Could you knowledgable people please clarify for me the lowered metabolic rate with exercise piece? I'm probably confusing lowered metabolic rate with lowered resting heart rate following exercise, which I always understood was a good thing. Are the two (metabolic and heart rates) linked?

Resting metabolic rate is how many calories you are burning while not engaged in activity. Resting heart rate is beats per minute while not engaged in activity.

Are they related? Interesting question. I could see the body burning fewer calories if it becomes more efficient with exercise, as the heart appears to.

I posted more details in another thread I started called "Aerobic exercise lowers resting metabolism" or something like that.

Thanks. I looked at the other thread and....yikes. I'm a walking fiend. I love to walk everywhere every day whenever possible. Hiking for hours is even better. It clears my head, helps me think through problems and it flat out feels good (endorphins I guess). Am I to believe it's been helping to keep me fat?!

Or our bodies are just swinging the pendulum for us and trying to compensate for the increased metabolic rate while exercising. Trying to hold on to its energy stores for when they might next be needed, particularly to fuel vigorous exercise. So perhaps the more you try to lose wt by exercising, the more the body tries to compensate to keep from losing your energy stores (fat). On the bright side lower metabolic rates seem to be associated with longer longevity, so while increasing exercise to lose wt might not be totally effective - it could help you live longer?!

Eout isn't dictated by an organ like the thyroid for example. But it can be limited by a restriction of Ein, or by an effect of the stuff we put in out mouth, like carbs for example. The study Phinney cited used caloric restriction to make their point. The Eout compensation that occurred after exercise didn't come from the exercise, but from the caloric restriction. But then, we get more hungry after exercise, that's also a compensation. This means if we don't compensate by eating more, we'll compensate by spending less energy.

Longevity is also associated with lower insulin. I'm more inclined to believe that than an association with lower metabolic rate. Though lower insulin means lower body weight, and lower body weight means lower total metabolic rate, so that might be where the association comes from. On the other hand, lower insulin means more fuel available, which should mean a higher metabolic rate per unit of body mass. We can lower insulin with caloric restriction, but we can do it just as easily with carbohydrate restriction, without restricting total food intake, therefore avoiding to compensate by lowering resting metabolic rate.

I can tell you for a fact.... I get hungry faster when I exercise hard or a lot.

The answer is "maybe". It depends on how long you exercise, how often, and your genetics.

Taken from 'The Art and Science of Low-Carbohydrate Performance':
(page 38, 2nd paragraph)

Cool information, Brigitta!

That paragraph doesn't say whether there is a reduction in the number of fat cells. The conclusion that "losing body fat means...but also the amount of the associated 'machinery'" does not follow: He said fat cells are replaced.

It seems to me that the idea that fat cells live forever is wrong considering that most other cells are replaced regularly. I don't know why that idea came about. Maybe because it's never been easy to reduce fat mass once it was established? The 'machinery' he speaks of is the supporting tissue like blood vessels that feed oxygen to those fat cells. Those don't go away just by eating low-carb either.

This brings us back to the idea of a set-point. There is no such thing from an organ point of view. There is no organ that regulates the amount of fat tissue we have. It's all done with hormones that are themselves regulated through feedback mechanisms on a system-wide scale, at the cellular level. Take the process of insulin-induced lipohypertrophy for example. It's not determined by a single organ, but by insulin alone, which itself is determined not by a single organ, but by many different agents, only one of which is dietary carbohydrate. Though insulin is secreted by a single organ, its regulation is not done by a single organ. Insulin resistance for example will affect insulin level independently of the rate of secretion of insulin by the pancreas, instead by affecting the rate of disposal of insulin by tissues that become insulin resistant.

The point is that individual cells don't know what the system is doing except through the hormones that flow through this system. In turn those hormones don't depend on individual cells, but on the total collection of cells. Take blood glucose for example. It's kept within a tight range by beta cells that sense directly the amount of glucose that comes in contact with each cell. Each beta cell will secrete X amount of insulin for X amount of glucose sensed. The glucose each beta cell senses is in the blood, and blood flows through the entire system, thus each beta cell actually senses the entire system's blood glucose level. It doesn't really matter much how many beta cells secrete insulin because each cell is built to secrete the same X amount of insulin based on the same X amount of glucose sensed. Though it matters if the system-wide amount of blood glucose surpasses the total insulin-secretion capacity of all beta cells combined, just to keep blood glucose within the acceptable range of each individual beta cell.

This brings an interesting side point. With diabetes type 2, it's often said that beta cells become tired, and that's why they can't secrete enough insulin anymore. But the real problem with diabetes type 2 is not the pancreas, it's insulin resistance in all other tissues, which reduces the rate of disposal of insulin, therefore the rate of disposal of blood glucose. This is seen as chronic hyperglycemia and chronic hyperinsulinemia. Incidentally, chronic hyperinsulinemia is exactly the hormonal signal needed for insulin-induced lipohypertrophy to occur. This means it all starts with insulin resistance. But that's besides the point.

I don't know of any physiological mechanism that can cause fat cells and its supporting tissues to die off just by eating low-carb. There's apoptosis but that's just when cells must die for some reason that is otherwise detrimental to the system. As far as I can see, surplus fat cells and surplus supporting tissue to those fat cells don't cause any harm that I can see, that would somehow trigger apoptosis of those cells. As each cell knows only what the system is doing except through the hormones that flow through this system, and if those hormones are returned to normal by eating low-carb, then all is fine as far as those surplus fat cells can see.

That's why I say we're stuck with that last 10-20 lbs. It won't go away just by eating low-carb.

M Levac, I am interested in knowing more about insulin-induced hypertrophy. Could you point me to any suggested reading? It could be from a link, scientific paper, or book. I always find a way to get my hands on information.

The reason why I pointed out that paragraph was particularly because of: "They (fat cells) will stay with us."

Again, I would like to read more so that I can educate myself. I'm only 24 years old, but all of my family have ****y metabolisms. For example, my dad hasn't lost any weight despite the fact that he's cut his carbs under 20 grams and eats high-fat. He does experience positive effects when he rides his road bike, and also doesn't get "the shakes" from not eating for a long time like he used to.

I wrote a post a while ago. It contains a link to google pictures. Here it is:

http://forum.lowcarber.org/showthread.php?t=423928

Here's a PubMed search of "insulin-induced lipohypertrophy":

http://www.ncbi.nlm.nih.gov/pubmed?...lipohypertrophy

There's a common theme here. Lipo-suction to treat insulin-induced lipohypertrophy. This means the condition is permanent, and the treatment must also be permanent. Adipotide is a new drug being tested with human subjects currently that has a permanent effect on fat tissue. I hadn't thought of this before but I think this would be quite an attractive alternative for diabetics type 1. Or even diabetics type 2 since more and more of them are prescribed insulin.

http://forum.lowcarber.org/showthread.php?t=435270

About your dad. If he eats low-carb, then everything should return to normal, including his perceived energy level. As I said earlier, if it doesn't, then obviously something else must be going on. Now if there's no initial loss, that's unlikely to be due exclusively to lipohypertrophy, more likely that insulin doesn't want to cooperate, maybe because insulin resistance doesn't want to drop, maybe indicating that something else must be taken care of first. Start with the easiest to address, try it for a week, and go on from there. Who knows, it might be something as simple as taking a supplement to help with insulin sensitivity, maybe by fixing a deficiency or something. Somebody else could come in and help with that cuz I'm out of my element there. Just shooting ideas.

M Levac, thank you for the link you posted on this topic. For some people, it must be a little bit of both lipid-induced hypertrophy and replacement of fat cells. I guess the correct way of putting it is that "The net count of fat cells remains constant. They're just replaced at a certain rate."

I forgot about how Taubes mentioned the fat accumulation on insulin injection sites over a period of decades. Anyway, I think this is a valid point for people who have had high insulin levels all their lives. I have heard that there are children who happened to have much higher insulin levels than other children their age who eat the same types of food.