Acute alcohol consumption aggravates the decline in muscle performance following strenuous eccentric exercise
Matthew. J. Barnes, a, , Toby Mündela and Stephen. R. Stannarda
aInstitute of Food, Nutrition, and Human Health, Massey University, Palmerston North, New Zealand
Received 23 July 2008; revised 8 December 2008; accepted 13 December 2008. Available online 20 February 2009.
Abstract
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 1 g/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 60 h following each exercise bout. All measures of muscle performance were significantly reduced at 36 and 60 h post-exercise compared to pre-exercise measures (all p < 0.05). The greatest decreases in peak strength were observed at 36 h 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.
Keywords: Ethanol; Creatine kinase; Muscle strength dynamometer; Athletic performance
Article Outline
-
Introduction
-
Methods
-
Results
-
Discussion
-
Conclusion
Practical implications
Acknowledgements
References
-
Introduction
Strenuous eccentric contractions produce micro-structural damage to skeletal muscle resulting in impaired muscular performance, inflammation, and soreness.1 Most running-based team sport events involve eccentric work and, particularly during competition, this results in varying levels of muscle damage.2 Rapid post-event recovery is necessary to enable adequate training and optimal performance during the following event, and consequently much effort is afforded to practices which enhance recovery processes.
However many sportspeople, particularly those involved in team-based sports, regularly ingest moderate to large volumes of alcohol (ethanol) in the hours after training or competition as a means of celebrating, socialising or bowing to sponsorship commitments.[3], [4] and [5] Yet, it is not known how this pattern of alcohol consumption affects recovery processes after eccentric exercise-induced muscle damage.
To date only one study has investigated the interaction of alcohol with recovery from eccentric exercise-induced muscle damage. Clarkson and Reichsman6 had subjects drinking either a beverage containing 0.8 g of ethanol/kg body weight or a non-alcoholic control beverage 35 min prior to performing 50 maximal eccentric contractions of the elbow flexor muscles. Although the exercise brought about significant amounts of muscle damage, as demonstrated by significant changes in all criterion measurements, no difference between treatments was evident in measures of plasma creatine kinase (CK) activity, muscle soreness, isometric strength or range of motion leading the authors to conclude that ingestion of alcohol does not impair recovery after eccentric exercise-induced muscle damage. As with much of the research into alcohol and physical performance7, in the Clarkson and Reichsman study alcohol was ingested prior to exercise rather during the much more common post-exercise period. Thus despite recommendations to the contrary, the available evidence does not seem to warrant abstinence from alcohol in the post-event period for the purposes of optimal recovery.
The purpose of this study was to compare the effects of post-exercise alcohol ingestion with that of an isocaloric non-alcoholic beverage on changes in muscle performance following a bout of strenuous eccentric exercise. We hypothesise that moderate amounts of alcohol ingested following eccentric exercise will not delay normal recovery of muscular performance.
- Methods
Eleven healthy males (23.9 ± 4.7 years; 87.6 ± 9.5 kg), who regularly participated in resistance training on a recreational basis and who were not naive to alcohol, volunteered to participate in this study. The protocol was approved by the Massey University Human Ethics Committee and written consent was obtained from each participant.
The study employed a one-legged model during each of two experimental trials (treatment and control) to enable a single cross-over on the contralateral leg. Leg and treatment were allocated randomly. The advantage of this design is that the participants are their own control, yet any residual effects in the muscle from the previous trial are negated. The latter is particularly important because of the well-described ‘repeated-bout’ adaptation which takes place following eccentric exercise-induced muscle damage.8
At least 1-week before the first experimental trial participants were familiarised with the Biodex® isokinetic dynamometer (Biodex Medical Systems, New York, USA) and the movements involved in the protocol. Participants were seated with the lateral femoral epicondyle aligned with the dynamometer axis of rotation and the ankle strap positioned approximately 5 cm proximal to the medial malleolus. Each participant’s seat position was recorded for subsequent trials.
At least two days later, participants attended the laboratory for the first experimental trial. Four hours prior to the start of each trial participants consumed a standard meal (4440 kJ). Immediately before testing participants warmed-up on a cycle ergometer (Monark, Varberg, Sweden) for 5 min at 100 W. Then once seated on the Biodex straps were fixed across the chest, hips and active leg to isolate movement to the quadriceps. Knee joint range of motion was set and recorded for use in follow-up tests. Five maximal isometric, concentric and eccentric contractions of the quadriceps muscles were then completed as tests of muscle performance. Isometric tension was measured 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)9. Absolute peak torque and average peak torque over five contractions was recorded. Each set was separated by 2 min of passive recovery.
Once performance tests were complete, participants remained on the Biodex and performed 300 maximal eccentric contractions using the quadriceps muscles of one leg. Participants were verbally encouraged to resist the downward action of the dynamometer arm as hard as possible and had access to visual feedback of their torque throughout the protocol to ensure continuous maximal effort. This eccentric exercise bout was divided into three sets of 100 repetitions separated by 5 min of passive recovery, during which time subjects remained seated. For the second trial the contralateral leg was damaged using the same protocol.
A 60° (1.05 rad) range of motion was set from maximal knee flexion (0°) using the dynamometers inbuilt goniometer. Repetitions were performed at an angular velocity of 30° s−1. Adapted from the work of MacIntyre and colleagues9, this protocol has previously been shown to bring about significant levels of muscle damage and soreness.
At the completion of the eccentric exercise bout participants consumed a standardised meal (1620 kJ). Then, 30 min after exercise, they began drinking a beverage containing either 1 g of alcohol per kg of body weight as vodka (Smirnoff, Australia) in orange juice (Frucor Beverages, New Zealand) (ALC) or a control beverage of orange juice alone (OJ). The treatment beverage was mixed in a 3.2:1 ratio of orange juice to vodka. Equivalent to 8.8 (±1) standard drinks, the mean volume of vodka consumed per participant was 235.9 ml (±25.5). The two beverages were balanced for fluid and energy value however participants consumed larger amounts of both vitamin C and carbohydrate in the OJ trial. Equal volumes of beverage were consumed every 15 min over a total time of 90 min. Once the required amount of beverage was consumed participants were driven home and instructed to go directly to bed. Participants returned to the laboratory for testing the following three mornings, having fasted overnight (≥12 h).
Ratings of muscle soreness were taken immediately post-drinking, and 12, 36, and 60 h later. Blood samples were collected prior to exercise, immediately post-drinking and 12 and 36 h later. Muscle performance tests, as described above, were repeated at 36 and 60 h post-drinking. Participants were instructed to abstain from any form of exercise and alcohol from 48 h before until 60 h after each damaging exercise bout and there were at least 10 days in between experimental trials.
Participants completed a questionnaire rating their current level of perceived muscle soreness on a subjective scale from 0 to 10 (0 = no soreness, 10 = very, very sore) as outlined by Sorichter et al.10 Soreness was rated while stepping up (concentric muscular contraction) onto a 40 cm box and lowering into a squatting position (eccentric contraction).
Each venous blood sample was obtained from the antecubital vein and collected into a 4 ml EDTA-containing vacutainer, placed on ice for 10 min, and centrifuged at 4 °C for 10 min at 805 × g. Plasma was aspirated into 300 μl aliquots and frozen at −80 °C for later analysis. CK activity was determined using a Vitalab Flexor clinical chemistry analyser (Vital Scientific NV, Netherlands) and a Roche CK-NAC liquid assay kit (Roche Diagnostics GmbH, Mannheim, Germany).
Data was 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 was used to compare conditions (alcohol and control) over time for each criterion measure. This analysis provided main effects of time and trial and the trial × time interaction. Paired-samples T-tests (two tailed) were carried out post-hoc to find the level of significance between each time point within a trial. To identify relationships between markers of muscle damage (muscle function, muscle soreness and CK activity) bivariate correlation tests were performed to find Pearson product correlation coefficients ®. Reported values are means ± 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, concentric and eccentric peak and average peak torque over time (all p < 0.001, Table 1). With the exception of average peak isometric torque, all post-exercise strength measures were significantly different between interventions (all p < 0.05) with the greatest decrements observed with ALC. After 36 h, all performance measures improved (p < 0.05) except ALC isometric peak torque and both OJ and ALC isometric average peak tension. Significant time × trial interactions were found for concentric (p = 0.02, Fig. 1), isometric, (p = 0.02) and eccentric (p = 0.01) peak torques as well as for concentric (p = 0.009) and eccentric (p = 0.008) average peak torque.
Table 1.
Changes in muscular performance following strenuous eccentric exercise.
Peak torque (Nm)
Average peak torque (Nm)
OJ
ALC
OJ
ALC
ISO
Pre 313.5 ± 5 6.5 311.8 ± 58.0 278.8 ± 46.1 271.8 ± 49.6
36 h 245.0 ± 21.2a 206.9 ± 21.2a,c 235.1 ± 45.6a 198.5 ± 46.5a
60 h 273.6 ± 50.7a,b 229.1 ± 57.3a,c 244.1 ± 42.8 210.4 ± 52.8a
CON
Pre 273.9 ± 50.1 274.0 ± 54.4 233.1 ± 46.8 245.5 ± 55.2
36 h 199.2 ± 45.0a 163.4 ± 45.9a,c 182.4 ± 69.2a 132.5 ± 39.6a,c
60 h 237.9 ± 44.5a,b 190.8 ± 40.7a,b,c 216.1 ± 65.6b 160.7 ± 40.2a,b,c
ECC
Pre 346.9 ± 68.8 353.0 ± 73.8 317.9 ± 69.1 325.1 ± 77.6
36 h 283.5 ± 74.1a 235.9 ± 45.8a,c 263.4 ± 77.5 217.4 ± 45.5a,c
60 h 323.3 ± 66.8b 289.3 ± 66.9a,b 303.7 ± 73.8b 261.4 ± 46.1a,b,c
Full-size table
Isometric (ISO), concentric (CON) and eccentric (ECC) force measurements made before and 36 and 60 h after 300 eccentric contractions of the quadriceps under control (OJ) and alcohol (ALC) conditions. All values are mean ± SD. Differences between time points were evaluated by post-hoc pairwise comparison. Significantly different from pre-exercise value – ap < 0.05. Significantly different from preceding value – bp < 0.05. Significant different from OJ treatment – cp < 0.05.
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Full-size image (4K)
Fig. 1. Peak concentric torque (mean ± SE) measurements made before and 36 and 60 h after 300 eccentric contractions of the quadriceps under control (OJ) and alcohol (ALC) conditions. Significant differences in values occur over time (p < 0.001) and between trials (p < 0.05) exist. A significant interaction effect exists (p < 0.05). Significantly different from preceding values – ap < 0.001, bp < 0.05.
View Within Article
Creatine kinase activity increased over time (p = 0.036) with all post-exercise values elevated above baseline levels. However, there was no trial × time interaction (p = 0.406), indicating that alcohol intake post-exercise does not modulate the increase in creatine kinase activity over time. Changes in CK activity appeared unrelated to alterations in muscular performance or ratings of muscle soreness.
Although soreness ratings while squatting and stepping up were higher (both p < 0.001) than pre-exercise values at all subsequent time points, no significant difference in ratings of soreness was evident between ALC and OJ conditions. Once elevated, above pre-exercise values ratings of soreness did not significantly change over time. Ratings of muscle soreness were unrelated to changes in muscular performance.
- Discussion
The primary purpose of this study was to investigate whether the consumption of alcohol after damaging exercise modulates muscle function during the subsequent 60 h. To our knowledge this is the first study to investigate this relationship, and contrary to our hypothesis, the first to show that alcohol consumed after heavy eccentric exercise leads to significantly greater decrements in dynamic and static torque when compared to an isocaloric non-alcoholic beverage. Warren et al.1 suggest that decreases in voluntary muscular strength best represent the magnitude of muscular damage occurring after eccentric exercise. Following this we could conclude that when combined with exercise-induced muscle damage, post-exercise alcohol consumption magnifies the damage, particularly over the first 36 h post-exercise. However, as mechanical damage to the muscle contractile elements can only occur during eccentric exercise, and because alcohol was provided after exercise, our results more accurately indicate that alcohol detrimentally affects the subsequent repair and recovery processes. Post-exercise alcohol consumption appears to have no effect on other commonly measured markers of muscle damage, namely ratings of muscle soreness and plasma CK activity.
Due to the study design, post-exercise carbohydrate and vitamin C intake was slightly different between trials, and this could potentially influence our results. However, this is unlikely as carbohydrate11 and vitamin C12 supplementation post-eccentric exercise have been found to have no effect on force recovery when compared to a placebo.
Completion of 300 maximal eccentric contractions of the quadriceps resulted in significant decreases in voluntary isometric, concentric and eccentric peak and average peak torques (Table 1). Greatest decreases in peak strength were observed at 36 h with losses of 12%, 28% and 19% occurring for OJ isometric, concentric and eccentric contractions, respectively. Peak strength loss was significantly larger in ALC with the same performance measures decreasing by 34%, 40% and 34%. The same trend was evident for concentric and eccentric average peak torque indicating that alcohol has an equally detrimental effect on repeated maximal muscular contraction, not just on single all out efforts. The greater loss of strength under ALC conditions over the first 36 h would likely result in delayed recovery of performance, even though strength improves at a similar rate to that seen in OJ between 36 and 60 h post-exercise.
Creatine kinase activity and ratings of perceived muscle soreness were both significantly elevated above pre-exercise values however no difference between interventions was evident. The absence of a significant difference in CK activity between trials may be due to large inter-subject variability. In the present study no more than three individual responses increased above 1000 U/L at any given time post-exercise. This corresponds with the observations of Nosaka and Clarkson13 and Miles et al.11 who found large inter-subject variability in CK activity following eccentric exercise-induced muscle damage in elbow flexors. Akin to the findings of Clarkson et al.14, Clarkson and Ebbeling15 and Nosaka et al.16 changes in CK activity observed in the present study were not associated with decreases in torque or to increases in ratings of perceived muscle soreness, further supporting the belief that CK activity is an unreliable indicator of the functional effects of muscle damage.1
As this is the first study of its kind, the mechanisms behind our findings are at this time unknown, however we can divide the observed effects of alcohol to its actions on central (nervous system) and/or peripheral (muscular) components of the contractile process. Prasartwuth et al.17 recently reported that decreased neural drive contributes to eccentric exercise-induced reductions in force for up to two days after a damaging bout of exercise. Alcohol consumed after damaging exercise may therefore, act directly on the central nervous system to further reduce the already depressed neural drive. Acute alcohol consumption has been shown to affect the innate immune system by altering the activity of a number of inflammatory proteins18, many of which play key roles in the damage and repair processes occurring after eccentric exercise.19 We can also speculate that an alteration in the activity of these proteins by alcohol may modify the inflammatory response and subsequent recovery of force. Further research is needed to identify the precise mechanism behind our findings.
The results of the present study are in contrast to those of Clarkson and Reichsman6 who found no effect of (prior) alcohol intake on eccentric-damage induced changes in strength, muscle soreness or CK activity over the 5 days following exercise. The important difference between the two studies is the timing of alcohol consumption with the present study better representing the drinking patterns of many sportspeople. That is, sports people are far more likely to consume large volumes of alcohol after undertaking strenuous exercise or competition than before. Although the volume of alcohol consumed in the present study is enough to be considered as binge drinking20, alcohol consumption by sportspeople often far exceeds these amounts.[3], [4] and [21] It may therefore prove beneficial to examine whether a dose–response effect exists whereby larger volumes of alcohol consumption are related to greater levels of muscle damage and accompanying loss of muscular function.
- Conclusion
Our observations that alcohol magnifies the severity of skeletal muscle injury and therefore delays recovery of strength over the following 24 h period suggests that participants in sports containing intense eccentric muscular work should be encouraged to avoid alcohol intake in the post-event period if optimal recovery is required.
Practical implications
• Post-exercise acute alcohol consumption magnifies exercise-induced muscle damage and related decrements in muscular performance.
Acknowledgements
This research was supported by a grant from Sport & Recreation (SPARC) New Zealand.
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