Aerobic training improves exercise-induced lipolysis in SCAT and lipid utilization in overweight men

2003 ◽  
Vol 285 (5) ◽  
pp. E984-E990 ◽  
Author(s):  
I. de Glisezinski ◽  
C. Moro ◽  
F. Pillard ◽  
F. Marion-Latard ◽  
I. Harant ◽  
...  

The aim of this study was to investigate whether endurance training improves lipid mobilization and oxidation in overweight subjects. Eleven young men (25.6 ± 1.4 yr and body mass index 27.7 ± 0.2) performed a 4-mo training program consisting of practicing aerobic exercise 5 days/wk. Before and after the training period, lipid oxidation was explored during a 60-min exercise at 50% of peak O2 consumption by use of indirect calorimetry. Lipid mobilization and antilipolytic α2-adrenoceptor effect were also studied using the microdialysis method in abdominal subcutaneous adipose tissue (SCAT). After training, plasma nonesterified fatty acid (NEFA) levels, at rest and during exercise, were significantly lower than before ( P < 0.001). Lipolysis in SCAT was significantly higher after than before training. An antilipolytic α2-adrenoceptor effect in SCAT was underlined during exercise before training and disappeared after. The respiratory exchange ratio was lower after training, i.e., the percentage of lipid oxidation was higher only at rest. The amount of lipid oxidized was higher after training, at rest, and during exercise. Although exercise power was higher after training, the relative intensity was equivalent, as suggested by a similar increase in plasma catecholamine concentrations before and after training. In conclusion, 4-mo training in overweight men improved lipid mobilization through a decrease of antilipolytic α2-adrenoceptor effect in SCAT and lipid oxidation during moderate exercise. Training induced a decrease of blood NEFA, predicting better prevention of obesity.

1994 ◽  
Vol 86 (1) ◽  
pp. 35-41 ◽  
Author(s):  
E. Carstensen ◽  
John S. Yudkin

1. Four studies were designed to test the hypothesis that platelet catecholamine levels may provide a stable index of circulating plasma catecholamine concentrations, and that these are unaffected by acute elevations of plasma levels with physical and psychological stress. 2. To assess the biological variability within individuals, ten subjects were sampled on five occasions over 8–30 h. The intra-individual coefficients of variation for plasma and platelet noradrenaline levels were 193 +10% and 9.5 +4.2%, respectively, and for plasma and platelet adrenaline levels 48.3 +22% and 25.3 +8.4%, respectively. 3. Three other studies investigating the response to physical and psychological stress were performed. In the first study, plasma and platelet catecholamine levels were studied in 12 healthy subjects before and after bicycle ergometry. Plasma catecholamine concentrations increased [noradrenaline by +346 + 323% (P = 0.002) and adrenaline by +314 + 352% (P -0.003)], whereas platelet concentrations showed little change [noradrenaline +4+18% (P = 0.94) and adrenaline +38+ 116% (P = 0.67)]. 4. In the study, catecholamine concentrations were measured in eight subjects after hand immersion in iced water. Plasma noradrenaline concentrations increased significantly (+58 +19%, P = 0.001), but no significant change was found in plasma adrenaline concentrations (+8+44%, P = 0.48). Platelet catecholamine concentrations showed no significant change (noradrenaline +15 +15%, P = 0.052, and adrenaline 19 +82%, P = 0.84). 5. In the third study, catecholamine concentrations were measured in 22 medical students before and after their end-of-year examination. There was no significant change in plasma noradrenaline or adrenaline concentrations (+20 +39%, P = 0.08, and −2 +33%, P = 0.36, respectively) nor in platelet concentrations (noradrenaline +6+19%, P = 0.15, and adrenaline +34 +72, P = 0.65). 6. In 53 subjects sampled between 08.00 and 12.00 hours, plasma and platelet noradrenaline concentrations were significantly correlated (r, = 0.47, P <0.001), but the relationship between plasma and platelet adrenaline concentrations in these subjects did not achieve significance (rs = 0.17, P <0.23). 7. In conclusion, platelet catecholamine concentrations seem to be unaffected by acute short-term stress and may provide a reliable indicator of chronic sympatho-adrenomedullary arousal.


2010 ◽  
Vol 299 (2) ◽  
pp. E258-E265 ◽  
Author(s):  
Katrien Koppo ◽  
Dominique Larrouy ◽  
Marie A. Marques ◽  
Michel Berlan ◽  
Magda Bajzova ◽  
...  

The aim of this study was to evaluate the relative contributions of various hormones involved in the regulation of lipid mobilization in subcutaneous adipose tissue (SCAT) during exercise and to assess the impact of obesity on this regulation. Eight lean and eight obese men performed a 60-min cycle exercise bout at 50% of their peak oxygen uptake on two occasions: during intravenous infusion of octreotide (a somatostatin analog) or physiological saline (control condition). Lipolysis in SCAT was evaluated using in situ microdialysis. One microdialysis probe was perfused with the adrenergic blockers phentolamine and propranolol while another probe was perfused with the phosphodiesterase and adenosine receptor inhibitor aminophylline. Compared with the control condition, infusion of octreotide reduced plasma insulin levels in lean (from ∼3.5 to 0.5 μU/ml) and in obese (from ∼9 to 2 μU/ml), blunted the exercise-induced rise in plasma GH and epinephrine levels in both groups, and enhanced the exercise-induced natriuretic peptide (NP) levels in lean but not in obese subjects. In both groups, octreotide infusion resulted in higher exercise-induced increases in dialysate glycerol concentrations in the phentolamine-containing probe while no difference in lipolytic response was found in the aminophylline-containing probe. The results suggest that insulin antilipolytic action plays a role in the regulation of lipolysis during exercise in lean as well as in obese subjects. The octreotide-induced enhancement of exercise lipolysis in lean subjects was associated with an increased exercise-induced plasma NP response. Adenosine may contribute to the inhibition of basal lipolysis in both subject groups.


2006 ◽  
Vol 91 (12) ◽  
pp. 5069-5075 ◽  
Author(s):  
Andreas L. Birkenfeld ◽  
Michael Boschmann ◽  
Cedric Moro ◽  
Frauke Adams ◽  
Karsten Heusser ◽  
...  

Abstract Context: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. Objective: The objective of the study was to determine the metabolic and cardiovascular interaction of β-adrenergic receptors and ANP. Design: This was a crossover study, conducted 2004–2005. Setting: The study was conducted at an academic clinical research center. Patients: Patients included 10 healthy young male subjects (body mass index 24 ± 1 kg/m2). Intervention: We infused iv incremental ANP doses (6.25, 12.5, and 25 ng/kg·min) with and without propranolol (0.20 mg/kg in divided doses followed by 0.033 mg/kg·h infusion). Metabolism was monitored through venous blood sampling, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings. Main Outcome Measures: Venous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured. Results: ANP increased heart rate dose dependently. β-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified fatty acid and glycerol concentrations. The response was not suppressed with propranolol. Venous glucose and insulin concentrations increased with ANP, both without or with propranolol. ANP induced lipid mobilization in sc adipose tissue. In skeletal muscle, microdialysate lactate increased, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation. Conclusions: Selected cardiovascular ANP effects are at least partly mediated by β-adrenergic receptor stimulation. ANP-induced changes in lipid mobilization and glycolysis are mediated by another mechanism, presumably stimulation of natriuretic peptide receptors, whereas substrate oxidation might be modulated through adrenergic mechanisms.


1992 ◽  
Vol 263 (3) ◽  
pp. E441-E447 ◽  
Author(s):  
F. Carli ◽  
J. Webster ◽  
P. Nandi ◽  
I. A. MacDonald ◽  
J. Pearson ◽  
...  

Body temperature, respiratory gas exchange, and plasma catecholamines were determined before and after surgery in three groups [control (C), warmed (W), and epidural (E) who received local anesthetic at T4-S5 dermatomes during and for 24 h after surgery] of patients undergoing colonic surgery under general anesthesia. At the end of surgery, group W were nursed in an ambient temperature of 28-30 degrees C, whereas the others were at 20-23 degrees C for a period of 24 h. Core (Tc) and dorsal hand temperature decreased during surgery in both C and E (P less than 0.05) but not in W. After surgery, Tc increased similarly in C and E and by a smaller amount in W. Plasma catecholamine concentrations increased significantly in C and W but not in E (P less than 0.001), with the greatest response occurring in C. Postoperative oxygen consumption and carbon dioxide production exceeded preoperative values (P less than 0.01) in C but not in W or E. After surgery, plasma albumin fell and C-reactive protein increased similarly in all three groups. Thus body heat conservation or epidural blockade attenuates or abolishes the rise in plasma catecholamines and oxygen consumption postoperatively but does not prevent the increase in Tc or the acute phase protein response.


2008 ◽  
Vol 295 (2) ◽  
pp. E505-E513 ◽  
Author(s):  
Cedric Moro ◽  
Fabien Pillard ◽  
Isabelle de Glisezinski ◽  
Eva Klimcakova ◽  
Francois Crampes ◽  
...  

Involvement of sympathetic nervous system and natriuretic peptides in the control of exercise-induced lipid mobilization was compared in overweight and lean men. Lipid mobilization was determined using local microdialysis during exercise. Subjects performed 35-min exercise bouts at 60% of their maximal oxygen consumption under placebo or after oral tertatolol [a β-adrenergic receptor (AR) antagonist]. Under placebo, exercise increased dialysate glycerol concentration (DGC) in both groups. Phentolamine (α-AR antagonist) potentiated exercise-induced lipolysis in overweight but not in lean subjects; the α2-antilipolytic effect was only functional in overweight men. After tertatolol administration, the DGC increased similarly during exercise no matter which was used probe in both groups. Compared with the control probe under placebo, lipolysis was reduced in lean but not in overweight men treated with the β-AR blocker. Tertatolol reduced plasma nonesterified fatty acids and insulin concentration in both groups at rest. Under placebo or tertatolol, the exercise-induced changes in plasma nonesterified fatty acids, glycerol, and insulin concentrations were similar in both groups. Exercise promoted a higher increase in catecholamine and ANP plasma levels after tertatolol administration. In conclusion, the major finding of our study is that in overweight men, in addition to an increased α2-antilipolytic effect, the lipid mobilization in subcutaneous adipose tissue that persists during exercise under β-blockade is not dependent on catecholamine action. On the basis of correlation findings, it seems to be related to a concomitant exercise-induced rise in plasma ANP when exercise is performed under tertatolol intake and a decrease in plasma insulin.


2006 ◽  
Vol 290 (5) ◽  
pp. E864-E869 ◽  
Author(s):  
Cédric Moro ◽  
Jan Polak ◽  
Jindra Hejnova ◽  
Eva Klimcakova ◽  
François Crampes ◽  
...  

Atrial natriuretic peptide (ANP) controls lipolysis in human adipocytes. Lipid mobilization is increased during repeated bouts of exercise, but the underlying mechanisms involved in this process have not yet been delineated. The relative involvement of catecholamine- and ANP-dependent pathways in the control of lipid mobilization during repeated bouts of exercise was thus investigated in subcutaneous adipose tissue (SCAT) by microdialysis. The study was performed in healthy males. Subjects performed two 45-min exercise bouts (E1 and E2) at 50% of their maximal oxygen uptake separated by a 60-min rest period. Extracellular glycerol concentration (EGC), reflecting SCAT lipolysis, was measured in a control probe perfused with Ringer solution and in two other probes perfused with either Ringer plus phentolamine (α1/2-AR antagonist) or Ringer plus both phentolamine and propranolol (β-AR antagonist). Plasma epinephrine, plasma glycerol, and EGC were 1.7-, 1.6-, and 1.2-fold higher in E2 than in E1, respectively. Phentolamine potentiated exercise-induced EGC increase during E2 only. Propranolol reduced the lipolytic rate during both E1 and E2 compared with the probe with phentolamine. Plasma ANP concentration increased more during E2 than during E1 and was correlated with the increase in EGC in the probe containing phentolamine plus propranolol. The results suggest that ANP is involved in the control of lipolysis during exercise and that it contributes to stimulation of lipolysis during repeated bouts of exercise.


2004 ◽  
Vol 82 (7) ◽  
pp. 465-473 ◽  
Author(s):  
S Marra ◽  
L Hoffman-Goetz

Catecholamines induce apoptosis in various lymphoid populations. This process can occur with both α- and β-adrenoreceptors. Heavy exercise increases plasma catecholamine concentrations, and is also a cause of lymphocyte apoptosis, a possible explanation for postexercise lymphocytopenia. The purpose of this study was to examine the effects of adrenoreceptor antagonism on exercise-induced decreases and apoptosis of intestinal lymphocytes. Mice received an intraperitoneal injection of phentolamine (a nonselective α-blocker), nadolol (a nonselective β-blocker), or saline (vehicle) prior to an exhaustive bout of exercise. Total intestinal lymphocyte numbers, percent and number of CD3+ lymphocytes, and cell viability were assessed. Neither α- nor β-antagonism prevented exercise-induced cell loss in the intestine; however, pretreatment with nadolol significantly reduced the number of apoptotic and necrotic cells. Phentolamine administration appeared to increase the incidence of cell death among intestinal lymphocytes. Both drugs decreased the percentage of CD3+ intestinal lymphocytes. Our study suggests that catecholamines are not responsible for postexercise lymphocytopenia, but β-adrenoceptor blockade may confer protection against exercise-induced apoptosis of intestinal lymphocytes.Key words: catecholamines, exhaustive exercise, apoptosis, intestinal lymphocytes, rodents.


2009 ◽  
Vol 587 (13) ◽  
pp. 3393-3404 ◽  
Author(s):  
I. De Glisezinski ◽  
D. Larrouy ◽  
M. Bajzova ◽  
K. Koppo ◽  
J. Polak ◽  
...  

1999 ◽  
Vol 87 (1) ◽  
pp. 317-324 ◽  
Author(s):  
K. Schaller ◽  
D. Mechau ◽  
H. Grosse Scharmann ◽  
M. Weiss ◽  
M. Baum ◽  
...  

The influence of increased training on the sympathoadrenergic system was investigated. Moderately trained male subjects ( n = 15) increased their training within 10 wk by 60%; eight of the subjects increased their training volume, and seven increased their training intensity. Before and after the training, an exhaustive treadmill exercise was carried out. Acute treadmill exercise increased β-adrenergic receptor number on mononuclear lymphocytes, isoproternol-stimulated cAMP production, and plasma catecholamine concentration. The increase of receptor number can at least partially be explained by a changed lymphocyte composition at rest and after exercise. After training, the exercise-induced increase of β-adrenergic receptor number was significantly blunted, and the exercise-induced increase of the isoproternol-stimulated cAMP production per β-receptor was enhanced. Subjects who experienced increased symptoms of physical discomfort and/or mood changes showed an enhanced cAMP production after training. These findings point to an altered regulation of the receptor and postreceptor mechanisms as an effect of a 10-wk period of hard training.


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