Training & Nutrition - Diet, exercise, weight loss, and insulin resistance

One of Enthalpic's comments got me surfing the PubMed database and I found these two tidbits which I think are worth remembering. "ad libitum" means "as desired" or "as much as you want" in this context, so no calorie restriction, which always reduces resting metabolic rate. Being a geezer, the ages of the study participants caught my eye.

From 2004:

"Effects of an ad libitum low-fat, high-carbohydrate diet on body weight, body composition, and fat distribution in older men and women: a randomized controlled trial.Hays NP, Starling RD, Liu X, Sullivan DH, Trappe TA, Fluckey JD, Evans WJ.
Nutrition, Metabolism, and Exercise Laboratory, Donald W Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock 72205, USA.

BACKGROUND: The efficacy of ad libitum low-fat diets in reducing body weight and fat in overweight and obese adults remains controversial. METHODS: We examined the effect of a 12-week low-fat, high-complex carbohydrate diet alone (HI-CHO) and in combination with aerobic exercise training (HI-CHO + EX) on body weight and composition in 34 individuals with impaired glucose tolerance (20 women and 14 men; mean +/- SEM age, 66 +/- 1 years). Participants were randomly assigned to a control diet (41% fat, 14% protein, 45% carbohydrates, and 7 g of fiber per 1000 kcal), a HI-CHO diet (18% fat, 19% protein, 63% carbohydrates, and 26 g of fiber per 1000 kcal), or a HI-CHO diet plus endurance exercise 4 d/wk, 45 min/d, at 80% peak oxygen consumption (HI-CHO + EX). Participants were provided 150% of estimated energy needs and were instructed to consume food ad libitum. Total food intake, body composition, resting metabolic rate, and substrate oxidation were measured. RESULTS: There was no significant difference in total food intake among the 3 groups and no change in energy intake over time. The HI-CHO + EX and HI-CHO groups lost more body weight (-4.8 +/- 0.9 kg [P=.003] and -3.2 +/- 1.2 kg [P=.02]) and a higher percentage of body fat (-3.5% +/- 0.7% [P=.01] and -2.2% +/- 1.2% [P=.049]) than controls (-0.1 +/- 0.6 kg and 0.2% +/- 0.6%). In addition, thigh fat area decreased in the HI-CHO (P=.003) and HI-CHO + EX (P<.001) groups compared with controls. High carbohydrate intake and weight loss did not result in a decreased resting metabolic rate or reduced fat oxidation. CONCLUSION: A high-carbohydrate diet consumed ad libitum, with no attempt at energy restriction or change in energy intake, results in losses of body weight and body fat in older men and women."

And from 2006:

"Effects of an ad libitum, high carbohydrate diet and aerobic exercise training on insulin action and muscle metabolism in older men and women.Hays NP, Starling RD, Sullivan DH, Fluckey JD, Coker RH, Williams RH, Evans WJ.
Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

BACKGROUND: Previous studies have demonstrated that aerobic exercise training and weight loss have independent effects on insulin-stimulated glucose disposal (ISGD). We hypothesized that ad libitum consumption of a high-carbohydrate diet would result in weight loss and improved ISGD, and that aerobic exercise training would facilitate greater improvements in ISGD compared with diet alone. METHODS: Older participants (13 women, 9 men; age = 66 +/- 1 year) with impaired glucose tolerance were randomly assigned to an ad libitum diet alone (18% fat, 19% protein, 63% carbohydrate) or this diet plus aerobic exercise training (4 d/wk, 45 min/d, 80% VO(2peak)) for 12 weeks. ISGD, abdominal fat distribution, muscle glycogen, and glycogen synthase activity were assessed pre- and postintervention. RESULTS: Consumption of the diet resulted in significant weight loss and an improvement in ISGD. Consumption of the diet plus exercise training also resulted in weight loss and increased ISGD, but results were not significantly different from those in the diet-alone group. Mean abdominal visceral and subcutaneous adipose tissue cross-sectional areas were smaller postintervention compared to baseline with no difference between groups. Exercise training and consumption of the diet increased muscle glycogen content (344.7 +/- 21.3 to 616.7 +/- 34.4 micromol.g(-1)) and decreased glycogen synthase activity (0.21 +/- 0.02 to 0.13 +/- 0.01) compared to the diet alone. CONCLUSIONS: These results demonstrate that consumption of an ad libitum, high-carbohydrate diet alone or in combination with aerobic exercise training results in weight loss and improved insulin sensitivity. Furthermore, exercise combined with this diet appears to limit additional increases in insulin sensitivity due to muscle glycogen supercompensation with a concomitant adaptive response of glycogen synthase."

This doesn't look good for the high protein diet crowd. However, the samples were small. We don't know if compliance was an issue or whether compliance was even monitored. The second study has no control group. And subjects all had some unspecified metabolic disorder. Still, interesting....

This doesn't look good for the high protein diet crowd. However, the samples were small. We don't know if compliance was an issue or whether compliance was even monitored. The second study has no control group. And subjects all had some unspecified metabolic disorder. Still, interesting....

In the first study all the food was supplied for the sample, and they could eat as much as they wanted.

In the first study all the food was supplied for the sample, and they could eat as much as they wanted.

I was assuming that they provided a variety of food, and subjects could select from the food that was provided. Maybe some subjects selected a lot of meat and not so much brown rice? I really don't know, but this is possible.

Without having read the entire OP....was there any adjustment for exercise level? Increased exercise amounts has been shown to reduce insulin resistance and this could be a source of variance within the study.

Without having read the entire OP....was there any adjustment for exercise level? Increased exercise amounts has been shown to reduce insulin resistance and this could be a source of variance within the study.

The second study was all about exercise. Older people on a high carb diet, who could eat as much as they wanted, lost weight and had better sugar metabolism, whether they exercised or not. But exercise increased a type of sugar used for energy by muscle cells (glycogen). Exercise also "decreased glycogen synthase activity", but I don't know what that means.

<<>> Exercise also "decreased glycogen synthase activity", but I don't know what that means.Well, there's this:

http://web.indstate.edu/thcme/mwking/glycogen.html

I read it and still don't know what they're talking about.

Since each study says the subjects were "provided" or "assigned" to a diet of precise composition, I would think the foods and proportions of those foods in that diet would be constant, no matter how much of that diet they chose to eat. Too bad it costs money to get the full study.

Well, there's this:

http://web.indstate.edu/thcme/mwking/glycogen.html

I read it and still don't know what they're talking about.

Since each study says the subjects were "provided" or "assigned" to a diet of precise composition, I would think the foods and proportions of those foods in that diet would be constant, no matter how much of that diet they chose to eat. Too bad it costs money to get the full study.

I think Someday RN might be able to email you the studies.

I can't picture how they could keep the composition the same while still allowing subjects to eat as much as they want. I suppose they could give them plates of all the foods as seconds. I doubt if they blended all the foods together, although that would explain the weight loss. ;) I'm a little leery of the studies, since they seem to have contradictory results to what you usually read.

<<>> I'm a little leery of the studies, since they seem to have contradictory results to what you usually read.Heh. Why I posted them. These are absolutely standard cyclists' diets, as recommended by exercise nutritionists. And low and behold, they have the results that we read about here. People lose weight, ride their bikes, and get stronger and healthier. Ride on.

Heh. Why I posted them. These are absolutely standard cyclists' diets, as recommended by exercise nutritionists. And low and behold, they have the results that we read about here. People lose weight, ride their bikes, and get stronger and healthier. Ride on.

I know that's what has worked for me. I lost more than 100 pounds on a high carb diet with much more exercise than is usually prescribed. My blood sugars also went from diabetic to normal, and LDL went from high to low. (I have to give statins some of the credit for the LDL.)

However, I know that what worked for me won't necessarily work for others. The sample (N = 1) just isn't large enough to draw any conclusions. We still need good science to tease out all the factors. Of course, in the meantime, I'll stick with what works for me. :)

exercise increases testosterone, which decreases insulin resistance.......

Not sure if this is exactly on your topic, but you will see metabolic syndrome (includes insulin resistance) treated with bioidentical testosterone back to optimal normal phsiological range very soon, I believe. In progressive medical circles anyway.

The second study was all about exercise. Older people on a high carb diet, who could eat as much as they wanted, lost weight and had better sugar metabolism, whether they exercised or not. But exercise increased a type of sugar used for energy by muscle cells (glycogen). Exercise also "decreased glycogen synthase activity", but I don't know what that means.


This is actually very interesting and a key component to why glucose tolerance is the same in the people who exercised and the people who did not.

Glycogen synthase is used to convert glucose into glycogen. It would seem that the more energy you use the more that would need to be replaced, therefore there should have been an increase in glycogen synthase.
But because the muscle has more glycogen stored in it it has decreased ability to uptake glucose because there is less room for it, thus not as much glucose can be taken up by the muscle.

They took muscle samples after an overnight fast, not after any activity, so since the exercised group had more glycogen stored there would be less need to uptake glucose from the blood. Plus the measurement of synthase was taken 3 days after the last exercise session. Because the tank is full you can't put more gas into it without it spilling over.

I would imagine that after exercising synthase activity would increase, thus decreasing glucose intolerance at that time. So it appears that they are saying that exercise will not decrease glucose intolerance globally, but it will increase glucose uptake after exercise.

They also looked at synthase activity only in the muscles. What effect would there be if you included the liver? and does exercise increase the amount of glycogen that the liver can store?

This is actually very interesting and a key component to why glucose tolerance is the same in the people who exercised and the people who did not.

Glycogen synthase is used to convert glucose into glycogen. It would seem that the more energy you use the more that would need to be replaced, therefore there should have been an increase in glycogen synthase.
But because the muscle has more glycogen stored in it it has decreased ability to uptake glucose because there is less room for it, thus not as much glucose can be taken up by the muscle.

They took muscle samples after an overnight fast, not after any activity, so since the exercised group had more glycogen stored there would be less need to uptake glucose from the blood. Plus the measurement of synthase was taken 3 days after the last exercise session. Because the tank is full you can't put more gas into it without it spilling over.

I would imagine that after exercising synthase activity would increase, thus decreasing glucose intolerance at that time. So it appears that they are saying that exercise will not decrease glucose intolerance globally, but it will increase glucose uptake after exercise.

They also looked at synthase activity only in the muscles. What effect would there be if you included the liver? and does exercise increase the amount of glycogen that the liver can store?


From my own experience as a diabetic I can tell you the effects of exercise seem to last about 24 hours. I could exercise everyother day and generally help to keep my blood sugars within a reasonable range (not perfect by any stretch of the imagination). If I skip 2 days, I can tell the difference, by about 30 mg/dl in the mornings when I test fasting bg's.

This is actually very interesting and a key component to why glucose tolerance is the same in the people who exercised and the people who did not.

Glycogen synthase is used to convert glucose into glycogen. It would seem that the more energy you use the more that would need to be replaced, therefore there should have been an increase in glycogen synthase.
But because the muscle has more glycogen stored in it it has decreased ability to uptake glucose because there is less room for it, thus not as much glucose can be taken up by the muscle.

They took muscle samples after an overnight fast, not after any activity, so since the exercised group had more glycogen stored there would be less need to uptake glucose from the blood. Plus the measurement of synthase was taken 3 days after the last exercise session. Because the tank is full you can't put more gas into it without it spilling over.

I would imagine that after exercising synthase activity would increase, thus decreasing glucose intolerance at that time. So it appears that they are saying that exercise will not decrease glucose intolerance globally, but it will increase glucose uptake after exercise.

They also looked at synthase activity only in the muscles. What effect would there be if you included the liver? and does exercise increase the amount of glycogen that the liver can store?

Thanks for the explanation. :)

I understand that glycogen storage is initiated by high levels of insulin. Type 2 diabetics and people with metabolic syndrome chronically have high levels of insulin, don't they? How does exercise affect insulin levels, and how does this fit into the issue of glycogen storage and insulin resistance?

I understand that glycogen storage is initiated by high levels of insulin.

For glycogen synthesis storage you need to have decreased glycogen in storage. If you stores are full then no amount of insulin would make a difference, the excess would get stored as fat.


Type 2 diabetics and people with metabolic syndrome chronically have high levels of insulin, don't they?

Yes and no. Type 2 DM is extremely complex, so I will try my best.

In some cases there is a normal amount of insulin, but the pathway has many steps and an error in the steps can contribute to DM2. Some of the errors can occur in the cell, after insulin has bound with the receptor sight, some sort of post receptor error. There can be chronically high insulin levels for years before the disease manifests, DM usually takes a decade or two to manifest, but this is also not a rule. The excess insulin can cause cells to down-regulate insulin receptor sights to prevent hypoglycaemia, and thus can cause insulin resistance.

After a while beta cells may not respond as well to glucose and put out less insulin, so in this case there would be chronically low levels of insulin in the blood. There is usually a decline in the weight and amount of beta cells in DMs. The beta cells also co-secrete amylin with insulin, which inhibits glucagon secretion.

Other factors include leptin, adiponectin, and restin. These adipokines have been proposed to be associated with insulin resistance. I think that these hormones function somewhat differently when someone is obese, and that is why when someone loses weight there is less insulin resistance. Don’t take my word on this one, I am getting out of my league here.

It is thought that problems with insulin secretion can lead to resistance and vice versa.


How does exercise affect insulin levels, and how does this fit into the issue of glycogen storage and insulin resistance?

I am not sure but this is something that I curious about. I am going to be working with a DSN tomorrow so I think I will ask about this. I would think that one would have trouble storing glycogen if you could not get glucose into the cell I don’t see how glycogen could be produced.

Remember that even though quite a bit is known about DM2, in reality relatively little is known, it is an extremely complex and interesting disease.