Why Exercise doesn't work

All the “experts” routinely suggest that the obese could ameliorate their problem or even prevent it if they merely exercised ninety minutes per day according to the USDA Dietary Guidelines. So the cure is to move more and to eat less, right? No matter where you look, there is advice to engage in daily physical activity. We see it in public health messages, popular writings, plastered on the back of food containers, etc. On exercise machines such as treadmills and stair climbers, we’re reminded of how many calories we allegedly expend while we workout. 

The problem is that this theory of physical activity has long been contradicted by the evidence. In Gary Taubes's great work, Good Calories, Bad Calories, we learned that in 1932, Russell Wilder noted that his patients tended to lose more weight with bed rest than they did with strenuous physical activity. He said, “The patient reasons quite correctly that the more exercise he takes the more fat should be burned and that the loss should be in proportion and he is discouraged to find that the scales reveal no progress.” 

In the 1960s, the “experts” continued to point out that moderate exercise would only lead to insignificant increases in energy expenditure and these could easily be matched by slight and comparatively effortless changes in diet.

As the old saying goes, “Those who do not know their history are destined to repeat it.” Nowadays, the government of the United States has a website that is dedicated to providing public information on small steps that the public can do to increase their physical activity. They advocate things such as taking the stairs, or parking the car further from the destination to promote walking. 

Even Louis Newberg, who is certainly not a fan of the alternative hypothesis, declared that “a 250-pound man will have to climb twenty flights of stairs to rid him of the energy contained one slice of bread.”

However, we’ve known since at least 1940 that a significant increase in energy expenditure also leads to an increase in appetite. Northwestern University endocrinologist Hugo Rony stated in 1940 that “vigorous muscle exercise usually results in immediate demand for a large meal.” Statistics support the fact that lumberjacks eat more than 5,000 calories while sailors eat only about 2,500. Most of us have seen the training tables of professional football players and boxers who eat tremendous amounts of food.

There is every reason to believe that if a sailor became a lumberjack, he would soon develop the appetite of his fellow lumberjacks. 

By at least 1960, it had been amply demonstrated that exercise is an ineffective method of increasing energy output and that physical exertion eventually evokes a desire for food such that the subsequent intake of calories may exceed that lost during exercise.

So what changed from 1960 until today where exercise is back in vogue and considered “indispensable” as a weight loss method? 

It was largely the work and influence of Jean Mayer who noted how overweight high school girls at several hundred calories less than those who weren’t. He also noted that those lean girls were more physically active than the obese. He chastised civilization for spending tends of billions annually on automobiles but unwilling to include a swimming pool and tennis courts in the plans of every high school.

It is common to observe that many obese persons are lazy, but most don’t stop to consider whether the weight has anything to do with the condition. If a lean person suddenly put on 20 pounds, would they not reduce their energy level somewhat? We also know of overweight people who participate in endurance running events yet they still remain obese. The same metabolic condition that leads to obesity could also lead to decreased physical activity. 

Another problem is that obesity is commonly associated with poverty. Those who earn their living through manual labor tend to be the less advantaged members of society in developed nations. They also tend to eat cheap carbohydrates. Go to any supermarket and it’s obvious which things are the least inexpensive. 

In 1965, there were physicians who challenged Mayer’s hypothesis and his faith in exercise. Physicians who treated obese patients called it unreasonable and that it “flouted common sense.” The only saving grace was that it came precisely at the time that Ancel Keys and Dennis Burkitt were gaining acceptance with two other bogus theories on fat and fiber respectively. Through 1972, he continued to argue that exercise would not increase appetite and even chaired President Nixon’s conference on nutrition and health. 

We have only to look at recent events to see the extremes of this bad advice. We’ve had runners die in marathons and world-class athletes develop heart disease and diabetes. Exercise cannot cover for a bad diet. Insulin remains the number one issue of our times and one cannot manage these levels through exercise. It has been demonstrated that insulin gets lowered by exercise, but if the next meal contains carbohydrates, that level will only rise to process the bad food. 

Through the 1970s, physiologists and biochemists worked out the mechanisms by which insulin and other hormones regulate not only the amount of fat we carry, but the distribution of that fat throughout the body. This all happens independently of how much we may or may not exercise. They can explain at both a hormonal and enzymatic level the entire corpus of lipophilia or “the exaggerated tendency of some tissues to store fat.” They found a critical enzyme in this process called lipoprotein lipase or LPL. Any cell that uses fatty acids for fuel or stores fatty acids uses LPL to make this happen.

When a triglyceride-rich lipoprotein passes by in the circulation, the LPL will grab on, and then break down the triglycerides inside into their component fatty acids. This increases the local concentration of free fatty acids flowing into the cells and these either go to storage (as triglycerides in fat cells) or for fuel. Basically, the more LPL activity on a particular cell type, the more fatty acids the cell will absorb and this is the reason that LPL is known as the gatekeeper for fat accumulation. 

It shouldn’t surprise you to know that insulin is the primary regulator of LPL activity, although not the only one. This regulation varies from tissue to tissue and from site to site. In fat tissue, insulin increases LPL activity; in muscle tissue, it decreases activity. Fat gets deposited in fat tissue when we secrete insulin and the muscle cells take up glucose instead of oxygen. When insulin levels drop, the LPL activity on the fat cells decrease and the LPL activity on the muscle cells increase. This causes the fat cells to release fatty acids and the muscle cells take them up for fuel. 

This orchestration of LPL activity by insulin and other hormones accounts for why some areas of the body will fatten differently than others, why women and men fatten differently, and how these distributions change with age. LPL activity also determines what happens during menopause and pregnancy as well as the fat deposition during nursing.

After M.R.C. Greenwood, a student of Jules Hirsch at Vassar College presented the “gatekeeper hypothesis” of obesity in 1981, Gary Taubes reported that researchers found that obese humans have increased LPL activity in their fat tissue. Moreover, they have found that LPL activity in fat tissue increases with weight loss on a semi-starvation diet and it decreases in muscle tissue. This will negate any negative energy balance that may be induced by semi-starvation (a low-fat diet). 

During exercise, LPL activity increases in muscle tissue to enhance the flow of fatty acids (the body’s preferred fuel) to the muscles for fuel. But when the workout is over, LPL activity in the fat tissue increases which serves to restock the fat tissue with whatever fat may have been lost to exercise. This led University of Colorado physiologist Robert Eckel to opine that “habitual carbohydrate intake may have a stronger effect on subcutaneous fat storage than does dietary fat intake.” 

This science is not controversial and it is hard to imagine why obesity researchers do not take seriously that carbohydrates have the unique ability to fatten humans. In 1991, the Belgian physiologist Henri-Gery Hers an authority on glycogen storage diseases, put it this way:

“Eating carbohydrates will stimulate insulin secretion and cause obesity. That looks obvious to me….”

But this simple chain of cause and effect has nonetheless been rejected out of hand by authority figures in the field of human obesity who believe the cause is overeating and under activity due to their flawed construction of the law of energy conservation.

Exercise, like most diet plans, does not control hunger and cravings and therefore it is ineffective as a means to weight loss. Having said that, I do recommend exercise as there clearly are benefits to being in shape. However, one should exercise because they enjoy it, not as a weight loss tool.



© ZIOH 2013