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Originally published In Press as doi:10.1194/jlr.M200436-JLR200 on December 1, 2002

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Journal of Lipid Research, Vol. 44, 522-526, March 2003
Copyright © 2003 by Lipid Research, Inc.

Single session exercise stimulates formation of preß1-HDL in leg muscle

Dmitri Sviridov1, Bronwyn Kingwell, Anh Hoang, Anthony Dart and Paul Nestel

Wynn Domain, Baker Medical Research Institute, PO Box 6492 St. Kilda Rd. Central, Melbourne, Victoria, 8008, Australia

Published, JLR Papers in Press, December 1, 2002. DOI 10.1194/jlr.M200436-JLR200

1 To whom correspondence should be addressed. e-mail: dmitri.sviridov{at}baker.edu.au


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 Results
 Discussion
 REFERENCES
 
Physical activity can raise the level of circulating HDL cholesterol. Preß1-HDL is thought to be either the initial acceptor of cellular cholesterol or virtually the first particle in the pathway of the formation of HDL from apolipoprotein A-I and cellular lipids. We have therefore sought to identify preß1-HDL in arterial and venous circulations of exercising legs in healthy individuals and in subjects with stable Type 2 diabetes mellitus. Blood samples were taken simultaneously from the femoral artery and vein before and after 25 min cycling exercise. The major findings were, first, that exercise significantly increased plasma concentration of preß1-HDL (20% increase, P < 0.05) and second, that the preß1-HDL concentration was significantly higher in the venous compared with the arterial blood both before and after exercise in both diabetics and controls.

In the combined population, formation of preß1-HDL at rest was 9.9 ± 5.2 mg/min and exercise enhanced preß1-HDL formation 6.6-fold in both groups.

Abbreviations: CETP, cholesteryl ester transfer protein; LBF, leg blood flow; LPL, lipoprotein lipase; PLTP, phospholipid transfer protein; RCT, reverse cholesterol transport; TRL, triglyceride-rich lipoproteins

Supplementary key words reverse cholesterol transport • high density lipoprotein • cholesterol • atherosclerosis


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 Results
 Discussion
 REFERENCES
 
Physically active people appear to be at reduced risk of cardiovascular disease (1, 2) although the required amount of exercise is uncertain (1, 3). The protective effect has been partially attributed to the increased concentration of HDL, which is inducible with regular, moderately intensive exercise (3, 4). The effect of exercise on HDL concentration is the most consistent and by far the most pronounced effect of exercise on lipoprotein metabolism (4–6). An increase in HDL cholesterol (HDL-C) was reported even after a single bout of intensive exercise (4). The mechanisms responsible for the effect of physical activity on HDL concentration are likely to be multiple. Lipids, mainly nonesterified cholesterol and phospholipid, are transferred to HDL during the catabolism of triglyceride-rich lipoproteins (TRL), which increases with exercise though the activation of lipoprotein lipase (LPL) (7, 8). Several other components of reverse cholesterol transport (RCT) that may affect HDL concentration, such as the activity of lecithin cholesterol acyltransferase (LCAT) and cholesteryl ester transport protein (CETP), are affected by exercise (9, 10). Additional sources of HDL-C might also be derived during acute exercise from cellular cholesterol especially from exercising muscle as other lipids become utilized for fuel. Muscle triglyceride becomes depleted with prolonged endurance exercise (8). It is possible that when cells become depleted of triglyceride, cellular cholesterol is also mobilized and released to its primary acceptor, HDL. In physically fit people, the HDL-C concentration correlates strongly with lean body mass (11).

The possibility that HDL-C might be generated in an exercising muscle has been investigated by Kiens and Lithell (12), who compared a pretrained leg muscle mass with its untrained pair during an acute period of exercise. In six healthy individuals, LPL activity and the uptake of triglycerides from TRL were greater in trained muscle. Importantly, there was a significantly higher venous-arterial difference in the HDL-C concentration across the leg in the trained muscle that correlated significantly with the arterial-venous difference in VLDL triglyceride. Thus, the production of HDL-C increased in the trained leg muscle and was ascribed to degradation of VLDL. A similar conclusion was drawn by Ruys et al. (13), who observed increased production of HDL in the exercising forearm of individuals who had eaten a fat meal.

Evidence for a contribution to circulating HDL of adaptive changes in the metabolism of exercising muscle would be strengthened by demonstrating net production of the earliest and smallest HDL particle, preß1-HDL, from such muscle. Preß1-HDL is considered as the initial acceptor of cellular cholesterol during RCT, or virtually the first particle in the pathway of HDL formation (14, 15). We have therefore sought to identify preß1-HDL in arterial and venous circulations of exercising legs in healthy individuals and in subjects with stable Type 2 diabetes mellitus. We chose to include diabetic patients in whom HDL metabolism is perturbed and because dyslipidemic patients have been shown to have raised concentrations of circulating preß1-HDL (16).


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
Results
 Discussion
 REFERENCES
 
Subjects
After providing written informed consent, nine type 2, noninsulin dependent diabetic males aged 48 ± 4 (mean ± SD) and seven controls (46 ± 5 years) participated in the study which was approved by the Alfred Hospital Ethics Committee, and conducted in accordance with the Declaration of Helsinki of the World Medical Association. All subjects were nonsmokers, free of overt coronary disease (stress ECG) with a body mass index of 25.9 ± 1.0 kg · m-2 for controls and 28.1 ± 1.4 kg · m-2 for diabetics (P = 0.25). Control subjects did not take any medication. Of the type 2 diabetics, seven were controlled by diet and two were medicated with metformin (half-life 3.5 h). Of those medicated, one was also taking gliclazide (half-life 12 h). Medication was not taken the night before or on the morning of the studies. All were normally active but were not specifically exercise trained.

Experimental procedures
The exact experimental procedures have been described previously (17). Briefly, after an overnight fast, subjects attended the Alfred Hospital at 0800 h. Teflon catheters were placed in the right femoral artery and right femoral vein under local anesthetic (1% lignocaine, Astra, Sydney, Australia) using strict aseptic conditions. A thermistor probe was inserted though the venous catheter and advanced ~8 cm beyond the catheter tip. The catheters were used for simultaneous arterial and venous blood sampling, arterial blood pressure measurement, and for venous blood flow measurement.

After resting for ~30 min, leg blood flow (LBF) was measured, heart rate and blood pressure were recorded, and blood samples were simultaneously obtained from the two catheters. Subjects then cycled supine at a predetermined workload eliciting 60 ± 2% pulmonary oxygen uptake (VO2) peak for 25 min. After 25 min of exercise, LBF was measured using continuous infusion thermodilution, as described previously (17).

Blood sampling and analysis
Simultaneous blood samples were drawn into EDTA tubes from the femoral artery and vein before and after 25 min of exercise. Blood was immediately placed on ice, then centrifuged at 1,500 g with the plasma frozen at -80°C for later analysis. It was demonstrated in preliminary experiments that under these conditions the concentration of preß1-HDL remains the same as in fresh samples and does not change for at least 1 year. These strict conditions were essential because keeping plasma at +4°C for more than 30 min as well as prolonged storage at -20°C or slow freezing lead to sharp elevation of preß1-HDL levels, probably due to decay of mature HDL particles. Plasma total cholesterol, triglycerides (TG), HDL-C, and apolipoprotein A-I (apoA-I) were measured using enzymatic spectrophotometric techniques with a Cobas-BIO centrifugal analyzer (Roche Diagnostic Systems, Basel, Switzerland). Preß1-HDL concentration was measured by ELISA (18) (Daiichi Pure Chemicals, Tokyo, Japan) (Inquiries about preß1-HDL ELISA assay and anti-preß1-HDL monoclonal antibody should be forwarded to Dr. Osamu Miyazaki, Diagnostics Research Laboratories, Daiichi Pure Chemicals Co., Ltd., 2117 Muramatsu Tokai Ibaraki 319-1182, Japan; Fax: +81-29-282-0402; e-mail: miyazaki-o{at}daiichichem.co.jp.)

Statistics
All results are expressed as mean ± SD. Group characteristics were compared by One Way ANOVA. Differences between parameters in venous and arterial blood and before and after exercise were analyzed by one way repeated measurements ANOVA with Bonferoni adjustment. Differences in preß1-HDL production before and after exercise were analyzed by Wilcoxon Signed Rank Test. Production of preß1-HDL was calculated by multiplying venous-arterial difference (µg/ml) by LBF (ml/min) to give a value in µg/min.


   Results
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 Results
Discussion
 REFERENCES
 
Measurements of preß1-HDL
Preß1-HDL concentration was expressed as apoA-I content of this subfraction, which was measured by ELISA utilizing specific anti-preß1-HDL monoclonal antibody (18). The preß1-HDL assay, as well as the specific anti-preß1-HDL antibody, has been characterized previously (18, 19). It was demonstrated that the monoclonal antibody reacts exclusively with preß1-HDL (18). Moreover, when used for the isolation of preß1-HDL the antibody completely removed preß1-HDL from human plasma and presented isolated preß1-HDL as a pure individual fraction (19). When several samples were analyzed both by ELISA and by nondenaturing two-dimensional electrophoresis, the relative abundance of preß1-HDL in plasma samples as well as differences between the samples were similar for both techniques (not shown).

The average concentration of preß1-HDL at rest found in this study was 130 ± 51 µg/ml (mean ± SD; n = 16). Although this is higher than average preß1-HDL concentration found in other healthy Australian individuals [82 ± 43 µg/ml (mean ± SD; n = 70)], it is within the range of previous measurements (13–207 µg/ml) and not dissimilar from that observed by others (20, 21). The proportion of apoA-I in the preß1-HDL subfraction (10.8%) is also similar to that found in our previous studies, when the relative concentration of preß1-HDL was measured using nondenaturing two-dimensional electrophoresis (22, 23). The reasons for higher average preß1-HDL concentration in the plasma of individuals examined in this study are not known, though they may fortuitous or related to the invasive nature of the procedure (see Materials and Methods).

The average plasma preß1-HDL concentration found in this laboratory both by ELISA and by nondenaturing two-dimensional electrophoresis as well as that reported from another laboratory using only the latter method (20, 21) is 4–5-fold higher than that reported by Miyazaki et al., using the ELISA method (18). The method was therefore cross standardized between the two laboratories (ours and that in Japan) by measuring the same plasma samples in a blinded study. Similar values were reported in both laboratories, excluding methodological variations and confirming good reproducibility. We hypothesize that the differences observed partly reflect ethnic differences between Australian and Japanese populations.

Formation of preß1-HDL in leg muscle
Plasma concentrations of total cholesterol, triglycerides, HDL-C, apoA-I, and preß1-HDL in blood taken from the femoral artery and vein before and after exercise were compared. Plasma total cholesterol concentration was 4.6 ± 0.7 mmol/l for controls and 4.1 ± 0.7 mmol/l for diabetics (P = 0.22). Compared with controls, the concentrations of apoA-I and HDL-C in both venous and arterial blood were lower in the diabetics whereas the concentration of triglycerides was higher; there was no statistically significant difference in preß1-HDL concentrations (Table 1). To study the response of lipid parameters to exercise, data from control and diabetic patients were combined. This was justified by the finding that both groups exercised at the same absolute and relative workload and changes in lipid parameters in response to exercise were similar in both groups.


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  		TABLE 1. Concentration of HDL-C, apoA-I, TG, and preß1-HDL in arterial and venous blood at rest and after single session exercise

 
The concentration of preß1-HDL on the venous side was significantly higher than on the arterial side at rest (P < 0.05)(Table 2, Fig. 1) , showing that preß1-HDL is formed during passage of blood from artery to vein. The magnitude of preß1-HDL formation at rest was calculated from the rate of blood flow and the venous-arterial difference in preß1-HDL concentration. Leg blood flow (LBF) was 403 ± 41 ml/min at rest and 3,053 ± 210 ml/min after exercise (mean ± SEM; n = 16). The formation of preß1-HDL during passage from artery to vein at rest was estimated as 9.9 ± 5.2 mg/min.


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  		TABLE 2. Effect of acute exercise on concentration of HDL-C, apoA-I, and preß1-HDL in arterial and venous blood

 


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  		Fig. 1. Arterio-venous difference in preß1-HDL concentration at rest. Preß1-HDL concentration in venous blood (V) was calculated as a percentage of that in arterial blood (A) for seven healthy controls (circle) and nine diabetic subjects (square).

 
Effect of exercise on preß1-HDL formation and its plasma levels
Acute exercise stimulated the formation of preß1-HDL by 6.6-fold when the increase in flows is considered (Fig. 2) . There was no difference between nondiabetic and diabetic patients in the ability to generate preß1-HDL (P = 0.2). No statistically significant difference between arterial and venous concentrations of triglycerides, HDL-C, and apoA-I was observed (Tables 1, 2).



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  		Fig. 2. Formation of preß1-HDL during passage from artery to vein at rest and after a 25 min bout of exercise at 60% VO2 peak. Preß1-HDL formation was calculated as preß1-HDL concentration in the vein minus preß1-HDL concentration in artery multiplied by leg blood flow. *P < 0.03 (Wilcoxon Signed Rank test, n = 16). Mean ± SEM are shown.

 
A single bout of moderate exercise raised the concentration of preß1-HDL in both arterial and venous blood both in absolute terms and as a proportion of total apoA-I (P < 0.04)(Tables 1, 2). A small increase of apoA-I concentration (3–4%) was also observed, which reached statistical significance in venous (P < 0.01), but not in arterial blood (Table 2). Exercise did not have a statistically significant effect on the levels of HDL-C or triglycerides in either venous or arterial blood, although there was a tendency to higher HDL-C levels after exercise (Tables 1, 2).


   Discussion
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 Results
 Discussion
REFERENCES
 
The major finding of this paper is that a substantial amount of preß1-HDL was generated during passage from the femoral artery to the femoral vein. The formation of preß1-HDL increased dramatically after a single bout of exercise. This suggests that a significant proportion of preß1-HDL, and consequently of mature HDL, might be formed extra-hepatically and its formation responds to a physiological stimulus such as exercise. The amount of preß1-HDL synthesized at rest was 9.9 mg/min, which would translate into 14.2 g of preß1-HDL a day. This may be an underestimate to the extent that some preß1-HDL may leave the tissue by way of lymph. Nanjee et al. (24) have found particles resembling preß1-HDL in the leg lymph, suggesting that it was formed extrahepatically. The rate of apoA-I synthesis in humans has been estimated to be about 700 mg/day (25, 26). Thus, if preß1-HDL is the sole precursor of HDL, and one leg represents about one-third of the total body muscle mass, then it follows that there is substantial recycling of apoA-I between nascent and mature HDL particles. This would be consistent with the recognized cycle of nascent to mature to nascent HDL mediated by CETP, PLTP, and hepatic lipase on the catabolic side and cholesterol efflux and LCAT on the anabolic side (16). Our data identify a major contributor to the anabolic phase, to which are added nascent HDL from liver and possibly other tissues. Muscat et al. (27) have recently suggested that muscle is a potential site for reverse cholesterol transport and may contribute to the control of HDL levels. The high rate of cycling appears to exceed significantly the net turnover of apoA-I and may be analogous to the higher rate of turnover of esterified cholesterol in plasma that reflects the activity of LCAT and exceeds that of total cholesterol net turnover (28). Contributing to this high flux of preß1-HDL may be a possible defect of removal of this particle from plasma. Chetiveaux et al. (29) have also demonstrated the existence of a separate pool of preß-HDL with kinetic parameters different from {alpha}-HDL. If formation of preß1-HDL and remodeling of preß1-HDL to {alpha}-HDL is accompanied by cholesterol efflux (16), that may represent a significant contribution to reverse cholesterol transport. However, it cannot be excluded that HDL may also be formed directly without the conversion from intermediate preß1-HDL.

The importance of preß1-HDL is that it is a metabolically active particle in the initial process of removal of cholesterol from cells (reverse cholesterol transport) (14, 16). It was suggested that preß1-HDL may be an initial acceptor of cellular cholesterol during cholesterol efflux (14, 30) and/or a first product of lipidation of lipid-free apoA-I by ABCA1-dependent formation of HDL (16). The role of preß1-HDL as a precursor of mature HDL has been strengthened by a recent finding of a greater rate of incorporation of newly synthesized apoA-I into preß-HDL (29). Its concentration increases with dyslipidemia (31) and with overweight (22). Whether these conditions are associated with increased efflux of cholesterol from cells, increased catabolism of triglyceride-rich lipoproteins (both of which generate more HDL-C) or through inefficient conversion of preß1-HDL particles to mature HDL is not known. The enhanced formation of preß1-HDL after a single bout of exercise may be related to metabolic events in highly active muscle and/or increased flow of blood though the muscles. Our data are generally consistent with those reported by Kiens and Lithel (12) and Ruys et al. (13) who demonstrated formation of HDL during passage of blood though muscle. However, in those papers HDL formation was accompanied by a rise in HDL-C and was apparently linked to increased lipolysis of triglyceride-rich lipoproteins that supply fatty acids to exercising muscle. In our studies, neither triglycerides nor HDL-C levels changed significantly. It must be noted, however, that even if all preß1-HDL was formed as a result of remodeling of HDL and/or triglyceride-rich lipoproteins, that would account for less than 1.5% change in the concentration of triglyceride and HDL-C; the change would not necessarily be detected by the methods employed.

In conclusion, we have demonstrated that preß1-HDL is formed during passage of blood though muscle and this process is stimulated by exercise.


   ACKNOWLEDGMENTS
 
This work was supported by grants from the National Health and Medical Research Council of Australia and Diabetes Australia. We are grateful to Dr. Osamu Miyazaki (Daiichi Pure Chemicals) for his help with preß1-HDL ELISA assay.

Manuscript received November 12, 2002


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TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 Results
 Discussion
 REFERENCES
 
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 Arterioscler. Thromb. Vasc. Bio.Home page
B. Olchawa, B. A. Kingwell, A. Hoang, L. Schneider, O. Miyazaki, P. Nestel, and D. Sviridov
Physical Fitness and Reverse Cholesterol Transport
Arterioscler. Thromb. Vasc. Biol., June 1, 2004; 24(6): 1087 - 1091.
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