Exercise and blood glucose levels: Insulin and glucose responses to exercise

The notion that exercise reduces blood glucose levels is widespread. That notion is largely incorrect. Exercise appears to have a positive effect on insulin sensitivity in the long term, but also increases blood glucose levels in the short term. That is, exercise, while it is happening, leads to an increase in circulating blood glucose. In normoglycemic individuals, that increase is fairly small compared to the increase caused by consumption of carbohydrate-rich foods, particularly foods rich in refined carbohydrates and sugars.

The figure below, from the excellent book by Wilmore and colleagues (2007), shows the variation of blood insulin and glucose in response to an endurance exercise session. The exercise session’s intensity was at 65 to 70 percent of the individuals’ maximal capacity (i.e., their VO2 max). The session lasted 180 minutes, or 3 hours. The full reference to the book by Wilmore and colleagues is at the end of this post.

As you can see, blood insulin levels decreased markedly in response to the exercise bout, in an exponential decay fashion. Blood glucose increased quickly, from about 5.1 mmol/l (91.8 mg/dl) to 5.4 mmol/l (97.2 mg/dl), before dropping again. Note that blood glucose levels remained somewhat elevated throughout the exercise session. But, still, the elevation was fairly small in the participants, which were all normoglycemic. A couple of bagels would easily induce a rise to 160 mg/dl in about 45 minutes in those individuals, and a much larger “area under the curve” glucose response than exercise.

So what is going on here? Shouldn’t glucose levels go down, since muscle is using glucose for energy?

No, because the human body is much more “concerned” with keeping blood glucose levels high enough to support those cells that absolutely need glucose, such as brain and red blood cells. During exercise, the brain will derive part of its energy from ketones, but will still need glucose to function properly. In fact, that need is critical for survival, and may be seen as a bit of an evolutionary flaw. Hypoglycemia, if maintained for too long, will lead to seizures, coma, and death.

Muscle tissue will increase its uptake of free fatty acids and ketones during exercise, to spare glucose for the brain. And muscle tissue will also consume glucose, in part for glycogenesis; that is, for making muscle glycogen, which is being depleted by exercise. In this sense, we can say that muscle tissue is becoming somewhat insulin resistant, because it is using more free fatty acids and ketones for energy, and thus less glucose. Another way of looking at this, however, which is favored by Wilmore and colleagues (2007), is that muscle tissue is becoming more insulin sensitive, because it is still taking up glucose, even though insulin levels are dropping.

Truth be told, the discussion in the paragraph above is mostly academic, because muscle tissue can take up glucose without insulin. Insulin is a hormone that allows the pancreas, its secreting organ, to communicate with two main organs – the liver and body fat. (Yes, body fat can be seen as an “organ”, since it has a number of endocrine functions.) Insulin signals to the liver that it is time to take up blood glucose and either make glycogen (to be stored in the liver) or fat with it (secreting that fat in VLDL particles). Insulin signals to body fat that it is time to take up blood glucose and fat (e.g., packaged in chylomicrons) and make more body fat with it. Low insulin levels, during exercise, will do the opposite, leading to low glucose uptake by the liver and an increase in body fat catabolism.

Resistance exercise (e.g., weight training) induces much higher glucose levels than endurance exercise; and this happens even when one has fasted for 20 hours before the exercise session. The reason is that resistance exercise leads to the conversion of muscle glycogen into energy, releasing lactate in the process. Lactate is in turn used by muscle tissues as a source of energy, helping spare glycogen. It is also used by the liver for production of glucose through gluconeogenesis, which significantly elevates blood glucose levels. That hepatic glucose is then used by muscle tissues to replenish their depleted glycogen stores. This is known as the Cori cycle.

Exercise seems to lead, in the long term, to insulin sensitivity; but through a fairly complex and longitudinal process that involves the interaction of many hormones. One of the mechanisms may be an overall reduction in insulin levels, leading to increased insulin sensitivity as a compensatory adaptation. In the short term, particularly while it is being conducted, exercise nearly always increases blood glucose levels. Even in the first few months after the beginning of an exercise program, blood glucose levels may increase. If a person who was on a low carbohydrate diet started a 3-month exercise program, it is quite possible that the person’s average blood glucose would go up a bit. If low carbohydrate dieting began together with the exercise program, then average blood glucose might drop significantly, because of the acute effect of this type of dieting on average blood glucose.

Still exercise is health-promoting. The combination of the long- and short-term effects of exercise appears to lead to an overall slowing down of the progression of insulin resistance with age. This is a good thing.

Reference:

Wilmore, J.H., Costill, D.L., & Kenney, W.L. (2007). Physiology of sport and exercise. Champaign, IL: Human Kinetics.

Interview with Jimmy Moore

About two months ago, I did an interview with Jimmy Moore of the Livin' la Vida Low Carb internet empire. I hardly remember what we talked about, but I think it went well. I enjoyed Jimmy's pleasant and open-minded attitude. Head over to Jimmy's website and listen to the interview here.

I do recall making at least one mistake. When discussing heart attacks,I said "atrial fibrillation" when I meant "ventricular fibrillation".

Compensatory adaptation as a unifying concept: Understanding how we respond to diet and lifestyle changes

Trying to understand each body response to each diet and lifestyle change, individually, is certainly a losing battle. It is a bit like the various attempts to classify organisms that occurred prior to solid knowledge about common descent. Darwin’s theory of evolution is a theory of common descent that makes classification of organisms a much easier and logical task.

Compensatory adaptation (CA) is a broad theoretical framework that hopefully can help us better understand responses to diet and lifestyle changes. CA is a very broad idea, and it has applications at many levels. I have discussed CA in the context of human behavior in general (Kock, 2002), and human behavior toward communication technologies (Kock, 2001; 2005; 2007). Full references and links are at the end of this post.

CA is all about time-dependent adaptation in response to stimuli facing an organism. The stimuli may be in the form of obstacles. From a general human behavior perspective, CA seems to be at the source of many success stories. A few are discussed in the Kock (2002) book; the cases of Helen Keller and Stephen Hawking are among them.

People who have to face serious obstacles sometimes develop remarkable adaptations that make them rather unique individuals. Hawking developed remarkable mental visualization abilities, which seem to be related to some of his most important cosmological discoveries. Keller could recognize an approaching person based on floor vibrations, even though she was blind and deaf. Both achieved remarkable professional success, perhaps not as much in spite but because of their disabilities.

From a diet and lifestyle perspective, CA allows us to make one key prediction. The prediction is that compensatory body responses to diet and lifestyle changes will occur, and they will be aimed at maximizing reproductive success, but with a twist – it’s reproductive success in our evolutionary past! We are stuck with those adaptations, even though we live in modern environments that differ in many respects from the environments where our ancestors lived.

Note that what CA generally tries to maximize is reproductive success, not survival success. From an evolutionary perspective, if an organism generates 30 offspring in a lifetime of 2 years, that organism is more successful in terms of spreading its genes than another that generates 5 offspring in a lifetime of 200 years. This is true as long as the offspring survive to reproductive maturity, which is why extended survival is selected for in some species.

We live longer than chimpanzees in part because our ancestors were “good fathers and mothers”, taking care of their children, who were vulnerable. If our ancestors were not as caring or their children not as vulnerable, maybe this blog would have posts on how to control blood glucose levels to live beyond the ripe old age of 50!

The CA prediction related to responses aimed at maximizing reproductive success is a straightforward enough prediction. The difficult part is to understand how CA works in specific contexts (e.g., Paleolithic dieting, low carbohydrate dieting, calorie restriction), and what we can do to take advantage (or work around) CA mechanisms. For that we need a good understanding of evolution, some common sense, and also good empirical research.

One thing we can say with some degree of certainty is that CA leads to short-term and long-term responses, and that those are likely to be different from one another. The reason is that a particular diet and lifestyle change affected the reproductive success of our Paleolithic ancestors in different ways, depending on whether it was a short-term or long-term change. The same is true for CA responses at different stages of one’s life, such as adolescence and middle age; they are also different.

This is the main reason why many diets that work very well in the beginning (e.g., first months) frequently cease to work as well after a while (e.g., a year).

Also, CA leads to psychological responses, which is one of the key reasons why most diets fail. Without a change in mindset, more often than not one tends to return to old habits. Hunger is not only a physiological response; it is also a psychological response, and the psychological part can be a lot stronger than the physiological one.

It is because of CA that a one-month moderately severe calorie restriction period (e.g., 30% below basal metabolic rate) will lead to significant body fat loss, as the body produces hormonal responses to several stimuli (e.g., glycogen depletion) in a compensatory way, but still “assuming” that liberal amounts of food will soon be available. Do that for one year and the body will respond differently, “assuming” that food scarcity is no longer short-term and thus that it requires different, and possibly more drastic, responses.

Among other things, prolonged severe calorie restriction will lead to a significant decrease in metabolism, loss of libido, loss of morale, and physical as well as mental fatigue. It will make the body hold on to its fat reserves a lot more greedily, and induce a number of psychological responses to force us to devour anything in sight. In several people it will induce psychosis. The results of prolonged starvation experiments, such as the Biosphere 2 experiments, are very instructive in this respect.

It is because of CA that resistance exercise leads to muscle gain. Muscle gain is actually a body’s response to reasonable levels of anaerobic exercise. The exercise itself leads to muscle damage, and short-term muscle loss. The gain comes after the exercise, in the following hours and days (and with proper nutrition), as the body tries to repair the muscle damage. Here the body “assumes” that the level of exertion that caused it will continue in the near future.

If you increase the effort (by increasing resistance or repetitions, within a certain range) at each workout session, the body will be constantly adapting, up to a limit. If there is no increase, adaptation will stop; it will even regress if exercise stops altogether. Do too much resistance training (e.g., multiple workout sessions everyday), and the body will react differently. Among other things, it will create deterrents in the form of pain (through inflammation), physical and mental fatigue, and even psychological aversion to resistance exercise.

CA processes have a powerful effect on one’s body, and even on one’s mind!

References:

Kock, N. (2001). Compensatory Adaptation to a Lean Medium: An Action Research Investigation of Electronic Communication in Process Improvement Groups. IEEE Transactions on Professional Communication, 44(4), 267-285.

Kock, N. (2002). Compensatory Adaptation: Understanding How Obstacles Can Lead to Success. Infinity Publishing, Haverford, PA. (Additional link.)

Kock, N. (2005). Compensatory adaptation to media obstacles: An experimental study of process redesign dyads. Information Resources Management Journal, 18(2), 41-67.

Kock, N. (2007). Media Naturalness and Compensatory Encoding: The Burden of Electronic Media Obstacles is on Senders. Decision Support Systems, 44(1), 175-187.

In Search of Traditional Asian Diets

It's been difficult for me to find good information on Asian diets prior to modernization. Traditional Chinese, Taiwanese and Japanese diets are sometimes portrayed as consisting mostly of white rice, with vegetables and a bit of meat and soy, but I find that implausible. Rice doesn't grow everywhere, and removing all the bran was prohibitively labor-intensive before the introduction of modern machine milling. One hundred years ago, bran was partially removed by beating or grinding in a mortar and pestle, as it still is in parts of rural Asia today. Only the wealthy could afford true white rice.

Given the difficulty of growing rice in most places, and hand milling it, the modern widespread consumption of white rice in Asia must be a 20th century phenomenon, originating in the last 20-100 years depending on location. Therefore, white rice consumption does not predate the emergence of the "diseases of civilization" in Asia.

In the book Western Diseases: Their Emergence and Prevention, there are several accounts of traditional Asian diets I find interesting.

Taiwan in 1980

The staple constituent of the diet is polished white rice. Formerly in the poorer areas along the sea coast the staple diet was sweet potato, with small amounts of white rice added. Formerly in the mountains sweet potato, millet and taro were the staple foods. During the last 15 years, with the general economic development of the whole island, white polished rice has largely replaced other foods. There is almost universal disinclination to eat brown (unpolished) rice, because white rice is more palatable, it bears kudos, cooking is easier and quicker, and it can be stored for a much longer period.

Traditionally, coronary heart disease and high blood pressure were rare, but the prevalence is now increasing rapidly. Stroke is common. Diabetes was rare but is increasing gradually.

Mainland China

China is a diverse country, and the food culture varies by region.

Snapper (1965)… quoted an analysis by Guy and Yeh of Peiping (Peking) diets in 1938. There was a whole cereal/legume/vegetable diet for poorer people and a milled-cereal/meat/vegetable diet for the richer people.

Symptoms of vitamin A, C and D deficiency were common in the poor, although coronary heart disease and high blood pressure were rare. Diabetes occurred at a higher rate than in most traditionally-living populations.

Japan

On the Japanese island of Okinawa, the traditional staple is the sweet potato, with a smaller amount of rice eaten as well. Seafood, vegetables, pork and soy are also on the menu. In Akira Kurosawa’s movie Seven Samurai, set in 16th century mainland Japan, peasants ate home-processed millet and barley, while the wealthy ate white rice. Although a movie may not be the best source of information, I suspect it has some historical basis.

White Rice: a Traditional Asian Staple?

It depends on your perspective. How far back do you have to go before you can call a food traditional? Many peoples' grandparents ate white rice, but I doubt their great great grandparents ate it frequently. White rice may have been a staple for the wealthy for hundreds of years in some places. But for most of Asia, in the last few thousand years, it was probably a rare treat. The diet most likely resembled that of many non-industrial African cultures: an assortment of traditionally prepared grains, root vegetables, legumes, vegetables and a little meat.

Please add any additional information you may have about traditional Asian diets to the comments section.

What about some offal? Boiled tripes in tomato sauce

Tripe dishes are made with the stomach of various ruminants. The most common type of tripe is beef tripe from cattle. Like many predators, our Paleolithic ancestors probably ate plenty of offal, likely including tripe. They certainly did not eat only muscle meat. It would have been a big waste to eat only muscle meat, particularly because animal organs and other non-muscle parts are very rich in vitamins and minerals.

The taste for tripe is an acquired one. Many national cuisines have traditional tripe dishes, including the French, Chinese, Portuguese, and Mexican cuisines – to name only a few. The tripe dish shown in the photo below was prepared following a simple recipe. Click on the photo to enlarge it.

Here is the recipe:

- Cut up about 2 lbs of tripe into rectangular strips. I suggest rectangles of about 5 by 1 inches.
- Boil the tripe strips in low heat for 5 hours.
- Drain the boiled tripe strips, and place them in a frying or sauce pan. You may use the same pan you used for boiling.
- Add a small amount of tomato sauce, enough to give the tripe strips color, but not to completely immerse them in the sauce. Add seasoning to taste. I suggest some salt, parsley, garlic powder, chili powder, black pepper, and cayenne pepper.
- Cook the tripe strips in tomato sauce for about 15 minutes.

Cooked tripe has a strong, characteristic smell, which will fill your kitchen as you boil it for 5 hours. Not many people will be able to eat many tripe strips at once, so perhaps this should not be the main dish of a dinner with friends. I personally can only eat about 5 strips at a time. I know folks who can eat a whole pan full of tripe strips, like the one shown on the photo in this post. But these folks are not many.

In terms of nutrition, 100 g of tripe prepared in this way will have approximately 12 g of protein, 4 g of fat, 157 g of cholesterol, and 2 g of carbohydrates. You will also be getting a reasonable amount of vitamin B12, zinc, and selenium.

Pretty faces are average faces: Genetic diversity and health

Many people think that the prettiest faces are those with very unique features. Generally that is not true. Pretty faces are average faces. And that is not only because they are symmetrical, even though symmetry is an attractive facial trait. Average faces are very attractive, which is counterintuitive but makes sense in light of evolution and genetics.

The faces in the figure below (click to enlarge) are from a presentation I gave at the University of Houston in 2008. The PowerPoint slides file for the presentation is available here. The photos were taken from the German web site Beautycheck.de. This site summarizes a lot of very interesting research on facial attractiveness.

The face on the right is a composite of the two faces on the left. It simulates what would happen if you were to morph the features of the two faces on the left into the face on the right. That is, the face on the right is the result of an “averaging” of the two faces on the left.

If you show these photos to a group of people, like I did during my presentation in Houston, most of the people in the group will say that the face on the right is the prettiest of the three. This happens even though most people will also say that each of the three faces is pretty, if shown each face separately from the others.

Why are average faces more beautiful?

The reason may be that we have brain algorithms that make us associate a sense of “beauty” with features that suggest an enhanced resistance to disease. This is an adaptation to the environments our ancestors faced in our evolutionary past, when disease would often lead to observable distortions of facial and body traits. Average faces are the result of increased genetic mixing, which leads to increased resistance to disease.

This interpretation is a variation of Langlois and Roggman’s “averageness hypothesis”, published in a widely cited 1990 article that appeared in the journal Psychological Science.

By the way, many people think that the main survival threats ancestral humans faced were large predators. I guess it is exciting to think that way; our warrior ancestors survived due to their ability to fight off predators! The reality is that, in our ancestral past, as today, the biggest killer of all by far was disease. The small organisms, the ones our ancestors couldn’t see, were the most deadly.

People from different populations, particularly those that have been subjected to different diseases, frequently carry genetic mutations that protect them from those diseases. Those are often carried as dominant alleles (i.e., variations of a gene). When two people with diverse genetic protections have children, the children inherit the protective mutations of both parents. The more genetic mixing, the more likely it is that multiple protective genetic mutations will be carried. The more genetic mixing, the higher is the "averageness" score of the face.

The opposite may happen when people who share many genes (e.g., cousins) have children. The term for this is inbreeding. Since alleles that code for diseases are often carried in recessive form, a child of closely related parents has a higher chance of having a combination of two recessive disease-promoting alleles. In this case, the child will be homozygous recessive for the disease, which will increase dramatically its chances of developing the disease.

In a nutshell: gene mixing = health; inbreeding = disease.

Finally, if you have some time, make sure to take a look at this page on the Virtual Miss Germany!

Low Micronutrient Intake may Contribute to Obesity

[2013 update: I'm skeptical of the idea that micronutrient insufficiency/deficiency promotes obesity.  Although the trial discussed below suggested it might be a factor, it has not been a general finding that micronutrient supplementation causes fat loss, and the result needs to be repeated to be believable in my opinion.  Also, conditions of frank micronutrient deficiency are not usually associated with fat gain]

Lower Micronutrient Status in the Obese

Investigators have noted repeatedly that obese people have a lower blood concentration of a number of nutrients, including vitamin A, vitamin D, vitamin K, several B vitamins, zinc and iron (1). Although there is evidence that some of these may influence fat mass in animals, the evidence for a cause-and-effect relationship in humans is generally slim. There is quite a bit of indirect evidence that vitamin D status influences the risk of obesity (2), although a large, well-controlled study found that high-dose vitamin D3 supplementation does not cause fat loss in overweight and obese volunteers over the course of a year (3). It may still have a preventive effect, or require a longer timescale, but that remains to be determined.

Hot off the Presses

A new study in the journal Obesity, by Y. Li and colleagues, showed that compared to a placebo, a low-dose multivitamin caused obese volunteers to lose 7 lb (3.2 kg) of fat mass in 6 months, mostly from the abdominal region (4). The supplement also reduced LDL by 27%, increased HDL by a whopping 40% and increased resting energy expenditure. Here's what the supplement contained:

Vitamin A(containing natural mixed b-carotene) 5000 IU
Vitamin D 400 IU
Vitamin E 30 IU
Thiamin 1.5 mg
Riboflavin 1.7 mg
Vitamin B6 2 mg
Vitamin C 60 mg
Vitamin B12 6 mcg
Vitamin K1 25 mcg
Biotin 30 mcg
Folic acid 400 mcg
Nicotinamide 20 mg
Pantothenic acid 10 mg
Calcium 162 mg
Phosphorus 125 mg
Chlorine 36.3 mg
Magnesium 100 mg
Iron 18 mg
Copper 2 mg
Zinc 15 mg
Manganese 2.5 mg
Iodine 150 mcg
Chromium 25 mcg
Molybdenum 25 mcg
Selenium 25 mcg
Nickel 5 mcg
Stannum 10 mcg
Silicon 10 mcg
Vanadium 10 mcg

Although the result needs to be repeated, if we take it at face value, it has some important implications:

• The nutrient density of a diet may influence obesity risk, as I speculated in my recent audio interview and related posts (5, 6, 7, 8, 9).
• Many nutrients act together to create health, and multiple insufficiencies may contribute to disease. This may be why single nutrient supplementation trials usually don't find much.
• Another possibility is that obesity can result from a number of different nutrient insufficiencies, and the cause is different in different people. This study may have seen a large effect because it corrected many different insufficiencies.
• This result, once again, kills the simplistic notion that body fat is determined exclusively by voluntary food consumption and exercise behaviors (sometimes called the "calories in, calories out" idea, or "gluttony and sloth"). In this case, a multivitamin was able to increase resting energy expenditure and cause fat loss without any voluntary changes in food intake or exercise, suggesting metabolic effects and a possible downward shift of the body fat "setpoint" due to improved nutrient status.

Practical Implications

Does this mean we should all take multivitamins to stay or become thin? No. There is no multivitamin that can match the completeness and balance of a nutrient-dense, whole food, omnivorous diet. Beef liver, leafy greens and sunlight are nature's vitamin pills. Avoiding refined foods instantly doubles the micronutrient content of the typical diet. Properly preparing whole grains by soaking and fermentation is equivalent to taking a multi-mineral along with conventionally prepared grains, as absorption of key minerals is increased by 50-300% (10). Or you can eat root vegetables instead of grains, and enjoy their naturally high mineral availability. Or both.