Ethanol use and abuse is at least as prevalent among athletes (especially men) as it is among nonathletes (35). Furthermore, the vast majority of athletes in the United States (approximately 80%) have begun drinking ethanol by the time they reach college/university (11). Although the number of National Collegiate Athletic Association athletes who use ethanol declined from 1997 to 2005, the incidence of binge drinking (more than five drinks in a sitting) increased significantly during the same period (11). In certain recreational sports settings, it is common for athletes to consume ethanol directly after or, in some cases, even during these events. Similarly, for the collegiate athletes who consume ethanol, approximately 50% reported doing so after competitions (33), and almost 60% believe that their use of ethanol does not affect their athletic performance or overall health (11).
Testosterone stimulates intramuscular uptake of amino acids and synthesis of muscle protein (16) and serves a vital role for the adaptations to resistance training (20,27). Acutely, heavy resistance exercise causes an elevation in serum total testosterone (TT) (39,40) and free testosterone (FT) (39,40) concentrations. Resistance exercise does not appear to change serum sex hormone-binding globulin (SHBG) concentration acutely unless combined with protein–carbohydrate supplementation (26). The testosterone-binding proteins, especially SHBG, regulate the biological activity of circulating testosterone. Approximately 44%–60% of TT is normally bound to SHBG (10,13), whereas the remainder is either bound loosely to other binding proteins or unbound (free); less than 2% of TT is free (13,39). SHBG effectively inhibits testosterone action, because only the testosterone not bound to SHBG is biologically active (36), with FT being the most active; thus, concentrations of SHBG and biologically active testosterone are inversely related.
At rest, ethanol intoxication in men acutely can suppress serum TT concentration for up to several hours after the ethanol ingestion (8,22,30,31). The effect of acute ethanol intoxication on SHBG is unclear; however, serum SHBG concentration is elevated in men who are alcoholics (3). Two different physiological effects of acute ethanol intoxication may be responsible for the reduction in TT: 1) Ethanol has an adverse acute effect on Leydig cell function (17), thus reducing testosterone production in the testes (18,37). 2) Ethanol increases the clearance of testosterone by conversion to dihydrotestosterone and estradiol by aromatase in the liver (7). The reduction in serum testosterone seen in men after ethanol intoxication may, therefore, be due to the combined effect of a lower synthesis rate and a higher clearance rate. Recently, several studies have found that acute high-dose ethanol ingestion (1 g of ethanol per kilogram body mass) disrupts muscle recovery (i.e., force production capability) from a bout of strenuous eccentric resistance exercise (5,6). Ethanol ingestion after a bout of resistance exercise could disrupt recovery by reducing the anabolic milieu (e.g., reduced testosterone bioavailability), which would lead to compromised adaptations from that exercise bout and, if repeated over time, to compromised training outcomes. Heikkonen et al. (19) found that ethanol ingestion (1.5 g of ethanol per kilogram body mass) after exhaustive cycle ergometer exercise had no apparent effect on the testosterone or cortisol response to exercise during the first 10.5 h postexercise, but it prolonged the depressant effect of alcohol on testosterone secretion (at approximately 21.5 h postexercise). In contrast to these findings, Koziris et al. (24) found that postexercise ethanol consumption (0.83 g of ethanol per kilogram body mass) resulted in higher TT and cortisol concentrations at 60–120 min into recovery from a bout of heavy circuit resistance exercise compared with when no ethanol was ingested.
Independently, resistance exercise and ethanol have opposite effects on circulating testosterone concentrations and its bioavailability. Despite the potentially important implications of acute alcohol ingestion for individuals involved in a physical conditioning program, only a single study (24) has examined the anabolic endocrine response to ethanol ingestion during the recovery from resistance exercise, and no investigations have examined the response on the bioavailable fraction of testosterone in this context. Thus, the purpose of this study was to examine the testosterone bioavailability and the anabolic endocrine milieu in response to acute ethanol ingestion after a bout of heavy resistance exercise.
MATERIALS AND METHODS
To examine the effect of ethanol ingestion after resistance exercise on testosterone bioavailability, a within-subjects repeated-measures design was used. Eight resistance-trained men completed two identical acute heavy resistance exercise tests (AHRET) separated by 1 wk. From 10 to 20 min post-AHRET, participants consumed either grain ethanol (EtOH condition) or no ethanol (placebo condition) diluted in an artificially sweetened and calorie-free beverage. Blood was collected before (PRE) and immediately after the AHRET (IP, before ethanol/placebo ingestion), and then every 20 min for 5 h. Blood collected after ethanol ingestion was pooled into three batches (phases: 20–40, 60–120, and 140–300 min postexercise) for biochemical analysis. PRE, IP, and pooled phases samples were analyzed for serum TT, FT, SHBG, cortisol, and estradiol concentrations; in addition, percent of TT that was free (%FTT), free androgen index (FAI), and testosterone-to-cortisol ratio (T:C) were calculated.
Eight men (21–34 yr; mean ± SD: 25.3 ± 3.2 yr, 87.7 ± 15.1 kg, 177 ± 7 cm, 15.1 ± 4.1% body fat) who were recreationally resistance trained (including the back squat) participated in this study. Participants were screened for any medical concerns that could confound the results of the study or place the participants at an elevated risk during the study. The participants were found to be free of relevant orthopedic and pathological conditions. To be included in the study, participants could not have used drugs such as glucocorticoids or anabolic–androgenic steroids within 1 yr before the start of the study.
Participants were screened for clinical signs of ethanol abuse using several questionnaires concerning their current and historic use of ethanol. To be considered for the study, the participants had to be low-to-moderate ethanol consumers (32). On the basis of the screening, participants were not ethanol dependent, did not have consumption-induced metabolic tolerance to ethanol, and were capable of tolerating the amount of ethanol ingestion required in this study without being affected in any extreme manner such as by nausea or flushing. After screening, fat-free body mass was measured using skin folds from seven sites (21). The study was approved by the University Institutional Review Board, and the volunteers provided written informed consent to participate.
Each participant completed both experimental treatments (EtOH and placebo) and thereby served as his own control. The treatments were performed 1 wk apart and administered in a balanced, randomized, crossover design. The participants were kept blind to the experimental conditions selected for that treatment day. To prevent participants from anticipating a particular treatment, they were informed that they could potentially receive the same treatment on both experimental treatments visits. Participants were required to consume the same diet for the 2 d before and the morning of each treatment visit (EtOH or placebo visit). Participants completed a diet record before the first treatment visit and were instructed to follow the same diet before the second treatment visit. All participants attested that they had complied with the diet instructions for their second visit.
Participants refrained from 1) eating or drinking anything (except for water and noncaffeinated diet drinks) during the 2 h leading up to each treatment visit, 2) any ingestion of ethanol for 84 h before each treatment visit, 3) consuming much caffeine on test day (no more than one cup of coffee allowed), 4) engaging in sexual activity for 24 h before each treatment period, and 5) performing any resistance exercise or intense aerobic exercise for 96 h before each visit. It was also required of the participants that they had not donated blood within 8 wk or plasma within 96 h of the laboratory visits. The participants attested that they had adhered to all instructions and that their records were accurate. All treatment visits began at the same time of day for each participant (1100 h arrival time for all participants) to avoid circadian influences.
An overview of the timeline for a treatment day is provided in Figure 1. Upon arrival at the laboratory on each treatment day, participants were screened for the presence of blood ethanol with a breathalyzer and were queried regarding compliance with study guidelines regarding diet, caffeine, sexual activity, ethanol, drugs, and exercise. Participants were asked to report to the laboratory in a euhydrated state. Upon arrival at the laboratory, hydration status was measured using urine refractometry; if participants presented with urine specific gravity ≥1.020, they were provided with cold water to drink. After the hydration status had been addressed, body mass was measured. Sixty-five minutes before the AHRET, participants consumed a standardized meal replacement drink (Ensure Plus®) containing 8 kcal·kg−1 body mass. After the meal replacement drink was ingested, a cannula was inserted in a superficial vein of the forearm.
Twenty-five minutes before the AHRET (40 min after the meal), participants completed a standardized warm-up, which consisted of 5 min of ergometer cycling at a low intensity followed by dynamic stretches (10 lunges, 20 heel kicks, 20 high knees, and 10 body weight moving squats). Fifteen minutes before the AHRET, participants completed a balance test and power tests (bench press throw and high pull at 30% of 1 repetition maximum (RM), maximal vertical jump), which were part of a different aspect of this project. Participants then completed 10 warm-up squats at 50% of 1 RM followed by the AHRET (39). The AHRET consisted of six sets of 10 repetitions of Smith machine squats starting at 80% of 1 RM and 2 min of rest between sets. If participants were not able to complete 10 repetitions on their own, they were assisted by the researchers to do so, and the load was reduced for subsequent sets. The same load for each set was used for both AHRET. After the completion of the AHRET, the participants sat quietly in a chair for the remainder of the test period and were not allowed to sleep. Blood ethanol concentration (BEC) was determined and blood samples were drawn according to the timeline presented in Figure 1. To prevent anxiety and boredom, the participants were permitted to read, write, or watch TV/movies during periods in which they sat quietly. They were asked not to become involved in any reading, writing, or TV/movie watching that would cause them to experience any form of stress, anxiety, or other strong emotions, either positive or negative.
The BEC was estimated from breath ethanol with an Alco-sensor IV (Intoximeters, St. Louis, MO). Standard gas was used to calibrate the instrument before and at regular intervals during each visit following manufacturer instructions. BEC was measured upon arrival at the laboratory, every 10 min from 40 to 100 min post-AHRET (measurement of BEC from breath immediately after ethanol consumption is not meaningful), and every 20 min from 100 to 300 min post-AHRET for both the EtOH and placebo condition. At no time were the participants allowed to know their BEC or whether they had received any ethanol during their visit. However, because of the obvious physiological and psychological effects of ethanol ingestion, participants were generally aware when they had received ethanol but could not easily discern when they had not received ethanol.
From 10 to 20 min post-AHRET, participants consumed either grain ethanol (EtOH condition) or no ethanol (Placebo condition) in an artificially sweetened and calorie-free beverage. For the EtOH condition, a dose of 1.09 g of ethanol (Everclear grain alcohol, 95% v/v ethanol; Luxco, St. Louis, MO) per kilogram of fat-free body mass (mean: 0.94 ± 0.05 g·kg−1 body mass; range: 0.84–1.01 g·kg−1 body mass, 82–122 mL of 95% v/v ethanol) was diluted to a concentration of 19% v/v absolute ethanol; for the placebo condition, the ethanol was substituted with an equal volume of water. The participants drank 1/10 of the drink each minute during the 10-min ingestion period. To reduce the ability of the participants to differentiate between the drinks (i.e., taste of EtOH), participants wore a nose clip during each drinking ingestion.
Heart rate and RPE
Upon arrival at the laboratory, immediately after each set of squats during the AHRET, and at each blood draw during recovery from exercise, heart rate was measured using a standard heart rate monitor with telemetry (Polar, Lake Success, NY). RPE was assessed at PRE and after each set of squats during the AHRET using the category-ratio (CR-10) scale of perceived exertion (34).
On treatment days, a Teflon-coated cannula (Vascular Access; Becton-Dickerson, Sandy, UT) was inserted in a superficial vein of the forearm while the participants were seated. Cannula patency was maintained with sterile saline (0.9% sodium chloride injectable, USP; Hospira Inc., Lake Forest, IL), and blood was drawn while participants were seated. Blood was collected 5 min before the AHRET (PRE), immediately after the AHRET (IP), and every 20 min for the 300 min after the AHRET (Fig. 1).
Blood was allowed to clot at room temperature (approximately 21°C) and subsequently was centrifuged at 1500g at 4°C for 15 min. The resultant serum was stored in several aliquots at −80°C until analysis. Samples for PRE and IP were analyzed individually. The remaining samples were pooled into three batches (phases: 20–40, 60–120, and 140–300 min postexercise) following the methods of Koziris et al. (24) for later hormone and binding protein analysis.
A small portion of whole blood obtained at PRE, IP, and 20, 40, 60, 120, 180, 240, and 300 min postexercise was analyzed immediately for lactate, hematocrit, and hemoglobin. Blood lactate was determined using an automated Lactate Plus analyzer (Sports Resource Group Inc., Hawthorne, NY) to characterize the metabolic demands of the exercise; the Lactate Plus analyzer has been validated against a standard bench top method (4). Hematocrit was measured by standard microcapillary technique, and hemoglobin concentration was determined using an automated analyzer (Hb201; HemoCue AB, Angelholm, Sweden). Plasma volume change (percent) was calculated using the hematocrit and hemoglobin values (12). Circulating hormone and binding protein concentrations were not corrected for plasma volume changes because of the molar exposure at the tissue level. The TT, FT, SHBG, cortisol, and estradiol concentrations were analyzed using commercially available enzyme-linked immunosorbent assays (Alpco, Salem, NH). The intraassay variances (CV) were as follows: TT, 8.8%; FT, 8.5%; SHBG, 4.8%; cortisol, 5.7%; and estradiol, 11.3%. The samples were not decoded until after the analysis was completed (blinded analysis). The FAI (ratio of TT to SHBG: 100 (TT) / (SHBG)) and the TT-to-cortisol ratio (T:C) (TT / cortisol) were calculated for all time point/phases examined. All samples for a particular time point/phase were analyzed in duplicate within the same assay batch to eliminate potential interassay variance for a particular variable.
Data for HR and RPE were each averaged across the six sets and the average value used for further analysis. Data for FAI and estradiol were log10 transformed before analysis. For each variable, data were analyzed using a two-way ANOVA (treatment × time phase/point) with repeated measures on both factors. Where appropriate, Fisher least significant difference post hoc test was used for pairwise comparisons. The α-level of significance was set at P ≤ 0.05. The Statistica software package (StatSoft, Inc., Tulsa, OK) was used for all statistical analysis. Data are presented as mean ± SD.
For all participants, BEC peaked (0.088 ± 0.015 g·dL−1) 60–90 min postexercise on ethanol ingestion days and gradually dropped to 0.033 ± 0.009 g·dL−1 at 300 min postexercise. BEC was 0.000 g·dL−1 at PRE for EtOH and at all time points for placebo. Significant main effects of time (P ≤ 0.05) were found for markers of metabolic demand (blood lactate, HR, and RPE). Blood lactate concentration, HR, and RPE increased significantly during the AHRET, peaking at IP (lactate: EtOH, 12.7 ± 1.6 mmol·L−1, placebo, 12.9 ± 1.5 mmol·L−1; HR: EtOH, 174 ± 13 bpm, placebo, 179 ± 8 bpm; RPE: EtOH, 7.8 ± 2.3, placebo, 7.4 ± 2.0), and then gradually decreased during recovery until reaching a plateau (at or below PRE values) 120 min post-AHRET (RPE) and 180 post-AHRET (HR and lactate). There was no difference for the lactate, HR, or RPE response between conditions. Plasma volume was significantly reduced at IP (EtOH, −11.5% ± 4.9%; placebo, −12.6% ± 7.1%) and returned to baseline at 20 min post-AHRET; there were no differences between conditions for plasma volume change throughout recovery.
A significant interaction effect (treatment–time phase/point) was found for TT (Fig. 2). Compared with PRE, serum TT was significantly elevated at IP for both conditions and at 140–300 min for EtOH; furthermore, compared with PRE, TT was significantly decreased at 60–120 and 140–300 min for placebo. Serum TT was significantly higher for EtOH than for placebo at 60–120 and 140–300 min. A significant interaction effect was also found for FT (Fig. 2). Compared with PRE, serum FT was significantly elevated at IP and 20–40 min for both conditions and at 60–120 min and 140–300 min for EtOH. Serum FT was significantly higher for EtOH than for placebo at 60–120 and 140–300 min. A significant main effect of time was found for %FTT (Table 1). Compared with PRE, %FTT was significantly higher at 140–300 min. No differences between conditions were noted for %FTT.
A significant main effect of time was found for SHBG (Table 1). Compared with PRE, SHBG was significantly elevated at IP and significantly decreased at 60–120 min. No differences between conditions were noted for SHBG. A significant interaction effect was observed for FAI (Table 1). Compared with PRE, the FAI was significantly higher at 20–40, 60–120, and 140–300 min for EtOH, and there was a trend (P = 0.06) for a higher FAI at IP compared with PRE for placebo. The FAI was also significantly higher for EtOH than for placebo at 140–300 min.
A significant main effect for time was found for cortisol (Table 1). Cortisol was significantly elevated at IP, 20–40 min, and 60–120 min and significantly decreased at 140–300 min compared with PRE. Cortisol concentrations were not affected by ethanol ingestion during recovery. A significant interaction effect was found for the T:C ratio (Table 1). Compared with PRE, the T:C ratio was significantly lower at 20–40 min for both conditions and at 60–120 min for placebo; furthermore, compared with PRE, the T:C ratio was significantly higher at 140–300 min for EtOH. In addition, the T:C ratio was significantly greater for EtOH compared with placebo at 140–300 min, and there was a trend (P = 0.08) for a greater T:C ratio for EtOH compared with placebo at 60–120 min. A significant main effect of time was found for estradiol (Table 1). Estradiol was significantly elevated at IP and 20–40 min compared with PRE. Estradiol concentrations were not affected by ethanol ingestion during recovery.
This is the first study to examine the effect of postresistance exercise ethanol ingestion on testosterone bioavailability in men. The findings from this investigation provide unique physiological insight regarding ethanol’s effect on the anabolic endocrine milieu during recovery from resistance exercise. The major finding of this study was that ethanol substantially elevated serum TT or FT concentrations during recovery from a bout of resistance exercise. Contrary to what was expected based on findings for ethanol ingestion in the absence of exercise, TT and FT concentrations were significantly higher for EtOH compared with placebo from 60 to 300 min post-AHRET (40 to 280 min after ethanol ingestion). Several confounding factors such as hydration state were controlled in this investigation to allow for the findings to be attributed to the ethanol ingested. It had been hypothesized that postexercise ethanol ingestion would significantly decrease TT and FT below the values observed for placebo at corresponding time points/phases due to the suppressive effect of ethanol on testosterone production in the Leydig cells of the testis (1,18,37) and the increased clearance of testosterone by aromatase in the liver (7). It appears that ethanol ingestion after heavy resistance exercise results in a testosterone response pattern that differs markedly from the pattern found when ethanol is ingested in the absence of prior resistance exercise.
Consistent with previous findings for TT and FT responses to an acute bout of heavy resistance exercise involving the lower body (2,39), serum TT and FT were elevated immediately after the AHRET (before drink ingestion). The elevation in TT and FT at IP was not accompanied by an elevation in the %FTT. This suggests that the acute bout of resistance exercise caused a similar relative elevation in the concentration of TT and the most bioactive portion of testosterone (i.e., FT) at IP. After ingestion of the placebo drink, TT and FT returned to or below PRE by 60–120 min and remained as such at 140–300 min. The return to or below baseline concentrations within 1 h postexercise is consistent with the TT and FT response observed previously after the AHRET and similar heavy resistance exercise protocols (2,39). For the EtOH condition, TT and FT were elevated at 60–120 and 140–300 min compared with corresponding PRE and time phase for placebo. Our findings are in contrast to those of Heikkonen et al. (20) who found that consuming a large dose of ethanol (1.5 g ethanol·kg−1 body mass, ingested over 3 h) after exhaustive cycle ergometer exercise did not affect TT during the first 10.5 h postexercise (measured every 2 h starting 30 min postexercise). In what appears to be the only previous study on the neuroendocrine response to postresistance exercise alcohol consumption, Koziris et al. (24) found that ethanol ingestion (0.83 g·kg−1 body mass, a dose slightly less than that used in the present study) prevented a drop below baseline (rebound low) in TT at 60–120 min after exercise compared with a no-exercise and placebo drink condition; FT was not investigated. Because a similar ethanol dose was used, the difference between the current findings for TT and those of Koziris et al. (24) is potentially due to the difference in the exercise protocols used by the two studies. Koziris et al. (24) used a circuit protocol that did not produce the large acute elevation in TT, which is usually found after heavy resistance exercise in men (as it was in the current study).
The mechanism for this prolonged elevated testosterone concentration after postexercise ethanol ingestion is not clear and thus remains speculative. The elevation in TT and FT found for EtOH could involve 1) increased testosterone production and release, 2) decreased testosterone clearance by liver, and/or 3) decreased uptake by muscle tissues. At rest, ethanol ingestion or injection of ≤1 g·kg−1 body mass can result in either no change or an elevation in TT for men, whereas doses >1 g·kg−1 body mass result in a reduction in TT (9,14,15,29). It is not known how lower doses of ethanol (≤1 g·kg−1 body mass) might cause an elevation in circulating testosterone, but large doses are known to suppress testosterone production in the Leydig cells of the testis (18,37). The current investigation involved ethanol ingestion of 0.84–1.01 g·kg−1 body mass over a short period (10 min). It is possible that the dose of ethanol used in this study was too low for an ethanol-induced decline in bioavailable testosterone to occur. Although the dose of ethanol ingested in the present study (approximately 5.3 drinks in 10 min for a 70 kg man with 15% body fat) was an appreciable amount, it was less than that often experienced in real-life settings (28). Future investigations should examine testosterone bioavailability after postexercise ingestion of larger doses (>1 g·kg−1 body mass) of ethanol.
Ethanol is known to increase the conversion of testosterone to estradiol by aromatase in the liver (7) and thus to increase testosterone clearance from circulation; a suppressive effect of ethanol on aromatase has not been demonstrated. In the current study, there were no differences in estradiol concentrations between conditions, although it could appear visually that the estradiol concentration was higher for EtOH in the latter phases of recovery. Thus, the elevation in testosterone likely is not due to a reduction in hepatic clearance. In the absence of ethanol ingestion, muscle androgen receptor content is elevated during later parts of recovery (60 min postexercise) from resistance exercise compared with immediately postexercise in men (25,39). Consistent with these findings (25,39), the reduction in TT for the placebo condition at 60–120 and 140–300 min postexercise could be caused by an increased testosterone uptake due to an increase in muscle androgen receptor content and potentially receptor affinity for testosterone. It has previously been found that chronic ethanol ingestion (approximately 6 wk) in male rats reduces the androgen receptor content of the predominantly Type II muscle fiber rectus femoris and prevents a training-induced increase in the androgen receptor content of the predominantly Type I muscle fiber soleus (38). It seems that ethanol interferes with the androgen receptor expression in muscle fibers. Therefore, the prolonged elevated concentrations of TT and FT after postexercise ethanol ingestion might be due to an acute ethanol-induced reduction in the muscle androgen receptor content compared with that after resistance exercise alone (i.e., placebo). Regardless of the mechanism involved, it appears that postexercise ethanol ingestion can cause an elevation in TT and FT during the later parts of recovery (60–300 min) from resistance exercise. Future research should examine potential mechanisms for this augmenting effect of ethanol ingestion on the testosterone response during recovery from heavy resistance exercise.
Ethanol ingestion had an effect on only one (i.e., FAI) of the two indirect measures of testosterone bioavailability (%FTT and FAI). Because SHBG binds to and prevents bioactivity of testosterone, the FAI has been used in lieu of FT as a measure of bioavailable testosterone, although the validity of FAI has long been questioned (23). Compared with PRE, FAI was higher at all time phases after alcohol ingestion; no changes over time were found for placebo. Despite this divergent response pattern, FAI was higher for EtOH compared with placebo only at 140–300 min. Because SHBG concentration and %FTT did not differ between conditions, the elevation found for measures of bioavailable testosterone (FT and FAI) with EtOH appears to be largely due an elevation in TT.
Cortisol was elevated during the first 2 h after the AHRET (i.e., at IP, 20–40 and 60–120 min), but no difference was noted between conditions. This cortisol response follows the pattern commonly found after acute heavy lower-body resistance exercise (2). The lack of difference between conditions is in contrast to the findings by Koziris et al. (24) who found that cortisol was elevated longer during recovery after postexercise ethanol ingestion; however, in that study, the cortisol concentration returned to or below baseline by 60–120 min for the placebo condition and by 140–300 min for the ethanol condition. In the current study, cortisol returned to (below) baseline by 140–300 min for both conditions, and thus, there is no difference between the two studies for the duration of the elevation in cortisol for the ethanol ingestion conditions. The T:C ratio is a crude measure of the anabolic/catabolic endocrine milieu. This ratio largely followed the response pattern of TT, with a greater T:C ratio for EtOH compared with placebo at 140–300 min postexercise. Although the T:C is a crude measure, its response shows that the elevation in testosterone in the latter stages of recovery after ethanol ingestion is not associated with a corresponding elevation in cortisol, a hormone with catabolic and antianabolic physiological effects. The results for the T:C ratio suggest that a more anabolic milieu exists during the latter stages of recovery from resistance exercise after ethanol ingestion. To date, no study has investigated the effect of postexercise ethanol ingestion on protein accretion, but negative effects of ethanol on muscle strength recovery have been found (5,6); unfortunately, in those studies, the hormonal response was not investigated. It remains unclear how the elevated testosterone bioavailability and anabolic milieu found with ethanol ingestion in the current study affect muscle adaptations to resistance exercise.
In conclusion, postexercise ethanol ingestion changed the total concentration and bioavailability of testosterone. The postexercise ingestion of ethanol elevated TT and FT concentrations at 60–300 min postexercise compared with ingestion of the placebo drink. The increase in testosterone bioavailability did not appear to be caused by changes in %FTT, SHBG, or hepatic clearance of testosterone because there were no differences between conditions for these variables at any time phase after ethanol ingestion. It follows that either testosterone release was increased by postexercise ethanol ingestion or that muscle uptake was reduced by postexercise ethanol ingestion (or both).
Thus, the primary finding of this study, that total and bioavailable testosterone concentrations were elevated acutely after postresistance exercise ethanol ingestion, should be interpreted with care. If testosterone release is increased, this could be beneficial; however, if muscle uptake is reduced, this could be detrimental to the desired adaptations. Acute ethanol ingestion has adverse consequences on muscle strength recovery from exercise (5,6) and on other aspects of the endocrine response (e.g., elevated acute cortisol) (24). Long-term ethanol use has negative effect on muscle tissue (e.g., preventing an increase in muscle androgen receptor content from resistance training) (38). Therefore, the findings of in the present study should not be seen by coaches and athletes as evidence that ethanol ingestion after resistance exercise is beneficial to their conditioning program.
J.V. was supported for this work by a Junior Faculty Summer Research Award from the University of North Texas. There is no conflict of interest to report for JV, DH, HB, and AD.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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Keywords:© 2013 American College of Sports Medicine
FREE TESTOSTERONE; SHBG; CORTISOL; ESTRADIOL; ALCOHOL; FREE ANDROGEN INDEX