endurance.
No differences in CK.
Small reduction in Ca2+only in
the ALC group.
Vingren et al.
[26] (2013)
8 To examine the
testosterone
bioavailability and the
anabolic endocrine
milieu in response to
acute ethanol ingestion
1.09 g/kg ALC was
diluted to a
concentration
of 19% v/v
absolute
ethanol in an
artificially
sweetened
and
calorie-free
beverage
The participants
drank 1/10 of the
drink each minute
during a 10-min
ingestion period.
-HR
-RPE
-Testosterone
-SHBG
-Lactate
-Cortisol
-Estradiol
6×10squats starting
at 80% of 1 RM and 2
min of rest between
sets.
Cross-Over No difference in HR, RPE and
lactate. Serum testosterone and
free testosterone was higher for
ALC at 300min post exercise. FAI
was higher in the ALC group.
No difference in cortisol levels.
No differences in estradiol.
Tot.
127
Mean 1.1g/kg
N=Number of participants; g/L=grams per liter; g/kg=grams per kilogram; ALC=Alcohol; CK=Creatine kinase; Ca
2+
=Calcium; MVC=Maximum voluntary contraction; ROM=Range
of movement; HR=Heart rate; RPE=Rating of perceived exertion; CMJ=Counter movement jump; HPO=Horizontal power output; RE=Resistance exercise; SHBG: Sex hormone-binding
globulin; RM=Repetition maximum; CRP=C-reactive protein; CHO=carbohydrate; PRO=Protein.; AA=Amino Acids; PPO=Peak power output; EAA =Essential amino acids; BCAA=
Branched Chain amino acids; FAI=Free androgen index.
J. Funct. Morphol. Kinesiol. 2019,4, 41 9 of 17
3.1.5. Urine Measures
Only Murphy et al. [
24
] included urine measures. Post-intervention urine output, nude mass and
urine-specific gravity were measured. No differences were found for nude mass and urine-specific
gravity between conditions. The ALC group had an increased total volume output overnight when
compared to the NO-ALC group.
3.1.6. Cortisol
Four studies included measures of cortisol [
19
,
21
,
24
,
26
]. In the study of Barnes et al. [
19
] the
cortisol levels increased after 12h after treatment in both conditions, after which at 24h returned to
baseline levels. A second rise in cortisol was seen at 36h under the ALC condition but not in the
NO-ALC condition. Haugvard et al. [
21
] showed that no differences were shown between the two
conditions at any specific time point after the intervention (12 and 24 h post-treatment). However, if
the 12 and 24 h cortisol values were combined and averaged, these resulted to be significantly elevated
only in the ALC condition at 24 h after the intervention. Murphy et al. [
24
] showed that a significant
decrease post-match was followed by a significant increase at 16h post intervention. No difference
was found in the levels of cortisol between the two interventions. However, a large effect size was
found between the %change from 2 to 16 h post-match for the increase in cortisol response after ALC
consumption. Vingren et al. [
26
] found that cortisol levels were not affected by ALC post intervention.
Cortisol was elevated immediately after, after 20, 40, 60, 120, 140 and 300 min post-intervention in both
ALC and NO-ALC conditions.
3.1.7. Testosterone
Four studies included measures of cortisol [
19
,
21
,
24
,
26
]. In the study of Barnes et al. [
19
] no
difference in the testosterone levels compared to baseline ware seen at any time point after the
intervention in either two conditions (12-24-36 and 48 h after the intervention). In the study of
Haugvard et al. [
21
] the levels of testosterone were not altered across trials neither for the ALC and
the NO-ALC condition. Calculated free testosterone (testosterone/SHBG multiplied by a factor of 10)
was not different between trials. However, if the measures at 12 and 24 h after the intervention were
combined and averaged the levels of testosterone resulted to be lower only in the ALC condition after
24 h. Murphy et al. [
24
] showed that a reduction in testosterone was present after 2 h post-match
followed by a significant increase 16h post-match. However, no differences were shown between the
testosterone levels for the two conditions neither between %changes from 2 to 16 h post-match. Vingren
et al. [
26
] found a significant effect for treatment for testosterone in which the levels were increased
immediately and 140 and 300 min after the intervention for the ALC group, whereas it appeared to be
decreased in the NO-ALC group between 60 and 300 min post-intervention. Free testosterone also
seemed to be increased between 60 and 300 min post-intervention for both conditions.
3.1.8. Estradiol
Only one study included measures of estradiol after ALC consumption [
26
]. The study indicates
that the levels of estradiol were elevated immediately after and between 20 and 40 min after the
intervention, when compared to baseline measures, in both groups, with no significant differences
between the ALC and the NO-ALC group. The results underlie that ALC has no effect on estradiol
during recovery from RT.
3.1.9. Sexual Hormone Binding Globulin
Two studies included measures of SHBG [
21
,
26
]. In none of the included records the levels of
SHBG seemed to be altered by ALC intake, neither by the acute bouts of exercise proposed by the two
authors. ALC does not seem to be a modulating factor for SHBG following RE.
J. Funct. Morphol. Kinesiol. 2019,4, 41 10 of 17
3.1.10. Leukocytes and Cytokines
Three of the included studies included measures of leukocytes and cytokines [
19
,
21
,
22
]. Barnes
performed analysis of total and differential leukocytes and found that total, neutrophil and monocyte
concentration increased after the intervention but decreased to baseline values after 12h. However,
no difference was present between the two conditions. Haugvard et al. [
21
] found no difference
between conditions regarding the white blood cell, neutrophils or monocytes count. Following RE both
conditions showed a sub-clinical leucocytosis 1h post-exercise. Levitt et al. [
22
] analysed inflammatory
markers in women post-exercise, in particular TNF-
α
, IL-1
β
, IL-6, IL-8 and IL-10 before, at 5, 24 and
48h post-intervention.IL-10, IL-8 and TNF-
α
increased after the intervention in both groups. IL-6 and
IL-1
β
remained unchanged over time for both conditions. No differences for cytokine was present
between the ALC and the NO-ALC condition. ALC doesn’t seem to affect neither leukocytes nor
cytokines after RE during recovery.
3.1.11. C-reactive Protein
C-reactive protein was evaluated only in the study of Murphy et al. [
24
], in which however no
significant difference was highlighted neither regarding time, when data was compared to baseline,
neither regarding condition, when ALC and NO-ALC where compared. The findings indicate that
post-match alcohol consumption did not unduly affect CRP markers of damage.
3.1.12. Plasma Amino Acids
Plasma amino acids (AA) have been included only in the study of Parr et al. [
9
], who evaluated
EEA, BCAA and leucine at 0, 1, 2, 4, 6 and 8 h after alcohol consumption following RE. It has to be
noted that Parr administered a concentration of alcohol in conjunction with either CHO or PRO. The
results were then compared to a control group who did not ingest ALC but consumed a single dose of
25 g of whey protein.
A significant effect for time and treatment were found. At all-time points the NO-ALC group had
significantly higher levels of essential AA (EEA), branched chain AA (BCAA) and leucine compared to
the ALC-PRO group. Both groups (the NO-ALC and the ALC-PRO) had at all-time points significantly
higher levels of AA compared to the ALC-CHO group. No difference in the levels of AA compared
to baseline was shown, at any time point, in the ALC-CHO group. Leucine, EEA and BCAA were
elevated compared to baseline at 1 and 6 h post-ALC ingestion for the NO-ALC and ALC-PRO group.
The data from the study of Parr et al. [
9
] indicates that ALC alone does not influence the levels of
plasma AA, however can be a factor that limits the rise of blood concentration of AA following
protein consumption.
3.1.13. Intracellular Signaling Proteins and Rates of Muscle Protein Synthesis
mTOR, p70S6K, eEF2, 4E-BP1, AMPK, MuRF-1 mRNA and fractional synthetic rate of myofibrillar
protein synthesis were analysed in the study of Parr et al. [
9
]. ALC and NO-ALC consumption
modalities have been described in the previous subsection. mTOR
Ser2448
phosphorylation was higher
in all groups at 2h post treatment. However, mTOR phosphorylation in the NO-ALC group was
higher than the ALC-CHO (76%) and ALC-PRO (54%) group at 2 and 8 h post-exercise. p70S6K
phosphorylation was greater after 2h post-exercise compared to baseline only in the NO-ALC and
the ALC-PRO groups. No differences were shown for the ALC-CHO group. eEF2 phosphorylation
decreased below rest values at 2 and 8 h in the ALC-CHO and ALC-PRO groups. No differences were
shown for the NO-ALC group at any time point.
No differences for time and condition were shown for 4E-BP1
Thr37/46
or AMPK
Thr172
phosphorylation. There were increases above rest in MuRF-1 mRNA at 2 h post- intervention
with no differences between treatments. All values returned to baseline at 8h post- intervention.
J. Funct. Morphol. Kinesiol. 2019,4, 41 11 of 17
Fractional synthetic rate of myofibrillar protein synthesis were increased above baseline for all
groups from 2 to 8 h post-intervention. However, a hierarchical reduction was shown when data was
compared to the NO-ALC group in the ALC-PRO (-24% compared to NO-ALC) and ALC-CHO (
−
38%
compared NO-ALC and
−
18% compared to ALC-PRO) groups. Data suggests that ALC consumption
impairs the response of muscle protein synthesis during recovery despite optimal nutrient provision.
3.1.14. Calcium
Only one study has evaluated the effects of ALC on Ca
2+
via blood sampling [
25
]. The authors
report that the Ca
2+
levels were similar before exercise for both conditions. A decrease of approximately
2% was observed following the exercise bouts. A further decrease was observed in the ALC condition,
and the difference with the NO-ALC condition was significant only after the strength evaluation.
Hypocalcaemia was not induced by ALC and no differences were shown for resting free Ca
2+
levels
indicating that free Ca2+concentrations were not affected by alcohol per se.
3.2. Physical Measures
3.2.1. Force
Nine studies have examined the effects of post-exercise ALC consumption on force [
18
,
20
–
25
,
27
,
28
].
McLeay et al. [
23
] evaluated maximal isometric, concentric and eccentric muscular contractions of
the quadriceps femoris using an isokinetic dynamometer for both lower limbs using one lower limb
as control. A significant difference between lower limbs was present post-treatment (exercised vs.
non-exercised lower limb) up to 60 h post-exercise regarding maximal isometric tension, concentric and
eccentric torque but no difference was observed between the ALC and the NO-ALC condition. Barnes
et al. [
18
,
27
] in both studies evaluated isometric, concentric and eccentric contractions of the quadriceps
muscles of both lower limbs using one lower limb as control. Isometric tension was measured at 75
◦
of knee angle. Concentric and eccentric torque was measured at an angular speed of 30
◦
/s. In both
studies a decrease in performance was seen in both the ALC and NO-ALC groups over time in the
exercised lower limb for all the evaluated measures (isometric and eccentric peak torques as well
as for isometric, concentric and eccentric average peak torques). A greater decrease in performance
was however seen in the ALC group in the first study [
27
] at 36h post-intervention (isometric and
eccentric peak torques were reduced 39 and 44% compared to pre-exercise measures, respectively,
with ALC whereas losses of 29 and 27% for the same measures in the NO-ALC group. Average peak
torque was reduced by 41% (isometric), 43% (concentric) and 45% (eccentric) with ALC compared
to 29, 32 and 26% with NO-ALC groups, respectively), while no differences were seen between 36
and 60h post-intervention. In the second study [
18
], except for average peak isometric torque, all
measures were different between interventions with the greatest decrements observed in the ALC
group. Greatest decreases in peak torque were observed at 36 h with losses of 12%, 28% and 19%
occurring in the NO-ALC group for isometric, concentric and eccentric contractions, respectively. Peak
torque loss was significantly larger in ALC with the same performance measures decreasing by 34%,
40% and 34%). Levitt et al. [
22
] measured peak torque for the knee extension exercise on each lower
limb using an isokinetic dynamometer. The same assessment procedure used by Barnes et al. [
18
,
27
]
was adopted. A reduction post-intervention was found for peak isometric, concentric and eccentric
torque between the exercised and not-exercised lower limb, but no difference was found between the
ALC and NO-ALC condition immediately post nor at 24 and 48 h post-intervention. Poulsen et al. [
25
]
evaluated isokinetic muscle strength of the dominant knee extensors and non-dominant wrist flexors.
No differences in isometric strength was observed immediately post, 4, 24 or 48 h post intervention,
neither regarding time, when compared to baseline, neither regarding ALC condition. Murphy et
al. [
24
] measured peak MVC of the knee extensors and found that a significant reduction compared to
baseline was evident at all measured time points (2 and 16 h post-intervention), but no differences
were present between the ALC and NO-ALC group. Haugvad et al. [
21
] have also measured isometric
J. Funct. Morphol. Kinesiol. 2019,4, 41 12 of 17
MVC of the knee extensors and the results reported by the authors showed stable values in all analysed
conditions (Low ALC dose, High ALC dose and NO-ALC). A decrease immediately after performance
and a recovery from immediately after to 12 and 24 h post intervention was seen in all groups, with no
significant differences between trials. Clarkson et al. [
20
] measured isometric strength of the elbow
flexors and the results are similar to those of Haugvad et al. with a reduction immediately post-exercise
but no difference between conditions. The level of isometric strength returned to baseline 5 days post-
intervention. Except for the studies of Barnes et al. no differences seem to be present following ALC
consumption on force during recovery following RE. It has to be noted that the ALC dose provided by
Barnes et al. is of 1g/kg, which is neither the minimum or maximum dose provided across the studies.
3.2.2. Power
Four studies [
19
,
24
,
28
,
30
] included measures of power following ALC consumption and RE.
Barnes et al. [
19
] have included measures of counter movement jump (CMJ) and horizontal power
output (HPO). HPO did not vary neither over time neither regarding condition. CMJ instead showed a
significant time x treatment effect, where a decrease in jump performance was observed after 24 and
48 h post-intervention only in the ALC group. However, the authors underline that the decrements
seen in performance are trivial as the decrease in the jumping performance of the CMJ was a mean
value of 12 cm. Murphy et al. [
24
] have included a measure of CMJ over time, where each participant
was required to perform 10-maximal repeated CMJs. The results of Murphy et al. do not show
any difference neither regarding time neither regarding condition. Levitt et al. [
28
] have included
measures of vertical power, and similarly to Barnes et al., the reported measures of power show a
time effect, with a reduction in vertical power output after 24 and 48 h post-intervention, but no effect
regarding condition. Haugvad et al. [
21
] included a measure of squat jump performed without any
counter movement on a force platform. Jump height was calculated for analysis. Jump height was
reduced immediately after and 12 h post-intervention in all groups (low-ALC, high-ALC and NO-ALC
condition). However, no difference between any group was present. ALC doesn’t seem to have an
effect on power output, at least in the 48 h following its consumption.
3.2.3. Muscular Endurance
Maximal isokinetic muscular endurance was calculated for the dominant knee extensors and
non-dominant wrist in the study of Poulsen et al. [
25
] using an isokinetic dynamometer. Thirty maximal
reciprocal movements were performed at a velocity of 180
◦
/s without any rest interval. Subjects were
instructed to exert maximal effort in every single movement and not to economise the muscle exertion.
An endurance index was calculated defined as the mean-peak torque of the last five repetitions as a
percentage of the mean-peak torque of the first five repetitions. The results obtained by the authors
show no differences in muscular endurance 4, 24 and 48h after treatment neither after ALC intoxication
neither in the NO-ALC group. No changes were evident neither in the leg extensors neither in the
wrist flexors or between the endurance index for both conditions for both muscle groups. The results
were also stratified according to gender and similar findings were achieved.
3.2.4. Soreness
Five studies included measures of soreness [
18
,
20
,
22
,
23
,
28
]. Barnes et al. [
18
] evaluated soreness
by asking each participant at different time points their levels of soreness by giving a value from 0
(no pain) to 10 (worst possible pain). Soreness was rated while stepping up (concentric muscular
contraction) onto a 40 cm box and lowering into a squatting position. Clarkson et al. [
20
] evaluated
soreness by questionnaire, measured for the forearm flexor muscles, using a scale of 1 to 10. Levitt et
al. [
22
] measured soreness applying on the vastuslateralis, in three different points along the muscle
belly, a pressure of 35N. Each participant rated the pain giving a value from 0 to 10. In a subsequent
study Levitt et al. [
28
] evaluated pain by asking the participants to self-report their level of pain using
a scale from 0 to 5. McLeay et al. [
23
] used the same protocol as above described in the study of Barnes
J. Funct. Morphol. Kinesiol. 2019,4, 41 13 of 17
et al. [
18
]. All the retrieved records show a time effect for muscle soreness related to the intervention
protocol, with increases over a period of 24 and 48 h after the training intervention, with no differences
between the ALC and the NO-ALC condition. The results indicate that RT is a factor responsible to
increase muscle soreness between 24 and 48 h post training, whereas ALC consumption is not.
3.2.5. Rate of Perceived Exertion
Rates of perceived exertion were measured in three of the retrieved studies [
19
,
24
,
26
]. The study of
Vingren [
26
], was the only one evaluating RPE before and after a single session of static RE. Barnes and
Murphy [
19
,
24
] evaluated RPE before and after a rugby match. In particular Murphy et al. evaluated
RPE after a competitive rugby league game, whereas Barnes et al. after a simulated rugby match. The
results of Vingren and Murphy highlight a significant time effect, with increases of RPE after the RT
and the rugby league game, but no significant differences between the RPE of the ALC or the NO-ALC
groups. The results of Barnes et al. are in line to those of the previous authors regarding the time
effect of RPE following the exercising protocol, however a difference was shown between conditions.
The ALC group reported lower levels of RPE at the end of the third quarter of the simulated game,
compared to the NO-ALC group at the same time measurement. Despite the significant results, the
mean difference between the two conditions is very small (ALC=15.2
±
1.6; NO-ALC=16.5
±
1.2) and
not present at any other time point.
3.3. Cognitive Function
Cognitive function was assessed only in the study of Murphy et al. [
24
] through a modified version
of the Stroop test. This test of cognitive function was a computer-based program requiring subjects
to react to repeated color and word stimuli. The program analyzed response time and accuracy for
congruent and incongruent stimuli. Measures of cognitive function were recorded before, immediately
post, 2 and 16 h intervention. The results provided by the authors show no difference over time for
cognition test time, congruent reaction time, or incongruent reaction time. However, the time required
to complete the cognition test significantly increased in the ALC compared to the NO-ALC group and
a large ES was shown for increased cognition test time, congruent and incongruent reaction time in the
ALC group compared to the NO-ALC group. The findings indicate that ALC consumption impairs
cognitive function during recovery, which may be a negative factor in sports where decision making
processes, speed and quality of responses to visual stimuli (especially team sports) are essential.
4. Discussion
By evaluating the effects of alcohol consumption on recovery following RE from biological,
physical and cognitive perspective, we have been able to provide a comprehensive description of the
multifactorial nature of alcohol consumption. Indeed, alcohol consumption is a common occurrence in
the general population on global scale and it is a phenomenon that has not been explored in depth
when it comes to post-exercise recovery, even more so in RE post-exercise recovery. The main findings
highlight that ALC cannot be considered as a modulating factor for the majority of the retrieved
biological measures. In fact, creatine kinase, heart rate, lactate, blood glucose, estradiol, sexual
hormone binding globulin, leukocytes and cytokines, C-reactive protein and calcium do not seem to
be modified following ALC consumption during the acute recovery phase post-resistance exercise.
Only cortisol levels seem to be increased, conversely testosterone, plasma amino acids, and rates of
muscle protein synthesis decreased. When considering the retrieved physical measures force, power,
muscular endurance, soreness and rate of perceived exertion also seem to be unmodified following
alcohol consumption during recovery. The general findings therefore highlight that muscle function is
not altered by alcohol consumption following exercise bouts, however the altered endocrinological
asset regarding cortisol and testosterone and the consequent suppressed rates of muscular protein
synthesis and reduced circulating levels of amino acids, suggest that long-term muscular adaptations
could be impaired.
J. Funct. Morphol. Kinesiol. 2019,4, 41 14 of 17
A trend of heart rate increase following the exercise intervention has been detected, however no
difference was shown between the ALC and the NO-ALC condition. This conclusion raises different
concerns since alcohol acts as a diuretic and it contributes to faster elimination of water content from
the bloodstream, leading to increased viscous blood plasma which is harder to pump and deliver to
the body tissues [
31
]. The heart has to adapt to these conditions to increase the cardiac output. There
seems to be a dose response relationship between the alcohol consumption and heart rate i.e., there is a
positive correlation between alcohol consumption and heart rate response [
32
]. Consequently, this has
the potential to alter individual RPE [
33
]. This latter parameter also seems to not be influenced by
alcohol consumption. Only one of the retrieved studies has shown there was a difference between
the ALC and NO-ALC group with the ALC group showing less perceived exertion compared to the
NO-ALC group.
As previously stated alcohol acts as a diuretic and thus can explain why in the study of Murphy
at al [
24
] the ALC group had an increased total volume output overnight when compared to the
NO-ALC group.
One of the most interesting findings of this review was found in the study by Parr et al. [
9
] who
demonstrated that blood glucose is affected by CHO but not ALC during recovery after RE. This is
in alignment with findings of Lustig [
34
] who claims that toxic effects of alcohol are very similar to
excessive sugar exposure mainly for its fructose content. Even though fructose does not show the same
acute toxic effects of ethanol, it encompasses all the chronic hazardous effects on long-term health [
34
].
Creatine kinase was also unmodified by ALC consumption. Such enzyme which is present
in the muscles, when detectable in the peripheral circulation, is commonly used as a measure of
muscle damage [
8
]. None of the authors which reported measures of CK showed differences between
groups, instead correlations were established between the ALC and the NO-ALC condition. ALC
cannot be considered as a modulating factor for CK following RE and the increases of CK shown are
the result of muscle damage following the exercise bouts. Neither leukocytes nor cytokines seem
to be changed following alcohol consumption, which means that the inflammatory response is not
modulated by alcohol consumption. Such is a controversial finding because as reported by different
authors [
35
,
36
] alcohol abuse not only increases inflammation but also alters the immune function of
the body. Probably healthy individuals, who regularly exercise, as those included in each study of
this review, do not express altered inflammatory or immune function following a single acute alcohol
intoxication. Same trend is shown by CRP, which confirms that muscle damage and inflammation are
not dependent, in the analyzed population, from the ingestion of alcohol [
24
]. Such findings may also
explain why perceived soreness was not different between the ALC and NO-ALC groups analyzed.
Cortisol and testosterone levels during post RE when compared between ALC and NO-ALC
groups appear to be altered. On average, the participants who consumed ALC expressed higher levels
of cortisol and lower levels of testosterone in comparison to the NO-ALC group. Decreased levels
of testosterone and increased levels of cortisol are suggested to be indicative for a disturbance in the
anabolic-catabolic balance, which likely leads to decreased recovery and therefore, decreased levels of
performance [
24
,
37
]. When present in excessive levels, cortisol is an overall catabolic hormone, which
decreases lean body and muscle mass and increases energy expenditure [
38
]. Conversely, testosterone
is an anabolic hormone, which may also explain why in the study of Parr et al. mTOR phosphorylation
in the NO-ALC group was higher than the ALC-CHO (76%) and ALC-PRO (54%) group at 2 and 8 h
post-exercise. In addition, also rates of muscle protein synthesis were higher in the NO-ALC group
when compared to those who ingested ALC. However, muscle protein synthesis may also appear
decreased because of the decreased plasma levels of AA showed following ALC consumption. These
findings can have major implications with regards to the recovery and performance of both non athletes
and professional athletes. An acute bout of vigorous RE can result in a transient increase in protein
turnover and until feeding, protein balance remains negative [
39
,
40
]. Protein ingestion post exercise
enhances muscle protein synthesis and net protein balance [
41
] by increasing myofibrillar protein
fraction with RE [
42
], but as seen in the study of Parr et al. alcohol ingestion after RE has the ability to
J. Funct. Morphol. Kinesiol. 2019,4, 41 15 of 17
disrupt this process. Beyond physical aspects, decreased protein synthesis leads to impaired long-term
memory in humans [
43
–
45
], which can be particularly important in professional athletes who have
many cognitive demands with respect to both short and long term memory [17].
In regards to measures of force only study of Barnes et al. [
18
] showed that following ALC
consumption the levels of isometric, concentric and eccentric torque decreased, while other studies in
this review that measured force production showed no differences between the ALC and NO-ALC
groups during recovery following RE. As depicted in the results section, with respect to muscle function
and force, only study by Barnes et al. has shown that moderate consumption of alcohol can amplify the
loss of force associated with strenuous eccentric exercise [
18
]. This particular study detected significant
decrements in average peak isometric, concentric and eccentric torques at 36 h post-exercise [
18
].
Clearly more research is needed since the outcomes among the mentioned studies are quite distinct.
All measures of force were assessed from 2 h to 48 h post RT or ALC ingestion and the measures all
appear decreased because of the exercise performed. The retrieved measures of performance returned
to baseline within 2 days following both ALC consumption and the exercise bouts. Same trend is
shown for the other two measures of performance retrieved: power and muscular endurance which
decreased following the exercise bouts in both groups with no difference between those who consumed
ALC and those who did not.
Several limitations have been encountered during the realization of this manuscript. Firstly, a
very limited body of evidence was present within each screened database, on the topic of alcohol
consumption following bouts of RE, therefore it is not possible to consider such review comprehensive
and definitive. Few studies have evaluated in depth biological measures of protein synthesis or specific
markers of muscular function. Other important limitation is the timely evaluation of each study. Each
included measure was evaluated in a timeframe ranging from 2 h to 48h post exercise or alcohol
consumption. Therefore, only acute modifications were evaluated and it was not possible to consider
hormonal fluctuations beyond 2 days and their relative effects. Lastly, the total sample size of each
study was small ranging between 8 and 19 participants.
5. Conclusions
Alcohol consumption following resistance exercise doesn’t seem to affect the majority of the
retrieved biological and physical measures. However, levels of cortisol were increased, and levels
testosterone and rates of muscle protein synthesis were decreased, which indicates that long term
muscular adaptations could be impaired if alcohol consumption during recovery is consistent. Muscle
function doesn’t seem to be influenced by alcohol consumption during recovery. Studies with larger
cohorts evaluating the effects of alcohol consumption during recovery following resistance exercise are
needed to further understand the long-term effects of alcohol ingestion.
Supplementary Materials:
Supplementary materials can be found at http://www.mdpi.com/2411-5142/4/3/41/s1.
Author Contributions:
Conceptualization, N.L.; Methodology, N.L.; Writing – Original Draft Preparation, N.L.;
Writing – Review & Editing, N.L;
Funding: This research received no external funding.
Acknowledgments:
I would like to thank Kaltrina Feka and Valerio Giustino from PhD program in Health
Promotion and Cognitive Sciences at University of Palermo for helping me to do the article search and assess risk
of bias.
Conflicts of Interest: The author declares no conflict of interest.
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