Slow Burn

In the immortal words of the short-lived marketing misstep that was Talking Barbie, "Math is hard." With a physique that would defy the physics of walking upright not to mention in heels, it's no wonder her creators found math challenging. But sometimes you just have to slog through the tough material just to know that you can rely on data that's proven. What I learned from Mrs. Lindsey, my 9th grade Elementary Functions teacher, is that proving theories with the 'Gibbons Theorem' just to imply I had a vague grasp of the material doesn't bring home the 'A', and hard candy for right answers doesn't make the task any more enjoyable. All that just to welcome you to the science of fat loss so that you can exercise strategically.

When reading scientific explanations there are two things to avoid. First, don't read with Carl Sagan-like inflection. Do try to liven up the material with zippy little exclamation points as necessary. Second, for the sake of retention, don't try to sing the text to the tune of any 'School House Rock' songs. The Declaration of Independence shouldn't have been reduced to a mere ditty and neither should the serious business of fat metabolism. So, put on your serious face and, for my Microsoft clients, pretend this is a Power Point presentation:

"Conjunction junction, what's your function . . . ."

We've talked about fast-twitch and slow twitch muscle fibers and no, this is not defined by relative coffee consumption. Fast Twitch, Type II, and Slow Twitch, Type I, needs little explanation. As Bruce W. Craig, PhD, Column Editor for NSCA's Strength and Conditioning Journal (Volume 28, Number 5, pages 70-71) and author of 'Fat Burning', "In short, your type I fibers have a slower chemistry than your type II fibers, and are the fiber of choice when the workload is lower." From here, Craig takes over to explain fat metabolism and the roll type I and type II fibers play:

Type I muscle fibers are classified as aerobic fibers and contain numerous mitochondria. Mitochondria contain a series of aerobic enzymes that represent a metabolic pathway called the Krebs cycle. The Krebs cycle within each mitochondrion is able to produce 1 ATP molecule directly and 8 hydrogen ions every time it cycles. The hydrogen ions this system produces then enter the electron transport system of the mitochondria, and their energy is used to rebuild the ATP broken down during muscle contraction. The metabolic pathways of the mitochondria can supply the ATP demands of the muscle at rest and during aerobic exercise if adequate oxygen is available. In the presence of oxygen, these 2 mitochondrial systems can make 12 ATP molecules for every turn of the Krebs cycle. The compound that starts the the Krebs cycle is called acetyl-CoA, and it can be formed from either carbohydrates or fats. The carbohydrate your muscles metabolize is a simple sugar called glucose, and it is either imported (blood glucose from dietary intake or liver) or taken from a local storage form (muscle glycogen) as a modified version of glucose. Glucose molecules consist of 6 carbons, and their complete breakdown produces 2 acetyl-CoA molecules. If both acetyl-CoA molecules enter the Krebs cycle, the ATP yield is 24. Fat, on the other hand, contains a lot more carbon and can produce more ATP than carbohydrates. The fat your muscle uses can come form many sources, such as plasma free fatty acids (FAs) and triglycerides, or the triglycerides stored within the muscle. Free FAs can be used directly, but triglycerides need to be broken down first. Triglycerides consist of glycerol molecule (alcohol compound) and 3 FA molecules. When you exercise, the body releases hormones that activate a fat cell enzyme that breaks triglycerides into glycerol and FA. The FA molecules that are released following this breakdown contain from 16 to 18 carbons, and the metabolism of just one 16-carbon palmitic acid (saturated FA) by the mitochondria will give you 129 ATP molecules. Given that there are 3 FA molecules per triglyceride, fats represent a major source of energy.

As indicated above, Type 1 Fibers can metabolize either carbohydrates or fats, and are more involved when exercise intensity is at or below 70% of your maximal aerobic capacity (VO2 max). If aerobic exercise is above 70% of VO2 max or you perform resistance training, the nervous system recruits more anaerobic muscle fibers (type II), which produce more and metabolize more carbohydrates. Type II muscle fibers do not contain as many mitochondria as type I fibers and use muscle glycogen as their primary fuel, so they are not as dependent on oxygen. The breakdown of glucose in type II fibers is faster than its usage in type I fibers because it occurs outside the mitochondria and does not produce as many acetyl-CoA molecules. The end result of glucose metabolism in type II fibers is lactic acid, and only 2 ATP molecules are produced per molecule of glucose. Therefore, when you increase exercise intensity, the muscle tends to burn (metabolize) more carbohydrate than fat because of the type of muscle fiber being used.

If your ability to burn fat were dependent solely on its progression through its metabolic pathways, 15 minutes of aerobic exercise might be adequate. However, fat metabolism is also dependent on the delivery of FAs to an active muscle, and the primary factor that influences fat usage during exercise is the time it takes to metabolize fats. The metabolization of fat represents its release from fat cells, and is hormonally regulated. Two hormones in particular, epinephrine from the adrenal gland and glucagon from the pancreas, are released into the bloodstream at the onset of exercise and activate hormone-sensitive lipase (HSL) in fat cells and muscle. Once activated, this enzyme breaks triglycerides into 3 FA molecules and glycerol, and the FA molecules enter the bloodstream (fat cells) or are available to the muscle (intramuscular triglyceride stores). The breakdown and usage of intramuscular stores of triglyceride during exercise is not well understood, and estimates of how much fat the muscle uses from this source are not possible with current research techniques. However, based on the appearance of FAs in the blood during steady-state aerobic exercise (70% of VO2 max) it takes approximately 20-30 minutes to get FAs to an active muscle, which represents the time it takes to release the HSL-activating hormones, the action of the HSL, and the transit time required for FAs to reach the muscle fromm fat cells. Even after FAs reach the muscle, they must cross the cell membrane, enter the mitochondria, and be converted into acetyl-CoA via a metabolic process called beta oxidation before they can be metabolized in the Krebs cycle. All of these steps increase the exercise time needed to utilize fat for ATP production from an external source. During this time, the muscle can use other fuels, and most likely metabolizes intramuscular fat, any free FAs in the blood, or glucose, but does not utilize a high percentage of the fat within the fat cells that diets and exercise programs target. Therefore, if your exercise goal is to reduce fat, exercising aerobically at 60 to 70% of your VO2 max for at least 20 minutes per day is one way to achieve that goal.

Well, that was one windy answer . . . .

It's likely that the clever little brainiacs who figured this out could easily be wrestled to the floor and robbed of their lunch money by bigger, stronger, faster hooligans who haven't listened to a word published about fitness. Though test tubes and microscopes are handy tools, so are dumbbells and a good sweat. As soundly reasoned as the above explanation is, it's the same thought process that brought us Nautilaus equipment - it's a localized approach that ignores the global result.

When queried in Fat Loss and Fitness, Patrick J. O'Shea, Ed.D, Professor Emeritus of exercise and sports science at Oregon State University and author of the book 'Quantum Strength and Power Training (Gaining The Winning Edge) (1996), talks about his observation that "Statistically, there is a close relationship between V02max and lean body mass." Note that O'Shea sees a forest where Craig only sees trees.

When asked in a Q&A by Clarence Bass about the research done by Angelo Tremblay that short intervals (30-90 Seconds) produced substanially more fat loss for each calorie burned exercising, O'Shea responded, "I was not surprised by Tremblay's findings showing that low intensity, long duration exercise is not as effective as short intense intervals in reducing body fat. It is relatively easy to explain why this is so. During strenuous exercise, the rate of metabolism rises, going to about 15 times the basal metabolic rate (BMR) and even higher during intense interval work. For example, running 5 mi/hr the oxygen uptake required is 28 ml 02/min/kg of body weight with 3.7 cal/hr./lb burned, while a short burst of intense interval work may require 100 ml 02/min/kg with 13.8 cal/hr/lb burned. By maintaining the high level of training over a 5 or 6 week period one would expect a significant increase in the ratio of lean body mass to fat."

"Intense interval work utilizes a greater percent of the body's muscles, both slow and fast twitch. Also, performing high intensity work places added energy demands on the respiratory system, cardiovascular system and nervous system. Thus more fat and glycogen are burned to support the expanding energy demands of the body during - and after - intense exercise. In other words, the cost of short intense interval exercise is very high in terms of energy demands in comparison to low intensity aerobic exercise. What's more, while at rest trained active muscles burn more fat night and day, contributing to further fat loss."

Hmmm, how many ways can I say this . . . .

Since Angelo Tremblay was referenced above, I dutifully tracked down the data and mercifully reprinted only the conclusion and results. You'll note you've read this before:

Impact of high-intensity exercise on energy expenditure, lipid oxidation and body fatness
A Tremblay, Division of Kinesiology, Physical Activity Sciences Laboratory, Laval University, Ste-Foy, Québec, Canada

RESULTS: Results from Study 1 showed that men who regularly take part in intense physical activities display lower fat percentage and subcutaneous adiposity than men who never perform such activities, and this was true even if the latter group reported a lower energy intake (917 kJ/day, P<0.05). In Study 2, the high-intensity exercise stimulus produced a greater post-exercise post-prandial oxygen consumption as well as fat oxidation than the resting session, an effect which disappeared with the addition of propranolol. In addition, the increase in post-prandial oxygen consumption observed after the high-intensity exercise session was also significantly greater than that promoted by the low-intensity exercise session.

CONCLUSION: These results suggest that high-intensity exercise favors a lesser body fat deposition which might be related to an increase in post-exercise energy metabolism that is mediated by -adrenergic stimulation.