@article{WiesnerBirkenfeldEngelietal.2010,
  author    = {Wiesner, Stefan and Birkenfeld, Andreas L. and Engeli, Stefan and Haufe, Sven and Brechtel, Lars and Wein, J. and Hermsdorf, Mario and Karnahl, Brita and Berlan, Michel and Lafontan, Max and Sweep, Fred C. G. J. and Luft, Friedrich C. and Jordan, Jens},
  title     = {Neurohumoral and metabolic response to exercise in water},
  issn      = {0018-5043},
  doi       = {10.1055/s-0030-1248250},
  year      = {2010},
  abstract  = {Atrial natriuretic peptide (ANP) stimulates lipid mobilization and lipid oxidation in humans. The mechanism appears to promote lipid mobilization during exercise. We tested the hypothesis that water immersion augments exercise- induced ANP release and that the change in ANP availability is associated with increased lipid mobilization and lipid oxidation. In an open randomized and cross-over fashion we studied 17 men (age 31 +/- 3.6 years; body mass index 24 +/- 1.7 kg/m(2); body fat 17 +/- 6.7\%) on no medication. Subjects underwent two incremental exercise tests on a bicycle ergometer. One test was conducted on land and the other test during immersion in water up to the xiphoid process. In a subset (n = 7), we obtained electromyography recordings in the left leg. We monitored gas exchange, blood pressure, and heart rate. In addition, we obtained blood samples towards the end of each exercise step to determine ANP, norepinephrine, epinephrine, lactate, free fatty acids, insulin, and glucose concentrations. Heart rate, systolic blood pressure, and oxygen consumption at the anaerobic threshold and during peak exercise were similar on land and with exercise in water. The respiratory quotient was mildly reduced when subjects exercised in water. Glucose and lactate measurements were decreased whereas free fatty acid concentrations were increased with exercise in water. Water immersion attenuated epinephrine and norepinephrine and augmented ANP release during exercise. Even though water immersion blunts exercise-induced sympathoadrenal activation, lipid mobilization and lipid oxidation rate are maintained or even improved. The response may be explained by augmented ANP release.},
  language  = {en}
}
@article{EngeliLehmannKaminskietal.2014,
  author    = {Engeli, Stefan and Lehmann, Anne-Christin and Kaminski, Jana and Haas, Verena and Janke, Urgen and Janke, J{\"u}rgen and Zoerner, Alexander A. and Luft, Friedrich C. and Tsikas, Dimitrios and Jordan, Jens},
  title     = {Influence of dietary fat intake on the endocannabinoid system in lean and obese subjects},
  series = {Obesity},
  volume    = {22},
  journal   = {Obesity},
  number    = {5},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {1930-7381},
  doi       = {10.1002/oby.20728},
  pages     = {E70 -- E76},
  year      = {2014},
  abstract  = {Objective: Endocannabinoid system (ECS) activation promotes obesity-associated metabolic disease. Increased dietary fat intake increases blood endocannabinoids and alters adipose and skeletal muscle ECS gene expression in human. Methods: Two weeks isocaloric low- (LFD) and high-fat diets (HFD) in obese (n = 12) and normal- weight (n = 17) subjects in a randomized cross-over study were compared. Blood endocannabinoids were measured in the fasting condition and after food intake using mass spectrometry. Adipose and skeletal muscle gene expression was determined using real-time RT-PCR. Results: Baseline fasting plasma endocannabinoids were similar with both diets. Anandamide decreased similarly with high- or low-fat test meals in both groups. Baseline arachidonoylglycerol plasma concentrations were similar between groups and diets, and unresponsive to eating. In subcutaneous adipose tissue, DAGL-alpha mRNA was upregulated and fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL) mRNAs were down-regulated in obese subjects, but the diets had no influence. In contrast, the HFD produced pronounced reductions in skeletal muscle CB1-R and MAGL mRNA expression, whereas obesity did not affect muscular gene expression. Conclusions: Weight-neutral changes in dietary fat intake cannot explain excessive endocannabinoid availability in human obesity. Obesity and dietary fat intake affect ECS gene expression in a tissue-specific manner.},
  language  = {en}
}