Cardiovascular disease (CVD) is a major cause of mortality in developed countries; hence, the establishment of effective measures for its prevention is the need of the hour. It is well known that fasting triglyceride (TG) concentrations are strongly associated with metabolic syndrome and CVD. In addition, growing evidence has shown that transient TG elevation for several hours after a high-fat meal is an independent risk factor for CVD (3,16,29). The elevation of postprandial TG leads to several physiological events, including the production of chylomicron (CM) remnants, a reduction in the content of HDL, activation of blood coagulation, stimulation of inflammatory cytokines and leukocytes, endothelial dysfunction, and formation of small LDL particles, which cause oxidative products to be generated (1,25,39). As a result, the atherogenic changes resulting from elevated postprandial lipemia can contribute to the causal role of TGs in the progression of CVD. Therefore, preventing the elevation of postprandial TG concentrations is important for the reduction of CVD risk.
Habitual exercise leads to lower postprandial lipemia and therefore decrease the risk of CVD (21,22). Furthermore, several studies have shown that even a single bout of exercise can suppress the elevation of postprandial TG concentration (27,35,37). This effect can be attended not only by moderate- to high-intensity aerobic exercise, such as running and cycling, but also by brisk walking and resistance exercise (33,37). In the previous studies, the effects of exercise, performed 8–16 h before (last day) meal intake on postprandial TG concentrations, have been examined; however, information regarding the effects of exercise on the day of a high-fat meal intake is limited, despite the importance of the timing of exercise and meal intake in gaining the benefits of exercise. Several studies have demonstrated that adequate meal timing on the day of exercise is important for glycogen loading, muscle building, and nutrient consumption (6,14,36), mainly due to the modification of hormone responses. The timing of exercise is therefore crucial to obtaining the maximum benefits of exercise and in the establishment of customized exercise programs for treating and preventing common diseases. It has previously been shown that a single bout of exercise drastically changes the secretion of several hormones, and that these effects often continue several hours after exercise according to the exercise type, intensity, and duration. Such hormone changes can acutely enhance nutrient metabolism in metabolic organs such as the skeletal muscles, liver, and adipose tissues. Therefore, we hypothesized that exercise on the day of meal intake may effectively suppress the elevation of postprandial TG.
A combination of aerobic exercise and resistance exercise has recently been recommended for better health and the prevention of common diseases. However, previous studies that have investigated the effects of single types of exercise on postprandial TG, such as aerobic or resistance exercise, have not examined the effects of a combination of both of these types of exercise. Resistance exercise, which the American College of Sports Medicine Position Stand recommends for all adult fitness programs (11), is characterized by high levels of muscle contraction and drastic secretion of growth hormone, even if performed at low intensity. Growth hormone increases lipid metabolism in the muscles, liver, and adipose tissues, which can lead to a reduction in the levels of circulating TG (7,38), as well as protein synthesis in the muscles. Although this effect has been unclear until now, this suggests that combined exercise may efficiently suppress postprandial lipemia, even when performed at low intensity. We therefore investigated postprandial TG concentrations after bouts of low-intensity exercise, consisting of brisk walking and light-resistance exercise, performed before or after meal intake.
Eleven healthy young subjects (five men and six women) who were not habituated to a regular exercise regimen were recruited to participate in this study, although one man retired before the completion of the study due to deconditioning unrelated to the study. Therefore, data obtained from 10 subjects were analyzed. The mean ± SD characteristics of the subjects were follows: men, age = 24.8 ± 5.5 yr, height = 176.9 ± 10.5 cm, body weight = 68.6 ± 11.9 kg, body mass index = 21.8 ± 2.0 kg·m−2, and body fat = 15.8% ± 5.5%; women, age = 21.8 ± 0.8 yr, height = 157.4 ± 4.5 cm, body weight = 52.4 ± 4.6 kg, body mass index = 21.2 ± 2.1 kg·m−2, and body fat = 24.7% ± 3.4%. All subjects were free of signs, symptoms, and history of any overt chronic disease. None of the participants had a history of smoking, and none were currently taking any medications or dietary supplements. This study was approved by the ethics committee of Kyoto Prefectural University, and all subjects signed a consent form after reading the design and protocol of the study.
All subjects participated in each of the three trials: rest, exercise before meal, and exercise after meal, in a repeated-measures experimental design. These trials were performed in random order and were separated by at least a week. All women participants performed the trials in each follicular phase to avoid the effects of the menstrual cycle. All subjects were asked to not perform vigorous exercise for 2 d before each trial and to refrain from drinking alcohol and smoking. Subjects also refrained from caffeine ingestion 24 h before each test and were asked to not to eat or drink anything except for water from 2200 h to the next morning. Food intake was recorded on the day before the trial, and the diet was repeated for each successive treatment.
On the day of each trial, subjects ate a breakfast of 200 g boiled rice at 0900 h in their individual homes. Subjects arrived at the laboratory at 1100 h and were provided with a meal at 1200 h, which was eaten for 10 min. The men ate a test meal containing 9.6% protein, 37.8% fat, and 52.8% carbohydrate (total energy = 1156 kcal), whereas the women ate a meal consisting of 10.6% protein, 39.1% fat, and 50.3% carbohydrate (total energy = 918 kcal). Blood samples were collected from the antecubital vein immediately before the test meal and 2, 4, and 6 h after meal intake. In the exercise before meal trial, subjects performed the exercise program at 1100 h, whereas in the exercise after meal trial, it was performed 1 h after meal intake (1310 h). With the exception of the duration of the exercise program, the subjects remained at rest (seated on a chair) and were asked to not drink or eat anything other than the drinking water supplied.
The exercise program consisted of brisk walking and light resistance exercise. First, subjects performed brisk walking in the university grounds for 2.0 km at the pace of two steps per second, which was completed in an average of 31 ± 0.8 min. Immediately after walking, the mean heart rate was 98 ± 6 beats per minute, and the rating of perceived exertion (Borg scale) was 9.6 ± 0.9. After a 2-min interval, participants performed light resistance exercises: squats, shoulder press, lateral side raise, bent over rowing, biceps curl, triceps extension, twist, side bend, push-up, and leg raise. With the exception of the push-up and leg raise exercises, all other exercises were performed using 2- and 3-kg dumbbells for women and men, respectively. The aforementioned exercises were repeated 15 times at a pace of one repetition per 4 s, with a 15-s interval between each exercise.
Blood glucose concentrations were determined using GluTest (Sanwa Kagaku Co., Ltd., Nagoya, Japan). Immediately after collection, each blood sample was centrifuged at 1900g for 15 min at 4°C. The analysis of the serum samples was entrusted to FALCO Biosystems Corporation (Kyoto, Japan), and measurements of total TG, total cholesterol, LDL cholesterol, HDL cholesterol, free fatty acid (FFA), and insulin were obtained. The concentration of TG contained in each lipoprotein fraction (CM, VLDL, LDL, and HDL) was measured using an agarose electrophoresis method, and the quantity of each lipoprotein was determined using densitometry and exclusive software (Choltri Combo; Helena Co. Ltd., Saitama, Japan). For the detection of the growth hormone, enzyme-linked immunosorbent assays were performed using a commercially available kit developed by R&D Systems (Minneapolis, MN), according to the manufacturer’s instructions. The absorbance was measured with a microplate reader, and the concentration was calculated by comparison with a calibration curve. The postexercise change in plasma volume was determined from hemoglobin and hematocrit concentrations, which were calculated using Dill and Costill’s (8) formula. The total TG response was determined as the area under the response curve (AUC) for the serum concentration versus time using the trapezoidal rule.
Indirect metabolic performance.
Indirect calorimetry analysis was performed for the assessment of metabolic performance for five subjects (two men and three women) who consented to the measurement. The subjects carried out three additional trials in the same way, and oxygen consumption (V˙O2) and carbon dioxide production (V˙CO2) were measured using a breath-by-breath respiromonitor system (MetaMax 3B, Cortex, Leipzig, Germany) for 30 min from 1400 h (10 min after the exercise program in the exercise after meal trial). The RER and the substrate use were calculated from the level of V˙O2 and V˙CO2, as described previously (2).
For time course comparisons of blood constituents, a repeated-measures two-factor ANOVA was used to examine differences among the three trials over time. When significant interactions were detected, post hoc multiple comparisons were made using Tukey’s HSD method. HSD Serum TG concentrations at each time point, AUC, and indirect metabolic parameters were analyzed using a repeated-measures one-factor ANOVA and Tukey’s HSD test for pairwise comparisons. A P value at the 5% level was accepted as statistically significant. To further assess the effects of exercise, the mean differences between the postprandial TG changes measured in the sedentary trial and each exercise trial, along with the 95% confidence intervals, were calculated. In addition, effect size (d) was determined using Cohen’s d. All data are reported as the mean ± SD.
Serum TG concentrations.
Compared with premeal in all three trials, serum TG concentrations were found to be markedly elevated 2 h after meal intake (Table 1). Although concentrations were reduced by 4 h after meal intake, when compared with the baseline, they remained at a higher level until 6 h. However, the postmeal exercise trial resulted in a reduction in the transient elevation in serum TG concentration observed 2 and 4 h after meal intake, judging by the 95% confidence interval of mean differences between the exercise and the sedentary trials. Large effect sizes were also observed (d < −1.0). With regard to the relative change ratio, exercise significantly suppressed the elevation of TG at 2 and 4 h after the meal in the exercise after meal intake trial when compared with the sedentary trial (P = 0.007 and P = 0.036, respectively), again with large effect sizes (d < −1.0) (Table 1). In addition, the AUC was significantly decreased by exercise postmeal compared with the sedentary trial (P = 0.012) (Table 1). In the premeal exercise trial, both the relative change ratio (2 h; P = 0.058) and the AUC (P = 0.067) reflected the tendency toward decreased TG concentrations in the premeal exercise trial, and medium effect sizes were observed (d = −0.47 to −0.74).
Lipoprotein fractions collected in this study were also examined to determine which steps from lipid intake to catabolism are involved in the suppression of postprandial TG due to exercise. After meal consumption, lipids are absorbed from the intestine and move into circulation as CM. Thereafter, TG are taken into the liver, synthesized to VLDL as a constitutive factor, and rereleased into circulation. Furthermore, VLDL-TG is converted to LDL and then HDL through catabolism. In the sedentary trials, the concentrations of TG in the VLDL, LDL, and HDL fractions were found to be significantly elevated 2 h after meal intake, after which they gradually returned to baseline (Figs. 1B–1D). In contrast, exercise after meal intake significantly suppressed the ratio of the LDL-TG increase (43% ± 37%, P = 0.028), and tendencies toward suppression in VLDL-TG (302% ± 334%, P = 0.056) and HDL-TG (55% ± 43%, P = 0.078) were observed 2 h after meal intake when compared with the sedentary trial (VLDL = 568% ± 727%, LDL = 109% ± 59%, HDL = 130% ± 78%). Exercise before meal intake also resulted in a tendency toward the suppression of TG concentrations in the VLDL (348% ± 342%, P = 0.071), LDL (48% ± 50%, P = 0.056), and HDL (57% ± 43%, P = 0.090) fractions. On the other hand, CM-TG concentrations were found to increase gradually after meal intake in a time-dependent manner but were not significantly affected by either meal intake or exercise (Fig. 1A).
Serum cholesterol, FFA, and blood glucose concentrations.
Total and HDL cholesterol concentrations were not changed by either meal intake or exercise (Figs. 2A and 2C), and although LDL cholesterol was slightly decreased 2 h after meal intake compared with baseline, exercise did not have an effect (Fig. 2B). Conversely, although the serum FFA concentration was not changed by meal intake, it was found to be significantly increased 6 h after meal intake in both exercise trials (preexercise [Pre-Ex] = 0.42 ± 0.12 mEq·L−1, postexercise [Post-Ex] = 0.49 ± 0.16 mEq·L−1) when compared with the value before meal (Pre-Ex = 0.27 ± 0.11 mEq·L−1, Post-Ex = 0.18 ± 0.05 mEq·L−1) (P = 0.007 and 0.003, respectively) (Fig. 2D). In addition, the FFA concentration measured 6 h after meal intake in the exercise after meal trial was significantly increased compared with that observed in the sedentary trial (0.29 ± 0.11 mEq·L−1) (P = 0.035). Finally, the blood glucose concentration was found to be elevated 2 h after meal intake, after which it gradually decreased in all three trials (Fig. 2E). No effects due to exercise were observed.
Serum hormone concentrations.
The concentrations of growth hormone in the sedentary trial were found to be 153 ± 63 ng·mL−1 before the meal and 104 ± 63 ng·mL−1 2 h after the meal. The concentrations were drastically elevated immediately after exercise in both the pre- and postmeal exercise trials, with levels of 2247 ± 772 ng·mL−1 before meal (P < 0.001) and 1840 ± 553 ng·mL−1 2 h after meal (P < 0.001) (Fig. 3B). On the other hand, although the insulin concentration was found to be significantly increased after meal intake, it was not affected by exercise (Fig. 3A).
The mean values obtained from the 30-min measurements of each parameter were compared between the three trials. The RER was found to be significantly lower in both exercise trials (Ex-Pre = 0.809 ± 0.012, P = 0.009; Ex-Post = 0.825 ± 0.018, P = 0.031) compared with the sedentary trial (0.854 ± 0.021) (see Figure, Supplemental Digital Content 1, http://links.lww.com/MSS/A189; comparison of metabolic performance after meal intake). Corresponding to the RER, fat use was demonstrated to be higher in the exercise trials (Ex-Pre = 0.83 ± 0.15 mg·(kg body weight·min−1)−1, Ex-Post = 1.00 ± 0.25 mg·(kg body weight·min−1)−1) than that in the sedentary trial (0.72 ± 0.26 mg·(kg body weight·min−1)−1), especially after meal consumption (see Figure, Supplementary Digital Content 1, comparison of metabolic performance after meal intake).
A single bout of exercise performed between 12 and 16 h before meal ingestion is known to reduce integrated TG concentrations by 16%–51% within the 6–8 h after a high-fat meal (27,35,37). However, little information regarding the effect of exercise on postprandial TG concentrations when performed on the day of meal intake has been published to date. Furthermore, until now, this effect has been observed only in response to relatively high-intensity exercise (>60% maximum oxygen uptake) for 30–90 min or low-intensity exercise performed for a long period (e.g., 180 min) (27,35,37). In contrast, the present study has revealed that the elevation in postprandial TG concentrations that occurs after meal consumption is suppressed after walking and light resistance exercise by integrated values of 25% before and 72% after a high-fat meal. Our observations provide the first evidence that exercise on the day of meal intake can suppress postprandial TG concentrations, even if the exercise is of low intensity and of a relatively short duration.
The habituation of an exercise program that combines low-intensity aerobic and resistance exercise has been recommended for efficient health promotion, as it improves cardiopulmonary function, body fat mass, insulin sensitivity, and muscle strength (9,15,18,30), which are closely related to mortality. Even single bouts of exercise can provide various health benefits, including improvements in peripheral blood flow, arterial stiffness, and insulin sensitivity, and these effects continue for 24–48 h after exercise (5,12). In addition to these effects, this study demonstrated that a single bout of exercise can suppress postprandial TG concentrations. As postprandial TG is an independent risk factor for CVD, exercise before and after a high-fat meal may be a countermeasure for the development of CVD. Furthermore, we have shown that exercise after meal intake is more effective at producing these effects than exercise carried out before meal intake. The effect sizes for both the peak concentration level and the AUC of postprandial TG indicate that the reduction in postprandial lipemia observed in the postmeal trial is approximately double that of the premeal trial, suggesting that exercise after meal intake elicits clinically significant changes that can lead to a reduction in CVD risk. Although it is known that exercise performed postmeal suppresses high levels of blood glucose, which contributes to the maintenance of metabolic and cardiovascular functions, our findings provide an additive benefit of postmeal exercise, that is, the suppression of TG concentration.
Previously, it has been reported that exercise both before and particularly after a high-fat meal increases postprandial fat use, with a decrease in RER (24). This is consistent with the results of the current study with regard to metabolic performance, which suggested that the catabolism and use of TG was accelerated by exercise. Thus, the elevation of fat use may have been the main cause of TG suppression in our exercise trials. Lipoprotein lipase (LPL) is the enzyme responsible for the hydrolysis of TG in lipoproteins. It has previously been shown that the activity of circulating LPL, which can reflect LPL in the capillary endothelium of metabolic tissues such as skeletal muscle, is negatively correlated with TG concentration (17,28). In skeletal muscles, a major tissue of TG catabolism, LPL is activated by reduced insulin and elevated growth hormone concentrations (31,40), changes which can be elicited by exercise. Several studies (19,32,34) have reported that LPL levels in both muscle and circulation are elevated by acute aerobic exercise. However, the increase of LPL that occurs in response to aerobic exercise has been reported to take several hours (33,34), leading previous studies to examine TG concentrations the day after the exercise. Although these studies have assessed the exercise-induced elevation of muscle LPL in association with the suppression of serum insulin levels, the exercise program in the present study did not significantly affect insulin and glucose levels. Because blood glucose generally reaches peak levels at 30 min after meal intake and returns to almost baseline levels after 1 h in healthy subjects, low-intensity exercise performed 1–2 h before or after meal intake has little effect on blood glucose and plasma insulin levels (26,27,33). Thus, the timing of exercise loading in the present study, even in the postmeal trial, may explain the low effect of exercise on the levels of these hormones, as they likely returned to near baseline levels. In contrast, the concentration of growth hormone was elevated drastically in response to combined aerobic and resistance exercise, probably leading to the activation of muscle LPL. Generally, the inhibitory effect of exercise on postprandial insulin is 20%–30%, whereas growth hormone concentrations are increased by more than 10-fold by resistance exercise (20). This is the case even when the resistance exercise is of low intensity, as shown in the present study. Thus, this drastic change in growth hormone concentration may lead to the suppression of postprandial TG expression on the day of exercise via the rapid activation of muscle LPL. We observed that FFA concentrations increased 6 h after meal intake in both exercise trials, which would be caused by the catabolism of adipose tissue, a major function of growth hormone when there are low levels of insulin, suggesting that secretion of growth hormone was enough to exert general effects including LPL activation. In addition, it has been shown that a single session of resistance exercise decreases the serum TG response to a high-fat meal to a greater extent than aerobic exercise of equal energy expenditure (23,33), which supports this hypothesis.
In our postmeal exercise trial, TG concentrations were already decreased 2 h after meal intake (15 min after exercise) when compared with the resting trial, suggesting that the suppression of postprandial TG had already occurred during exercise and that other factors may also be associated with this suppression. Hamilton et al. (13) have reported that muscle LPL can be directly activated by the local contractile activity of muscle, especially in the fast-twitch fibers of muscles. As resistance exercise produces high muscle contraction regardless of intensity, this may be one way in which it leads to the activation of muscle LPL. In addition, a possible determining factor of the postprandial TG response may be the entry speed of CM or VLDL into circulation, as the level of postprandial TG can be reduced if the time of ingestion and absorption in the gastrointestinal tract is slow. The normal flow of blood in skeletal muscle is also decreased in the gastrointestinal system during exercise in a process known as “blood flow redistribution” (10), which may delay ingestion and absorption. However, because very little redistribution occurs during low-intensity exercise, and because exercise in this study was not found to change TG concentrations in the CM fraction, it is difficult to associate a delay in the movement of CM with circulation. As another possibility, the decrease in postprandial plasma TG concentrations due to exercise may be a result of a decrease in VLDL secretion from the liver into the blood. A previous study has reported that total VLDL concentration is decreased for several hours after a single bout of exercise (4), which is consistent with our finding that TG in the VLDL fraction as well as the LDL and HDL fractions, was markedly decreased in both exercise trials when compared with the resting trial. In addition, Magkos et al. (23) have reported that resistance exercise suppresses postprandial VLDL secretion from the liver to a great extent when compared with aerobic exercise, which supports this hypothesis. Growth hormone may also affect the secretion of VLDL from the liver, and treatment with growth hormone has previously been shown to reduce serum TG and improve lipid metabolism (7). Furthermore, growth hormone-deficient adolescents present an abnormal postprandial and basal lipemia (7,38), whereas treatment with recombinant growth hormone has been shown to decrease serum TG in growth hormone-deficient adults (38). Therefore, this change in growth hormone concentration may be at least partly responsible for the suppression of postprandial TG via a decrease in VLDL-TG secretion from the liver into circulation, although the detailed mechanism remains unclear.
In conclusion, we found that low-intensity exercise that combines walking and light resistance exercise suppresses the elevation of postprandial TG concentration when performed after the ingestion of a high-fat meal, and to a lesser extent when performed before meal intake, in healthy young subjects. This effect was observed in the VLDL, LDL, and HDL fractions, but not in the CM fraction, and was particularly apparent in the postmeal exercise trial. In addition, exercise was shown to increase serum FFA and growth hormone concentrations, although no effect on insulin was detected. These observations suggest that low-intensity exercise performed on the day of meal intake can effectively suppress postprandial TG concentrations, especially when performed after meal intake. Further research is required to examine whether these findings can be generalized to the larger public.
This study was supported by Grants-in-Aid from the Japan Society of the Promotion of Science (23700776) from the Ministry of Education, Culture, Sports, Science and Technology of Japan and by research grants from the Uehara Memorial Foundation.
None of the authors have a personal or financial conflict of interest. The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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