Purpose: The purpose of this study was to examine the effects of previous exercise on metabolic, hormonal, and endothelial responses to an oral fat-tolerance test (OFTT).
Methods: Twelve healthy, recreationally trained men (age = 22.3 ± 2.5 yr, weight = 80.7 ± 12.4 kg, BMI = 25.1 ± 3.1 kg·m−2) volunteered for this study. In a crossover fashion, subjects completed three OFTT trials that involved no exercise (NoEx) or exercise performed 16 h (EX-16) or 4 h (EX-4) before the ingestion of a meal (13 kcal·kg−1 and 1.4 g of fat per kilogram of body weight). Blood was collected before and after the meal and hourly for 6 h. Brachial artery reactivity was measured using ultrasound before and at 2, 4, and 6 h after the meal. Dietary intake and exercise were standardized 4 d before the OFTT. The exercise session consisted of six resistance exercises and 30 min of running on a treadmill. The washout period between trials was, on average, 5 d.
Results: Compared with NoEx, there were significant (P < 0.05) decreases in triglyceride area under the curve (AUC) during EX-16 (−26%) and EX-4 (−15%). Compared with NoEx, there were decreases in insulin AUC during EX-16 (−7%, P < 0.05) and EX-4 (−5%, NS). EX-4 resulted in a significantly larger fasting arterial diameter than EX-16 and NoEx, but there were no other significant effects on endothelial function. Lipemic variables did not show correlations with endothelium function for any of the trials.
Conclusion: An acute exercise session, regardless of the time point chosen (i.e., EX-16 or EX-4), reduced to a similar extent the total and incremental lipemic responses compared with the NoEx condition.
1Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, CT; 2Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT; 3Department of Nutritional Sciences, University of Connecticut, Storrs, CT; and 4 Preventive Cardiology, Henry Low Heart Center, Division of Cardiology, Hartford Hospital, Hartford, CT
Address for correspondence: William J. Kraemer, Ph.D., Professor, Human Performance Laboratory, Department of Kinesiology-Unit 1110; The University of Connecticut, Storrs, CT 06269-1110; E-mail: william.kraemer@.uconn.edu.
Submitted for publication June 2007.
Accepted for publication September 2007.
Regular exercise decreases the risk of cardiovascular disease, coronary heart disease (CVD), non-insulin-dependent diabetes mellitus, selected cancers, and all-cause mortality. One mechanism by which exercise may decrease risk of chronic disease is by reducing postprandial lipemia (PPl). Abnormal PPL is an exaggerated and prolonged elevation in triglyceride (TAG) after a meal and is associated with a host of atherogenic events, including endothelial dysfunction, that predispose individuals to CVD (35). An acute bout of aerobic (12,18) or resistance exercise (23) lowers postprandial TAG concentrations after a fat-rich meal. The majority of studies have evaluated acute exercise performed about 16 h before the test meal (i.e., exercise was performed the night before a morning oral fat tolerance test (OFTT)) (12,18,23), with little attention given to shorter time periods between exercise and feeding.
There is a logical physiologic basis to hypothesize an improved postprandial lipemic response when exercise is performed closer to a meal. An exercise-induced reduction in the lipemic response may be attributable to increased clearance of TAG by the action of lipoprotein lipase (LPL) (23,27). The time course of LPL upregulation after exercise has only been examined in a few studies, with skeletal muscle LPL mRNA increasing approximately 4 h after exercise, followed by an increase in the enzyme mass around 8 h after exercise (27,28). On the basis of this response, and the fact that TAG concentration reaches a peak at about 4 h after meal ingestion, an exercise bout performed about 4 h before a meal would theoretically elevate muscle LPL coincidentally with the peak postprandial TAG response. However, no studies have evaluated the effect of exercise performed 4 h before a meal on (PPL).
Endothelial dysfunction is one of the earliest events in the development of atherosclerosis in populations at risk, but also in young healthy men (15). Distortion of endothelial cells by a sudden increase in blood flow causes an increase in vessel diameter, termed flow-mediated dilation (FMD), which is an essential mechanism that opposes neurogenic and myogenic vasoconstriction. A decrease in the normal dilatory response to the release of brachial arterial occlusion has been taken as a marker of such dysfunction (13). In young, healthy subjects without cardiovascular risk factors, endothelial dysfunction is related to the magnitude of PPL after a fat load (19). In contrast, acute exercise, if timed properly before the ingestion of a meal, can reduce PPL, thereby preserving FMD (32).
The timing of exercise in relation to fasting and postprandial measures of FMD has not been examined. We hypothesized that a time point closer to exercise, such as 4 h, would have a favorable effect on endothelial function because of enhanced blood flow and increases in vasodilator substances (32). To date, no studies have investigated the effects of the timing of prior exercise on PPL. In addition, few studies have evaluated the effects of exercise at any time on postprandial endothelial function. Therefore, the purpose of this study was to analyze the effects of whole-body exercise (aerobic plus resistance) at different times (4 and 16 h) before OFTT on PPL and endothelial function in healthy, recreationally active young men.
Twelve healthy men participated in this study after giving written informed consent, approved by the institutional review board of the University of Connecticut. Subject characteristics are shown in Table 1. All subjects were physically active and recreationally trained nonsmokers, and none took vasoactive medication or nutritional supplements known to affect lipid metabolism. Recreationally trained was characterized as subjects performing aerobic training at least three times a week and strength training twice a week. This information was obtained via questionnaire completed during each subject's first visit to the laboratory. Subjects were very fit; however, their values for body mass index (BMI) were slightly above the normal range, thus categorizing the subjects as overweight. This apparent discrepancy was explained by the subjects' more muscular body composition profiles, which were evident in the subjects' low percentages of body fat. All enrolled subjects completed the study.
A crossover design was used, with subjects performing three different trials in a random order: no-exercise (NoEx), exercise the night before (EX-16), and exercise the same day (EX-4). Each trial included an oral fat-tolerance test (OFTT) that began around 1115 h. After ingestion of the meal, blood was obtained each hour, and endothelial function was assessed every 2 h, for a total of 6 h. For the NoEx trial, subjects abstained from exercise for 74 h before the OFTT. For EX-16, subjects exercised the day before from 1800 to 1915 h (i.e., 16 h before the OFTT). For EX-4, subjects exercised from 0600 to 0715 h the day of the OFTT (i.e., 4 h before the OFTT). To ensure standardization between trials, subjects followed a strict exercise and dietary regimen in the days leading up to the OFTT trials. The washout period between trials was, on average, 5 d. An exercise session similar to the one used for data collection was planned 48 h before the EX-16, 60 h before the EX-4, and 74 h before the NoEx. This exercise session (STEX) started at 1800 and finished at 1915 h. Participants were asked to avoid structured exercise or highly demanding physical activity in the 2 d before the STEX and between STEX and the exercise session for data collection. The same control extended to nutritional intake. The subjects recorded their dietary intake for 4 d, leading to the day of data collection. In the first OFTT day, the dietary records were retrieved from the subjects and copied. The original was stored in the subject's file, and a copy was given to the participant for replication on the next trial. A graphic representation of the study design is presented in Figure 1.
Aerobic exercise has been shown to be an effective mode to reduce PPL (12,18). It also has been proposed that muscle contraction may induce LPL expression through the depletion of energy stores, increased concentration of oxygen-derived free radicals, increased hydrogen ions, and increased calcium (28). The guidelines of the American College of Sports Medicine recommend that resistance training and aerobic training should be a part of fitness programs developed for adults (25). Therefore, the exercise session proposed for this study included both modes to augment the possibility of a treatment effect on PPL.
An initial strength testing session was performed to determine the 10-repetition maximum (10RM) in the squat, bench press, leg curls, rowing, and shoulder press exercises. The protocol used to determine the 10RM consisted of an initial dynamic warm-up, followed by a first set of 10 repetitions with a light load (50% of the predicted maximum provided by the participant). The participant would then perform progressive 10RM sets with increased loads until the research team determined the 10RM load.
The treatment exercise session duration was 75 min and consisted of resistance exercise followed by treadmill running. The session started with dynamic warm-up exercises (lunges, butt-kicks, high knees, jumping jacks, squatting movement with no bar) and flexibility exercises. After warm-up, resistance exercises were performed in sequence: squat, bench press, leg curls, rowing exercise, shoulder press, and sit-ups; three sets of 10 repetitions were completed for each exercise. The three sets were performed at 95% of the 10RM load determined in preliminary testing. For the first two exercises (squat and bench), a first set of 10 repetitions with 60% of the weight was used as a specific warm-up. Squat and bench exercises had a 120-s rest period between sets (including from warm-up to the first set). For leg curls, rowing, and shoulder press, the rest period between sets and between exercises was 90 s. At the end of the resistance exercise session, subjects were asked to perform two sets of continuous sit-ups for 60 s. If participants were not capable of performing sit-ups continuously for 60 s, the participant would complete as many sit-ups as possible during the same 60-s period. For sit-ups, the time of rest between sets was 60 s. Subjects then ran for 30 min on a treadmill at velocity that was calculated, according to body weight, to result in a caloric expenditure of approximately 450 kcal (1). Exercise energy expenditure (EE) for the resistance exercise portion of the session was estimated at 9.75 kcal·min−1 (2). After the treadmill run, subjects provided their ratings of perceived exertion and ratings of soreness resulting from the exercise session. The rating of perceived exertion ranged from 0 ("nothing at all") to 10 ("very, very strong") [with magnitude estimation] (21). The rating of general soreness ranged from 0 ("no pain") to 10 ("highest possible pain") (22).
Subjects consumed a standardized high-fat meal for each trial, consisting of whipping cream and sugar-free pudding. The meal was scaled to each subject's body weight to provide 13 kcal·kg−1 and 1.4 g of fat per kilogram of body weight. Subjects arrived at the laboratory after abstaining from food for 12 h and alcohol and strenuous exercise for 24 h (except in the exercise trials). A flexible catheter was inserted into a forearm vein, and blood samples were obtained from a three-way stopcock connected to the end of the catheter. Blood was collected with a syringe and transferred to appropriate tubes for processing, for determination of lipids and hormones. The catheter was kept patent with a constant saline drip. Subjects rested quietly for 10 min in the supine position before blood collection. Blood samples were obtained before, immediately after the test meal, and at every hour thereafter, for a total of 6 h. The test meal was tolerated well by all the subjects. No subjects reported any gastrointestinal discomfort in the hours after ingestion.
Brachial artery reactivity (BAR) was assessed using standardized procedures for performing high-frequency ultrasonographic imaging before (PRE) and at 2, 4, and 6 h after OFTT. The technique provokes the release of nitric oxide, resulting in vasodilation that can be quantitated as an index of vasomotor function (5). All tests were performed in a quiet, temperature-controlled room. A blood pressure cuff was placed on the right forearm for occlusion. ECG leads were attached to monitor heart rate throughout the procedure. Subjects rested for 10 min in a supine position before data collection.
The brachial artery was imaged above the antecubital crease, and the transducer was placed to image the brachial artery in a longitudinal axis with clear visualization of the anterior and posterior vessel walls. When a clear image of the anterior and posterior walls of the artery was obtained, the transducer was held by a stereotactic clamp and the position held constant for the duration of the data collection. After the image was deemed optimal, baseline brachial artery diameter was recorded. A mark was made on the arm where the image was collected. The cuff was inflated to 200 mm Hg for 5 min to occlude the brachial artery, and then released. Arterial diameter was then assessed continuously for about 5 min after occlusion (5). Images of the brachial artery were obtained using an Acuson 13.0-MHz linear array transducer and an Aspen cardiac ultrasound system (Acuson Corp, Elmwood Park, NJ). After the trial was completed, measurements were taken in a two-dimensional plan to ensure data collection in the same place in subsequent trials.
Image analysis was performed using MIA software (Medical Imaging Applications, Iowa City, IA) software. For baseline, the average diameter taken from 30 frames was used. Three hundred frames were recorded for postocclusion. One-minute postocclusion diameter (1-min) was calculated by averaging the vessel diameter 10 frames immediately before the 1-min mark and the 10 frames immediately after the same mark. Brachial artery FMD was calculated and expressed as a percentage of the baseline diameter (29). Coefficients of variation for arterial diameter on repeat scans with repositioning on a group of men and women (N = 10) in our laboratory were 2.2% for measurements made the same day, and 2.2% for measurements made on two consecutive days.
Blood was collected into tubes with no preservative for serum and tubes coated with EDTA for plasma. Blood collection tubes were centrifuged at 1520g at 4°C for 15 min, with the resulting serum being stored frozen in microcentrifuge tubes at −80°C. After plasma was isolated, a preservation cocktail was added to the samples (5 mL·L−1 aprotinin, 1 mL·L−1 PMSF, and 1 mL·L−1 sodium azide) and stored in microcentrifuge tubes and frozen at −80°C. Samples were only thawed once for analysis. Serum glucose was determined in duplicate with the use of an YSI Lactate/Glucose Analyzer; model 2300 STAT (YSI Incorporated, Yellow Springs, OH). Serum insulin was measured in duplicate with DSL's human insulin ELISA (Diagnostic Systems Laboratory, TX). Nonesterified fatty acids (NEFA) were analyzed with an ACS-ACOD method from Wako (Wako Chemicals USA, Richmond, VA). Triglycerides were measured with an in vitro test for quantitative determination of triglyceride (Roche Diagnostics USA, Indianapolis, IN). Intraassay coefficients of variation were 2.0% for TAG, 5.4% for insulin, and 3.3% for NEFA.
Body composition was measured in the morning after an overnight fast. Body mass was recorded to the nearest 100 g on a calibrated digital scale, with subjects wearing only underwear. Whole-body and regional body composition were assessed using a fan-beam densitometer (Prodigy, Lunar Corporation, Madison, WI). Scan analyses were performed according to anatomical landmarks by the same technician using computer algorithm commercial software (enCORE version 6.00.270). Coefficients of variation for lean body mass and fat mass on repeat scans with repositioning on a group of men in our laboratory were 0.4 and 1.4%, respectively.
Subjects received detailed written and verbal instructions on how to properly complete the dietary food and beverage record. A 1-d "practice" dietary record was completed and discussed with the dietitian to ensure proper detailed recording. When the participant started the first trial, a 4-d diet record was performed. The participant was then requested to replicate the nutritional intake for each day exactly as the correspondent day in the previous trial. Subjects were instructed to maintain their usual diet and choose foods that were easily reproducible for 4 d before each trial. They were encouraged to consume 64 fluid ounces of water each day. To ensure each trial was identical, the subjects were required to duplicate their dietary intake and time of consumption for 4 d before each testing day. The day before the testing day was particularly tightly controlled to ensure uniformity in the metabolic and hormonal variables. The daily caloric requirements were calculated based on active individuals (35 kcal·kg−1) for each subject. The participant was instructed to consume two-thirds of this daily requirement on their own before 1600 h. A dietitian provided a sample meal plan for breakfast, lunch, and two snacks that met this caloric goal and was low in fat and glycemic carbohydrates. Each subject was also provided with a list of acceptable foods. The other third of the daily caloric requirements was provided by our laboratory in the form of shakes (54% carbohydrate, 23% fat, and 21% protein) (Ensure High Protein, Ross Laboratories, Columbus, OH). Seventy percent of these calories were consumed at 1630 h, and 30% were consumed at 2230 h, to ensure they received sufficient calories throughout the evening. Food diaries were analyzed for energy and macro/micronutrient content (NUTRITIONIST PRO, Version 1.3, First Databank Inc., The Hearst Corporation, San Bruno, CA). The database was modified by our group to include new foods and recipes; there were no missing values for the nutrients reported.
Data were analyzed for normality of distribution. When normal distribution was not observed, data were log transformed. Total area under the curve (AUC; concentration × time) was calculated by connecting all the time points before and after OFTT using the trapezoidal method (20). Differences within subjects were tested using 3 × 8 repeated-measures ANOVA for TAG, and a 3 × 4 repeated-measures ANOVA for insulin, glucose, and NEFA. Differences within AUC were measured using 3 × 1 repeated-measures ANOVA. In the case of an interaction, as indicated by a significant F-ratio, Fisher's least significant difference post hoc procedures were employed to determine pairwise differences between means. Selected bivariate correlations were determined with Pearson r correlation coefficients. Differences were considered significant at a P value less than or equal to 0.05. Effect sizes were calculated as Cohen's d. A sample size of 12 subjects was determined to be adequate to detect a 10% difference in the primary variable PPL and a 2% difference between exercise groups in the secondary variable FMD during the BAR tests, according to the coefficients of variation in a small reliability study we performed with repeated measures and prior studies in the literature (5). Statistica 5.5 for windows (StatSoft Inc, Tulsa, OK) was used for all statistical analyses. Data are presented as means ± standard errors (SE).
There were no differences in the participants' dietary intake between trials (Table 2). For exertion and soreness perception (Table 3), no differences were found between the exercise sessions in the three trials. The perceived exertion was considered to be strong (range 4.6-5.3), and soreness was perceived to be moderate (4-4.7), with no outliers. These results indicate that the participants were in a similar condition between trials. Total mean exercise energy expenditure was 888 kcal per session (3.7 MJ), including 450 kcal for the 30-min aerobic session, and 438 kcal for the resistance exercise.
Metabolic and hormonal responses.
Postabsorptive (premeal) serum TAG levels were significantly lower for EX-16 compared with the other trials. TAG concentrations were significantly lower at 2 and 4 h postmeal for both exercise conditions compared with NoEx (Fig. 2A). The results show that exercise significantly decreased the TAG concentration. Values for AUC were decreased by 26% for EX-16 and by 15% for EX-4, but there was no difference between exercise conditions. Compared with the NoEx trial, the majority of subjects had a lower TG AUC during EX-4 (9 of 12 subjects) and EX-16 (10 of 12 subjects) (Fig. 2B).
The results show that there were no treatment or trial effects for serum insulin concentrations (Fig. 3A); however, a significant difference in insulin AUC was observed between the EX-16 and NoEx (−7%, P < 0.001, effect size = 0.3). These results show that exercise caused a decrease in postprandial insulin concentrations. Qualitative examination of individual responses reveal that compared with the NoEx trial, the majority of subjects had lower insulin AUC during EX-4 (7 of 12 subjects) and EX-16 (11 of 12 subjects); furthermore, insulin AUC concentrations were higher for EX-4 compared with EX-16 in 8 of 12 subjects (Fig. 3B).
There were no premeal differences for glucose values between the three trials. During the postprandial period, the results show that the EX-16 trial had a consistent and significantly lower concentration than NoEx. This shows that exercise in the EX-16 improved serum glucose regulation when compared with no exercise. The EX-4 trial did not differ from the NoEx or the EX-16 (Fig. 4A). Similar to insulin, the glucose AUC for EX-16 had a significantly decreased total response compared with NoEx (−7%), but not with EX-4. Compared with NoEx, 10 of 12 subjects had a lower glucose AUC response during EX-16 (Fig. 4B).
The NEFA values for the EX-4 trial had a significantly increased concentration before the OFTT compared with the other two conditions (P = 0.002 vs EX-16 and P = 0.000 vs NoEx). After the OFTT, the values for EX-4 were still significantly increased compared with NoEx at 2 h, but not with EX-16. On the other hand, the EX-16 trial had a similar NEFA concentration to the NoEx at PRE (EX-16 = 0.35 μEq·L−1 vs NoEx = 0.36 μEq·L−1), but it had significant increases at 2 h and 6 h (Fig. 5A). For the AUC, both exercise conditions had significantly more NEFA than the NoEx (9%, P = 0.000 for EX-4; and 11%, P = 0.010 for EX-16) (Fig. 5B). Compared with NoEx, all but one subject had a higher NEFA AUC during EX-4, likely signifying an upregulation of lipolysis during the initial hours after exercise.
Pre- and postocclusion brachial artery diameters, as well as percent dilation, are shown in Figure 6. Premeal, preocclusion brachial artery diameter was significantly greater in the EX-4 trial (4.50 mm) (Fig. 6B) compared with the EX-16 and NoEx trials (EX-16 = 4.38 mm, NoEx = 4.32 mm). The larger preocclusion diameter before the meal during EX-4 resulted in a significantly lower percent dilation (1.4%) compared with the NoEX trial (2.7%). Diameter at 1-min postocclusion for the EX-16 trial progressively increased during the postprandial lipemic period (Fig. 6C), reaching a significantly increased value when compared with NoEx (but not with EX-4).
Metabolic variables and endothelial function.
Correlations between concentrations of TAG, NEFA, and insulin, and diameter at baseline, diameter at 1-min postocclusion, and percent change in dilation were calculated. Triglycerides showed a weak correlation with markers of endothelial function. NEFA correlated significantly with baseline diameter for EX-4 (r = 0.598, P < 0.05) and postocclusion for EX-16 (r = −0.578, P < 0.05). These results show that circulating TAG wasnot associated with endothelial function in this study, and NEFA was only marginally related to endothelial function.
The major finding of this study is that acute exercise, performed 16 or 4 h before eating, reduced both the total and peak postprandial lipemia compared with the NoEx condition. The exercise session used in this study complied with guidelines of the American College of Sports Medicine, which call for the inclusion of resistance and aerobic training as a part of fitness programs for adults (25). Previous studies of exercise effects on PPL have used either aerobic exercise or resistance exercise alone (12,18,23). The present study is, therefore, the first to our knowledge to assess the effects of a combination of aerobic and resistance exercise. The exercise energy expenditure of 888 kcal (3.7 MJ) was in line with the volume recommended for exercise benefits on PPL responses (24).
Similar to previous studies, there was a significant decrease in PPL when comparing exercise with NoEx. Those differences were seen at individual time points in the postprandial period (2, 3 and 4 h) and as a total lipemic response during the 6-h period. The relative decrease in PPL AUC for EX-16 (−26%) is similar to the results of other investigations (12,23). This observation reinforces the positive effects of exercise, particularly by decreasing the magnitude of PPL in response to a fat-rich meal. Notably, there was no significant difference in the reduction of PPL when exercising at 16 h versus 4 h before the meal.
Decreases in PPL after exercise could be attributable either to increased rates of clearance of triglyceride-rich lipoproteins from the circulation associated with an exercise-induced increased in LPL (26) and/or a reduced rate of appearance of the same lipoproteins (12). In this investigation, it is not possible to ascertain whether clearance was enhanced, appearance was decreased, or some combination of both occurred. Factors that influence the appearance of postprandial TAG are the rates of digestion and intestinal absorption of the meal leading to the primary appearance of intestinally derived TAG, and the rate of secondary release of TAG of hepatic origin, which occurs after hepatic uptake of chylomicron remnants. It is unclear whether exercise affects the secondary release of hepatic-derived TAG. Acute exercise decreases postprandial insulin, leading to less suppression of hepatic release of VLDL. Thus, prior exercise may actually augment the postprandial TAG response.
Peripherally, acute exercise induces a temporal upregulation of muscle LPL and a temporal increase in muscle blood flow. The rate of clearance of circulating TAG is strongly dependent on these two factors (27). These responses are probably not coupled. Although LPL activity peaks at about 8 h after aerobic exercise (26), it is doubtful that muscle blood flow remains elevated this late into recovery. In response to intensive forearm exercise, brachial artery diameters were elevated above baseline out to 20 min after exercise, with forearm blood flow returning to baseline even before that time (30). In a study with exhaustive knee extensor exercise, blood flow to the quadriceps was also reported to return to baseline values after 30 min postexercise (3). Without measurements of tissue blood flow and skeletal muscle tissue LPL activity, any mechanistic explanation remains purely speculative.
An increase in postexercise, pre-OFTT plasma NEFA in the EX-4 trial may also contribute to the lack of differences between exercise sessions in TAG concentration after the OFTT (Fig. 5A). Exercise causes a release of NEFA from adipocytes attributable to the hormonal milieu created by the exertion. Some of the responsible agents in this NEFA release are catecholamines, which increase after exercise (23). The significantly increased concentration of NEFA in the EX-4 compared with the EX-16 at PRE could have been associated with an increased fat oxidation that is augmented acutely after a high-intensity exercise (8). Enhanced adipocyte lipolysis creates an increase in serum NEFA, and there is a linear relationship between plasma NEFA concentration and the rate of plasma NEFA oxidation (11). In addition, skeletal muscle hormone sensitive lipase activity is increased by exercise and remains active for 2 h after exercise (33). Release of NEFA from adipose tissue with concomitant esterification in the liver could have caused the increased concentration of TAG in the plasma, mainly because of an increase in VLDL (14) in EX-4. In support of this possibility, there was a significantly increased TAG concentration at PRE (Fig. 2A) for EX-4 compared with EX-16. Although this compensation was still active in the EX-4 at the time of the OFTT, the time elapsed from the EX-16 could have been sufficient to cause reesterification of NEFA into TAG in adipose tissue and intramuscular TAG stores.
Exercise causes decreases in postprandial insulin concentrations (18), causing a reduced uptake of NEFA into adipocytes after the OFTT. Even if no statistical significant differences were noted between exercise conditions, it is interesting that EX-16 had a lower AUC compared with EX-4 (Fig. 3B) and a decreased concentration at PRE, 4, and 6 h (Fig. 3A). However, it is unclear whether insulin changes after exercise contribute directly to a triglyceride reduction. Gill et al. (7) have demonstrated that the effects of exercise on postprandial lipemia may not be related to exercise effects on increased insulin sensitivity.
Time of exercise may have played the most important role for glucose concentrations. Intense exercise is associated with an increase in the rate of gluconeogenesis that can last up to 4 h after exercise (6) to compensate for decreases in glycogen stores. This helps explain the consistent increased concentration of glucose in EX-4 when compared with EX-16 (Fig. 4A) and in the AUC (Fig. 4B). In addition, Bielinsky et al. (4) have shown that respiratory exchange rates could be suppressed for up to 14 h after exercise. Exercise can lead to increased use of fatty acids for oxidation processes, which diverts NEFA away from the pathway of esterification, decreasing VLDL production and secretion (17). This represents a shift toward fat oxidation attributable to increased use of carbohydrates for restoration of muscle glycogen stores (16). This phenomenon can account for the decreased presence of NEFA, insulin, glucose, and TAG at PRE for the EX-16 trial. Compared with NoEx, EX-16 had a significantly decreased AUC for glucose, parallel to significant decreases in insulin AUC. This shows that EX-16 increased insulin sensitivity and improved serum glucose regulation compared with NoEx.
Studies show that FMD is impaired after an experimental fat-rich meal in young, healthy men (9,15,19). Although several investigations have shown an acute impairment in endothelial function after ingestion of an OFTT, and this impairment is closely related to postprandial hypertriglyceridemia (19,31), others have not observed this effect (34). Triglyceride-rich remnant lipoproteins have been shown to impair endothelium-dependent vasodilation of arterial rings, and it can be speculated that oxidation of chylomicron remnants trapped in the vessel wall was responsible for the endothelial dysfunction (10). Associations between TAG concentrations after OFTT and FMD are usually moderate to large and inverse, with one study reaching an r = −0.70 (19). Circulating TAG was not associated with endothelial function in this study. Postocclusion FMD in young healthy men can decrease up to 10% after an OFTT (19,31). In this study, decreases in values for percent change were approximately 1%, with a noticeable variability within and between trials from pre-OFTT to the 6-h period. Subjects' brachial artery diameters ranged from 4.3 to 4.5 mm, depending on the trial (larger in exercise trials). In other studies with a population similar to that of this investigation, values for diameter were consistently lower than 4 mm (15,19). This difference is of great importance, because an increased diameter before occlusion will cause a decreased FMD after reactive hyperemia, particularly when it is measured as a percentage of the baseline change (9). A smaller vessel at baseline will register a larger increase in diameter after the occlusion, thus increasing the percent change in FMD. This occurrence can help explain the small percent changes in FMD in this study. Furthermore, elevated plasma TAG is known to dilate the brachial artery without affecting the diameters after occlusion, thereby resulting in a decrease in the percent dilation (9). We also have shown a gradual increase in preocclusion diameters during the postprandial period; however, the postocclusion vessel responses generally mirrored the preocclusion pattern, resulting in a fairly stable percent dilation during the postfeeding period for all treatments (Fig. 6). Given the lack of published studies in this area, we can only speculate as to the nature of this response. The elevated level of fitness of the subjects could override the effect of the fat load in FMD, the OFTT could have caused a stimulus that prevailed over exercise benefits, and the mean size of the brachial artery for the subjects was considerably elevated.
Because of a lack of statistical differences between trials, it is not possible to ascertain whether the timing of exercise can play a role in endothelial function by way of affecting PPL. Exercise seems to have a dual positive effect: it increases the protein expression of vasodilator substances within minutes of the shear stress, and it has a lingering effect (around 2 h) with an enhancement of the message for further increases in protein expression (32). The results from this study suggest that acute benefits from exercise in increases in vessel size can extend longer than 2 h in a young, healthy population, maybe because of an increased endothelial nitric oxide synthase expression with consequent increases in the production of nitric oxide (32).
In conclusion, this study reinforces the positive effects of exercise, particularly by decreasing the magnitude of PPL in response to a fat-rich meal. Notably, there was no significant difference in the reduction of PPL when exercising the night before or on the same day of a fat load. Furthermore, assessment of endothelial function with the help of a BAR test may be dependent on artery diameter at baseline. Finally, exercise may increase arterial diameter up to 4 h after exercise in young, healthy population.
The primary author wishes to thanks the Foundation for Science and Technology-Ministry of Science, Technology and Higher Education (FCT-MCTES) from the Portuguese government, and the support from the POCI2010 and from the FSE. In addition, this study was also supported in part by a grant from the National Strength and Condition Association, Colorado Springs, CO.
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Keywords:©2008The American College of Sports Medicine
HEALTHY YOUNG MEN; FLOW-MEDIATED DILATION; METABOLIC SUBSTRATES