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J Appl Physiol 91: 1760-1765, 2001;
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Vol. 91, Issue 4, 1760-1765, October 2001

Lack of alpha 2-adrenergic antilipolytic effect during exercise in subcutaneous adipose tissue of trained men

I. De Glisezinski1,2, F. Marion-Latard1, F. Crampes1,2, M. Berlan2,3, J. Hejnova4, J. M. Cottet-Emard5, V. Stich4, and D. Rivière1,2

1 Laboratoire des Adaptations de l'Organisme à l'Exercice Musculaire, Centre Hospitalier Universitaire Purpan, 31059 Toulouse Cedex; 3 Laboratoire de Pharmacologie Médicale et Clinique, Faculté de Médecine, 31073 Toulouse Cedex; 2 Institut National de la Santé et de la Recherche Médicale, Université Paul Sabatier, 31403 Toulouse Cedex; 5 Laboratoire de Physiologie de l'Environnement, Université Claude Bernard Lyon Grange Blanche, 69373 Lyon Cedex 08, France; and 4 Department of Sport Medicine, Charles University, 100 00 Prague 10, Czech Republic


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

The aim of this study was to investigate the involvement of the antilipolytic alpha 2-adrenergic receptor pathway in the regulation of lipolysis during exercise in subcutaneous abdominal adipose tissue (SCAAT). Seven trained men and 15 untrained men were studied. With the use of microdialysis, the extracellular glycerol concentration was measured in SCAAT at rest and during 60 min of exercise at 50% of maximal oxygen consumption. One microdialysis probe was perfused with Ringer solution; the other was supplemented with phentolamine (alpha 2-adrenergic receptor antagonist). No differences in baseline extracellular or plasma glycerol concentrations were found between the two groups. The exercise-induced extracellular and plasma glycerol increase was higher in trained compared with untrained subjects (P < 0.05). Addition of phentolamine to the perfusate enhanced the exercise-induced response of extracellular glycerol in untrained subjects but not in trained subjects. The exercise-induced increase in plasma norepinephrine and epinephrine concentrations and the decrease in plasma insulin were not different in the two groups. These in vivo findings demonstrate higher exercise-induced lipolysis in trained compared with untrained subjects and show that, in trained subjects, the alpha 2-mediated antilipolytic action is not involved in the regulation of lipolysis in SCAAT during exercise.

microdialysis; catecholamines; phentolamine; glycerol; nonesterified fatty acids


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

CATECHOLAMINES ARE OF MAJOR IMPORTANCE in the regulation of lipolysis in adipose tissue (20, 24) and in the increase of nonesterified fatty acid (NEFA) supply to the working muscle (6, 7). The presence of beta - and alpha 2-adrenergic receptors (AR) has been demonstrated by functional in vitro assays in isolated human fat cells and binding studies with selective ligands (9, 23, 25). The coexistence of beta -AR that increase and alpha 2-AR that decrease the rate of lipolysis in human fat cells still raises questions about their physiological relevance. In vitro, at low epinephrine concentrations, the preferential recruitment of the alpha 2-AR inhibits lipolysis (28).

Physical exercise promotes lipolysis by increases of both plasma norepinephrine and epinephrine and the decrease of plasma insulin. It was demonstrated that, during exercise, epinephrine activates alpha 2-AR and that this pathway inhibits lipolysis in subcutaneous abdominal adipose tissue (SCAAT) (30). This is particularly the case in obese subjects (29), in agreement with in vitro studies, which show the high alpha 2-mediated antilipolytic action of catecholamines in SCAAT from the obese subjects (27). It was indicated previously, in vitro, that endurance training induces a decrease of the antilipolytic alpha 2-mediated action of epinephrine, both in longitudinal studies (10) and in cross-sectional studies (28). Moreover, higher lipid mobilization was found in vitro in trained subjects compared with untrained subjects in relation to an increased response of the beta -adrenergic pathway (8).

Microdialysis appears to be an alternative method to study the lipolytic response of adipose tissue, in vivo, during exercise (1, 11); it allows local infusion of pharmacological drugs (2) and, in particular, AR antagonists to explore the efficiency of the alpha 2-adrenergic pathway.

Therefore, in the present study, by using a physical exercise model, we investigated the involvement of alpha 2-adrenergic lipolysis regulation. The aim of the present study was to compare the alpha 2-AR activity in subcutaneous adipose tissue of trained and untrained men during adrenergic stimulation. For that purpose, subjects performed a prolonged exercise bout, and lipid mobilization was assessed by the microdialysis method. The alpha 2-AR effect was explored by perfusing the microdialysis probe with phentolamine, an alpha 2-AR antagonist.


    MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Subjects

Seven trained men [mean age (± SE) = 25.9 ± 2.2 yr] and 15 lean untrained men (25.0 ± 0.2 yr) participated in the study. The untrained subjects exercised <3 h/wk. The trained subjects were high-level cyclists. The mean body-mass index was 21.8 ± 0.3 and 23.6 ± 0.5 kg/m2 for trained and untrained subjects, respectively, and the percentage of fat mass was 7.9 ± 1.1 and 13.6 ± 1.1%, respectively. The maximal oxygen uptake (VO2 max) was 72.6 ± 3.3 and 46.4 ± 5.3 ml · min-1 · kg-1 for trained and untrained subjects, respectively. All were drug free and had a stable weight for at least 3 mo before the beginning of the study. All subjects had given their written, informed consent before the study. The studies were performed according to the Declaration of Helsinki and approved by Ethics Committees of the Third Faculty of Medicine, Prague (Czech Republic) and Toulouse I (France) University Hospital.

Study Procedure

The subjects were studied at 8:00 AM after an overnight fast. After determination of body composition using skinfold thickness (12), they were placed in a semirecumbent position. Microdialysis probes (Carnegie Medecin, Stockholm, Sweden) of 20 × 0.5 mm and 20,000-MW cutoff were inserted percutaneously after epidermal anesthesia (200 µl of 1% lidocaine; Roger-Bellon, Neuilly-s-Seine, France) into the abdominal SCAAT at a distance of 10 cm immediately to the right of the umbilicus. Two probes, separated by at least 5 cm, were connected to a microinjection pump (Harvard apparatus, SARL, Les Ulis, France). One probe was perfused with Ringer solution (in mM: 139 sodium, 2.7 potassium, 0.9 calcium, and 140.5 chloride), and the second with Ringer plus 0.1 mM phentolamine (alpha -AR antagonist). This nonselective alpha 1/alpha 2-antagonist is the only agent allowed by the Ethics Committees for microdialysis assays in humans. The two perfusate solutions were supplemented with ethanol (1.7 g/l). Ethanol was added to the perfusate to estimate changes in the blood flow, as previously described (13, 14, 16, 19).

The calibration procedure using various perfusion rates was applied for interstitial glycerol concentration determination in SCAAT and as previously described by our group (2, 11). A simplified but relevant and less time-consuming method was selected in this study. The estimated extracellular glycerol concentrations were calculated by plotting (after log transformation) the concentration of glycerol in the dialysate measured at 0.5 and 2.5 µl/min against the perfusion rates. For this, after a 30-min equilibration period, a 30-min fraction of dialysate was collected at a flow rate of 0.5 µl/min. Then, after a 5-min flush at 10 µl/min, the perfusion was set at 2.5 µl/min for the remaining experimental period. At this flow rate, a 15-min collection was not kept, and then two 15-min fractions were kept at rest, which were used for the calibration and the basal concentration values. Therefore, the probe recovery was only evaluated at rest because it is not possible to do this during exercise.

After the calibration of the probes and the two 15-min fraction collections at rest, the subjects started a bout of exercise on an electromagnetically braked bicycle ergometer (Ergometrics 800s, Ergoline, Jaeger, Germany) at a workload corresponding to 50% of their VO2 max. Exercise duration was 60 min. Heart rate was continuously monitored with a Polar Accurex Plus Cardiometer (Monitor, Bayonne, France) during the exercise. The subjects then rested in the semirecumbent position for 60 min. Water intake was allowed ad libitum during the exercise and recovery periods. During the exercise and recovery periods, 15-min fractions of the dialysate were collected.

Before exercise and every 15 min during exercise and recovery, 5 ml of blood were collected from an indwelling polyethylene catheter inserted into an antecubital vein for glycerol determination. Every 30 min, an additional 5 ml of blood were collected for other plasma determinations. Blood was collected on 50 µl of an anticoagulant and antioxidant cocktail (Immunotech, Marseille, France) to prevent oxidation of catecholamines and was processed immediately in a refrigerated centrifuge. The plasma was stored at -80°C until analysis.

Drugs and Biochemical Determinations

Phentolamine methansulfonate (Regitine) was obtained from Ciba-Geigy (Reuil-Malmaison, France). Glycerol in dialysate (10 µl) and in plasma (20 µl) was analyzed with an ultrasensitive radiometric method (5), and the intra- and interassay variabilities were 5.0 and 9.2%, respectively. Ethanol in dialysate and perfusate (5 µl) was determined with an enzymatic method (4), and the intra- and interassay variabilities were 3.0 and 4.5%, respectively. Plasma glucose and NEFA were determined with a glucose-oxidase technique (Biotrol kit, Merck-Clevenot, Nogent-s-Marne, France) and an enzymatic procedure (Wako kit, Unipath, Dardilly, France), respectively. Plasma insulin concentrations were measured using RIA kits from Sanofi Diagnostics Pasteur (Marnes la Coquette, France). Plasma epinephrine and norepinephrine were assayed in 1-ml aliquots of plasma by high-performance liquid chromatography using electrochemical (amperometric) detection (22). The detection limit was 20 pg/sample. Day-to-day variability was 4%, and within-run variability was 3%.

Statistical Analysis

Values are means ± SE. The responses to exercise were analyzed using a paired t-test for plasma values and ANOVA (doubly multivariate repeated-measures design) for extracellular glycerol concentrations with statistical software (SAS, proc GLM). During exercise, plasma values and extracellular glycerol concentration response curves (in µmol · l-1 · h-1) were calculated as the total integrated changes over baseline values [area under curves (AUC)] using a trapezoidal method. P < 0.05 was considered statistically significant.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

General Observations

Body mass index, percentage of fat mass, and VO2 max were significantly different between trained and untrained subjects (P < 0.01, P < 0.001, and P < 0.001, respectively).

The power developed was regularly adjusted to maintain the oxygen uptake constant over the exercise bout. The power developed during exercise by the untrained subjects was significantly lower (102 ± 8 W) than that developed by trained subjects (169 ± 13 W; P < 0.01), whereas heart rate was not significantly different (138 ± 3 and 124 ± 2 beats/min for untrained and trained subjects, respectively).

Plasma Catecholamine Concentrations

At rest, plasma norepinephrine and epinephrine concentrations were not different between the two groups. During exercise, the plasma norepinephrine concentrations were significantly higher than baseline at minute 30 (P < 0.001) and afterward did not change until the end of exercise in either group. After the 60-min recovery period, norepinephrine concentrations decreased to a value that did not differ from that measured at rest (Table 1). The plasma epinephrine concentrations increased until the end of exercise (P < 0.05 for trained and P < 0.001 for untrained). After 60 min of recovery, the epinephrine concentrations decreased to a value that did not differ from that measured at rest (Table 1). AUC calculated for norepinephrine and epinephrine increase in plasma during the exercise bout showed no significant differences between the two groups.

                              
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  		Table 1.   Effect of 60-min exercise and recovery on plasma catecholamines, glucose, and insulin concentrations in untrained and trained men

Plasma Glucose and Insulin Concentrations

In the baseline period, the plasma concentrations of glucose and insulin were similar in both groups. No significant variation of plasma glucose level was observed during the exercise bout. A significant decrease in plasma insulin concentrations was observed at the end of the exercise (P < 0.05) in trained and untrained subjects (Table 1). AUC calculated for glucose and insulin variations in plasma during the exercise bouts showed no significant differences between the two groups.

Plasma NEFA and Glycerol Levels and Extracellular Glycerol Concentrations in Adipose Tissue

Baseline values. During the baseline period, plasma NEFA concentrations were significantly higher in untrained than in trained subjects (386 ± 44 vs. 137 ± 25 µmol/l, respectively; Fig. 1). Plasma glycerol concentrations did not differ between the two groups (68 ± 10 vs. 62 ± 4 µmol/l, respectively); the same was true for the corresponding baseline extracellular glycerol concentrations in SCAAT in the probe perfused with Ringer solution, i.e., the control probe (170 ± 21 and 144 ± 34 µmol/l in untrained and trained subjects, respectively). The baseline extracellular glycerol concentrations in the probe with phentolamine were not different from those in the control probe (227 ± 33 and 149 ± 43 µmol/l in SCAAT of untrained and trained subjects, respectively; Fig. 2).


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  		Fig. 1.   Time course changes of plasma glycerol (A) and nonesterified fatty acid (NEFA; B) concentrations during the 60-min cycle-ergometer exercise in untrained (open circle ) and trained () subjects. Data are means ± SE. *Significantly different compared with corresponding values measured before exercise (P < 0.05).



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  		Fig. 2.   Time course of calculated interstitial glycerol concentration (extracellular glycerol) changes in subcutaneous adipose tissue calculated from glycerol in dialysate during the 60-min cycle-ergometer exercise in untrained (A) and trained (B) subjects. open circle , Results from the probe with phentolamine; , results from control probe. Data are means ± SE. *Significantly different compared with corresponding values measured before the exercise (P < 0.05).

Exercise values. In both groups, plasma NEFA concentrations changed weakly during the exercise period. After 15 min of recovery, NEFA concentration increased (671 ± 89 and 406 ± 61 µmol/l in untrained and trained subjects, respectively) and then decreased to values not different from those found at rest (Fig. 1). Plasma glycerol level increased during exercise in both groups and then, after a 1-h recovery period, decreased to values not significantly different from those found at rest (Fig. 1). The calculated AUC of plasma glycerol increase was lower for untrained than for trained subjects (3,762 ± 618 vs. 7,793 ± 1,470, respectively; P < 0.003).

During exercise, extracellular glycerol concentrations increased during the first 15 min of the control probe for the two groups (Fig. 2) and continued to increase until the end of exercise. However, the exercise-induced increase tended to be lower in untrained than in trained subjects (497 ± 60 vs. 605 ± 68 µmol/l after 60 min of exercise), but the difference was not significant. The calculated AUC of extracellular glycerol response to exercise was significantly lower in untrained than in trained subjects (11,025 ± 1,612 vs. 15,638 ± 2,371, respectively; P < 0.05). In the probe supplemented with phentolamine in untrained subjects, the extracellular glycerol concentrations increased significantly starting from 15 min and was 758 ± 118 µmol/l after 60 min of exercise (Fig. 2). The glycerol increase was ~1.5-fold higher in the probe with phentolamine than in the control probe. The corresponding calculated AUC of glycerol increase was 17,564 ± 3,530 with phentolamine vs. 11,025 ± 1,612 in control (P < 0.05). On the other hand, in trained subjects, the exercise-induced response of extracellular glycerol was not different in the phentolamine-supplemented probe from that in the control probe (corresponding calculated AUC of glycerol increase was 15,055 ± 2,397 vs. 15,638 ± 2,371; Fig. 2). During exercise, there was no significant interaction between group and treatment (P = 0.112).

Ethanol Outflow-to-Inflow Ratio in Adipose Tissue

Ethanol outflow-to-inflow ratios (expressed as a percentage, i.e., the ethanol concentration in the dialysate divided by the ethanol concentration in the perfusate × 100) from control and phentolamine-added probes are depicted in Fig. 3. In the control probe, the ethanol ratio was not different in the two groups at rest (52.2 ± 4.9 and 51.6 ± 6.1 for untrained and trained subjects, respectively). At rest, phentolamine did not induce changes in the ethanol ratio in either group (53.5 ± 4.6 and 50.5 ± 6.7 for untrained and trained subjects, respectively). A slight decrease in the ethanol outflow-to-inflow ratio was observed during the first 30 min of exercise in untrained subjects and during the first 15 min in trained subjects. The addition of phentolamine induced a more marked and prolonged decrease in the ethanol outflow-to-inflow ratio, which occurred during the whole exercise period in untrained subjects and during the first 30 min of exercise in trained subjects (Fig. 3).


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  		Fig. 3.   Time course of ethanol ratio (ethanol dialysate concentration/ethanol perfusate concentration × 100) changes in subcutaneous adipose tissue calculated from the control probe () or the probe with phentolamine (open circle ) during the 60-min cycle-ergometer exercise in untrained (A) and trained (B) subjects. Data are means ± SE. *Significantly different compared with corresponding values measured before the exercise (P < 0.05).


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

The present study demonstrates that, in the trained unlike in the untrained subjects, alpha 2-AR are not involved in the regulation of lipolysis during exercise. The lack of alpha 2-AR involvement might contribute to the higher exercise-induced lipolysis in trained subjects.

The exercise-induced increase in lipolysis is promoted by increased catecholamine levels (and lowered insulinemia). It has been shown that the hormonal response to exercise is determined by relative, not absolute, intensity (15). Therefore, in the present study, both groups exercised at the same percentage of VO2 max. The exercise-induced responses of both catecholamines and insulin were similar in the two groups. Consequently, in trained subjects, the increased exercise-induced lipolysis was not associated with a different catecholamine stimulation (or insulin inhibition) of lipolysis. In fact, the exercise-induced rise of extracellular glycerol was higher in trained compared with untrained subjects. However, the concentration of glycerol in the extracellular space is not determined solely by the rate of lipolysis in adipocytes; it is also influenced by local blood flow. Pharmacological studies have shown that local blood flow modifies glycerol levels in adipose tissue, i.e., that vasoconstriction increases and vasodilatation decreases extracellular glycerol concentration in adipose tissue (13). During exercise, the increase in extracellular glycerol concentration could be due to changes in blood flow in adipose tissue. The measurement of ethanol escape through the dialysis probe is a validated nonquantitative method used to estimate the changes in vasomotricity in aerobic threshold (14). In agreement with some authors (17, 30), the stability of the ethanol outflow-to-inflow ratio found during the exercise bouts indicated that vasomotricity did not change during exercise. Consequently, exercise-induced changes in extracellular glycerol concentration are not influenced by local blood flow changes and, consequently, reflect changes in local lipolysis in SCAAT. In the presence of phentolamine, there was a slight decrease in the ethanol ratio (alpha 2-AR blockade involving vasodilatation), but the difference with the control probe was not significant. Furthermore, it appears that, without the weak vasodilatation found in untrained subjects, the extracellular glycerol increase would have been higher, confirming our results.

Hydrolysis of triglyceride produces glycerol and NEFA. Glycerol gives the best index of lipid mobilization because it cannot be used by adipocyte or muscle, unlike NEFA. In this experiment, the exercise-induced increase of extracellular and plasma glycerol concentrations was lower in untrained subjects; therefore, we can conclude that a lower lipolytic response occurred during exercise in this group vs. trained subjects. Conversely, results concerning NEFA were different (plasma NEFA concentrations were found to be higher in untrained than in trained fasting subjects); this can be explained by lower NEFA oxidation in muscle of nontrained subjects (21, 32).

The catecholamines (epinephrine and norepinephrine) control lipolysis by a dual action: stimulation via beta -AR and inhibition via alpha 2-AR. The resulting effect of catecholamines is determined by the relative contribution of the two pathways (24). As demonstrated previously, epinephrine shows an antilipolytic action mediated by alpha 2-AR during exercise (30). This antilipolytic action of epinephrine did not appear significant (although it was present) during a single bout of exercise in untrained subjects (30), perhaps because the untrained population is in fact very heterogeneous on account of the variability of the spontaneous activity. Therefore, in the present study, a large group of untrained subjects (15) was studied to better evaluate the statistical significance of the antilipolytic effect during exercise. Consequently, the blockade of alpha 2-AR by phentolamine produced an enhancement of lipolytic responses to exercise in the group of untrained but not trained subjects, whereas the epinephrine responses in the trained and untrained subjects were identical. This indicates an absence of alpha 2-regulation of lipolysis during exercise in the trained group. Moreover, the higher alpha 2-adrenergic responsiveness in untrained subjects might contribute to a lower lipid mobilization. However, our study was restricted to male subjects, so we cannot conclude about women. Indeed, Hellström et al. (17) showed a different response of alpha 2-AR between men and women; in women, only beta -AR were activated. Similarly, only SCAAT was investigated, and we cannot say whether these data are available to other adipose tissue sites. For example, an in vitro study with isolated abdominal or gluteal adipose cells in obese women showed an alpha 2-AR affinity and density that differed between abdominal and gluteal subcutaneous fat depots (3). It has been demonstrated that, during exercise, the stimulation effect of catecholamines on lipolysis is mediated by the beta -adrenergic pathway (1). In cross-sectional (8) as well as in longitudinal (31) in vitro studies, it has been shown that the responsiveness of isolated adipocytes to beta -adrenergic lipolysis stimulation is higher in trained subjects. Consequently, the lower beta -adrenergic responsiveness in untrained subjects might also contribute to their lower exercise-induced lipolysis.

The present results show that training induces a weakening of the alpha 2-mediated antilipolytic action. This appears to support results of in vitro longitudinal studies (10) in which obese subjects were trained for 12 wk; the training elicited a decrease of the alpha 2-antilipolytic action of epinephrine in vitro. Moreover, when interpreting the present results, we must consider the differences in fat mass between the two groups. Higher fat mass suggests a higher adipocyte volume in the untrained subjects, and this could be a reason for the higher alpha 2-AR activity, as it was shown that the alpha 2-AR activity depends on fat cell size (26). Similarly, in another experiment, we found that alpha 2-AR activity was more striking in obese subjects than in nonobese subjects independent of endurance training (29), and Hellström et al. (18) showed that, after weight loss during very-low-calorie diet, alpha 2-AR sensitivity decreased. However, when obese subjects were trained for 3 mo, although their weight did not change, the antilipolytic effect of alpha 2-AR in vitro was decreased (10); this illustrates the effect of training on AR activity.

In summary, the present study demonstrates that, in trained subjects, the antilipolytic action of catecholamines mediated by alpha 2-AR is not involved in the regulation of lipolysis in SCAAT during exercise. This absence of alpha 2-AR involvement differentiates trained from untrained subjects and, in conjunction with a more efficient beta -adrenergic pathway, can contribute to the higher exercise-induced lipolysis in trained subjects. This study underscores the role of the alpha 2-adrenergic pathway in the effects of training on the regulation of lipolysis in SCAAT and indicates the importance of physical training for the regulation of fat mass in humans. It would be tempting to confirm these findings by a longitudinal study involving training of sedentary subjects.


    ACKNOWLEDGEMENTS

The authors express their gratitude to M. T. Canal and S. Parizkova for contribution to the study and M. Meste for statistical analysis.


    FOOTNOTES

The study was partially supported by Grant GAUK 199 of Charles University, Czech Republic, and the laboratories involved in the study participated in the Commission of the European Communities, Agriculture and Fisheries specific RTD program CT98-4141 (FATLINK: dietary fat, body weight control, and links between obesity and cardiovascular disease).

Address for reprint requests and other correspondence: I. de Glisezinski, Service d'Exploration de la Fonction Respiratoire et de Médecine du Sport, CHU Purpan, 31059 Toulouse Cedex, France (E-mail: crampes.f{at}chu-toulouse.fr).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 10 May 2000; accepted in final form 20 May 2001.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

1.   Arner, P, Kriegholm E, Engfeldt P, and Bolinder J. Adrenergic regulation of lipolysis in situ at rest and during exercise. J Clin Invest 85: 893-898, 1990.

2.   Barbe, P, Millet L, Galitzky J, Lafontan M, and Berlan M. In situ assessment of the role of the beta 1-, beta 2- and beta 3-adrenoceptors in the control of lipolysis and nutritive blood flow in human subcutaneous adipose tissue. Br J Pharmacol 117: 907-913, 1996[Web of Science][Medline].

3.   Berman, DM, Nicklas BJ, Rogus EM, Dennis KE, and Goldberg AP. Regional differences in adrenoceptor binding and fat cell lipolysis in obese, postmenopausal women. Metabolism 47: 467-473, 1998[Web of Science][Medline].

4.   Bernst, E, and Gutmann I. Ethanol determination with alcohol dehydrogenase and NAD. In: Methods of Enzymatic Analysis, edited by Bergmeyer HU.. New York: Academic, 1974, p. 1499-1505.

5.   Bradley, DC, and Kaslow HR. Radiometric assays for glycerol, glucose and glycogen. Anal Biochem 180: 11-16, 1989[Web of Science][Medline].

6.   Bülow, J. Lipid mobilization and utilization. In: Principles of Exercise Biochemistry, (2nd ed.), edited by Poortmans JR.. Basel: Karger, 1993, p. 158-185.

7.   Christensen, NJ, and Galbo H. Sympathetic nervous activity during exercise. Annu Rev Physiol 45: 139-153, 1983[Web of Science][Medline].

8.   Crampes, F, Beauville M, Rivière D, and Garrigues M. Effect of physical training in humans on the response of isolated fat cells to epinephrine. J Appl Physiol 61: 25-29, 1986[Abstract/Free Full Text].

9.   Crampes, F, Beauville M, Rivière D, Garrigues M, and Lafontan M. Lack of desensitization of catecholamine-induced lipolysis in fat cells from trained and sedentary women after physical exercise. J Clin Endocrinol Metab 67: 1011-1017, 1988[Abstract/Free Full Text].

10.   De Glisezinski, I, Crampes F, Harant I, Berlan M, Hejnova J, Langin D, Riviere D, and Stich V. Endurance training changes in lipolytic responsiveness of obese adipose tissue. Am J Physiol Endocrinol Metab 275: E951-E956, 1998[Abstract/Free Full Text].

11.   De Glisezinski, I, Harant I, Crampes F, Trudeau F, Felez A, Cottet-Emard JM, Garrigues M, and Riviere D. Effect of carbohydrate ingestion on adipose tissue lipolysis during long-lasting exercise in trained men. J Appl Physiol 84: 1627-1632, 1998[Abstract/Free Full Text].

12.   Durnin, JVG, and Womersley J. Body fat assessed from total body density and its estimation from skinfold thickness: measurements on 418 men and women aged from 16 to 72 years. Br J Nutr 32: 77-97, 1974[Web of Science][Medline].

13.   Enocksson, S, Nordenstrom J, Bolinder J, and Arner P. Influence of local blood flow on glycerol levels in human adipose tissue. Int J Obes 19: 350-354, 1995[Web of Science].

14.   Felländer, G, Linde B, and Bolinder J. Evaluation of the microdialysis ethanol technique for monitoring of subcutaneous adipose tissue blood flow in humans. Int J Obes 20: 220-226, 1996[Web of Science].

15.   Galbo, H, and Gollnick MD. Hormonal changes during and after exercise. Med Sport Sci 17: 97-100, 1984.

16.   Galitzky, J, Lafontan M, Nordenström J, and Arner P. Role of vascular alpha 2-adrenoceptors in regulating lipid mobilization from human adipose tissue. J Clin Invest 91: 1997-2003, 1993.

17.   Hellström, L, Blaak E, and Hagström-Toft E. Gender differences in adrenergic regulation of lipid mobilization during exercise. Int J Sports Med 17: 439-447, 1996[Web of Science][Medline].

18.   Hellström, L, Rossner S, Hagström-Toft E, and Reynisdottir S. Lipolytic catecholamine resistance linked to alpha 2-adrenoceptor sensitivity: a metabolic predictor of weight loss in obese subjects. Int J Obes Relat Metab Disord 21: 314-320, 1997[Web of Science][Medline].

19.   Hickner, RC, Rosdahl H, Borg I, Ungerstedt U, Jorfeldt L, and Henriksson J. Ethanol may be used with the microdialysis technique to monitor blood flow changes in skeletal muscle: dialysate glucose concentration is blood flow-dependent. Acta Physiol Scand 143: 355-356, 1991[Web of Science][Medline].

20.   Hodgetts, V, Coppack SW, Frayn KN, and Hockaday TDR Factors controlling fat mobilization from human subcutaneous adipose tissue during exercise. J Appl Physiol 71: 445-451, 1991[Abstract/Free Full Text].

21.   Klein, S, Coyle EF, and Wolfe RR. Fat metabolism during low-intensity exercise in endurance-trained and untrained men. Am J Physiol Endocrinol Metab 267: E934-E940, 1994[Abstract/Free Full Text].

22.   Koubi, HE, Desplanches D, Gabrielle C, Cottet-Emard JM, Sempore B, and Favier RJ. Exercise endurance and fuel utilization: a reevaluation of the effects of fasting. J Appl Physiol 70: 1337-1343, 1991[Abstract/Free Full Text].

23.   Lafontan, M, and Berlan M. Evidence for the alpha 2-nature of the alpha-adrenergic receptor inhibiting lipolysis in human fat cells. Eur J Pharmacol 66: 87-93, 1980[Web of Science][Medline].

24.   Lafontan, M, and Berlan M. Fat cell adrenergic receptors and the control of white and brown fat cell function. J Lipid Res 34: 1057-1091, 1993[Abstract].

25.   Lafontan, M, and Berlan M. Fat cell alpha 2-adrenoceptors: the regulation of fat cell function and lipolysis. Endocr Rev 16: 716-738, 1995[Abstract/Free Full Text].

26.   Mauriège, P, Després JP, Prud'homme D, Pouliot MC, Marcotte M, Tremblay A, and Bouchard C. Regional variation in adipose tissue lipolysis in lean and obese men. J Lipid Res 32: 1625-1633, 1991[Abstract].

27.   Mauriège, P, Galitzky J, Berlan M, and Lafontan M. Heterogeneous distribution of beta - and alpha 2-adrenoceptor binding sites in human fat cells from various fat deposits: functional consequences. Eur J Clin Invest 17: 156-165, 1987[Web of Science][Medline].

28.   Rivière, D, Crampes F, Beauville M, and Garrigues M. Lipolytic response of fat cells to catecholamines in sedentary and exercise-trained women. J Appl Physiol 66: 330-335, 1989[Abstract/Free Full Text].

29.   Stich, V, De Glisezinski I, Crampes F, Cottet-Emard JM, Galitzky J, Lafontan M, Rivière D, and Berlan M. Physiological activation of alpha 2-adrenergic receptors impairs exercise-induced lipolysis in subcutaneous adipose tissue of obese subjects. Am J Physiol Regulatory Integrative Comp Physiol 279: R499-R504, 2000[Abstract/Free Full Text].

30.   Stich, V, De Glisezinski I, Crampes F, Suljkovicova H, Galitzky J, Rivière D, Hejnova J, Lafontan M, and Berlan M. Activation of antilipolytic alpha 2-adrenergic receptors by epinephrine during exericse in human adipose tissue. Am J Physiol Regulatory Integrative Comp Physiol 277: R1076-R1083, 1999[Abstract/Free Full Text].

31.   Stich, V, De Glisezinski I, Galitzky J, Hejnova J, Crampes F, Rivière D, and Berlan M. Endurance training increases the beta -adrenergic lipolytic response in subcutaneous adipose tissue in obese subjects. Int J Obes 23: 374-381, 1999.

32.   Turcotte, LP, Richter EA, and Kiens B. Increased plasma FFA uptake and oxidation during prolonged exercise in trained vs. untrained humans. Am J Physiol Endocrinol Metab 262: E791-E799, 1992[Abstract/Free Full Text].

J APPL PHYSIOL 91(4):1760-1765
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