Calorie Partitioning: Part 1

At a very fundamental level, the problem that natural bodybuilders and athletes have is one of partitioning; that is, where the calories go when you eat more of them or come from when you eat less of them. In an ideal universe, every calorie you ate would go to muscle tissue, with none going into fat cells; you’d gain 100% muscle and no fat. In that same ideal universe, every calorie used during dieting would come from fat stores; you’d lose 100% fat and no muscle. Unfortunately, we don’t live in an ideal universe.

Bodyweight Regulation: Leptin Part 6

I talked a little bit about #1 in a previous post, when I talked about refeeds. At this point, and this topic is discussed to some degree in nearly every book I’ve written at this point, interjecting high carbohydrate, high calorie refeeds of varying lengths (anywhere from 5 hours to 3 days) is (currently) the best way to raise leptin while dieting.

Bodyweight Regulation: Leptin Part 5

Leptin and insulin also both change with changing food intake; leptin levels can drop significantly within a few days of dieting even with no change in body fat levels. Insulin changes meal to meal.

Bodyweight Regulation: Leptin Part 4

Basically, the body appears to be sensing ‘energy availability’ (defined as energy intake minus expenditure) and adjusting things based on that. I’d, of course, note that exercise still plays plenty of other crucial roles (including psychological, which I am getting back to slowly but surely) in terms of dieting and fat loss.

Bodyweight Regulation: Leptin Part 3

When it was originally discovered, leptin was originally conceived as an ‘anti-obesity’ hormone, it was thought that leptin should act to prevent weight gain. This led one researcher to quip (and I’m paraphrasing here) that “If leptin is meant to act as an anti-obesity hormone, it has to go down in history as the most ineffective hormone in the human body” or something roughly to that effect.

Bodyweight Regulation: Leptin Part 2

In the last post, I talked primarily about leptin (and a bit about insulin,and a very little bit about the other hormones) and its discovery and how it may be the (or at least one of the) long-sought after hormones involved in regulating bodyweight.

Bodyweight Regulation: Leptin Part 1

With early research (I’m talking the 1950’s) having established the existence of some type of setpoint (again, primarily in animal models), early researchers had to sort of guess what might be going on in terms of regulating body fat levels.

Homeostatic and Non-Homeostatic Pathways Involved in the Control of Food Intake and Energy Balance.

The homeostatic system has to do with the idea that the body tries to maintain some specific ‘set point’ in terms of bodyweight or body fat. Basically this system takes incoming signal (from hormones like leptin, insulin, blood glucose, ghrelin, peptide YY and a host of other stuff) and makes adjustments in appetite, hormones, metabolic rate and activity to compensate.

Crosstalk Between Estrogen and Leptin Signalling in the Hypothalamus

First things first, let me talk about leptin and the hypothalamus. I feel like I’ve been thumping on about leptin for years now, probably because I have. In many ways, it is the single most important hormone when it comes to problems with dieting and body recomposition. Released from body fat (and scaling frighteningly well with body fat levels), leptin signals the brain about two things which are

AMPK: Master Metabolic Regulator

The molecule I want to talk about is called AMP-activated protein kinase or AMPk for short, a compound that is turning out to be one of the major metabolic regulators in the liver, skeletal muscle, fatty acids, and the brain. This is especially true if you’re talking about the regulation of glucose uptake and utilization, fatty acid intake and oxidation, and appetite. Ok, maybe I have your attention again.