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J Appl Physiol 85: 1169-1174, 1998;
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Vol. 85, Issue 3, 1169-1174, September 1998

Effects of four different single exercise sessions on lipids, lipoproteins, and lipoprotein lipase

Michael A. Ferguson1,2, Nathan L. Alderson1, Stewart G. Trost1, David A. Essig1, Jeanmarie R. Burke1, and J. Larry Durstine1

1 Department of Exercise Science, University of South Carolina, Columbia, South Carolina 29208; and 2 Georgia Prevention Institute, Medical College of Georgia, Augusta, Georgia 30912

    ABSTRACT
Top
Abstract
Introduction
Methods
Results
Discussion
References

The purpose of this study was to determine the threshold of exercise energy expenditure necessary to change blood lipid and lipoprotein concentrations and lipoprotein lipase activity (LPLA) in healthy, trained men. On different days, 11 men (age, 26.7 ± 6.1 yr; body fat, 11.0 ± 1.5%) completed four separate, randomly assigned, submaximal treadmill sessions at 70% maximal O2 consumption. During each session 800, 1,100, 1,300, or 1,500 kcal were expended. Compared with immediately before exercise, high-density lipoprotein cholesterol (HDL-C) concentration was significantly elevated 24 h after exercise (P < 0.05) in the 1,100-, 1,300-, and 1,500-kcal sessions. HDL-C concentration was also elevated (P < 0.05) immediately after and 48 h after exercise in the 1,500-kcal session. Compared with values 24 h before exercise, LPLA was significantly greater (P < 0.05) 24 h after exercise in the 1,100-, 1,300-, and 1,500-kcal sessions and remained elevated 48 h after exercise in the 1,500-kcal session. These data indicate that, in healthy, trained men, 1,100 kcal of energy expenditure are necessary to elicit increased HDL-C concentrations. These HDL-C changes coincided with increased LPLA.

energy expenditure; lipase; triglyceride; high-density lipoprotein cholesterol; kilocalories

    INTRODUCTION
Top
Abstract
Introduction
Methods
Results
Discussion
References

BLOOD LIPID AND LIPOPROTEIN concentration changes have been observed after a single exercise session (16, 17). Reductions in triglycerides (TG) and increases in high-density lipoprotein cholesterol (HDL-C) concentration by as much as 10-25% have been noted after a single exercise session, and these changes may play a role in the improvements in lipid and lipoprotein profiles observed in trained individuals (8). Little information exists as to the amount of exercise necessary to mediate these changes. Additionally, different exercise thresholds may exist for various populations. Crouse et al. (3) found an increased HDL-C concentration the day after exercise in untrained hypercholesterolemic men when completing an exercise session requiring 350 kcal of energy expenditure. Differing results have been observed in other studies. Davis et al. (4) found no change in lipid and lipoprotein concentrations in trained men with normal blood cholesterol after two treadmill exercise sessions (subjects expended 950 kcal during each exercise session) at intensities of 50 and 75% of maximal oxygen consumption (VO2 max). Visich et al. (27) examined the effects of treadmill running at 75% of VO2 max during separate treadmill exercise sessions that required caloric expenditures of 800 and 1,600 kcal. No changes in lipid and lipoprotein concentrations were found in the 800-kcal session, whereas HDL-C concentration was significantly elevated 48 h after exercise in the 1,600-kcal session. This information suggests that an energy expenditure threshold may exist during exercise that would elicit blood lipid and lipoprotein concentration changes in trained individuals. Therefore, the purpose of this study was to determine in healthy, trained men the energy expenditure necessary to alter plasma lipid and lipoprotein concentrations and lipoprotein lipase activity (LPLA) after a single exercise session.

    METHODS
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Abstract
Introduction
Methods
Results
Discussion
References

Subjects. Eleven trained men, ages 21-44 yr, served as subjects. Subjects were recruited from the University of South Carolina. Physical and physiological characteristics are presented in Table 1. Criteria for inclusion in the study included having participated in structured exercise programming 3-5 times/wk (between 90 and 150 min of weekly aerobic activity) over the previous year, being a nonsmoker, consuming <4 alcoholic drinks/wk, and not taking any medications affecting lipid or lipoprotein metabolism. Five of the 11 subjects were previously collegiate runners, and the remaining six were recreational athletes. The purpose of the project was explained to each subject, and before participatin in the study, each gave written informed consent in accordance with the University of South Carolina College of Public Health Ethics Committee.

                              
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  		Table 1.   Descriptive characteristics of subjects

Experimental design. During their first laboratory visit, subjects completed a health-risk questionnaire, a personal interview, anthropometric measures, and a maximal treadmill exercise test to ascertain VO2 max (description to follow). The work rate for the four experimental exercise protocols that each subject completed was determined during a second laboratory visit. Treadmill speed was adjusted until 70% of VO2 max was obtained. Each experimental exercise protocol was completed at least 2 wk apart. A 2-wk interval was chosen to prevent any carryover effects from the previous experimental treatment, and normal exercise training was maintained between experimental treatments. The experimental exercise protocols consisted of continuous treadmill running at 70% of VO2 max, with caloric expenditures of 800, 1,100, 1,300, and 1,500 kcal. After subjects completed a 12-h fast, blood samples for each experimental exercise protocol were collected 24 h before exercise, immediately before exercise, immediately after exercise, 24 h after exercise, and 48 h after exercise. Subjects were asked to maintain their normal eating habits for 2 wk before and during each experimental time period to minimize the lipoprotein changes resulting from dietary variations. To ensure compliance, subjects maintained diet records for each 4-day experimental exercise protocol period. Subjects were asked to refrain from alcohol consumption 72 h before any blood collection. Subjects were also asked to maintain their regular exercise habits, and an exercise training log was kept over the duration of the study. Subjects refrained from exercise for 3 days before the start of any given exercise protocol to minimize any carryover effects from a previous exercise effort.

Anthropometric measures. Body weight and height were determined by using standard physician scales. Percent body fat was estimated with the Jackson-Pollock equation by using skinfold measures of the chest, abdomen, and thigh (15).

Maximal exercise test. VO2 max was determined by using a modified Åstrand protocol on a motorized treadmill (1). This protocol began with a 1-min warm-up at a speed that was 2.5 miles/h (mph) slower than the subjects' estimated 10-km road-racing speed at 0% grade. Speed was increased 0.5 mph every minute for a total of 5 min, until treadmill speed matched the subjects' 10-km road-racing pace. After the 5-min warm-up, treadmill grade was progressively increased 2.5% every 2 min until VO2 max was obtained. Criteria for attainment of VO2 max included a <2 ml/kg increase in oxygen consumption (VO2) with an increased work rate, a respiratory exchange ratio (RER) greater than or equal to 1.1, and/or the subject's inability to maintain this work rate (24). Ametek S-3A/I oxygen and Ametek CD-3A carbon dioxide analyzers were used during VO2 max measurements. Known concentrations of carbon dioxide and oxygen were used for calibration before and during each exercise session. Heart rate was monitored during exercise with a Polar XL heart rate monitor (Polar Electro, Port Washington, NY).

Experimental exercise protocols. The kilocalorie equivalent that corresponded to the RER value obtained at 70% VO2 max was multiplied by the VO2 value obtained during exercise to determine energy expenditure (kcal/min) (20). For each experimental exercise protocol, the calculated energy expenditure was used to determine the exercise time required to expend 800, 1,100, 1,300, or 1,500 kcal of energy at 70% of VO2 max.

During each exercise session, VO2 was measured after the first 15 min of exercise and every 30 min thereafter. Work rates were adjusted when VO2 was not within 5% of the desired value. Subjects were given water during exercise (4 ml/kg body weight every 30 min) to help maintain hydration.

Blood collection. Venous blood samples were collected from fasted subjects 24 h before and immediately before exercise, immediately after exercise, 24 h after exercise, and 48 h after exercise for all four exercise protocols. Subjects were seated for 15 min before and during resting phlebotomy. An indwelling catheter was used to collect blood samples into tubes containing EDTA. After the blood sample for lipid and lipoproteins was obtained (excluding the time immediately before exercise), an intravenous injection of heparin (sodium-heparin, 75 IU/kg body weight, delivered in a 1- to 2-ml volume) was administered (26). Ten minutes after this injection, blood samples for determination of the measurement of total lipase activity (TLA) and hepatic lipase activity (HLA) were collected in heparinized tubes. Catheter patency was maintained by a heparin well. After they were collected, blood samples were placed in an ice bath until centrifugation. Samples were separated by low-speed centrifugation (20 min at 3,000 g), with plasma placed in plastic vials and stored at -70°C until analysis. Time-of-day variations for lipid and lipoprotein concentrations were reduced by collecting blood samples at the same time of day for each subject. All samples were collected in the morning.

Blood analysis. Hematocrit was obtained with the microcapillary technique. The Drabkin and Austin (6) cyanmethemoglobin technique was used to measure hemoglobin concentration. Hematocrit and hemoglobin concentrations were used to account for plasma volume changes to prevent overestimation of TG and underestimation of HDL-C concentration changes after exercise (5).

Spectrophometric analysis, using a stable Lieberman-Burchard reagent, was used to determine total cholesterol (TC), HDL-C, and subfraction HDL3-C (18). HDL-C was determined with the manganese chloride procedure (29). HDL3-C concentration was determined by precipitation of the supernatant with 1.5 M magnesium chloride-dextran sulfate solution (30) and centrifugation (3,000 g for 30 min). Subfraction HDL2-C was calculated by subtracting HDL3-C from HDL-C. Low-density lipoprotein-cholesterol (LDL-C) and very-low-density lipoprotein cholesterol (VLDL-C) were estimated using the technique of Friedewald et al. (10). TG concentration was measured enzymatically by using a commercialized kit (procedure no. 339-10, Sigma Diagnostics, St. Louis, MO). All samples for each exercise protocol were analyzed in one laboratory session to reduce interassay variation. Primary standards of cholesterol and TG lipid concentrations prepared by Sigma Diagnostics served as internal controls for lipid and lipoprotein measures. Interassay variation for the respective analyses were TC (2.1%), TG (0.8%), HDL-C (1.4%), and HDL3-C (5.8%).

Lipase activity was measured in postheparin plasma with a modified Belfrage and Vaughan (2) radioenzymatic procedure, as described by Thompson et al. (26). The emulsion contained triolein (100 mg, no. T-7140; Sigma Diagnostics), glycerol tri[9, 10(n)-3H]oleate (25 µCi, no. TRA 191 B100; Amersham, Arlington Heights, IL), egg lecithin (0.8 mg, no. P-3556; Sigma Diagnostics), fatty acid-free bovine serum albumin (600 mg, no. A-6003; Sigma Diagnostics), Triton X-100 [0.6 ml of a 1% (vol/vol) aqueous solution, no. T-8787; Sigma Diagnostics], and 10 ml of Tris·HCl (0.194 M, pH 8.6, 0.15 M NaCl; Trizma reagent grade no. T-5503, preset crystals, pH 8.6; Sigma Diagnostics). The substrate was kept on ice during sonication, and it was sonicated for a total of 3 min by using the microtip of a model W-385 cell disrupter (Heat Systems-Ultrasonics) set at 5. After each minute of sonication, a 30-s period followed during which sonication was suspended to reduce excess heat production. The emulsion was stable for 6 h. Samples were measured in a reaction mixture containing 20 µl of postheparin plasma, 80 µl of Tris·HCl buffer (0.194 M, pH 8.6 with 0.19 M NaCl), and 100 µl of substrate. The mixture was incubated for 45 min with agitation at 37°C. The enzymatic reaction was stopped, and free fatty acids were extracted with a methanol-chloroform-heptane reagent. HLA was determined in the presence of 1.0 M NaCl, whereas LPLA was determined as the difference between the TLA and HLA (E. E. Shoup, S. L. Durstine, J. M. Davis, R. R. Pate, and W. P. Bartoli, unpublished observations). Pooled heparinized plasma samples were used for internal control measures for lipase determinations. Interassay variation for both TLA and HLA was 7.8%.

Dietary analysis. To ensure subjects' eating patterns were similar throughout the study, subjects completed dietary diaries for 4 days during each experimental protocol. To reinforce dietary compliance, feedback from the first dietary analysis was given to subjects before each experimental exercise protocol. A commercially available software program (Nutritionist III software package; N-Squared Computing, Silverton, OR) was used to analyze total caloric intake, choles-terol, and dietary carbohydrate, fat, and protein content.

Statistical analysis. Within each treatment, differences over time were tested by using ANOVA with repeated measures. Duncan's multiple-comparison test was used to determine the location of significant differences within treatments. Correlation analysis was completed with Pearson correlation. Data are presented as means ± SE. The level of significance was P < 0.05 for all statistical tests.

    RESULTS
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Abstract
Introduction
Methods
Results
Discussion
References

Subjects' baseline characteristics are presented in Table 1. VO2 during the 800-, 1,100-, 1,300-, and 1,500-kcal-expenditure exercise sessions ranged from 67 to 69% of maximum (Table 2). There were no significant changes in any dietary variable examined during any of the exercise protocols (Table 3). This reduced the likelihood of dietary modification as a confounding factor in the interpretation of any lipid and lipoprotein concentration change. Plasma volume decreased significantly immediately after exercise (from 6 to 13% in the four exercise treatments), followed by a nonsignificant increase of 1-6% in the days after exercise. Blood lipid and lipoprotein concentrations as well as lipase activity are presented as corrected values for exercise-induced plasma volume change (Tables 4 and 5). Pearson correlations were used to examine the relationship between the change in HDL-C concentration and LPLA after exercise in each of the four treatments. None of these correlations was significant.

                              
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  		Table 2.   Exercise kilocalorie expenditure, time, and distance

                              
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  		Table 3.   Dietary variables

                              
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  		Table 4.   Corrected lipid concentrations before and after exercise

                              
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  		Table 5.   Corrected lipase activity before and after exercise

No changes were observed immediately after exercise in the 800-kcal-exercise session. However, 24 h after the 800-kcal-exercise session, TG concentration decreased 26% and VLDL-C concentration decreased 22% (P < 0.05), but these changes were no longer significant at 48 h. At 24 h after the 1,100-kcal-exercise session, TG concentration decreased 30%. VLDL-C concentration also decreased (P < 0.05) at this time point, whereas HDL-C concentration increased 15% and LPLA increased 33% (P < 0.05). None of these changes existed 48 h after the 1,100-kcal-exercise session. Immediately after the 1,300-kcal-exercise session, TC and LDL-C concentration, as well as TLA and HLA, were decreased (P < 0.05). At 24 h after the 1,300-kcal-exercise session, TG concentration decreased 28%, whereas VLDL-C concentration and HLA were decreased (P < 0.05). Also, at this time point, HDL-C concentration increased 15% and LPLA increased 31% (P < 0.05). Immediately after the 1,500-kcal-exercise session, HDL-C and HDL2-C concentrations increased by 21 and 29%, respectively (P < 0.05), whereas LDL-C concentration decreased (P < 0.05). At 24 h after the 1,500-kcal-session, TG concentration decreased by 36%, and VLDL-C and LDL-C concentrations decreased (P < 0.05). Additionally, at this same time point, HDL-C concentration increased 29% (12 mg/dl), HDL2-C concentration increased by 36%, HDL3-C concentration increased by 25%, and LPLA increased by 49% (P < 0.05). At 48 h after the 1,500-kcal-exercise session, TG (20%) and VLDL-C concentrations remained decreased (P < 0.05), whereas HDL-C (24%) and HDL2-C (43%) concentration and LPLA (47%) remained increased (P < 0.05).

    DISCUSSION
Top
Abstract
Introduction
Methods
Results
Discussion
References

Four different exercise sessions were used to determine whether an energy-expenditure threshold exists for change in blood lipids and lipoprotein concentrations in trained men. Plasma HDL-C concentrations were significantly elevated in treatments that had energy expenditures of 1,100 kcal or more. The magnitude of HDL-C concentration change ranged from 15 to 28%. Delayed change (24 and 48 h after exercise) in HDL-C concentration occurred when LPLA increased (Figs. 1 and 2).


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  		Fig. 1.   Change in high-density lipoprotein-cholesterol (HDL-C) and lipoprotein lipase activity (LPLA) after exercise sessions in which subjects expended 800 (top) and 1,100 (bottom) kcal (n = 11 subjects). Data are means ± SE. FFA, free fatty acid; 24 Pre, 24 h before exercise; Imm Pre, immediately before exercise; Imm Post, immediately after exercise; 24 Post, 24 h after exercise; 48 Post, 48 h after exercise. * Significantly different from Imm Pre for HDL-C, P < 0.05; dagger  significantly different from 24 Pre for LPLA, P < 0.05.


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  		Fig. 2.   Change in HDL-C and LPLA after exercise sessions in which subjects expended 1,300 and 1,500 kcal (n = 11 subjects). Data are means ± SE. * Significantly different from Imm Pre for HDL-C, P < 0.05; dagger  significantly different from 24 Pre for LPLA, P < 0.05.

Results presented in previous studies are inconsistent regarding changes in HDL-C after a single exercise session (4, 12, 28). Some studies have found increased HDL-C concentrations after a single exercise session (16, 17) whereas others have not (4). Visich et al. (28) observed 24 h after exercise an increased HDL-C concentration and LPLA, whereas HLA decreased in trained individuals when an exercise energy expenditure of 800 kcal was achieved. Kantor et al. (16, 17) found increased LPLA and increased HDL-C concentration 24-48 h after prolonged exercise (running a marathon and riding a cycle ergometer) in studies with both trained and untrained individuals. Gordon et al. (13) found a significant increase in LPLA after exercise at 75% of VO2 max, but not after exercise at 60% of VO2 max, when energy expenditures of the two different exercise sessions were both held at 800 kcal. HDL-C concentration was significantly elevated 48 h after exercise at 75% of VO2 max, whereas HDL-C concentration was unchanged after exercise at 60% of VO2 max. However, Davis et al. (4) found no change in HDL-C concentration after a single exercise session completed at both 50 and 70% of VO2 max when the energy expenditure for both exercise sessions was 950 kcal. Individuals in the study by Davis et al. (4) were trained runners and had baseline HDL-C concentrations near 60 mg/dl. In addition, Visich et al. (28) compared the effects of treadmill running at 75% of VO2 max in college-age men who completed exercise sessions of 800 and 1,600 kcal. HDL-C concentration was increased after the 1,600-kcal-exercise session but not after the 800-kcal-exercise session.

An explanation for these inconsistencies may be related to one or more factors and includes the use of different exercise intensities, different exercise time durations, different subject training statuses, and different baseline lipoprotein values. Crouse et al. (3) have illustrated the importance of baseline values. Their subjects were sedentary and hypercholesterolemic men with mean baseline cholesterol values of 245-263 mg/dl. HDL-C concentrations were increased 24 h after exercise after a 350-kcal treadmill energy expenditure at 50 and 80% of VO2 max. Their data suggest that a different exercise threshold for HDL-C concentration increase may exist for hypercholesterolemic men.

A potential mechanism for increased HDL-C concentrations in the present study may be increased LPLA. LPL is involved with TG degradation, provides substrate material for HDL-C production, and is known to become metabolically active several hours after exercise cessation (16). TG concentration was significantly decreased 24 h after exercise in all four treatments. In addition, the decreased TG persisted for 48 h after exercise in the 1,500-kcal-exercise session. Decreased TG concentrations routinely have been observed in the days after exercise that requires subjects either to expend 800 kcal of energy or to exercise for 1 h or more (11, 16, 22, 25). TG concentration reductions in the present study were concurrent with the postexercise increased HDL-C production. In addition to providing substrate material for HDL-C production, LPLA-mediated TG hydrolysis can also aid in replenishment of intramuscular TG used during exercise (21). However, because LPLA was measured in plasma, we were unable to distinguish between muscle or adipose tissue LPLA and can only speculate on the contribution of fat mobilized from either site. Because our subjects were trained, we believe a greater percentage of the increased LPLA was from increased skeletal muscle LPLA (14).

A second potential mechanism for our finding of increased HDL-C concentrations may be decreased cholesterol ester transport protein (CETP) activity. CETP facilitates the transfer of cholesterol ester and triglyceride between HDL2 and other lipoproteins (VLDL-C and LDL-C). Föger et al. (9) found decreased CETP activity in combination with an increased HDL-C concentration 24 h after a very long cycling session of 230 km. If CETP activity were partially inhibited or slowed as a result of exercise, increased HDL-C concentration would be observed after exercise. Because HDL2-C in the present study was significantly increased immediately after the 1,500-kcal-exercise session and LPLA was not increased immediately after exercise, these two factors together suggest that CETP activity may have been decreased immediately after exercise.

Another enzyme involved in HDL-C metabolism is hepatic lipase. In the present study, a significant decrease in HLA was found immediately after and 24 h after the 1,300-kcal-exercise session. Although it was not statistically significant, HLA was also decreased after exercise in most of the exercise protocols by 10-20% and might be an indication of significant physiological change. A decreased HLA would slow hepatic HDL2-C uptake and result in higher plasma HDL-C concentrations. These results are consistent with those reported by others (13, 17).

Given the results seen in our data and those of others, there appears to be an energy threshold for an increase in plasma HDL-C concentration in trained individuals. This threshold is ~1,100 kcal or more of energy expenditure while exercising at 70% VO2 max. Additionally, a threshold for decreased TG concentrations occurred with an energy expenditure as small as 800 kcal.

LDL-C and TC concentration changes were noted after exercise in the present study. LDL-C significantly decreased immediately after the 1,300- and 1,500-kcal-exercise sessions and probably accounted for the decrease in TC concentration. These decreases persisted for 24 h in the 1,500-kcal session only. The magnitude of these changes was 17-18%. Some studies have found a decrease (9, 16, 17, 22) or no change (3, 4, 7, 12) in LDL-C concentration after exercise. Studies that have found decreased LDL-C concentrations have typically used prolonged exercise in which 1,000 kcal were expended (9, 16, 17, 22). A possible explanation for decreased LDL-C concentrations after exercise may be increased uptake of LDL-C by peripheral tissue. Although it is not commonly measured after exercise, increased uptake of LDL-C has been observed after prolonged exercise (19). Therefore, if TC or LDL-C concentrations are to change after a single exercise session, an energy expenditure of 1,300 kcal or more during exercise is probably necessary.

Conclusion. Our results indicate an exercise-induced change in blood lipid and lipoprotein concentrations after a single exercise session and the conclusion that, in trained individuals, energy thresholds for these changes do exist. An energy expenditure of 1,100 kcal or more was necessary for increased HDL-C concentration, whereas 1,300-kcal energy expenditure was necessary for a decreased LDL-C concentration. An 800-kcal energy expenditure was necessary for a decreased TG concentration after a single exercise session. Because each experimental exercise protocol was completed at least 3 days after each subject's last regular exercise session, the changes noted in lipid and lipoprotein concentrations were probably not related to the last exercise session but rather related to the single exercise intervention.

    ACKNOWLEDGEMENTS

The authors give special thanks to Dr. Linda Bausserman and the Lipid Laboratory at Miriam Hospital in Providence, RI, for guidance with the LPL assay and to Bill Bartoli for assistance with manuscript preparation.

    FOOTNOTES

Address for reprint requests: J. Larry Durstine, Dept. of Exercise Science, Univ. of South Carolina, 1300 Wheat St., Columbia, SC 29208 (E-mail: ldurstine{at}sophe.sph.sc.edu).

Received 20 June 1997; accepted in final form 19 May 1998.

    REFERENCES
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Abstract
Introduction
Methods
Results
Discussion
References

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J APPL PHYSIOL 85(3):1169-1174
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