Dynamic strength training improves insulin sensitivity and functional balance between adrenergic alpha 2A and beta pathways in subcutaneous adipose tissue of obese subjects.
OBJECTIVE
The aim of this study was to investigate whether dynamic strength training modifies the control of lipolysis, with particular attention paid to the involvement of the antilipolytic adrenergic alpha 2A receptor (ADRA2A) pathway.


METHODS
Twelve obese men (age: 47.4+/-2.8 years; BMI: 32.7+/-0.9) were investigated during a 210-min euglycaemic-hyperinsulinaemic clamp conducted before and after 3 months of dynamic strength training. Before and during the third hour of the clamp, the lipolytic effect of a perfusion of isoproterenol or adrenaline (epinephrine) alone or associated with the ADRA2A antagonist phentolamine was evaluated using the microdialysis method of measuring extracellular glycerol concentration (EGC) in subcutaneous abdominal adipose tissue (SCAAT). In addition, biopsies of SCAAT were carried out before and after training to determine mRNA levels


RESULTS
The training increased insulin sensitivity in adipose tissue. The decrease of EGC was more pronounced during the clamp conducted after the training period than during the clamp done in pre-training conditions. Before and after the training, catecholamines induced an increase in EGC, the increase being lower during the clamp on each occasion. The isoproterenol-induced increase in EGC was higher after the training. Adrenaline-induced lipolysis was potentiated by phentolamine after but not before the training. There were no training-induced changes in mRNA levels of key genes of the lipolytic pathway in SCAAT.


CONCLUSIONS
In obese subjects, dynamic strength training improves whole-body and adipose tissue insulin responsiveness. It increases responsiveness to the adrenergic beta receptor stimulation of lipolysis and to the antilipolytic action of catecholamines mediated by ADRA2As.
Polak
J
J
Franco-Czech Laboratory for Clinical Research on Obesity, French Institute of Health and Medical Research (Inserm U586) and 3rd Faculty of Medicine, Charles University, Prague, Czech Republic.
Moro
C
C
Klimcakova
E
E
Hejnova
J
J
Majercik
M
M
Viguerie
N
N
Langin
D
D
Lafontan
M
M
Stich
V
V
Berlan
M
M
D015105:3',5'-Cyclic-AMP Phosphodiesterases / Q000235:genetics / Q000502:physiology; D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D058666:Adrenergic beta-2 Receptor Agonists; D000328:Adult; D054684:Cyclic Nucleotide Phosphodiesterases, Type 3; D004837:Epinephrine / Q000494:pharmacology; D015444:Exercise / Q000502:physiology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D015309:Glucose Clamp Technique; D005990:Glycerol / Q000032:analysis / Q000097:blood; D006801:Humans; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance / Q000502:physiology; D007545:Isoproterenol / Q000494:pharmacology; D050356:Lipid Metabolism; D008066:Lipolysis; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism / Q000503:physiopathology*; D010646:Phentolamine / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis; D018341:Receptors, Adrenergic, alpha-2 / Q000235:genetics / Q000378:metabolism*; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics / Q000378:metabolism*; D002787:Sterol Esterase / Q000235:genetics / Q000502:physiology; D050507:Subcutaneous Fat, Abdominal / Q000737:chemistry / Q000378:metabolism*
D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D058666:Adrenergic beta-2 Receptor Agonists; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D012333:RNA, Messenger; D018341:Receptors, Adrenergic, alpha-2; D018343:Receptors, Adrenergic, beta-2; D002787:Sterol Esterase; D015105:3',5'-Cyclic-AMP Phosphodiesterases; D054684:Cyclic Nucleotide Phosphodiesterases, Type 3; D007545:Isoproterenol; D005990:Glycerol; D004837:Epinephrine; D010646:Phentolamine