Förbränning vid viktnedgång?

[RandomC]

Vad ska man tycka om detta påstående? Stämmer det? Jag inbillar mig att det tidigare länkats till en studie som visade på att det i första hand är fett som förbränns vid en viktnedgång?

"Vidare bränner kroppen i första hand muskler vid viktnedgång delvis beroende på att aminosyror är det primära substratet för glukosproduktionen i levern."

[myling]

Känns som citatet är ryckt ur sitt sammanhang på nåt sätt. Du måste ju tänka på att du också nybildar ungefär samma mängd musklelprotein hela tiden (om du t ex styrketränar), under kalorirestriktion gäller ju inte det för fett.

[Eddie Vedder]

Det är främst fett som utnyttjas vid svält. Muskelmassa ryker förstås även det, ju större underskott desto mer, men fortfarande är fettet det främsta substratet att utnyttjas vid lågt energiintag.

http://www.ncbi.nlm.nih.gov/books/bv.fcgi?indexed=google&rid=stryer.section.4355

Under normal circumstances, approximately 50% of daily energy expenditure is derived from carbohydrate, thus for a daily expenditure of 8 MJ, the carbohydrate store will only last for 1-2 d of fasting-starvation before carbohydrate supply becomes dependent on gluconeogenesis. In reality, it is probable that the glycogen store is only depleted after several days of starvation, because even after an overnight fast, gluconeogenesis makes a significant contribution to hepatic glucose production (for review, see Shulman & Landau, 1992). In addition, as starvation proceeds there is less dependence on glucose as a metabolic fuel and a major focus of the first part of the present paper will be the control of substrate supply and utilization in fasting and starvation.
Adipose tissue lipolysis increases substantially in the first few days of starvation. Using stable-isotope-tracer methods, Wolfe et al. (1987) showed 2-3-fold increases in the rates of appearance of glycerol and palmitate in plasma. Interestingly, the lipolytic response to starvation was much less marked in the obese, although in both groups of subjects there was a similar starvation-induced enhancement of the lipolytic response to an adrenaline infusion. In the non-obese, the increased rate of lipolysis in starvation releases non-esterified fatty acids (NEFA) at a much greater rate than that needed for energy metabolism. Thus, there is a substantial amount of re esterification, and the energy costs of this fatty acid-triacylglycerol recycling can account for 2-3% of resting energy expenditure in the starving individual (Klein et al. 1989). Although the lower rate of lipolysis in the obese releases fatty acids in excess of the rate of fat oxidation, the surplus is smaller than that in the non-obese and so the energy cost of fatty acid-triacylglycerol recycling will be substantially lower in the obese.
The increase in lipolysis in the early stages of fasting seems most likely to be due to a variety of factors, including an increase in p-adrenoceptor sensitivity and a reduction in plasma insulin concentration.

[...]

The hypoinsulinaemia occurring during fasting contributes to the rise in basal lipolysis, but is not critical for the enhanced lipolytic responses to infused adrenaline seen after 4 d of starvation (Jensen et al. 1987). Further evidence of the importance of hypoinsulinaemia comes from a study by Klein et al. (1990), where infusion of glucose to maintain euglycaemia during fasting reduces the fall in plasma insulin and the magnitude of the enhanced lipolytic response to adrenaline.
The time-courses of the changes in glucose and fatty acid metabolism during the early stages of fasting-starvation provide some insight into the possible controlling mechanism. Klein et al. (1993) showed a 35% fall in plasma insulin during the first 24 h of fasting with 50-80% increases in the rates of lipolysis. By contrast, there was no change in the rate of glucose production. Thus, a rise in fat mobilization precedes any fall in glucose release. However, this takes no account of the likelihood that the mechanisms of glucose production alter during the fast, such that gluconeogenesis is the principal source of glucose at 24 h of fasting. Further evidence supporting this comes from the observations by Romijn et al. (1990) and Klein et al. (1993) that net glucose oxidation approaches zero within the first 24 h of starvation. This apparent paradox has a simple explanation, in that oxidation of glucose produced via gluconeogenesis from amino acids would not appear through whole-body indirect calorimetry as net glucose oxidation, but rather as protein oxidation. The subsequent reductions in glucose production and oxidation in later starvation are probably a result of increased fat oxidation, leading to inhibition of pyruvate dehydrogenase complex activity (see Denton & McCormack, 1995).

http://journals.cambridge.org/download.php?file=%2FPNS%2FPNS54_01%2FS00296651950 00255a.pdf&code=a54bad50024670306cb278dbfe6e39fd

Feeding, fasting and starvation: factors affecting fuel utilization. Proceedings of the Nutrition Society (1995), 54, 267-274


Men även om kroppen effektivare förbränner fett vid viktnedgång innebär inte det att muskelproteinbalansen inte blir negativ. Att muskelproteinnedbrytning inte blir jättemycket högre är EN sak, men man får inte glömma att man vid svältintag får en väldigt dålig stimulering av muskelproteinsyntesen samtidigt.

Muskelnedbrytningen som enskild process förväxlas ofta med det som egentligen är en negativ nettobalans mellan nedbrytning och nysyntes.