Regular exercise is an important aspect of a healthy lifestyle for the prevention of diseases related to a sedentary lifestyle like coronary heart disease (CHD), Type II diabetes, and obesity (5). Classic physical activity recommendations for endurance exercise have been 20–60 min of moderate-to-vigorous intensity continuous exercise (CON-EX) per day, performed at least 3 d·wk−1(16). Intermittent exercise (INT-EX) guidelines state that health can be improved through multiple 10-min exercise bouts that accumulate to at least 30 min of moderate intensity lifestyle activities on most, if not all, days of the week (9,12,16,24). For individuals who are unable to exercise for long durations due to low fitness levels or busy lifestyles, these recommendations offer an alternative method to increase daily caloric expenditure and promote a physically active lifestyle. INT-EX has been shown to lower postprandial triglyceride (TG) accrual and to attenuate postprandial lipemia (PPL) (11,15), a factor that plays a role in CHD.
Epidemiological studies have indicated that fasting TG concentrations are related to the development of CHD (14,21). Patsch et al. (17) stated that prolonged elevation of TG after a meal increases the susceptibility of atherosclerotic development and is negatively associated with high-density lipoprotein cholesterol (HDL-C) concentrations. Due to high fat diets and repeated feeding, most people have elevated TG during the majority of a day.
To combat PPL, exercise in various combinations of intensity and duration effectively lowered PPL (2,10,11,23,28) and increased HDL-C (2,26,28). Zhang et al. (28) reported that continuous jogging for 60 min at 60% V̇O2max decreased postprandial TG incremental area under the curve (AUCI) by 51% compared with a control trial. To our knowledge, only two studies have compared PPL responses using single sessions of CON-EX and multiple INT-EX bouts. Murphy et al. (15) reported that both CON-EX and INT-EX significantly reduced PPL as compared with a control trial in hypercholesterolemic subjects, but PPL lowering was not different between 30 min of CON-EX and 30 min of INT-EX. Likewise, 90-min CON-EX and three 30-min INT-EX bouts decreased PPL in physically fit males (11). Both researchers (11,15) separated INT-EX bouts by 4 h, and
Murphy et al. (15) followed each exercise bout with a PPL test meal. These studies (11,15) show that INT-EX attenuates PPL, but neither study can definitively conclude that INT-EX was accumulated because food was consumed between INT-EX bouts (11,15), which might confound PPL (18). A comparison of CON-EX and INT-EX on PPL has not been reported in low-fit, normolipidemic populations without interruption due to feeding.
Pate et al. (16) emphasized that 200 kcal should be expended daily through accumulated INT-EX, which is realistic for inactive people. Petitt and Cureton (18) stated that energy expenditure appears to be a common link for PPL lowering. If energy expenditure is equal between CON-EX and INT-EX, it is plausible that these exercise methods would attenuate PPL equally. The purpose of this study was to compare postprandial TG responses in inactive, normolipidemic subjects after performing a single session of CON-EX and accumulated short bouts of INT-EX.
Eighteen inactive, normolipidemic males and females (7 males and 11 females) ages 18–45 yr volunteered for the study (1). Subjects were screened with questionnaires on physical activity history, medical and health history, and dietary habits. At initial screening, subjects were given a description of the research and were informed of the risks and benefits associated with the study. Subjects were excluded from the study if they were participating in a regular exercise program consisting of more than 2 d·wk−1 and >20 continuous minutes per session, had known cardiovascular or metabolic disease, were currently smoking, were taking any lipid-altering medications, were ingesting cold-water fish more than 3 d·wk−1, or if known to be pregnant. All female subjects were eumenorrheic, and all but two females reported use of oral birth control. Subjects were screened for habitual alcohol intake and were excluded if consuming excessive alcohol. A multi-vitamin/mineral was allowed if it contained no more that 150% of the RDA for any nutrient. Before participation in the study, subjects signed informed consent documents approved by the Health Sciences IRB at the University of Missouri-Columbia, Columbia, Missouri.
Body composition was assessed using the sum of three skin-fold measurements specific for males (chest, abdomen, thigh) and females (triceps, suprailium, thigh). The mean of three measurements at each site was used to estimate body density and percent body fat (1). Body mass index and waist-to-hip ratio were also measured and calculated using known methods (1).
Maximal oxygen uptake testing.
Subjects performed an exhaustive treadmill test to determine the exercise intensity for the subsequent submaximal exercise trials. This protocol has been described previously (22,23,28,29). After a warm-up at a self-selected pace, treadmill speed was increased to 3.5 mph for females and to 4.0 mph for males for 2 min, and was increased by 0.5 mph each until 6.0 mph and 6.5 mph was reached for females and males, respectively. After maximal speed was achieved, treadmill grade was increased 2% each min until exhaustion. Metabolic data were collected using open-circuit spirometry, and heart rate was measured via ECG using a single-lead attachment. The highest 30 s V̇O2 during the test was determined as being the VO2max of the subject. All subjects stated that they had previous experience with treadmill running.
Dietary habits were recorded for 3 d that included two weekdays and one weekend day. Subjects were instructed to record their foods as they were eaten. Diet records were analyzed using the Food Processor software, version 7.8 (Esha, Salem, OR).
Subjects performed three separate trials with a standardized high-fat meal (HFM) in random order: 1) a control trial of no exercise (NOEX), 2) 30-min CON-EX, and 3) 30-min INT-EX. Exercise trials were performed at 60% V̇O2max, occurred in the evenings, and ended 12 h before the HFM. Subsequent HFM trials were performed approximately 7–10 d apart. Female subjects did not perform trials during menses or the 5 d before menses (19). Subjects were free-living during all PPL trials, and the three trials were scheduled on days with similar routines (i.e., work schedule, low-intensity ambulation). Throughout each trial, subjects were quizzed about their daily activities and were reminded to maintain their typical daily routine with minimal ambulation.
Forty-eight hours before each HFM trial, subjects were instructed to continue with their typical routines but to abstain from both moderate and vigorous activity. Subject activity levels were not directly monitored or recorded during the 48 h preceding or during PPL trials. Twenty-four hours before the first HFM trial, each subject consumed meals typical of individual subject eating habits with no dietary restrictions. Foods were recorded as they were eaten. This diet was replicated before subsequent trials with respect to portion sizes, preparation, and times food was consumed. Subjects were quizzed concerning their dietary preparations, and trials were rescheduled if the pretrial diet was not replicated. The pretrial diet included a 12-h overnight dietary fast in which subjects were instructed to only consume water and maintain activity restriction. Subjects were instructed to not ingest alcohol in the 48 h before HFM trials and to abstain from caffeine in the 24 h prior and during the HFM trials. At 72 h before each trial, subjects were contacted daily by telephone and e-mail to remind them of the activity-control period, repeated diet, and dietary fast.
In the three trials with the HFM, subjects ingested a shake composed of heavy whipping cream and specialty ice cream that has been used previous by our lab (22,23,28,29). Caloric composition was based on body weight and contained 1.5 g fat, 0.05 g protein, and 0.4 g of carbohydrate per kilogram body weight. Total fat content was 88% of calories, and the shake was well tolerated by all subjects. Upon morning arrival at the lab, a fasting (0 h) blood sample was collected, and the subject was given the HFM, which was ingested within 10 min. After consuming the HFM, subjects returned to the lab every 2 h, for a total of 8 h, for blood sampling. During this time, subjects were instructed to consume only water. Fluid intake was not monitored.
Subjects performed treadmill jogging for 30 min at 60% of their individual V̇O2max. Both sub-maximal CON-EX and INT-EX trials used a treadmill speed that was closely correlated with 60% V̇O2max derived from the V̇O2max trial, and treadmill speed was titrated to maintain 60% V̇O2max. The CON-EX trial began with a 9-min warm-up that started with walking at 2.5 mph with increases in speed each minute for the duration of the warm-up. Subjects began jogging in the sixth minute of the warm-up. The INT-EX trial was performed in three 10-min bouts. Each INT-EX bout started with a 3-min warm-up that began with walking at 2.5 mph with increases in speed every 30 s for the duration of the warm-up. Subjects began jogging in the third minute of warm-up. The three short bouts were separated by 20-min rest periods in which subjects were seated and were allowed to do paperwork. In both exercise sessions, total time at 60% V̇O2max was 30 min, not including the 9-min warm-up. During the exercise sessions, expired gases were measured continuously with open-circuit spirometry and HR was measured with wireless telemetry (Polar Electro, Inc., Woodbury, NY). V̇O2 and HR were recorded every 30 and 60 s, respectively. Rating of perceived exertion was recorded at 10, 20, and 30 min after the warm-up, which corresponded to the end of each 10-min INT-EX bout. Caloric expenditure was calculated for the 30 min at target intensity in both exercise trials using the average RER and V̇O2 (L·min −1) (22).
Blood collection and preparation.
All blood samples were collected via a butterfly needle inserted into an antecubital vein after subjects were in a semisupine position for 3–5 min. Samples were collected into 10-mL tubes containing EDTA, and were separated by centrifugation at 4°C for 15 min at 2000μg in a refrigerated centrifuge. Separated plasma was transferred to labeled cryogenic vials and was stored at −80°C until analyzed. To eliminate intra-assay variability, all samples from a single subject were analyzed together for each assay, and all samples were analyzed in duplicate or triplicate.
Plasma TG analysis.
TG was measured enzymatically using a diagnostic kit (Infinity TG Reagent 344, Sigma, St. Louis, MO). Mean coefficient of variation (cv) for this assay was 1.3%. TG concentration was measured in all samples during the postprandial period at 0, 2, 4, 6, and 8 h to determine the PPL response. Quantified using the trapezoidal rule, total area under the curve (AUCT) was calculated using the actual value of all TG responses, and AUCI was calculated using the difference between all TG responses from the 0 h (pre-HFM) sample (28,30). TG peak responses were quantified as total peak (PeakT) being the highest TG value and incremental peak (PeakI) being the difference between the highest TG value during the postprandial period and the 0-h sample.
Total cholesterol and HDL-C analysis.
Zero-hour total cholesterol (TC) was analyzed using a diagnostic kit (Infinity Cholesterol Reagent 402, Sigma). Mean cv for this assay was 0.9%. Plasma HDL-C and subfractions were determined using a modified heparin-MnCl2-dextran sulfate method (8). Cholesterol content of HDLTotal-C and HDL3-C were determined with the same procedure as TC, and HDL2-C was calculated. HDL-C and its subfractions were analyzed with the 0 h (fasting) and 8 h post-HFM. Mean cv were 1.6%, 1.4%, and 0.6% for HDLTotal-C, HDL2-C, and HDL3-C, respectively.
An independent t-test was used to analyze gender differences in subject characteristics and PPL variables of the NOEX trial only. A two-way (gender × trial) ANOVA with repeated measures analyzed all post-prandial TG values, and fasting (0 h) TC and TC:HDL ratio. PPL responses respective of genders were analyzed with a one-way ANOVA with repeated measures for the main effect of trial. Because no gender × trial interactions were discovered for PPL variables, TC, or the TC:HDL ratio, genders were combined to analyze the main effect of trial with a one-way ANOVA with repeated measures. A three-way (gender × trial × time) ANOVA with repeated measures on trial and time analyzed HDL-C and its subfractions at the times of pre-HFM (0-h) and 8-h post-HFM. Significant F-test for main effects was followed by a Bonferroni multiple comparison test. Probability was set at P ≤ 0.05.
Subject characteristics by gender and the combined group are reported in Table 1. One-day and 3-d dietary records were not different in caloric composition or dietary constituents (Table 2). Males consumed significantly more kilo-calories and carbohydrates in the 3-d dietary record compared with females, but other dietary constituents were not different between genders or between diet records (Table 2). Exercise trial data are reported in Table 3. Average V̇O2 of CON-EX and INT-EX was 62.5% and 62.2% V̇O2max, respectively, and was not significantly different between the exercise trials. Caloric expenditure and RER were not different between CON-EX and INT-EX trials, but HR and RPE were significantly higher in CON-EX compared with INT-EX.
Plasma-derived variables are reported without plasma volume calculations since Murphy et al. (15) found no change in plasma volume using a similar exercise protocol. When averaged across all three trials, fasting TG values were not different among trials (Table 4), but females were 42% lower than males. In the NOEX trial only, TG AUCI (P = 0.139), AUCT (P = 0.131), PeakI (P = 0.133), and PeakT (P = 0.099) were not significantly different between genders. Two-way (gender × trial) results for TG AUC are reported in Figure 1, and TG Peak results are reported in Figure 2. Female TGAUCI and AUCT was 51.8% and 42.1% lower, respectively, compared with males (Fig. 1). TG PeakI and PeakT of females were 47.2% and 42.4% lower and significantly different compared with males (Fig. 2). The main effect of trial observed no difference among NOEX, CON-EX, and INT-EX for any PPL variables, and no trial × gender interaction was discovered.
Because no gender × trial interaction was found, genders were combined and analyzed by trial. TG AUCI and AUCT for each trial are reported in Figure 3. TG AUCI of INT-EX was 26.9% lower and significantly different from NOEX. AUCI of CON-EX was 15.9% lower than NOEX but not different than NOEX. TG AUCI of INT-EX and CON-EX were not different from each other. TG PeakI and PeakT by trials are reported in Figure 4. INT-EX TG PeakI was 23.0% lower and was significantly different than NOEX. CON-EX TG PeakI was 10.1% lower than NOEX but not different than NOEX. TG PeakI was not different between CON-EX and INT-EX trials. Among trials, absolute TG values of AUCT or PeakT were not significantly different.
Fasting lipoproteins are reported in Table 4. Averaged across all trials, females had significantly higher fasting (0-h) HDLTotal-C, HDL2-C, and HDL3-C by 29.7%, 55.7%, and 19.9%, respectively, compared with males. Because no gender × trial interaction was discovered, genders were combined to compare trials. HDLTotal-C, HDL2-C, and HDL3-C were not different among trials, and a comparison of fasting (0-h) and 8-h post-HFM did not change HDLTotal-C, HDL2-C, and HDL3-C (8-h data not shown). Fasting TC and fasting TC:HDL ratio were not different among trials or between genders.
To our knowledge, only two other studies have reported PPL comparisons between acute INT-EX and CON-EX sessions. In agreement with previous research (11,15), the INT-EX trial of the present study effectively attenuated PPL compared with a control trial, and CON-EX and INT-EX did not affect PPL differently. In contrast with previous data (11,15), the CON-EX trial of the present study did not significantly attenuate PPL as compared with NOEX. The present study also differs from previous reports (11,15) in relation to feeding status exercise sessions, rest between bouts, and subject populations. Both Gill et al. (11) and Murphy et al. (15) fed subjects between INT-EX bouts, which could confound subsequent PPL measurements (18). Gill et al. (11) studied males involved in a regular personal exercise program and tested an exercise volume beyond the INT-EX recommendations (16). Murphy et al. (15) implemented walking in an older, hypercholesterolemic population. Due to the absence of food between INT-EX bouts, the present results indicate that short moderate-intensity exercise bouts are additive and attenuate the effects of a HFM to a greater degree than CON-EX in inactive, normolipidemic subjects.
Caloric expenditure has been emphasized as being a primary factor in decreasing PPL (13,18), and Dunn et al. (9) showed similar caloric expenditure between CON-EX and INT-EX. In the present study, the 30 min of CON-EX and INT-EX were not different in caloric expenditure, but only INT-EX significantly reduced AUCI and PeakI as compared with NOEX. Pate et al. (16) recommended that INT-EX should expend at least 200 kcal·d−1. In the present study, CON-EX and INT-EX expended slightly greater than recommended (16), which is attainable is for most inactive populations. The present results demonstrate that INT-EX bouts are additive and show a compounding effect for lowering PPL compared with a CON-EX session. Based on the results of the present study, caloric expenditure cannot be assumed as the sole influence on PPL, and the TG-lowering effects of INT-EX might work on a different mechanism(s) compared with CON-EX.
Single sessions of endurance exercise have been shown to increase TG removal through amplification of the enzyme lipoprotein lipase (LPL) (20,22,29). Seip and colleagues (20) reported that LPL accumulated after moderate-intensity exercise was performed for five consecutive days, and Zhang et al. (29) reported that LPL remained elevated at 24 h postexercise. It remains unclear whether CON-EX and INT-EX affect LPL differently, and the low exercise volume of the present study might not be sufficient to elicit differences between CON-EX and INT-EX in LPL. If LPL is the responsible mechanism for enhanced TG clearance in INT-EX, the timing of the present protocol would have captured peak LPL levels in both exercise trials (29).
Another plausible INT-EX mechanism responsible for PPL attenuation could be excess postexercise oxygen consumption (EPOC). Borsheim and Bahr (6) reported that each short exercise bout has an individual oxygen deficit that affects the EPOC that follows differently. A single CON-EX bout compared with multiple INT-EX bouts of similar duration could yield a small energy difference due to EPOC (4,6). Murphy et al. (15) reported no EPOC differences between CON-EX and INT-EX trials, but did not report their warm-up procedures. The present study began each short INT-EX bout with a 3-min warm-up that progressed more rapidly compared with the 9-min warm-up before CON-EX. We believe that the rapid INT-EX warm-up would cause only a minimal difference between CON-EX and INT-EX because total warm-up of both trials was 9 min. Almuzaini and colleagues (3) reported 40% greater EPOC when comparing two 15-min cycling bouts with a single 30-min session. PPL changes of the present INT-EX protocol could be a result of the rapid INT-EX warm-up progression or the brief rest between bouts. Nonetheless, the magnitude of PPL lowering associated with INT-EX is supportive of the accumulation of exercise throughout a day.
Other INT-EX research that studied PPL is difficult to interpret because food was consumed between bouts (11,15), or PPL was measured after each short bout (15). Thus, it is unclear whether the PPL lowering of previous research (11,15) was a result of INT-EX accumulation or due only to the most recent short exercise bout. The present results suggest that PPL decreases are magnified after all INT-EX bouts are accumulated. The 1:2 exercise-to-rest ratio removed food consumption between bouts, which can confound PPL (18). Our results support the conceptual model of Dunn et al. (9), in which INT-EX may compound resting metabolism during the recovery after INT-EX bouts. This unique 1:2 ratio has not been reported previously in the literature and merits further investigation in its possible effect on EPOC and LPL.
Like postprandial TG caloric expenditure through exercise affects HDL-C metabolism (25). Crouse et al. (7) and Visich et al. (27) suggested that at least 350 kcal must be expended in a single exercise session to cause lipoprotein changes. This caloric threshold is much greater than the recommended daily 200 kcal expended through INT-EX (16). Our results partially confirm this threshold because 200 kcal was not adequate to affect TC or HDL-C or its subfractions.
In conclusion, our data suggest that accumulated short bouts of INT-EX are effective in lowering PPL as compared with a CON-EX or control trial in inactive, normolipidemic subjects. Our data also suggest that a single 30-min session of cardio-respiratory exercise at 60% V̇O2max, performed continuously or intermittently, is inadequate to cause changes in TC, HDL-C and its subfractions, or the TC:HDL ratio.
Thank you to Dr. Ying Liu, Scott Rector, and Brianne Giles for their assistance with subject preparation and assisting with performing analytical techniques, Dr. Steven W. Edwards for statistical insight, and Dr. Bryan K. Smith for reviewing this manuscript.
This study was supported by NIH T32 Postdoctoral Training Grant, University of Missouri-Columbia Foods for the 21st Century, University of Missouri-Columbia Alumni Grant, and a grant from the Elizabeth Hegarty Foundation.
1. ACSM. ACSM's Guidelines for Testing and Prescription
, 6th Ed. Baltimore: Lippincott, Williams & Wilkins, 2000, pp. 24, 63–66.
2. ALDRED, H. E., I. C. PERRY, and A. E. HARDMAN. The effect of a single bout of brisk walking on postprandial lipemia in normo-lipidemic young adults. Metabolism
3. ALMUZAINI, K. S., POTTEIGER J. A., and S. B. GREEN. Effects of split exercise sessions on excess postexercise oxygen consumption and resting metabolic rate (RMR). Can J. Appl. Physiol.
4. BAHR, R., I. INGNES, O. VAAGE, O. M. SEJERSTED, and E. A. NEWSHOLME. Effect of duration of exercise on excess post exercise O2
consumption. J. Appl. Physiol.
5. BOOTH, F. W. Waging war on modern chronic diseases: primary prevention through exercise biology. J. Appl. Physiol.
6. BORSHEIM, E., and R. BAHR. Effect of exercise intensity, duration, and mode on post-exercise oxygen consumption. Sports Med.
7. CROUSE, S. F., B. C. O'BRIEN, P. W. GRANDJEAN, R. C. LOWE, J. J. ROHACK, and J. J. GREEN. Effects of training and a single session of exercise on lipids and apolipoproteins in hypercholesterolemic men. J. Appl. Physiol.
8. DIAS, V. C., H. G. PARSONS, N. D. BOYD, and P. KEANE. Dual-precipitation method evaluated for determination of high-density lipoprotein (HDL), HDL2
, and HDL3
cholesterol concentrations. Clin. Chem.
9. DUNN, A. L., R. E. ANDERSEN, and J. M. JAKICIC. Lifestyle physical activity interventions: history, short- and long-term effects, and recommendations. Am. J. Prev. Med.
10. GILL, J. M. R., and A. E. HARDMAN. Postprandial lipemia: effects of exercise and restriction of energy intake compared. Am. J. Clin. Nutr.
11. GILL, J. M. R., M. H. MURPHY, and A. E. HARDMAN. Postprandial lipemia: effects of intermittent versus continuous exercise. Med. Sci. Sports Exerc.
12. HARDMAN, A. E. Issues of fractionization of exercise (short vs long bouts). Med. Sci. Sports Exerc.
13. HARDMAN, A. E. The influence of exercise on postprandial triacylglycerol metabolism. Atherosclerosis
14. JEPPESEN, J., H. O. HEIN, P. SUADICANI, and F. GYNTELBERG. Triglyceride concentration and ischemic heart disease: an eight-year follow-up in the Copenhagen Male Study. Circulation
15. MURPHY, M. H., A. M. NEVILL, and A. E. HARDMAN. Different patterns of brisk walking are equally effective in decreasing post-prandial lipemia. Int. J. Obes.
16. PATE, R. R., M. PRATT, S. N. BLAIR, et al. Physical activity and public health: A recommendation from the centers for disease control and prevention and the American college of sports medicine. JAMA
17. PATSCH, J. R., G. MIESENBOCK, T. HOPFERWIESER, et al. Relation of triglyceride metabolism and coronary artery disease. Studies in the postprandial state. Arterioscler. Thromb.
18. PETITT, D. S., and K. J. CURETON. Effects of prior exercise on postprandial lipemia: a quantitative review. Metabolism
19. REED, R. G., P. KRIS-ETHERTON, P. W. STEWART, and T. A. PERASON. Variations of lipids and lipoproteins in premenopausal women compared with men and postmenopausal women: DELTA (dietary effects on lipoproteins and thrombogenic activity. Metabolism
20. SEIP, R. L., K. MAIR, T. G. COLE, and C. F. SEMENKOVICH. Induction of human skeletal muscle lipoprotein lipase gene expression by short term exercise is transient. Am. J. Physiol.
21. STAMPFER, M. J., R. M. KRAUSS, J. MA, et al. A prospective study of triglyceride level, low-density lipoprotein particle diameter, and risk of myocardial infarction. JAMA
22. THOMAS, T. R., K. E. HORNER, M. M. LANGDON, et al. Effect of exercise and medium-chain fatty acids on postprandial lipemia. J. Appl. Physiol.
23. THOMAS, T. R., B. A. FISCHER, W. B. KIST, K. E. HORNER, and R. H. COX. Effects of exercise and n-3 fatty acids on postprandial lipemia. J. Appl. Physiol.
24. THOMPSON, P. D., D. BUCHNER, I. L. PINA, et al. Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: a statement from the council on clinical cardiology (subcommittee on exercise, rehabilitation, and prevention) and the council on nutrition, physical activity, and metabolism (subcommittee on physical activity). Circulation
25. THOMPSON, P. D., S. F. CROUSE, B. GOODPASTURE, D. KELLEY, N. MOYNA, and L. PESCATELLO. The acute versus the chronic response to exercise. Med. Sci. Sports Exerc.
26. TSETSONIS, N. V., A. E. HARDMAN, and S. S. MASTANA. Acute effects of exercise on postprandial lipemia: a comparative study in trained and untrained middle-aged women. Am. J. Clin. Nutr.
27. VISICH, P. S., F. L. GOSS, P. M GORDON, et al. Effects of exercise with varying energy expenditure on high-density lipoprotein-cholesterol. Eur. J. Physiol.
28. ZHANG, J. Q., T. R. THOMAS, and S. D. BALL. Effect of exercise timing on postprandial lipemia and HDL cholesterol subfractions. J. Appl. Physiol.
29. ZHANG, J. Q., B. SMITH, M. M. LANGDON, et al. Changes in LPLa and reverse cholesterol transport variables during 24-h postexercise period. Am. J. Physiol. Endocrinol. Metab.
30. ZIOGAS, G. G., T. R. THOMAS, and W. S. HARRIS. Exercise training, postprandial hypertriglyceridemia, and low density lipoprotein (LDL) subfraction distribution. Med. Sci. Sports Exerc.