Elevated postprandial triacylglycerol (TAG) concentration is considered as an independent risk factor for cardiovascular disease (2,28). One of the interventions shown to decrease postprandial lipemia (PPL) is low-to-moderate intensity aerobic exercise performed 12-24 h before the consumption of a high-fat meal (15,37). Although the mechanisms involved have not been fully elucidated, exercise energy expenditure is considered an important factor because it has been shown that the effects of exercise on PPL are related to the energy expended during exercise (15,29). It has been demonstrated that the energy expenditure of prior aerobic exercise must be at least 2.0 MJ to reduce PPL on the next day and that there is a dose response above that energy threshold (15,40). However, there is evidence suggesting that attenuation in PPL can occur with energy expenditure as low as 0.9 MJ (27).
Resistance exercise (RE) is an alternative form of training whose popularity has increased considerably over the past few years (8). The American College of Sports Medicine has recommended RE as an effective means of improving muscular strength and endurance, fat-free mass, and bone mineral density (31). Also, RE is recommended for people with and without cardiovascular disease by the American Heart Association as complementary to aerobic exercise to reduce cardiovascular disease risk factors (38). It has also been suggested that a bout of RE is even more effective than aerobic exercise of the same energy expenditure in reducing PPL on the following day (30). However, no sound conclusions can be drawn yet about the effect of acute RE on PPL because there are only five more studies on this topic. Two of those studies showed a similar positive effect of RE on PPL with energy expenditures ranging from 0.76 (39) to 5.1 MJ (7). Interestingly, the other three studies showed either no effect (6,35) or an increase in PPL 1 h after RE (5).
One speculation that was put forward to explain the results from studies finding no effect or even an increased PPL after RE is the possible detrimental effect of muscle damage caused by this form of exercise on TAG metabolism (5,6). This may counteract or even surpass the positive effect of exercise on TAG levels and result in similar or even greater PPL compared with control. One of the mechanisms involved in the possible negative effect of muscle damage on TAG metabolism is the transient insulin resistance lasting up to 48 h after muscle damaging exercise (1,21) because there is evidence that impaired insulin action is linked to impaired TAG postprandial metabolism (19).
Despite this theoretical background and the suggestion that muscle damage adversely affects PPL (5,6), there is no evidence linking muscle damage due to RE with impaired TAG metabolism. Therefore, the main purpose of the present study was to clarify whether muscle damage affects postprandial TAG metabolism when exercise energy expenditure is minimal. Furthermore, a secondary purpose was to determine whether insulin resistance due to muscle damage is related with changes in PPL. For these reasons, we have used an eccentric RE protocol known to cause muscle damage in untrained individuals (11) while keeping the total volume of exercise low. PPL was measured for two consecutive days after exercise because muscle damage indices remain elevated for more than 24 h after exercise (9). We hypothesized that if muscle damage had a detrimental effect on PPL, this would have been more evident on the second day after exercise.
Nine male volunteers aged 27.2 ± 1.1 yr took part in the study, which was approved by the institutional ethics committee. Participants gave written consent after being informed about the procedures, the risks involved, and their right to terminate participation at will. Participants were nonsmokers, without known history of cardiovascular disease, and were not taking any medication or nutritional supplements known to affect lipid or carbohydrate metabolism. In addition, participants were selected only if they had refrained from regular RE for the past 12 months. None of the participants performed more than 2 h·wk−1 of recreational physical activities (e.g., walking, cycling, swimming) as reported in personal interviews. Some physical characteristics of the participants are shown in Table 1.
Height and body mass were determined using standard methods. Body mass index was calculated by dividing body mass by the square of height (kg·m−2). Skinfold thickness was measured at seven sites (chest, midaxillary, triceps, subscapular, abdominal, anterior suprailiac, and thigh) using a Harpenden skinfold caliper, and body composition (fat and fat-free mass) was then calculated (18). Fat-free midthigh cross-sectional area (CSA) was calculated from midthigh circumference and anterior thigh skinfold measurements (16).
Study design and procedures.
Each participant took part in two conditions separated by 1 wk in random order. The control condition (C) involved only the consumption of the high-fat meal at 0800 h. In the exercise condition, participants performed the eccentric RE protocol at 1600 h and then consumed the high-fat meal in the in the morning (0800 h) of the next 2 d, that is, 16 (day 1) and 40 h (day 2) postexercise.
In the morning of C, day 1 and day 2 participants reported to the laboratory after a 12-h overnight fast and body mass was recorded. Then, they rested in a seated position for 10 min before the measurement of resting metabolic rate (Cosmed K4b2 portable metabolic unit; Cosmed, Rome, Italy). Afterward, a cannula was inserted into an antecubital vein and a baseline blood sample was obtained before the consumption of the high-fat meal. All participants consumed the test meal within 15 min and none reported any gastrointestinal discomfort.
The meal consisted of white bread, jam, margarine, and full fat milk and was given according to body mass (1.2 g fat, 1.2 g carbohydrate, 0.22 g protein, and 68.6 kJ·kg−1 body mass). The meal energy derived 65.9% from fat, 29.2% from carbohydrate, and 4.9% from protein.
Upon completion of the meal, a clock was started and further blood samples were taken at 0.5 h and hourly for 6 h. The cannula was kept patent by flushing with 0.9% sodium chloride. The first 2 mL of blood withdrawn was always discarded to avoid dilution of the sample. Water was available ad libitum the first time of the consumption of the high-fat meal, and the volume ingested was replicated during the subsequent tests. Participants remained at rest in the laboratory during the 6 h and were seated for at least 10 min before each blood sample was obtained.
Control of diet and exercise.
Participants were asked to refrain from any form of physical exercise for 2 d before each condition. They were also instructed to refrain from alcohol and caffeine intake and to record their diet for 2 d before consuming the high-fat meal for the first time (C or day 1). This diet was replicated for 2 d before the other condition 1 wk later. In the exercise condition that involved consuming the high-fat meal for two consecutive days (day 1 and day 2), food intake for the rest of day 1 (after the consumption of the test meal) was prescribed individually so that the total daily energy and macronutrient intake for each participant was the same as in the previous day. By doing this, energy intake and diet composition were standardized for the day before each test meal. Dietary analysis was done using a commercially available nutritional software program (Nutritionist V. CN-Squared; Computing Inc., San Bruno, CA). The mean daily energy intake was 9.48 ± 1.04 MJ (15.1 ± 0.5% protein, 39.7 ± 3.3% fat, and 47.1 ± 3.4% carbohydrate). The macronutrient content of the diet was kept constant before all trials so its influence on the postprandial lipid response would be the same for all trials.
Eccentric RE Protocol
After a standardized warm-up (5 min jogging on a treadmill at 8 km·h−1 and 5 min of stretching), participants performed eight sets of six repetitions of leg presses that emphasized the eccentric movement using a load equal to the individual six repetition maximum (6-RM) on a 45° inclined leg press machine (leg press; Super Sport, S.A., Athens, Greece), with a 3-min break between sets. Two spotters ensured that the required repetitions were executed in all sets by assisting during the concentric phase when the participant was unable to lift the weight. Participants were instructed to lower the weights in 4 s and to perform a forceful push when reversing from the eccentric to the concentric movement. The mechanical stops of the machine were adjusted so that knee angle (between femur and tibia) at the bottom of the downward movement was 60°. This exercise protocol has been previously shown to induce muscle damage in the leg extensors, especially in untrained individuals (11).
The 6-RM load was estimated from the CSA using the regression equation for untrained individuals developed by Dolezal et al. (11). The predicted 6-RM weight was used for the first set, and the participant was instructed to perform as many repetitions as possible. If the number of repetitions was different from six, then the load was adjusted for the remaining sets (3). A separate 6-RM test was not performed to avoid the repeated bout effect that would reduce the extent of muscle damage in the main trial (32). Muscle soreness was evaluated 24 and 48 h after the RE session using a visual analog scale that had a continuous 100-mm line with "no pain" on one end and "extremely sore" on the other. Participants were asked to rate soreness levels upon palpation of the knee extensor muscles and during one knee extension movement from a seated position. The average soreness rating of the right and left leg was used.
Duplicate 20-μL capillary blood samples were taken before exercise in the middle of the rest period between sets 4 and 5 immediately after the last set and 3 min into recovery. Samples were deproteinized in 0.3 M perchloric acid, and lactate was measured enzymatically at a later date (Sigma Diagnostics, St Louis, MO).
Estimation of energy expenditure during RE.
Throughout the exercise and for 3 min into the recovery, expired air was analyzed breath by breath using the Cosmed K4b2 portable metabolic unit. For the estimation of energy expenditure, aerobic plus anaerobic energy were summed, whereas protein contribution was ignored. Aerobic energy was calculated using an equivalent of 21.1 kJ·L−1 of oxygen consumed, whereas anaerobic energy was estimated by converting the increase in lactate concentration (from rest to the peak value) to oxygen equivalents values assuming that 1 mmol·L−1 of lactate is equivalent to 3 mL O2 kg−1 body mass (33).
At each sampling point, 5 mL of blood was placed into a 10-mL nonheparinized tube and left to clot for 1 h before being centrifuged for preparation of serum. Serum was then stored at −20°C for the later (within 3 months) determination of triacylglycerol (TAG), insulin, nonesterified fatty acids (NEFA), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), lactate dehydrogenase (LDH), and creatine kinase (CK) using an automated analyzer (ACE® Clinical Chemistry System; Alfa Wasserman, Inc., West Caldwell, NJ) with kits provided by the manufacturer. Analysis of insulin was done by an immunoenzymetric fluorescent method using a commercially available kit (ST AIA-PACK IRI; Tosoh Bioscience, Tessenderlo, Belgium) on an automated analyzer (Tosoh AIA 360; Tosoh Bioscience).
Another 2 mL of blood was placed in KF + Na2 ethylenediaminetetraacetic acid tubes to prevent further oxidation of glucose. From this sample, duplicate 20-μL aliquots were taken at the beginning and the end of the 6-h period for the colorimetric determination of hemoglobin concentration using the cyanmethemoglobin method (17) available from a commercial kit (Mallinckrodt Baker, B.V., Deventer, Holland). Hematocrit was also determined in triplicate at the same time points after centrifugation in a microcentrifuge. Changes in plasma volume were estimated from the changes in hematocrit and hemoglobin (10). Duplicate 20-μL aliquots were also taken from this tube at 0, 2, 4, and 6 h for lactate determination. Samples were deproteinized in 0.3 M perchloric acid, and lactate was measured enzymatically at a later date (Sigma Diagnostics). The remaining blood was immediately centrifuged, and plasma was collected and stored at −20°C for later glucose analysis.
Samples from the same participant were assayed on the same run. Intraassay coefficients of variation were as follows: TAG, 1.9%; NEFA, 1.24%; TC, 1.0%; LDH, 4.8%; CK, 1.99%; HDL-C, 1.6%; glucose, 1.8%; insulin, 2.8%; and lactate, 3.1%.
The total lipemic, insulinemic, and glucose responses were determined as the area under the curve (AUC) for the serum and the plasma concentration versus time by using the trapezoidal rule. The incremental areas were determined by subtracting the area corresponding to the fasting TAG concentration from the total area (i.e., normalization to the 0-h concentration).
Normal distribution of the data was verified using the Kolmogorov-Smirnov test. Comparisons of fasting values and summary postprandial responses were made using one-way ANOVA, whereas changes over the postprandial period were assessed by two-way ANOVA (trial × time) with repeated measures on both factors. Differences between means were located using Tukey's post hoc tests. Relationships between variables were evaluated using Pearson's product-moment correlation coefficient. Effect size was estimated for main effects and interaction by calculating partial eta squared (η 2) values using the Statistical Package for the Social Sciences (Version 15; SPSS Inc., Chicago, IL). Effect size for pairwise comparisons of days 1 and 2 with C was assessed with Cohen's d using the pooled SD of the two means compared. Effect sizes were classified as small (0.2), medium (0.5), and large (>0.8). Significance was accepted at the P < 0.05 level, and data are presented as mean ± SE, unless otherwise stated.
The total duration of the exercise session (including rest intervals) was 25.6 ± 0.2 min, whereas the net exercise time was 4.6 ± 0.2 min. The 6-RM load was 217 ± 27 kg. The calculated gross energy expenditure was 0.64 ± 0.04 MJ, and the net energy expenditure (gross minus resting) was 0.46 ± 0.03 MJ. Preexercise blood lactate concentration was 1.7 ± 0.3 mmol·L−1, whereas peak lactate concentration was observed immediately after the end of the exercise session (13.6 ± 1.1 mmol·L−1). There were no differences between trials in resting metabolic rate before the consumption of the meal (C: 7871 ± 463 MJ; day 1: 8593 ± 404 MJ; day 2: 8465 ± 487 MJ; P = 0.31, η 2 = 0.31).
Fasting and postprandial serum and plasma concentrations.
Serum and plasma concentrations in the fasted state are shown in Table 2. Fasting serum TAG concentration was significantly different between the three trials (P < 0.02, η 2 = 0.42). Post hoc tests revealed that fasting TAG concentration was lower on day 2 compared with C (P < 0.05, d = 0.66) but did not differ between C and day 1. Resting CK (Table 2) was significantly higher on both days after exercise compared with C (η 2 = 0.42; d = 1.47 for day 1 and d = 1.11 for day 2), whereas LDH was higher on day 2 compared with C (η 2 = 0.33; d = 0.88; Table 2). As shown in Figure 1, muscle soreness ratings for palpation and extension increased significantly after exercise and peaked on day 2.
Changes in plasma volume were less than ±1% and did not differ between trials, and thus no adjustments were made to the measured concentrations. Postprandial TAG responses and total and incremental AUC are shown in Figure 2. There were significant main effects of trial (P < 0.02, η 2 = 0.41) and time (P < 0.001, η 2 = 0.59), but no Trial × Time interaction (P = 0.31, η 2 = 0.14) for postprandial TAG concentration was found. Post hoc tests for the trial main effect revealed that the TAG curve for day 1 was lower compared with C (P < 0.02) with no significant difference between C and day 2 (P = 0.19) and between day 1 and day 2 (P = 0.42). Total TAG AUC differed between the 3 d (8.54 ± 0.99, 7.51 ± 0.99, 7.94 ± 1.13 mmol·L−1·6 h−1 for C, day 1, and day 2, respectively; P < 0.05; η 2 = 0.36). Total TAG AUC was 12.1% lower on day 1 (P < 0.05, d = 0.35) and 7.0% lower on day 2 (P = 0.27, d = 0.19) compared with C (Fig. 2). Incremental TAG AUC did not differ between trials (P = 0.25; Fig. 2). There were no significant correlations between indices of PPL (total and incremental TAG AUC) and CK or LDH concentration on day 1 (r = 0.07-0.21, P > 0.60). Also, indices of PPL on day 1 were not related to exercise energy expenditure (r = −0.42 to −0.34, P > 0.26).
Fasting and postprandial plasma glucose and serum insulin responses are shown in Figure 3. There was a main effect for time (P < 0.001, η 2 = 0.66) but no main effect for trial or Trial × Time interaction for glucose. There was no between-trial difference for total and incremental glucose AUC.
There was a main effect for time (P < 0.001, η 2 = 0.82) and a trial × time interaction for insulin (P < 0.02, η 2 = 0.21) but no main effect of trial (P = 0.18; Fig. 3). Post hoc tests for the trial × time interaction revealed that insulin concentration was higher on the second hour of day 2 compared with C (Fig. 3). A significant effect of trial was found for insulin incremental AUC (P < 0.05, η 2 = 0.33), with insulin incremental AUC being greater on day 2 compared with C (726.3 ± 67.9 vs. 553.6 ± 53.1 pmol·L−1·6 h−1, P < 0.05, d = 0.94; Fig. 3). Despite significant changes in PPL on day 1, insulin response remained unchanged, and there were no significant correlations between insulin and indices of PPL (r = 0.21-0.49, P > 0.20). NEFA postprandial responses were similar in all three trials whereas there was a main effect of time (P < 0.01, η 2 = 0.90).
The main finding of the present study was that low-volume eccentric RE caused a significant decrease in postprandial TAG concentration 16 h postexercise despite the large increase of indirect indices of muscle damage. Also, the further increase of indirect indices of muscle damage and the consequent transient increase in insulin on day 2 did not impair PPL. To the knowledge of the authors, this is the only study that has examined the effects of muscle damage caused by eccentric RE on PPL for two consecutive days after exercise. The results of the present study suggest that muscle damage does not have a negative effect on postprandial TAG metabolism, as previously suggested (5,6).
We sought to find evidence linking muscle damage due to RE with impaired TAG metabolism based on the results of previous studies by Burns et al. (5,6), who suggested that PPL may be negatively affected by the metabolic consequences of muscle damage. In one of those studies (5), muscle damage was documented based on increased plasma myoglobin, whereas in the other (6) it was argued that participants were not accustomed to RE, without providing any evidence for muscle damage. The present study was designed to cause significant muscle damage by using a previously validated protocol of eccentric low-volume RE (11) and participants who were not accustomed to RE. The magnitude of muscle damage caused by this protocol was indicated by the large increases in serum CK and ratings of perceived muscle soreness (Table 2, Fig. 1), which were equal or greater compared with the values reported for the validated protocol (11). However, in contrast with the findings of Burns et al. (5) who found increased PPL 1 h after RE, the present study showed attenuation in PPL 16 h after exercise that was not correlated with any of the indirect indices of muscle damage. The different findings of Burns et al. (5) and our study may be attributed to the timing of the meal in relation to the exercise (1 vs. 16 h postexercise). This discrepancy may indicate a time-course phenomenon dependent on the progression of muscle damage over the hours after exercise (9).
A secondary purpose of the study was to determine whether insulin resistance due to muscle damage is related with changes in PPL as suggested by Burns et al. (5,6) who speculated that insulin resistance, developed due to muscle damage, may impair the uptake of TAG into adipose tissue/skeletal muscle. A transient insulin resistance, lasting up to 2 d, is a common finding after muscle damaging exercise (1,21). In our study, although the insulin response after the meal on day 1 was identical with the control trial (Fig. 3), a transient increase in insulin concentration was observed 2 h after the consumption of the meal on day 2, resulting in an increase of the incremental insulin AUC (Fig. 3). Nevertheless, contrary to our hypothesis, PPL on day 2 was not different from C, and there were no significant correlations between indices of PPL and insulin response. This provides further evidence dissociating the metabolic consequences of muscle damage from the beneficial effects of RE on PPL.
The 12.1% lower total TAG AUC on day 1 compared with C is an interesting finding because the total energy expenditure during exercise was only 0.64 ± 0.04 MJ. This energy expenditure is the lowest reported to have a beneficial effect on PPL and was achieved by only eight sets of six repetitions of leg press against a load of 6-RM, with 3-min rest intervals between sets. This resulted in a pure exercise time of only 4.6 min, during which ∼50 muscle contractions were performed, whereas the remaining 21 min constituted the rest intervals between sets. It is noteworthy that the characteristics of this exercise program are typical of maximal strength training session (23). The attenuation of PPL with such a short exercise time is a novel concept and is in agreement with the idea that the intermittent exercise of low volume may have similar metabolic effects to the traditional continuous exercise (26). There is also evidence to suggest that repeated bouts of anaerobic exercise may have similar metabolic effects with aerobic exercise (4). A recent study demonstrated that six sessions of four to six sprints lasting 30 s each with 4 min of recovery between repetitions spread over 2 wk induced similar metabolic adaptations with six 90- to 120-min sessions of endurance cycling at 65% V˙O2max (13). The mechanisms for this time-efficient strategy have not been elucidated yet, but the combination of high metabolic stress of each exercise bout together with the elevated metabolism during the recovery intervals may result in activation of intracellular signaling pathways that may be involved in adaptations usually seen after endurance exercise (36). In the present study, the magnitude of metabolic stress was reflected by the high blood lactate concentration at the end of exercise (13.6 mmol·L−1). Also, due to the intermittent nature of exercise, the greater part of energy expenditure was accounted for by elevated oxygen consumption during recovery between sets. Although the effects of exercise intensity on PPL have been examined only for submaximal efforts and were found nonsignificant (37), the present results suggest that very intense muscle contractions may have an effect through a mechanism that seems to be less related to energy expenditure. The dissociation of energy expenditure from the magnitude of PPL attenuation during RE has been previously demonstrated by Zafeiridis et al. (39), who reported a similar 20-24% decrease in total TAG AUC after two protocols with different energy expenditure (0.76 and 1.40 MJ).
Contrary to the total TAG AUC, incremental AUC was not significantly affected by exercise on day 1 (Fig. 2). This has also been observed after RE of low volume, whereas both total and incremental TAG AUC were reduced when the exercise volume was doubled (39). These findings may suggest that the attenuation of the net lipemic response to a fat meal, as reflected by a decrease in the incremental TAG AUC, may require a greater exercise stimulus. Nevertheless, the reduction of the total TAG AUC on day 1 clearly demonstrates that our low-volume RE protocol has a positive effect on health by lowering the level of circulating TAG after the consumption of a high-fat meal.
The possible mechanisms for the decrease in PPL in the present study may involve both local (i.e., intramuscular) and systemic (i.e., hormonal) changes (14). One mechanism that may explain the attenuated levels of PPL could involve increased TAG clearance from the bloodstream due to enhanced muscle lipoprotein lipase (LPL) activity (20). Although the role of eccentric RE on LPL regulation has not been studied, however, data from aerobic exercise studies show increased plasma LPL concentration the day after aerobic exercise (25). Also, an increase in muscle LPL content and/or activity has been found after an acute 1-h bout of knee extensors exercise (20). The increase in muscle LPL activity may be modulated by circulating levels of insulin and/or by a tissue specific effect through transcriptional regulation of the LPL gene (20,24). In the present study, insulin response on day 1 was identical with C, suggesting that muscle LPL activity could not have been modified by this hormonal mechanism. However, it is possible that eccentric exercise may have a significant local effect on the previously exercised muscles through gene regulation (24,34). This effect may be related with the high levels of loading and the associated metabolic and ultrastructural changes seen in this type of exercise. An up-regulation of the LPL gene through these local effects may also explain the decrease in PPL after exercise of such a low volume and energy expenditure.
Another attractive theory to explain the reduced PPL is that intramuscular lipids are depleted by exercise and are subsequently replenished by the fat contained in the test meal (15). RE results in a significant reduction of intramuscular TAG (by 27%) as well as glycogen stores (22). However, intramuscular TAG are replenished within 2 h after RE (22), and thus it is not likely that this mechanism may be the cause of the reduced PPL observed 16 h after RE. Alternatively, heavy eccentric RE may have influenced hepatic secretion of VLDL-TAG. Although there is some evidence suggesting that aerobic exercise may modify VLDL-TAG secretion by the liver (12,25), the possible effects of RE remain to be elucidated.
In conclusion, eccentric RE involving only eight sets of leg presses against a load of 6-RM caused a significant decrease in postprandial TAG concentration 16 h postexercise, despite the low energy expenditure of 0.64 MJ and the large degree of muscle damage. In addition, contrary to our hypothesis, the transient insulin resistance 2 d after exercise did not have a detrimental effect on PPL. These results lend further support to the notion that RE with heavy loads may also be used to promote cardiovascular health.
The authors report that no professional relationships with companies or manufacturers who will benefit from the results of the present study exist.
The authors report no conflict of interest or endorsement by ACSM.
1. Asp S, Daugaard JR, Kristiansen S, Kiens B, Richter EA. Eccentric exercise decreases maximal insulin action in humans: muscle and systemic effects. J Physiol
2. Boquist S, Ruotolo G, Tang R, et al. Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men. Circulation
3. Brzycki M. Strength testing-predicting a one-rep max from reps-to-fatigue. J Phys Educ Recreat Dance
4. Burgomaster KA, Howarth KR, Phillips SM, et al. Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. J Physiol
5. Burns S, Broom DA, Miyashita M, Ueda C, Stensel DJ. Increased postprandial lipaemia following a bout of resistance exercise. Med Sci Sports Exerc
6. Burns SF, Corrie H, Holder E, Nightngale T, Stensel DJ. A single session of resistance exercise does not reduce postprandial lipaemia. J Sports Sci
7. Burns SF, Miyashita M, Ueda C, Stensel DJ. Multiple bouts of resistance exercise and postprandial triacylglycerol and serum c-reactive-protein concentrations. Int J Sport Nutr Exerc Metab
8. Centers for Disease Control and Prevention. Trends in strength training-United States, 1998-2004. MMWR
9. Clarkson PM, Hubal MJ. Exercise-induced muscle damage in humans. Am J Phys Med Rehabil
. 2002;81(Suppl 11):S52-69.
10. Dill DB, Costill DL. Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. J Appl Physiol
11. Dolezal BA, Potteiger JA, Jacobsen DJ, Benedict SH. Muscle damage and resting metabolic rate after acute resistance exercise with an eccentric overload. Med Sci Sports Exerc
12. Fukuda N, Tojho M, Hidaka T, Sho H, Sugano M. Reciprocal responses to exercise in hepatic ketogenesis and lipid secretion in the rat. Ann Nutr Metab
13. Gibala MJ, Little JP, van Essen M, et al. Short-term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance. J Physiol
14. Gill JMR, Hardman AE. Exercise and postprandial lipid metabolism: an update on potential mechanisms and interaction with high carbohydrate diets (Review). J Nutr Biochem
15. Gill JM, Herd SL, Hardman AE. Moderate exercise and post-prandial metabolism: issues of dose-response. J Sports Sci
16. Housch DJ, Housch TJ, Weir JP, Weir LL, Johnson GO, Stout JR. Anthropometric estimation of thigh muscle cross-sectional area. Med Sci Sports Exerc
17. International Committee for Standardization in Hematology. Recommendations for reference method for hemoglobinometry in human blood (ICSH 1986) and specifications for international hemoglobobincyanide reference preparation, 3rd ed. International Committee for Standardization in Hematology; Expert Panel on Haemoglobinometry. Clin Lab Haematol
18. Jackson AS, Pollock ML. Generalized equations for predicting body density of men. Br J Nutr
19. Jeppesen J, Hollenbeck CB, Zhou M-Y, et al. Relation between insulin resistance, hyperinsulinemia, postheparin plasma lipoprotein lipase activity, and postprandial lipemia. Arterioscler Thromb Vasc Biol
20. Kiens B, Lithell H, Mikines KJ, Richter EA. Effects of insulin and exercise on muscle lipoprotein lipase activity in man and its relation to insulin action. J Clin Invest
21. Kirwan JP, Hickner RC, Yarasheski KE, Kohrt WM, Wiethop BV, Holloszy JO. Eccentric exercise induces transient insulin resistance in healthy individuals. J Appl Physiol
22. Koopman R, Manders RJF, Jonkers RAM, Hul GBJ, Kuipers H, van Loon LJC. Intramyocellular lipid and glycogen content are reduced following resistance exercise in untrained healthy males. Eur J Appl Physiol
23. Kraemer WJ, Ratamess NA. Fundamentals of resistance training: progression and exercise prescription. Med Sci Sports Exerc
24. Ladu MJ, Kapsas H, Palmer WK. Regulation of lipoprotein lipase in muscle and adipose tissue during exercise. J Appl Physiol
25. Magkos F, Wright DC, Patterson BW, Mohammed S, Mittendorfer B. Lipid metabolism response to a single, prolonged bout of endurance exercise in healthy young men. Am J Physiol Endocrinol Metab
26. Miyashita M, Burns SF, Stensel DJ. Exercise and postprandial lipemia: effect of continuous compared with intermittent activity patterns. Am J Clin Nutr
27. Miyashita M, Tokuyama K. Moderate exercise reduces serum triacylglycerol concentrations but does not affect pre-heparin lipoprotein lipase concentrations after a moderate-fat meal in young men. Br J Nutr
28. Patsch JR, Miesenbock G, Hopferwieser T, et al. Relation of triglyceride metabolism and coronary artery disease. Studies in the postprandial state. Arterioscler Thromb
29. Petitt DS, Cureton KJ. Effects of prior exercise on postprandial lipemia: a quantative review. Metabolism
30. Petitt DD, Sigurborn A, Arngrimsson A, Cureton KJ. Effect of resistance exercise on postprandial lipemia. J Appl Physiol
31. Pollock ML, Gaesser GA, Butcher JD, et al. American College of Sports Medicine position stand on the recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness, and flexibility in adults. Med Sci Sports Exerc
32. Proske U, Allen TJ. Damage to skeletal muscle from eccentric exercise. Exerc Sport Sci Rev
33. Scott CB. Contribution of blood lactate to the energy expenditure of weight training. J Strength Cond Res
34. Seip RL, Angelopoulos TJ, Semenkovich CF. Exercise induces human lipoprotein lipase gene expression in skeletal muscle but not adipose tissue. Am J Physiol Endocrinol Metab
. 1995;31(2 Pt 1):E229-36.
35. Shannon KA, Shannon RM, Clore JN, Gennings C, Warren BJ, Potteiger JA. Resistance exercise and postprandial lipemia: the dose effect of differing volumes of acute resistance exercise bouts. Metabolism
36. Terada S, Kawanaka K, Goto M, Shimokawa T, Tabata I. Effects of high-intensity intermittent swimming on PGC-1a protein expression in rat skeletal muscle. Acta Physiol Scand
37. Tsetsonis NV, Hardman AE. Reduction in postprandial lipemia after walking: influence of exercise intensity. Med Sci Sports Exerc
38. Williams MA, Haskell WL, Ades PA, et al. American Heart Association scientific statement. Resistance exercise in individuals with and without cardiovascular disease: 2007 update. Circulation
39. Zafeiridis A, Goloi E, Petridou A, Dipla K, Mougios V, Kellis S. Effects of low- and high-volume resistance exercise on postprandial lipaemia. Br J Nutr
40. Zhang JQ, Ji LL, Fogt DL, Fretwell VS. Effect of exercise duration on postprandial hypertriglyceridemia in men with metabolic syndrome. J Appl Physiol
Keywords:©2009The American College of Sports Medicine
TRIACYLGLYCEROL; MUSCLE DAMAGE; PLYOMETRIC EXERCISE; FAT TOLERANCE TEST