Velen hier (waaronder ik) nemen vaak vetten, zoals nootjes, voor het slapen gaan om hun kwark/nightprotein langer te laten verteren. Onderzoeken die ik tegenkwam tonen echter aan dat vetten voor het naar bed gaan een negatieve invloed hebben op je groeihormoon (HGH). Minder HGH betekent minder spier gains en meer fat gains. Ook speelt HGH een belangrijke rol in het fit voelen na je ontwaken.
Deze onderzoeken suggereren dat je het beste een aantal uren voor het naar bed gaan geen vetten nuttigt, wil je optimale werking van je groeihormoon hebben.
Deze onderzoeken suggereren dat je het beste een aantal uren voor het naar bed gaan geen vetten nuttigt, wil je optimale werking van je groeihormoon hebben.
Clin Invest. 1972 Sep;51(9):2388-98.
Studies on the relationship between plasma free fatty acids and growth hormone secretion in man.
Quabbe HJ, Bratzke HJ, Siegers U, Elban K.
The influence of plasma free fatty acid (FFA) concentration on the secretion of human growth hormone (HGH) was investigated. (a) FFA depression was produced by means of a nicotinic acid (NA) infusion for either 1 or 5 hr in the presence of glucose-induced hyperglycemia. Controls received only saline. (b) FFA depression was also produced by a 90 min NA infusion and then rapid FFA elevation by a lipid-plus-heparin (lipid) infusion. This procedure was compared with a similar NA infusion not followed by lipid. (c) FFA elevation was produced either by a lipid or by a norepinephrine (NE) infusion and then HGH secretion was stimulated by insulin-induced hypoglycemia. Each subject in this group received both the lipid and the NE infusion on seperate days as well as two control tests (insulin alone and NE alone).Depression of FFA resulted in an increase of HGH with a lag period of approximately 2 hr. Maximal HGH rise after 1 hr NA infusion was 7.7+/-1.9 ng/ml and with 5 hr NA infusion 14.3+/-3.6 ng/ml (both significantly higher than during saline infusion, P < 0.025 and < 0.005 respectively) and occurred despite continuous hyperglycemia. Lipid infusion just before the expected HGH increase prevented the HGH response to FFA depression. HGH rise during insulin hypoglycemia (32.2+/-6.5 ng/ml) was significantly inhibited by prior FFA elevation whether achieved by lipid infusion (maximum HGH rise 11.4+/-1.6 ng/ml) or by NE infusion (maximum HGH rise 19.0+/-6.2 ng/ml).The results are suggestive of a negative feedback loop between plasma FFA and HGH secretion, of importance for subacute rather than acute changes in the plasma FFA concentration. FFA lack itself seems to be the signal for HGH release despite the lag period between FFA decrease and HGH increase. Glucose and FFA can at least not fully replace each other in their respective influence on HGH release.
J Appl Physiol. 2008 Mar;104(3):724-8. Epub 2008 Jan 10.
The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men.
Stokes KA, Tyler C, Gilbert KL.
Sport and Exercise Science, School for Health, University of Bath, Bath, UK. k.stokes@bath.ac.uk
A single 30-s sprint is a potent physiological stimulus for growth hormone (GH) release. However, repeated bouts of sprinting attenuate the GH response, possibly due to negative feedback via elevated systemic free fatty acids (FFA). The aim of the study was to use nicotinic acid (NA) to suppress lipolysis to investigate whether serum FFA can modulate the GH response to exercise. Seven nonobese, healthy men performed two trials, consisting of two maximal 30-s cycle ergometer sprints separated by 4 h of recovery. In one trial (NA), participants ingested NA (1 g 60 min before, and 0.5 g 60 and 180 min after sprint 1); the other was a control (Con) trial. Serum FFA was not significantly different between trials before sprint 1 but was significantly lower in the NA trial immediately before sprint 2 [NA vs. Con: mean (SD); 0.08 (0.05) vs. 0.75 (0.34) mmol/l, P < 0.05]. Peak and integrated GH were significantly greater following sprint 2 compared with sprint 1 in the NA trial [peak GH: 23.3 (7.0) vs. 7.7 (11.9) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 316 (527) microg.l(-1).60 min(-1), P < 0.05] and compared with sprint 2 in the Con trial [peak GH: 23.3 (7.0) vs. 5.2 (2.3) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 206 (118) microg.l(-1).60 min(-1), P < 0.05]. In conclusion, suppressing lipolysis resulted in a significantly greater GH response to the second of two sprints, suggesting a potential role for serum FFA in negative feedback control of the GH response to repeated exercise.
Inhibition of Sleep-Related Growth Hormone Release by Elevated Free Fatty Acids
Growth hormone release was measured in four normal young men during normal sleep and during sleep in which free fatty acids (FFA) were elevated by the administration of oral Lipomul? and iv heparin. No correlation was found during normal sleep between plasma glucose and free fatty acid levels and the release of growth hormone coincident with control deep sleep periods. Elevation of FFA levels resulted in a suppression of growth hormone release with deep sleep with a mean peak level of 2.3 ? 0.7 ng/ml as compared to a mean peak of 29.4 ? 1.6 ng/ml obtained during normal sleep nights. Analysis of the data suggests that growth hormone secretion during deep sleep can be influenced by FFA which affect growth hormone secretion in the wake state.
http://jcem.endojournals.org/cgi/content/abstract/35/4/592


Vetten voor het slapen, een must of net niet?
