CYCLING PERFORMANCE TIPS
The foods we eat provide these three energy containing compounds: carbohydrates, fats, and protein. Carbohydrates are the primary energy source for short, maximum performance events (sprints at or near 100% VO2 max). Both fats and carbohydrates can serve as an energy source for the cell in endurance events (generally performed at less than 50% VO2 max.) Proteins are used to maintain and repair body tissues, and are only rarely used as an energy source to power muscle activity (almost always when severe Calorie restrictions are in effect such as with starvation or malnutrition).
The cardiovascular system delivers the oxygen necessary for oxidation. Oxygen is extracted by the lungs from the air we breathe and then transported via the circulatory system (bound to hemoglobin) to the cells where it will be utilized. One of the end products of energy production, carbon dioxide, is transported from the cell back to the lungs by the circulating blood and then leaves the body in expired air.
The two limiting factors in cellular energy production are:
When we exercise, the cells begin to recruit anaerobic metabolic pathways at approximately 50% VO2max. and are almost entirely using these anaerobic pathways when exercise is at 90 to 100% VO2max. When glycogen energy stores are depleted, and the cells only have fat as a fuel, they can only function aerobically (thus at a maximum of about 50% VO2max). As a result we have "hit the wall" or "bonked" and are markedly limited in our exercise capacity.
OXIDATION & ATP
Food energy is released via oxidation - a chemical reaction with oxygen. When oxidation
occurs outside the body - for example in the burning of oil (a fat)
in a lamp, or the use of a flaming sugar cube (a carbohydrate) as a decoration in a
dessert - the energy is released as heat and light. In the cell, this same energy from
carbohydrates and fats in food is released more slowly and in a form that can be harnessed
to support basic cell functions or transformed into mechanical movement by muscle cells.
Controlled oxidation in the cell is accomplished by "refining" these three basic compounds (carbohydrates, fats, and proteins), to a single common chemical compound adenosine triphosphate (ATP). It is ATP, the intermediate synthesized as the cell metabolizes (or breaks down) these three basic compounds that actually transfers the energy content of all foods to muscle action.
ATP is composed of a base (adenosine), a sugar (ribose) and three phosphate groups. The chemical bonds between the phosphate groups contain the energy stored in this molecule, and it is the breaking of these bonds (as ATP is converted into ADP or adenosine diphosphate) that provides the energy to power muscle contractions and other cellular functions.
PRODUCTION OF ATP - THREE PATHWAYS
There is a limited storage capacity for ATP in the cell, and at maximum work levels the
ATP stored in the muscle cells will be depleted in a few seconds at most. Thus, to sustain
physical activity, the cells need to continually replenish (resynthesize) their ATP.
There are three pathways for ATP synthesis, and the one used by the cell depends
on both the degree and duration of the physical activity.
The first pathway involves the metabolism of phosphocreatine - another high energy molecule found in all muscle cells - to directly resynthesize and resupply cellular ATP. But phosphocreatine is also in limited supply and provides at most another 5 to 10 seconds of energy which limits its usefulness to sprint activities. Once phosphocreatine supplies have been depleted, the cells must switch to one of the other two pathways that regenerate ATP - one requiring oxygen (an aerobic pathway) and another that does not (anaerobic).
Aerobic metabolism, which requires oxygen (is oxygen dependent) refers to several different chemical processes in the cell, which produce ATP from all three food elements - carbohydrates, fats, and protein. Aerobic metabolism supplies the ATP needed for endurance activities.
Glycolysis, also known as anaerobic metabolism, occurs in the absence of oxygen and is limited to carbohydrates (glucose, glycogen) as a fuel source. Anaerobic metabolism is limited by the buildup of excess protons (H+ ions, acidic compounds) in the cell within minutes. This acidic environment then impairs muscle cell contraction and producing actual physical discomfort or pain resulting in a degradation of athletic performance. Anaerobic is generally the source of energy only for short bursts of high level activity lasting several minutes at most (sprints). At one time it was thought that lactic acid was THE acidic compound responsible for muscle pain and impaired muscle cell function (and physical performance). However recent work has shown that to be untrue. Although lactic acid is produced in the cell during energy production, it appears to be an intermediary in glucose metabolism serving an additional protective function to prevent the development of excessive acidity, while other acidic compounds are actually responsible for the impairment of muscle cell function.
FUEL FOR THE MUSCLE CELL - CARBOHYDRATES, FATS, AND "THE BONK"
So far we have learned that muscle cell contraction is powered by ATP Ð an energy transfer
molecule produced in the oxidation of carbohydrates and fat. Only in times of starvation is
protein a significant fuel source. The production of ATP takes place in mitochondria (the cell
powerhouse) and is most efficient when adequate oxygen is present.
Carbohydrate "fuel" is stored in the muscle cell in the form of glycogen as well as extracted from circulating blood where it is being transported as glucose. Blood glucose comes from non-muscle stores (mainly glycogen in the liver) and glucose absorbed from the digestive tract. Fat is stored within the muscle cell as triglycerides and is transported from fat cells throughout the body as free fatty acids (FFA) in the blood. These FFAs, just as with blood glucose, are available to the muscle cell as an energy source.
Triglycerides within the muscle cells contain 2,000-3,000 kcal of stored energy, making them a larger source of potential energy than muscle glycogen, which can contain only about 1,500 kcal of energy. Yet, even though both might provide significant amounts of ATP to the exercising muscle, glycogen is the preferred energy source at higher levels of exertion. There have been a number of suggestions as to why this might be the case.
This graph (from Romjin et al http://jap.physiology.org/content/88/5/1707.long) shows the relative contribution of energy Calories from glycogen and triglycerides (in the muscle cell) versus energy that is available from the glucose and FFAs (in the blood) as the level of exertion increases. What I found most interesting is the plateau in fat Calories utilized as VO2 increased and as a result the falling percent of total expended Calories as muscle cell energy needs increased. The ability to extract FFA to support exercise appears limited and the total Calories provided from this energy source actually go down at higher levels of exertion. Training can modify this triglyceride/glycogen relationship. To quote: "As discussed in a recent issue of Sports Science Exchange (Terjung, 1995), one of the most functional adaptations to endurance training is an increase in the size and number of muscle mitochondria to greatly enhance aerobic metabolism, i.e., the ability of muscles to use oxygen to metabolize fat and carbohydrate for energy. The reduction in muscle glycogen oxidation as a result of endurance training was directly associated with an increase in oxidation of triglycerides derived from within muscle, but not from plasma......Therefore, it appears that intramuscular triglyceride is the primary source of the fat that is oxidized at a greater rate as an adaptation to endurance training and that it is the oxidation of this intramuscular fat that is associated with a reduction in muscle glycogen utilization and with improved endurance performance."
What points can we take away from this?
THE BALANCE OF AEROBIC AND ANAEROBIC METABOLISM
As one begins to exercise, the anaerobic pathways provide for the initial ATP needs while
the body shifts into gear to increase adequate oxygen to the cell - increasing both breathing and
heart rates. As more oxygen is transported to the exercising muscle cell, the aerobic
pathways (metabolizing both fats and carbohydrates) pick up the slack and anaerobic
metabolism tapers off. However, anaerobic pathways
continue to provide a small amount of ATP energy, and small
amounts of lactic acid are still being produced. At this level of production,
lactic acid is actually a source of cell energy as it is metabolized
by liver and muscle cells. It is only as cell
energy needs rise (as in a sprint, for example) and a significant shift occurs towards anaerobic
metabolism as the more dominant metabolic pathway for energy production that lactic acid
levels begin to rise (paralleling the rise in other intracellular acidic compounds).
Aerobic pathways are used by the muscle cells for energy production (metabolizing both fats and carbohydrates as an energy source) up to exercise levels of approximately 50% VO2 max. At that point (called the "crossover point" ), although metabolism is still oxygen based (aerobic), it shifts towards glycogen as an energy source (and fat metabolism decreases). Then, as 100% VO2max is approached, and the cardiovascular system can no longer provide adequate oxygen to the muscle cell to continue aerobic ATP production, either the phosphocreatine system, or anaerobic metabolism pathways once again cover the cells energy needs. When the level of activity drops back to less than 100% VO2max, and oxygen is once again available to the cells, metabolism once again shifts away from anaerobic pathways, and excess oxygen is available to regenerate phosphocreatine and metabolize (clear) the excess acids produced during the anaerobic sprint type activity. With training, changes occur in the cardiovascular system and muscle cells that support higher levels and longer duration of physical activity before anaerobic pathways are needed, and also clear lactic acid more quickly leading to faster recovery from anaerobic sprints.
LACTIC ACID - AND THE "SECOND WIND" PHENOMENA
Lactic acid accumulation, an important intermediate in glycogen/glucose
metabolism in the muscle, which may help to protect the cell from
the excess acidity of anaerobic metabolism is often blamed for the "burn" experienced with
anaerobic metabolism. However
of ATP metabolism (free H+ ions) also increase in the anaerobic environment and are
more likely to be the real the culprit. Rather than being a negative for performance,
lactate (the Na+ or K+ salt of lactic acid) is a positive, fueling the exercising
muscle with glycogen sparing effects.
Two relevant articles:
These 2 studies support the contention of Dr. Mirkin that the second wind phenomena is a result of this increased lactic acid metabolism with a slight slowing in the cyclists (or runners) speed (below LT, I presume).
To quote: "Your muscles get their energy from each of several successive chemical reactions, called the Krebs cycle. The Krebs cycle requires large amounts of oxygen to burn carbohydrates, fat and protein for energy.... However, if you run so fast that your muscles do not get all the oxygen that they need, you develop an oxygen debt that slows down the successive reactions of the Krebs cycle. This causes lactic acid to accumulate in your muscles to make them acidic. It is the acidity that makes muscles burn, and you gasp for air, trying to get more oxygen.
The muscle burning and shortness of breath caused by the accumulation of lactic acid forces you to slow down....Your muscles switch to burning more lactic acid for energy, you need less oxygen and then you pick up the pace. You tell everyone that you suddenly got your "second wind", but actually:
Carbohydrate metabolism is much more efficient than fat metabolism assuming adequate oxygen is available (ie aerobic metabolism). But once VO2max has been reached, and anaerobic metabolism takes over, the efficiency of carbohydrate metabolism drops off dramatically. Carbohydrate will produce 19 times as many units of ATP per gram when metabolized in the presence of adequate cell oxygen supplies (aerobic) as opposed to its metabolism in an oxygen deficient (anaerobic) environment.
In the well fed and rested state, the human body contains approximately 1500 carbohydrate Calories (stored as glycogen) in the liver and muscle tissue, and over 100,000 Calories of energy stored as fat. The muscles are the main glycogen repository containing anywhere from 300 - 600 grams of glycogen (which equates to 1200 to 2400 Calories) while the liver contains 80 to 110 grams (300 to 400 Calories). The exact numbers are less important than the concept that internal carbohydrate stores are only adequate for several hours of brisk cycling (80 to 100 % VO2max). On the other hand, there is enough stored fat to continue to cycle at a reduced speed (50 - 60% VO2@max) for days.
If one is not supplementing their internal carbohydrates with oral supplements, the muscles first use their internal glycogen reserves for fuel, then call upon liver glycogen which has been maintaining a constant blood sugar level, and finally, when there is no more glucose as an energy source, the muscles switch to fat metabolism and you " bonk". This term describes the fatigue resulting from muscle glycogen depletion. Without adequate carbohydrate to fuel continues high level muscle activity, it is impossible to maintain a high level of energy output and one has to slow to speeds of 50% VO2max where fat metabolism can provide the needed Calories. Any oral supplements delay the onset of this mandatory switch in energy source and associated inability to maintain a high level of performance. The bonk can be delayed by using oral sugars to supplement muscle glycogen stores. Thus, on a long ride, a rider that snacks will have more glucose remaining in the body to fuel that final sprint than one who cuts corners on their nutrition.
Two other strategies are to 1) minimize extremely energy inefficient anaerobic sprints earlier in the ride (remember they are very inefficient in terms of ATP production) and 2) whenever possible, ride closer to 50% VO2max to take advantage of supplemental Calories available from fat metabolism. In addition to eating while riding, these two strategies will help to save a few more grams of muscle glycogen for that final sprint to the line.
THE ROLE OF INSULIN IN ENERGY PRODUCTION AT THE CELLULAR LEVEL
Insulin is made by special cells in the pancreas, is released when they sense a
rise in the blood glucose level, and works by stimulating the cells of the
body to extract that extra glucose from the blood stream. Insulin is essential
to the normal functioning of exercising muscle cells - and the replenishment
of glycogen post exercise.
The disease of diabetes, at its most basic, is the result of a lack of glucose inside the cells to power them. The blood glucose level is usually elevated but it can't get into the cells where it is needed to supply the energy they need.
Exercise moves carbohydrates into the cell, where it is needed to produce the energy to power the cell, in 2 ways.
The traditional teaching has been that the stress of aerobic training leads to adaptive changes in the muscle cell that improve performance. This article suggests that the physiology behind training improvements is slightly more complex than previously suspected.
Mitochondria are the powerhouses of our muscle cells. They contain the enzymes that convert glycogen and fats into the ATP needed to power muscle contraction. With aerobic training, we know the mitochondria increase in both size and number increasing the amount of ATP that can be produced per minute (assuming there is sufficient fuel (carbohydrates) and oxygen delivered to the exercising cell.)
We also knew that regular aerobic training changes the types and numbers of bacteria in our colon (the microbiome) https://www.ncbi.nlm.nih.gov/pubmed/28360096 I never understood why exercise might have this effect. Was it the fact that athletes see diet as part of a training program and eat healthier with more fiber and vegetables (which we also know changes the composition of the microbiome)?
The bacteria of the microbiome metabolize unabsorbed food material from our diet (generally fiber), in turn manufacture short chain fatty acids (which are absorbed and provide a modest amount of additional energy for our cells) as well as producing various small molecules that can affect energy metabolism.
This article puts forth a good argument that our mitochondria in some way affect colon bacterial composition which in return produces molecules that will positively influence mitochondrial metabolism and growth. A positive feedback loop which magnifies the benefits of aerobic training.
So what, you might ask., is the point? There are no clear training take-aways......yet. But if we can isolate the bacterial products that stimulate mitochondrial growth, we may have a cue as to how we might magnify the benefits of aerobic training. And as we know our diet can directly affect the microbiome, perhaps we will find helpful or harmful diets that should be included/avoided to maximize a training benefit.
So no recommendations yet. Just a nice example demonstrating how complex physiology can be, and illustrate how a clear understanding could give us clues to provide a competitive edge.