Journal of the American College of Nutrition, Vol. 20, No. 1, 58-64 (2001)
Published by the American College of Nutrition
Effect of Alcohol on Postprandial Lipemia with and without Preprandial Exercise
Paolo M. Suter, MD, MS, FACN,
Margreta Gerritsen-Zehnder, MD,
Erik Häsler, MD,
Magdalen Gürtler, MD,
Wilhelm Vetter, MD and
Edgar Hänseler, PhD
Medical Policlinic, Department of Internal Medicine (P.M.S., M.G.-Z., E.H., M.G., W.V.), Zürich, Switzerland
the Institute of Clinical Chemistry (E.H.), University Hospital, Zürich, Switzerland
Address correspondence to: Paolo M. Suter, MD, MS, Medizinische Poliklinik, Universitätsspital, Rämistrasse 100 8091 Zürich, Switzerland. E-mail:polpms{at}usz.unizh.ch.
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ABSTRACT
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Objective: Different factors such as exercise habits and alcohol consumption may modulate postprandial lipid metabolism. What are the effects of alcohol on postprandial metabolism in untrained and trained individuals?
Methods: The postprandial lipid response to an oral fat load (1 g fat per kg body weight (bw)) with and without alcohol (0.5 g/kg bw) was evaluated in physically trained healthy young men (T, n=12, mean ±SD age 27 ±3 years, BMI 21.6 ±1.4 kg/m2) after a premeal running session and in untrained healthy young men (UT, n=8, age 24 ±1 years, BMI 23.2 ±1.8 kg/m2) without a premeal exercise session. The T subjects ingested 35.5 ±2.7 g alcohol, the UT subjects 38 ±0.6 g. Fat was given as butter and the carbohydrates as marmalade and zwieback (rusk). The T subjects received 1.20 ±0.05 g fat and 1.02 ±0.04 g carbohydrates per kilogram lean body mass. The corresponding numbers for the UT subjects were 1.28 ±0.08 g and 1.20 ±0.06 g. The postprandial lipemia was observed for an eight-hour period.
Results: Alcohol led to an increase to the triacylglycerol area under the curve (AUC) in the T subjects from 7.4 ±0.4 mmol/L * h on the control day to 11.3 ±0.9 mmol/L * h (p=0.001). The corresponding numbers in the UT subjects were 13.4 ±2.3 mmol/L * h to 19.4 ±3.5 mmol/L * h (p=0.004). Alcohol intake and physical activity training were the major determinants of the triacylglycerol (TG) AUC in these subjects.
Conclusion: The ingestion of a high fat meal in combination with alcohol leads to an increased in the postprandial lipemia independently from the level of training. It is suggested that this unfavorable effect of alcohol and a high fat diet could be modified by fat restriction or a combination of a premeal exercise session and a higher level of physical activity training.
Key words: postprandial lipemia, alcohol, triacylglycerol, exercise, dietary fat, atherosclerosis
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INTRODUCTION
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More than 20 years ago, Zilversmit postulated that postprandial metabolic phenomena may play a role in the pathogenesis of atherosclerosis [1]. The latter concept has been supported by different studies [2–6]. Lipid changes during the postprandial phase, such as an increase in the concentration of chylomicrons and triacylglycerol, may play a causal role in the development and the progression of atherosclerosis. Exercise and physical activity represent an important element in the prevention of atherosclerosis and coronary artery disease [7,8]. Favorable alterations of the postprandial lipid metabolism have been found in physically-active subjects [9–12]. Alcohol may have cardioprotective effects [13–15] and has been reported to lead to an increase in fasting and postprandial triacylglycerol levels [16,17]. Many healthy individuals follow the recommendation of exercise to lower the risk of coronary artery disease, and quite a few sportsmen ingest food in combination with alcoholic beverages after their exercise sessions [18,19]. Accordingly, we evaluated the postprandial lipid response to an oral fat load with and without alcohol in trained healthy young men after an exercise session (Study 1) and in untrained healthy young men without prior exercise (Study 2).
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MATERIAL AND METHODS
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Study 1
Subjects.
Twelve young healthy men were studied. Their mean age was 27.5 ±2.5 years (mean ±SD), mean body weight 69 ±5 kg, mean body mass index 21.6 ±1.4 kg/m2 and fat mass of 11.5 ±2.5 kg. All subjects were physically well trained (abbreviation for this group "T" for trained) and reported regular (i.e., nearly daily) jogging and running as their predominant type of physical activity. Six of them were moderately trained, i.e., pursuing running only three to five times per week in the form of short distance jogging sessions of about 30 to 50 minutes; six of the subjects were highly trained, i.e., pursuing a running training on five to seven days per week of approximately 40 to more than 60 minutes a day. The characteristics of the subjects are summarized in Table 1. Their body weight had been stable for the previous three months, they underwent a normal physical examination and medical history and did not take any medications, and their usual ethanol intake was 49 ±9 grams per week. All were non-smokers. The study protocol was approved by the Ethics Committee of the Medical Faculty of the University Hospital Zürich, and each man gave written consent before entering the study. The participation in the study was voluntary. During the study period the subjects had to pursue their usual life style and especially their usual physical activity pattern and level of exercise training. Three days before each test they had to abstain from any strenuous physical activity as well as sports activity, and they were not allowed to ingest any alcoholic beverages.
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Table 1. Age, Anthropometric Characteristics, Usual Physical Activity and Usual Alcohol Intake of the Participants in Study 1 (Trained) and Study 2 (Untrained) (Mean ±SD)
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Study Design
After an overnight fast of at least 12 hours, the men were studied for an eight-hour postprandial period on two different days, separated by 13 ±6 days. On the test day subjects were admitted to the University running track at 7:00 am. After a resting period of about 30 minutes, a first sample of blood was drawn by venipuncture immediately before the start of the exercise session. On each morning of the two testing days subjects had to run 5.4 km. On the first test day, subjects were instructed to run at a speed at which they would feel comfortable and could maintain for the entire distance. After each lap, the lap time was recorded. Heart rate was monitored using a commercial heart rate monitor (Polar Vantage NVTM, Polar Electro Oy, Kempele, Finland). On the second test day, subjects had to run at the same speed and same constant heart rate. Since intermediate times were taken the subjects could run at a constant speed. On the alcohol and the control day mean running time (23:55 ±01:25 vs. 25:00 ±01:08 minutes:seconds), speed (13.75 ±0.9 vs. 13.15 ±0.6 km/hour) and the heart rate (170 ±8 vs. 171 ±6 beats per minute) were statistically not different. After the exercise session, subjects were relocated from the running track to the University Hospital. There, the subjects were placed in a semi-recumbent position on a bed and a cannula was inserted into a cubital vein and a fasting postexercise (premeal) blood sample was taken (corresponding to time point "0" in Fig. 1). About 40 ±5 minutes after termination of the exercise session, the meal was given to the subjects. The meal contained one g of fat per kg body weight either with or without ethanol. The sequence of the experiments (i.e., with or without alcohol) was conducted in random order. The energy content of the meal was 3602 ±83 kJ and the proportions of protein, carbohydrates and lipids of the meal were identical on both test days: 3% (6 ±0 g protein), 27% (59 ±1 g carbohydrates) and 70% (69 ±5 g fat), respectively. The energy substrate intake (mean ±SD) for protein, carbohydrates and fat was 0.10 ±0.01 g, 1.02 ±0.04 g and 1.20 ±0.05 g per kilogram lean body mass (LBM), respectively. Fat was given as butter and the carbohydrates as marmalade and zwieback (rusk) (all products from Migros Genossenschaftsbund, Zürich, Switzerland). The energy content of the table butter used was 742 kcal/100 g (the fat content 82 g/100 g), the carbohydrate and protein content 0.5 g/100 g. The energy content of the zwieback was 416 kcal/100 g (the fat content was 6 g/100 g; the carbohydrate content 79 g/100 g and the protein content 10 g/100 g). The marmalade was given as quince jelly containing 268 kcal/10 g with a carbohydrate content of 66 g/100 g. On the ethanol day, the men received 0.5 g ethanol per kg bw. Mean intake of ethanol was 34.5 ±2.7 g as a 10% (v/v) water solution. On the control day, the same meal with an identical volume of normal tap water was given (427 ±33 mL). The meal including the drink had to be ingested within five minutes. One third of the drink was taken before, one third during and the remaining third after the meal.
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Fig. 1. Time course of the serum triacylglycerol concentration for eight hours after the ingestion of the test meal with (•) and without ( ) alcohol. The "0" time-point corresponds to the fasting concentration just before the meal for the untrained (n=8, Study 2 left graph). For the trained subjects the "0" time-point corresponds to the fasting value before the meal after the exercise session (n=12, Study 1 right graph). All values are mean ±SEM.
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The first two postprandial blood samples were drawn at 30 and 60 minutes after the ingestion of the meal, thereafter hourly except at the 5th and 7th postprandial hours when no blood was drawn. EDTA plasma was immediately analyzed for lipid composition and ethanol. During the test, the subjects were seated in a semi-recumbent position on a bed and were allowed to read, study or sleep. Walking or any other type of physical activity was not allowed. On both test days, 200 mL of normal tap water was given to the subjects hourly to maintain an adequate hydration state. During the interval between the two test days the subjects were instructed to pursue their usual diet and physical activity patterns.
Study 2
This study was performed to evaluate the effect of alcohol on the postprandial metabolism in untrained (UT) healthy young men without a premeal exercise session (n=8). "Untrained" was defined as no regular leisure time physical activity, in particular no regular aerobic endurance training in the form of running and/or jogging. All subjects reported themselves not to be sportsmen. Age and anthropometric characteristics of UT subjects are summarized in Table 1. The usual alcohol intake of these subjects was 40 ±9 grams of ethanol per week.
The design of the Study 2 was identical to that of Study 1, except that there was no exercise session before the ingestion of the test meal. Body weight was stable for three months preceding the study. All subjects had normal results from a physical examination and medical history, and none took any medications. All subjects were non-smokers, except one man who smoked irregularly and did not smoke during the entire study period. The two test days were 8 ±2 (mean ±SD) days apart. The sequence of the test days (i.e., alcohol vs. control) was randomized. The energy content of the meals in Study 2 was 4137 ±115 kJ, and the proportions of protein, carbohydrates and lipids of the meal were identical on both test days: 2% (5 ±0 g), 28% (71 ±2 g), and 70% (76 ±8 g), respectively. The energy substrate intake (mean ±SD) for protein, carbohydrates and fat was 0.08 ±0.01 g, 1.20 ±0.06 g and 1.28 ±0.08 g per kilogram LBM, respectively. Food items were identical to those in Study 1. On the alcohol day, the men also received 0.5 g ethanol/kg bw. The mean (± SD) intake of ethanol was 38 ±0.6 grams, which was ingested as a 10% (by vol) water solution (518 ±8 mL). The same volume was ingested as plain water on the control day. The procedures of the blood sampling and handling as well the methodology of the biochemical determinations and statistical analysis were identical to those in Study 1, except that during the initial five postprandial hours blood was drawn every 30 minutes.
Biochemical tests
The plasma triacylglycerol (TG), free fatty acid (FFA), insulin, glucose and ethanol were analyzed immediately in the Institute of Clinical Chemistry of the University Hospital, Zürich, using standard techniques [20]. The between-batch analytical variations (CVs) for triacylglycerol, glucose, insulin and FFA in our assays were 2% to 4%.
Body Composition
Body weight and height were measured by standard devices used in our hospital. Body composition was determined following the methodology of Durnin and Womersley based upon the measurement of four skinfolds [21].
Statistical Analysis
All values are expressed as mean ±SEM except where stated. The postprandial responses of the different parameters were evaluated as absolute values at each time point and as area under the curve for each period of one hour (AUC) and for the eight-hour postprandial period (AUC8, i.e., sum of each one hour AUC over the eight-hour period), following the trapezoidal rule [22]. For the AUC data we used a repeated measures design to study the effects of alcohol and exercise/training. In addition the results from the control day and the days when ethanol was ingested were compared by standard statistical methods, including the paired t-test when applicable. All p values are two tailed. All statistical tests were performed with JMPTM (SAS Institute, Cary, NC, USA) and SPSS Advanced Statistics (Chicago, IL) statistical software programs for PC.
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RESULTS
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Study 1
Table 2 summarizes the fasting concentration of selected variables for the control and alcohol days. The AUC of the selected parameters for the eight-hour period on the different test days are summarized in Table 3. The triacylglycerol AUC on the alcohol day increased by 54 ±11% over the AUC of the control day. The time course of the triacylglycerol concentration on the different test days is shown in Fig. 1. The exercise session led to a decline of the serum triacylglycerol concentration of 0.16 ±0.03 mmol/L on the control day (p < 0.001, as compared to the preexercise concentration) and of 0.17 ±0.03 mmol/L on the alcohol day (p < 0.001); the exercise induced reduction on the two test days was identical. On the alcohol day the triacylglycerol concentration was significantly higher at the end of the test as compared to the (postexercise) premeal value (difference 0.27 ±0.11, p < 0.05), but not statistically different from the preexercise concentration (Fig. 1). At the end of the eight-hour period on the control day, the triacylglycerol levels were not different from the concentration after the exercise but significantly lower than before the exercise (difference 0.23 ±0.07, p=0.007). There was a nonsignificant relationship between the fasting triacylglycerol concentration (before and/or after the exercise) and the maximal postprandial response on neither test day. The maximal alcohol concentration was 12.0 ±1.1 mmol/L.
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Table 2. The Fasting Concentration for Selected Biochemical Variables on the Two Test Days in the Trained and Untrained Subjects1
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Table 3. Area Under the Curve (AUC) over the Eight-Hour Postprandial Period for Selected Biochemical Plasma Parameters for the Control and Alcohol Meals in the Trained and Untrained Subjects1
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Study 2
Fasting (i.e., levels before the meal) concentrations of selected biochemical variables on the two test days are summarized in Table 2. The time course of the serum triacylglycerol concentrations in the fasting state and for eight hours after the ingestion of the test meal with and without alcohol are shown in Fig. 1. The area under the curve for selected parameters is summarized in Table 3. The triacylglycerol AUC on the alcohol day increased by 46 ±10% over the AUC of the control day. There was a significant relationship between the fasting triacylglycerol concentration and the following maximal postprandial response on the alcohol (r=0.74, p < 0.05) and the control day (r=0.73, p < 0.05). The maximal alcohol concentration in the UT subjects was 13.9 ±2.8 mmol/L.
As shown in Table 3, alcohol affected the AUC of triacylglycerol, FFA and glucose significantly independently from the study group. The factor exercise and training affected the triacylglycerol AUC and insulin AUC significantly.
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DISCUSSION
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Accumulating evidence indicates that increased triacylglycerol levels, especially during the postprandial period, may promote the development and progression of atherosclerosis [1–6]. This descriptive study shows that the ingestion of alcohol with a high fat meal led to an increased postprandial triacylglycerol response in physically trained subjects performing a premeal exercise jogging session (Fig. 1). In Study 2 the same pattern of response, although with higher levels of the postprandial lipemia, was found in physically untrained subjects.
In both studies alcohol induced an increase in the postprandial lipemia. Several factors may contribute to the alcohol effects on postprandial lipemia: alcohol suppresses lipid oxidation [23] and leads thus to a higher availability of lipids which compete for the lipoprotein lipase. In addition the acute ingestion of alcohol leads to a suppression of the extrahepatic lipoprotein lipase (LPL) activity, thus slowing down the clearance of serum triacylglycerol [24]. Although we do not have any specific biochemical measurements of the LPL activity, it can be assumed that both factors have been operational independently from the study group.
Physical active individuals do have a more favorable fasting as well as postprandial lipid profile [9,12,25,26]. Exercise may affect postprandial lipemia by several mechanisms: Regular physical activity leads to an increase in the lipoprotein lipase activity, increased lipid oxidizing capacity and thus enhanced clearing of triacylglycerol [27,28]. An acute bout of physical activity leads to a reduction of intramuscular storage lipids thus enhancing the clearance of triacylglycerol after a fat load due to an increased muscular uptake of these lipids during the postprandial lipemia [12,27,29]. Given the present evidence it can be assumed that in our subjects in Study 1 all of these mechanisms have been operating.
Because of the study design we cannot make a statement about how much the postprandial lipemia could have been influenced favorably in the untrained subjects by a premeal exercise session. According to the evidence from the literature [9,12,25–27], as well the results from the present study, it seems that exercise and regular physical activity training may attenuate the postprandial lipemia (Table 3 and Fig. 1), independently from the intake of alcohol. The differences in the running time on the alcohol and the control day were not significantly different and probably do not explain the metabolic differences found on the two days.
In both studies, one g of fat per kilogram body weight was given. Since body weight and also body composition differed in our two study groups the intake of macronutrients per kilogram body weight as well as per kilogram lean body mass was different. Since the postprandial lipemia is influenced by the absolute amount of fat [30] and carbohydrates ingested it is conceivable that the difference of the postprandial lipemia in the two studies may be due to differences in amount of macronutrients ingested. Although, as stated above, we cannot compare the two study populations directly, the differences in the triacylglycerol AUC are of such a kind that they are unlikely caused by the comparatively small differences in the macronutrient intake only. Nevertheless, the subjects in Study 1 were well trained, a circumstance which is also reflected in their rather high running speed of over 13.0 km/hour. Since physical exercise leads in a dose-dependent manner to an improvement of the postprandial lipid profile [9,11,12,31], the present findings suggest that the major part of the different behavior of the postprandial lipemia may be due to the level of usual training and the effect of the premeal exercise session.
Fasting triacylglycerol level represents an important predictor of the postprandial triacylglycerol peak concentration and clearance rate [22]. This second relationship was also observed in our study, but only reached significance in the untrained subjects. The latter suggests that fasting triacylglycerol concentration may not be a good correlate of postprandial lipemia in trained subjects. This can be explained by miscellaneous aforementioned exercise and training which induced favorable metabolic alterations [9,12,25–27]. The lack of association between the fasting and maximal triacylglycerol concentration in trained individuals highlights the role of exercise as a modulator of postprandial lipemia [26] and thus also the risk of atherosclerosis.
The combination of a high fat meal with alcohol represents an important sensorial aspect of eating for many people [32] and an important component of their lifestyles. In view of the present evidence our study suggests that the unfavorable effects of this combination can be counteracted by regular physical training and preprandial aerobic exercise. However, the higher the fat intake and/or alcohol intake the higher the intensity and/or duration of the required exercise to counterbalance some of the unfavorable effects of this combination [9,23,30,33,34]. In view of the effects of alcohol on lipid oxidation as well as the alcohol effects on the postprandial lipids, the no-effect level of fat intake in combination with alcohol may be lower than the suggested 15 grams [30]. The percentage increase of the triacylglycerol AUC due to the ingestion of alcohol was similar in the untrained and trained subjects (46% vs. 54%). This suggests that the alcohol effects occur independently from the premeal exercise and/or training level. These results even suggest that the alcohol associated LPL inhibition [24] cannot be compensated by exercise training and/or a premeal exercise session.
For both studies we chose the subjects based upon the history of their usual physical activity training and not according to exercise testing and Vo2max measurements. Further the exercise sessions were not standardized. We are well aware of the limitations of this approach; however, the running times were quite reproducible on the two days in Study 1, and the non-significant differences in the running time do not account for the observed differences. This approach with the rather crude means of standardization was chosen to imitate the situation in daily clinical practice and counseling, where no extensive fitness testing can be pursued routinely. Despite the limitations of this methodology, we found clear-cut differences in the postprandial response, which supports the validity of our overall approach and which cannot be solely explained by the anthropometric differences, differences in macronutrient intake or differences in running speed.
How much exercise is needed to counterbalance the effects of fat and alcohol? Our data do not permit to answer this question. Nevertheless, only in the trained subjects did triacylglycerol levels return to the fasting (pre-exercise) concentration on the alcohol day. These subjects pursued a nearly daily exercise regimen, and the mean running speed on the track during the test sessions was slightly over 13.0 km/hour. This training intensity is rather high and difficult to maintain in daily life for the average individual. Accordingly, the ideal approach to control these postprandial metabolic changes would be to sustain moderate levels of physical activity in combination with a reduced fat intake and moderate or even only light alcohol consumption.
Since most individuals spend up to 50% of the day in a postprandial state, the development and the progression of atherosclerosis may be enhanced. Accordingly one major strategy to control the risk of atherosclerosis may be modulation of the postprandial metabolism by different means including a preprandial session of aerobic exercise as reported by Tsetsonis et al. [11]. Physically active people have a more favorable postprandial metabolic profile independently of a preprandial exercise session [26].
The ingestion of alcoholic beverages for rehydration and for social reasons after exercise is a common practice of many sportsmen [18,19]. Our data show that a high-fat meal in combination with alcohol enhances postprandial lipemia in untrained and physically trained individuals. This unfavorable effect of alcohol and a high fat diet could be modified by fat restriction or a higher level of physical activity training and a premeal exercise session.
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FOOTNOTES
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The data from Study I have been presented in abstract form at the Experimental Biology Meeting, Washington, DC, April 18, 1999.
Received March 9, 2000.
Accepted September 26, 2000.
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TOP
ABSTRACT
INTRODUCTION
