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00005768-199610000-0000500005768_1996_28_1235_tsetsonis_postprandial_10article< 97_0_6_10 >Medicine & Science in Sports & Exercise©1996The American College of Sports MedicineVolume 28(10)October 1996pp 1235-1242Reduction in postprandial lipemia after walking: influence of exercise intensity[Clinical Sciences: Clinically Relevant]TSETSONIS, NATASSA V.; HARDMAN, ADRIANNE E.Department of Physical Education, Sports Science and Recreation Management, Loughborough University, Loughborough, Leicestershire LE11 3TU UNITED KINGDOMSubmitted for publication November 1995.Accepted for publication June 1996.The authors are grateful to Dr. S. S. Mastana and Mrs. A. Packynko of the Department of Human Sciences, Loughborough University, for determinations of aplipoprotein E phenotypes. Natassa V. Tsetsonis was supported by a British Council (Greece) Fellowship.Address for correspondence: Dr. A. E. Hardman, Department of Physical Education, Sports Science and Recreation Management, Loughborough University, Loughborough, Leicestershire LE11 3TU, UK. E-mail:a.e.hardman@lut.ac.uk.ABSTRACTThis study compared the effects of low and moderate intensity walking on postprandial lipemia, holding energy expenditure constant. Nine healthy normolipidemic subjects (5 men, 4 women; age 27.7 ± 0.9, fasting plasma triacylglycerol 0.95 ± 0.18 mmol·1-1, mean ± SEM) who were physically active but not endurance-trained undertook three trials, each over 2 d, in a balanced design. On the afternoon of day 1 they either refrained from exercise (Control), walked for 3 h at low intensity (Walk low, 32 ± 1% ˙VO2max), or walked for 1.5 h at moderate intensity(Walk moderate, 63 ± 1% ˙VO2max). The following morning, after a 12-h fast, they consumed a high-fat meal (1.3 g fat, 1.2 g carbohydrate, 0.2 g protein, 76 kJ energy per kg body mass). Blood and expired air samples were obtained before the meal and for 6 h afterward. Postprandial lipemia (total area under triacylglycerol concentration vs time curve) was lower than control after low intensity walking as well as after moderate intensity walking (both P < 0.05) but did not differ between the two walking trials (Control, 8.09 ± 1.09 mmol·1-1·h; Walk low, 5.46 ± 0.63 mmol·1-1·h; Walk moderate, 5.53 ± 0.58 mmol·1-1·h). The increase in energy production following the test meal did not differ between trials, but fat oxidation was increased in the fasting and postprandial states for both walking trials, compared with control (P < 0.05).In the fasted state, endurance-trained individuals exhibit low plasma concentrations of triacylglycerol (TAG) and high concentrations of high density lipoprotein (HDL) cholesterol compared with their more sedentary counterparts (9). This may be in part because the trained men and women possess high rates of clearance of exogenous TAG(21,25), the link being that the intravascular hydrolysis of TAG-rich lipoproteins proceeds with the transfer of surface material to nascent HDL.A capacity for rapid removal of TAG-rich lipoproteins could contribute to the low level of coronary heart disease risk reported in physically active(18) or fit (3) individuals; in the last few years case-control studies have shown that a high and prolonged plasma TAG response to an oral fat load is a strong predictor of the presence of coronary artery disease (e.g., 12). This may either be because chylomicron remnants themselves are atherogenic(31) or because the persistence in the circulation of high concentrations of chylomicrons causes perturbations of lipoprotein metabolism, which hasten the progression of atherosclerosis(10). People spend the majority of each day in the postprandial state and repeated, prolonged elevations of plasma TAG could constitute an important atherogenic stimulus. The potential of exercise to influence postprandial lipemia therefore justifies examination.We have previously shown that a prolonged bout of walking (2 h) at 30% of maximal oxygen uptake (˙VO2max) reduced by one third the lipemic response to a high-fat meal consumed the following morning (15 h later) after an overnight fast (2). In a subsequent study using the same design, a shorter bout of walking (1.5 h) had a significant effect on lipemia only when its intensity was higher, i.e., 60% ˙VO2max, a walk of the same duration at 30% ˙VO2max, with correspondingly lower energy expenditure, having no significant effect(29). These observations collectively suggest that the energy expenditure of an exercise bout may be the main determinant of its potential to reduce postprandial lipemia and, by inference, its potentially atherogenic sequelae. If this is the case, then “trading off' longer or more frequent bouts of lower intensity exercise for fewer or shorter bouts of higher intensity exercise may have comparable effects, in line with views advanced by Haskell (13).The purpose of the present study was therefore to test the hypothesis that the attenuation of postprandial lipemia evident after a bout of walking is independent of its intensity when energy expenditure is held constant. Walking was selected as the mode of exercise because it is attainable and socially acceptable for so many people. We employed a high-fat, mixed meal because it is more palatable, and more comparable to a normal meal, than fat alone.METHODSSubjects. Nine normolipidemic volunteers (5 men) took part. All subjects were physically active in their leisure time (2/3 h·wk-1 of recreational sport or jogging) but could not be described as well-trained. Some of their physical characteristics are presented in Table 1. None was taking drugs known to affect lipid or carbohydrate metabolism. The study was approved by the university's Ethical Advisory Committee and all subjects were fully informed of the procedures and risks involved before giving their written consent to take part.TABLE 1. Some physical characteristics of the nine subjects; mean and range.Design. Subjects took part in two exercise trials and a control trial at intervals of 7 d in a balanced design, each trial being conducted over 2 d (Fig. 1); on the afternoon of day 1, subjects either rested quietly (Control), walked for 3 h at 30% ˙VO2max(Walk low), or walked for 1.5 h at 60% ˙VO2max (Walk moderate). After eating their evening meal on day 1, subjects fasted overnight (>12 h) before reporting to the laboratory on the morning of day 2 for an oral fat tolerance test.Figure 1-Study protocol. Each trial conducted over 2 d. Evening meal on day 1 standardized between trials. Test meal on morning of day 2 comprised 1.28 g fat, 1.24 g carbohydrate, 0.19 g protein, and 76 kJ energy per kg subject's body mass. Baseline measurements on day 2 (fasted state) made ≈16 h after end of exercise on day 1.Each subject performed two preliminary exercise tests; in the first,˙VO2max was determined with the Douglas bag method during uphill walking at a constant speed (range, 1.34-1.88 m·s-1), using a modification of the Taylor treadmill test (28). At least two of the following criteria had to be met for the test to be considered valid: a rating of perceived exertion ≥18, a respiratory exchange ratio of>1.1, maximal heart rate within 10 beat·min-1 of age-predicted maximum, or a plateau in ˙VO2 (increase of ≤2.0 ml·kg-1·min-1 with increase in treadmill grade). In the second preliminary test the relationship between steady state˙VO2 and treadmill grade was established using a submaximal, incremental walking test. The grades needed to elicit 30% and 60% of˙VO2max were interpolated for each individual. Subjects walked at the same speed for each of their two long walks (range 1.47-1.83 m·s-1).During the long walks, expired air samples were collected at 15-min intervals; heart rate (ECG, modified lead I) and ratings of perceived exertion(4) were recorded at the same times. Duplicate 20-μl capillary blood samples were taken from the thumb before exercise and every 30 min during exercise. Water was provided ad libitum, the volume consumed being recorded.Oral fat tolerance tests. On day 2, i.e. for the exercise trials 16 h after the completion of the bout of walking (same interval for both exercise trials, Fig. 1), subjects came to the laboratory at 8 a.m. after an overnight fast. A cannula was placed in a forearm or antecubital vein and, after a 10-min interval, a baseline blood sample was obtained. The test meal was then ingested within 15 min. Further blood samples(10 ml per occasion) were obtained after 0.5, 1, 2, 3, 4, 5, and 6 h while subjects rested quietly. The cannula was kept patent by flushing with nonheparinized saline (9 g·1-1). During the observation period subjects consumed only water, ad libitum on the first trial, the volume being recorded and replicated for the two remaining trials. Expired air samples were collected into Douglas bags for 5 min immediately before each blood sample.Dietary control. Subjects weighed and recorded all food and drink consumed for the 3 d before their first oral fat tolerance test and replicated this diet during the 3 d immediately preceding their second and third tests, refraining from alcohol during all these days. Food diaries were analyzed using a computerized version (COMPEAT, Nutrition Systems, London) of food composition tables (14). No exercise was performed during the 2 d preceding day 1 of each trial.Test meal. This was given according to body mass (1.3 g fat, 1.2 g carbohydrate, 0.2 g protein, and 76 kJ energy per kg body mass) and consisted of whipping cream, cereal, fruits, chocolate, and nuts. The energy value was 5.31 ± 0.23 MJ, of which 67% was derived from fat (29% from carbohydrate). No subject reported nausea or other gastrointestinal discomfort.Analytical procedures. Capillary blood samples obtained during exercise were immediately deproteinized in 2.5% perchloric acid and stored at-70°C until analyzed for lactate using a fluorimetric micromethod(17). Hemoglobin concentration and hematocrit were measured before and after oral fat tolerance tests for estimation of plasma volume changes (8).One milliliter of whole blood was dispensed into sodium fluoride tubes and plasma was immediately separated and stored at -70°C for determination of blood glucose (Boehringer-Mannheim; Mannheim, Germany). Five milliliters of blood was dispensed into an EDTA tube; after separation of plasma, sodium azide was added prior to storage at -70°C for later determination of apo E phenotypes. Remaining blood was allowed to clot and serum was separated and stored at -70°C until analysis. Samples from each subject for all trials were analyzed in the same run wherever possible. Cholesterol, TAG, glucose(Boehringer-Mannheim; Mannheim, Germany) and nonesterified fatty acids (NEFA)(Wako; Neuss, Germany) were determined by enzymatic, colorimetric methods using a centrifugal analyzer (Cobas-Bio, Roche; Basel, Switzerland). High density lipoprotein cholesterol was determined in the supernatant after precipitation of low and very low density lipoproteins (VLDL), using magnesium and phosphotungstate (Boehringer-Mannheim; Mannheim, Germany). Insulin was measured by radioimmunassay (Diagnostic Products; Los Angeles, USA). Accuracy was maintained using quality control sera (Roche and Boehringer-Mannheim). Within-batch coefficients of variation were 1.0% for total cholesterol, 1.2% for HDL cholesterol, 1.0% for TAG, 1.1% for NEFA, 1.2% for glucose, and 4.5% for insulin. Phenotypes of apolipoprotein E, which affect exogenous fat clearance, were determined by isoelectric focusing using Western blot techniques.Statistical analysis. Statistical comparisons between trials were made using ANOVA, with Tukey post-hoc tests where significant differences were found. Relationships between variables were evaluated using Pearson's product-moment correlation coefficient. Tests were considered statistically significant at the 5% level. Values are presented as mean and standard error of the mean (mean ± SEM) or as mean and range.RESULTSInspection of the main outcome measures, i.e. fasting and postprandial concentrations of TAG, NEFA, insulin, fasting and postprandial values for the respiratory exchange ratio, revealed no substantive differences between the responses of men and women. Data for all nine subjects are therefore presented together.Responses during treadmill walking. Average oxygen uptake represented 32 ± 1% of ˙VO2max during low intensity walking and 63 ± 1% of ˙VO2max during moderate intensity walking, with heart rates of 102 ± 4 beat·min-1 and 150 ± 3 beat·min-1, respectively. Average values for blood lactate concentration (1.74 ± 0.29 mmol·1-1 and 2.76 ± 0.27 mmol·1-1 for low and moderate intensity, respectively), respiratory exchange ratio values (0.88 ± 0.0 vs 0.92 ± 0.01), and ratings of perceived exertion (9.3 ± 0.7 vs 13.0 ± 0.8) were of the order expected for the relative intensities of the exercise bouts.Serum and plasma concentrations. Changes in plasma volume during the oral fat tolerance tests were small and did not differ significantly between trials (-2.1 ± 1.8%, -3.6 ± 0.8%, and -0.9 ± 0.9% for control, low intensity, and moderate intensity trials, respectively). No adjustments were made, therefore, to measured concentrations.The serum TAG responses to the test meal are shown inFigure 2. TAG concentration in the fasted state was significantly lower than control after low intensity walking and after moderate intensity walking. Postprandial lipemia was evaluated as the total and incremental (above baseline) areas under the TAG versus time curve. Both indices of lipemia were significantly reduced by low intensity walking as well as by moderate intensity walking (Fig. 3), the magnitude of these reductions being strikingly similar. Serum concentrations of total and HDL cholesterol are presented in Table 2. No differences between trials in the response over time were apparent.Figure 2-Serum concentration of triacylglycerol measured in the fasted state and for 6 h after consumption of a high-fat meal. Three trials: Control (○), after a day of minimal physical activity; Walk low (□), after a 3-h walk at 30% ˙VO2max; and Walk moderate (▵), after a 1.5-h walk at 60% ˙VO2max; N = 9; mean and SEM.Figure 3-Incremental and total areas under the 6-h serum triacyl-glycerol concentration-time curves. Three trials: Control (▪), after a day of minimal physical activity); Walk low ([light shade square]), after a 3-h walk at 30% ˙VO2max; and Walk moderate (▨), after a 1.5-h walk at 60%˙VO2max; N = 9; mean and SEM.* significantly different from Control, P < 0.05.TABLE 2. Serum concentrations of total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) in the fasted state and during the 6 h after consumption of a high-fat meal.The serum insulin and NEFA and plasma glucose responses to the test meal are shown in Figure 4. The total area under the insulin concentration-time curve was significantly lower for the moderate intensity trial than for the other two trials (Fig. 5). Plasma glucose concentration changes were modest and did not differ between trials. The concentration of NEFA fell during the hour after eating, rising again thereafter. The incremental area under the NEFA versus time curve was lower than control (P < 0.05) for each exercise trial (control 0.78± 0.17 mmol·1-1·h, low intensity 0.08 ± 0.22 mmol·1-1·h, moderate intensity 0.14 ± 0.31 mmol·1-1·h).Figure 4-Serum and plasma concentrations measured in the fasted state and for 6 h after consumption of a high-fat meal. Three trials: Control, after a day of minimal physical activity); Walk low, after a 3-h walk at 30%˙VO2max; and Walk moderate, after a 1.5-h walk at 60%˙VO2max; N = 9; mean and SEM.Figure 5-Incremental and total areas under the serum insulin concentration vs time curves. Three trials: Control (▪), after a day of minimal physical activity); Walk low ([light shade square]), after a 3-h walk 30%˙VO2max; and Walk moderate (▨), after a 1.5-h walk at 60%˙VO2max; mean and SEM. *significantly different from Control, P < 0.05. + significantly different from Walk low, P < 0.05.Apolipoprotein E plays an important role in receptor-mediated clearance of lipoprotein particles from plasma but genetic variation exists, with three alleles coding for proteins called E2, E3, and E4. In vitro, E2 binds poorly and heterozygosity for this form of apo E delays the clearance of dietary fat; by contrast, E4 increases clearance (31). In the present study, eight subjects possessed the (commonest) E3/E3 apo E phenotype and one, a woman, the E2/E3 phenotype.Indirect calorimetry. Rates of whole body substrate oxidation and energy expenditure were calculated from the indirect calorimetry data, without direct measurement of protein oxidation (6). Gross energy production during walking on day 1 was then calculated from ˙VO2 and ˙VO2 was 4.18 ± 0.40 MJ for low intensity and 4.28± 0.45 MJ for moderate intensity (NS). Total fat oxidation was 43.2± 5.4 g and 28.8 ± 4.5 g during low and moderate intensity walking (NS, P = 0.07), respectively, representing 40 ± 5% and 25 ± 3% of total energy produced (P < 0.05).No significant differences were observed between trials in the˙VO2 response to the meal (Fig. 6) but respiratory exchange ratio values were significantly lower than control after low intensity walking and after moderate intensity walking, both in the fasted state and over the postprandial period (mean value over 6 h)(Fig. 6). Whole body fat oxidation, calculated over the 6-h period, was greater after walking than after a day of rest but this did not differ between the two walking trials (Table 3). Net fat balance was calculated as the difference between the amount of fat ingested and the total amount oxidized over the observation period, assuming that the amount of dietary fat which had left the intestine within 6 h did not differ between trials. This was lower than control after both low and moderate intensity walking (Table 3). There were no significant between trial differences in postprandial carbohydrate oxidation or storage.Figure 6-Oxygen uptake (upper panel) and respiratory exchange ratio (lower panel) in the fasted state and for 6 h after consumption of a high fat meal. Three trials. Control, after a day of minimal physical activity); Walk low, after a 3-h walk 30%˙VO2max; and Walk moderate, after a 1.5-h walk at 60%˙VO2max; mean and SEM.TABLE 3. Calculated energy production from fat and carbohydrate (CHO) and whole-body net substrate oxidation and storage† over the 6-h postprandial period.Dietary analysis. Average daily dietary intakes of energy and selected nutrients consumed during the 3 d leading up to the oral fat tolerance tests are presented in Table 4. Similar analysis was undertaken for food consumed after walking (or comparable period for the control trial) on day 1. No significant between-trial differences were observed.TABLE 4. Dietary intakes of energy and major nutrients prior to oral fat tolerance tests.DISCUSSIONSingle bouts of low and moderate intensity exercise of equivalent energy expenditure had strikingly similar effects on the plasma TAG response to a high-fat, mixed meal when this was consumed 16 h after walking: post-prandial lipemia was reduced by nearly one third during both walking trials. This finding confirms the considerable potential of nonintense exercise to influence post-prandial lipemia and, by inference, the ensuing atherogenic disturbances of lipoprotein metabolism.On the mornings after walking plasma TAG concentration in the fasting state was markedly reduced, the magnitude of the reduction (one third or 0.3 mmol·1-1) being independent of the relative intensity of the prior bout of walking. This confirms a recent report in healthy but hypercholesterolemic men (7), which found that decreases in fasting TAG measured 24 h after cycling were independent of exercise intensity (80% and 50% ˙VO2max). Lower fasting TAG concentrations will have contributed to the lower lipemic responses to dietary fat in the present study. There is competition for clearance between chylomicrons and VLDL (5), and the size of the fasting TAG pool has been reported to be positively related to indices of postprandial lipemia(20,22). Our findings are in agreement with these earlier reports, with strong relationships found between between fasting TAG concentration and the total lipemic response (r = 0.95, 0.96, 0.90 for Control, Walk low, and Walk moderate trials, respectively). The effect of exercise cannot, however, be attributed solely to its influence on fasting TAG pool size as the incremental area (above baseline) under the TAG-time curve was also reduced, by 27-28% compared with control.The lower postprandial TAG concentrations after walking probably reflect enhanced rates of removal by peripheral tissues of TAG-rich lipoproteins. A decreased rate of appearance cannot be ruled out because our methodology precludes this but rates of appearance of exogenous fat should not differ between trials with such a long interval between exercise and the ingestion of the meal. A lower VLDL secretion is unlikely explanation for the lower TAG response because NEFA tended to be higher and insulin lower during the exercise trials. Moreover, an earlier study found that the rate of clearance of TAG introduced intravenously was enhanced during recovery from a bout of exercise (marathon running) (25).Skeletal muscle is the likely site of enhanced TAG uptake; at rest this tissue is reported to be the main determinant of clearance rate, clearing 50% of a dose of intravenous fat emulsion compared with 13% by adipose tissue(24). Moreover, the capacity to clear TAG appears to relate to the activity of lipoprotein lipase (LPL) in muscle but not to its activity in adipose tissue (30). Exercise stimulates an increase in LPL activity which is characteristically “local, delayed, and transient” (16). The rate of TAG hydrolysis would be enhanced, with the resulting NEFA either entering muscle (for oxidation or storage) or perhaps escaping into the circulation if the muscle's capacity to “entrap” NEFA is exceeded (11). This might be thought of as a mechanism for the directed storage of TAG during recovery in order to replenish skeletal muscle TAG which was degraded during exercise (19).However, our subjects consumed a normal meal on the evening of day 1. This included about 50 g of fat, compared with the 43 g and 29 g which we estimate was degraded during low and moderate intensity walking, respectively. Based on our findings on day 2, some additional fat oxidation may have occurred after walking during the hours following the evening meal on day 2. Even so, it is difficult to argue that there would have been an important skeletal muscle“fat deficit” on the exercise trials by the morning of day 2. Furthermore, the decrease in the serum TAG response to the meal was the same for both exercise trials, despite the fact that degradation of skeletal muscle TAG would probably have been greater during moderate intensity walking than in low intensity walking (23); this also argues against enhanced storage of TAG in muscle as an important determinant of the exercise-induced reduction in postprandial lipemia.Our estimates of substrate storage and oxidation during the postprandial period (Table 3) show a reduction for the exercise trials in (whole body) fat storage during the 6 h period after consuming the meal. Fat oxidation was approximately 30% (approximately 6 g over 6 h) greater for the walking trials than for the control trial so, as the same amount of fat was consumed on each trial, storage was correspondingly reduced. There is evidence that “storage” in blood was decreased because serum TAG concentrations were lower throughout the observation period, but this cannot be quantified and we cannot say whether storage was reduced also in other tissues. Skeletal muscle is an unlikely site of reduced storage and, given its mass, was probably the main site of increased postprandial fat oxidation; decreased storage in adipose tissue seems a possibility. Whatever the site(s), this reduction in storage appears to be independent of qualitative differences in the utilization of particular substrates between the two different exercise intensities because the decreases in lipemia and the increases in postprandial fat oxidation were remarkably similar for the two walking trials.Enhanced fat oxidation in skeletal muscle could compensate for an increase in the nonoxidative disposal of glucose. This would link enhanced postprandial oxidation of fat to the extent of glycogen degradation during exercise; glycogen utilization during walking is poorly described, however, and we have no data. What information there is suggests that it may have been greater for the (shorter) bout of walking at 60% ˙VO2max than for the (longer) bout at 30% ˙VO2max (26). Moreover, carbohydrate intake after walking on day 1 (141 g and 173 g for low and moderate intensity trials, respectively) was probably sufficient to replenish muscle glycogen stores; this intake was of the same order of magnitude as estimates of total carbohydrate oxidation (from muscle and from blood-borne glucose) during walking (149 g and 182 g, respectively).Although neither bout of walking influenced total energy expenditure immediately before or during the 6 h after the meal, the effect of exercise on fat storage following fat ingestion may still be important for energy balance. In contrast to carbohydrate and protein, fat intake has no influence on fat oxidation and is almost exclusively used or stored in response to day-to-day fluctuations in energy balance (1). Consequently, it has been argued that energy balance is virtually equivalent to fat balance(27). If this reasoning is correct, for body weight to fall there must be an imbalance between fat intake and oxidation. Enhanced fat oxidation during exercise will have a role, but our data suggest that exercise may also have an effect on fat balance through promoting fat oxidation during the hours following a fat-containing meal.It has recently been suggested that insulin resistance plays a role in regulating the postprandial concentrations of TAG-rich lipoproteins(15). In our study the plasma insulin response, reported to be highly correlated with insulin resistance, was not strongly related to indices of lipemia. Moreover, the area under the insulin concentration-time curve was significantly reduced by moderate exercise but not by low intensity exercise of equivalent energy expenditure so changes in the biological actions of insulin do not appear to be important determinants of the exercise-induced decrements in lipemia that we observed. Our young subjects had much lower fasting TAG concentrations than the older (mean age 59 yr) subjects studied by Jeppesen and colleagues (15), however, and it may not be surprising that insulin sensitivity did not appear to exert a strong influence on lipemia in the present study.Our study cannot shed light on the mechanisms responsible for the decrease in lipemia after the prolonged walking bouts, but it does show clearly that this effect is independent of relative exercise intensity (in the low/moderate range) when an equivalent amount of energy is expended.REFERENCES1. Abbott, W. G., B. V. Howard, L. Christin, et al. Short-term energy balance: relationship with protein, carbohydrate and fat balances. Am. J. Physiol. 255:E332-E337, 1988. [Medline Link] [Context Link]2. Aldred, H. E., I. Perry, and A. E. Hardman. The effect of a single bout of brisk walking on postprandial lipemia in normolipidaemic young adults. Metabolism 43:836-841, 1994. [Context Link]3. Blair, S. N., H. W. Kohl, R. S. Paffenbarger, D. G. Clark, K. H. Cooper, and L. W. Gibbons. Physical fitness and all-cause mortality: a prospective study of healthy men and women. J.A.M.A. 262:2395-2401, 1989. [CrossRef] [Medline Link] [Context Link]4. Borg, G. Perceived exertion: A note on history and methods. Med. Sci. Sports 5:90-93, 1973. [Full Text] [Medline Link] [Context Link]5. Brunzell, J. D., W. R. Hazzard, D. Porte, and E. L. Bierman. Evidence for a common, saturable, triglyceride removal mechanism for chylomicrons and very low density lipoproteins in man. J. Clin. Invest. 52:1578-1585, 1973. [CrossRef] [Medline Link] [Context Link]6. Consolazio, C. F., R. E. Johnson, and L. J. Pecora.Physiological Measurements of Metabolic Functions in Man. New York: McGraw Hill, 1963, pp. 313-319. [Context Link]7. Crouse, S. F., B. C. O'Brien, J. J. Rohack, et al. Changes in serum lipids and apolipoproteins after exercise in men with high cholesterol: influence of intensity. J. Appl. Physiol. 79:279-286, 1995. [Context Link]8. Dill, D. B. and D. L. Costill. Calculation of percentage changes in volumes of blood, plasma and red cells in dehydration. J. Appl. Physiol. 37:247-248, 1974. [Medline Link] [Context Link]9. Durnstine, J. L. and W. L. Haskell. Effects of exercise training on plasma lipids and lipoproteins. Exerc. Sports Sci. Rev. 22:477-521, 1994. [Context Link]10. Ebenbichiler, C. F., R. Kirchmair, C. Egger, and J. R. Patsch. Postprandial state and atherosclerosis. Curr. Opinion Lipidol. 6:286-290, 1995. [Context Link]11. Griffiths, A. J., S. M. Humphreys, M. L. Clark, B. A. Fielding, and K. N. Frayn. Immediate metabolic availability of dietary fat in combination with carbohydrate. Am. J. Clin. Nutr. 59:53-59, 1994. [Medline Link] [Context Link]12. Groot, P. H. E., W. A. H. J. Van Stiphout, H. J. Krauss, et al. Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease. Arteriosclerosis Thrombosis 11:653-662, 1991. [Full Text] [Medline Link] [Context Link]13. Haskell, W. L. Health consequences of physical activity: understanding and challenges regarding dose-response. Med. Sci. Sports Exerc. 26:649-660, 1994. [CrossRef] [Full Text] [Medline Link] [Context Link]14. Holland, B., A. A. Welch, I. D. Unwin, D. H. Buss, A. A. Paul, and D. A. T. Southgate. McCance and Widdowson's “The Composition of Foods”, 5th Ed. London: Royal Society of Chemistry and Ministry of Agriculture, Fisheries and Food, 1991, 23-385. [Context Link]15. Jeppesen, J., C. B. Hollenheck, M.-Y. Zhou, et al. Relation between insulin resistance, hyperinsulinemia, postheparin plasma lipoprotein lipase activity, and postprandial lipemia. Arteriosclerosis Thromb. Vasc. Biol. 15:320-324, 1995. [Context Link]16. Kiens, B., H. Lithell, K. J. Mikines, and E. A. Richter. Effects of insulin and exercise on muscle lipoprotein lipase activity in man and its relation to insulin action. J. Clin. Invest. 84:1124-1129. 1989. [Context Link]17. Maughan, R. J. A simple, rapid method for the detection of glucose, lactate, pyruvate, alanine, 3-hydroxybutyrate and acetoacetate on a single 20 μl blood sample. Clin. Chim. Acta 122:231-240, 1982. [CrossRef] [Medline Link] [Context Link]18. Morris, J. N., D. G. Clayton, M. G. Everitt, and E. H. Burgess. Exercise in leisure time: coronary attack and death rates. Br. Heart J. 63:325-334. 1990. [Context Link]19. Nikkila. E. A. Role of lipoprotein lipase in metabolic adaptation to exercise and training. In: Lipoprotein Lipase, J. Borensztajn (Ed.). Chicago: Evener, 1987, pp. 187-199. [Context Link]20. Patsch, J. R., J. B. Karlin, L. W. Scott, L. C. Smith, and A. M. Gotto. Inverse relationship between blood levels of high density lipoprotein subfraction 2 and magnitude of postprandial lipemia. Proc. Natl. Acad. Sci. USA 80:1449-1453, 1983. [CrossRef] [Medline Link] [Context Link]21. Podl, T. R., J. M. Zmuda, S. M. Yurgalevitch, et al. Lipoprotein lipase activity and plasma triglyceride clearance are elevated in endurance-trained women. Metabolism 43:808-813, 1994. [CrossRef] [Medline Link] [Context Link]22. Potts, J. L., S. M. Humphreys, S. W. Coppack, R. M. Fisher, G. F. Gibbons, and K. N. Frayn. Fasting plasma triacylglycerol concentrations predict adverse changes in lipoprotein metabolism after a normal meal. Br. J. Nutr. 72:101-109, 1994. [CrossRef] [Medline Link] [Context Link]23. Romijn, J. A., E. F. Coyle, L. S. Sidossis, et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am. J. Physiol. 265:E380-E391, 1993. [Medline Link] [Context Link]24. Rossner, S. Studies on an intravenous fat tolerance test: Methodological, experimental and clinical experiences with Intralipid.Acta Med. Scand. 564(suppl.):3-24, 1974. [Context Link]25. Sady, S. P., P. E. Thompson, E. M. Cullinane, M. A. Kantor, E. Domagala, and P. N. Herbert. Prolonged exercise augments plasma triglyceride clearance. J.A.M.A. 256:2552-2555, 1986. [CrossRef] [Medline Link] [Context Link]26. Saltin, B. and J. Karlsson. Muscle glycogen utilization during work of different intensities. In: Muscle Metabolism During Exercise, B. Pernow and B. Saltin (Eds.). New York: Plenum, 1971, pp. 289-299. [Context Link]27. Swinburn, B. and E. Ravussin. Energy balance or fat balance? Am. J. Clin. Nutr. 57(suppl.):766S-771S, 1993. [Medline Link] [Context Link]28. Taylor, H. L., E. Buskirk, and A. Henschel. Maximal oxygen intake as an objective measure of cardio-respiratory performance.J. Appl. Physiol. 8:73-80, 1955. [Medline Link] [Context Link]29. Tsetsonis, N. V. and A. E. Hardman. Effects of low and moderate intensity treadmill walking on postprandial lipaemia in healthy young adults. Eur. J. Appl. Physiol. 73:419-426, 1996. [CrossRef] [Medline Link] [Context Link]30. Vessby, B., I. Selinus, and H. Lithell. Serum lipoprotein and lipoprotein lipase in overweight, type II diabetics during and after supplemented fasting. Arteriosclerosis 5:93-100, 1985. [Full Text] [Medline Link] [Context Link]31. Weintraub, M. S., S. Eisenberg, and J. L. Breslow. Dietary fat clearance in normal subjects is regulated by genetic variation in apolipoprotein E. J. Clin. Invest. 80:1571-1577, 1987. [CrossRef] [Medline Link] [Context Link]32. Zilversmit, D. B. Atherogenic nature of triglcyerides, postprandial lipemia, and triglyceride-rich remmant lipoproteins. Clin. 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