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  Last updated:11/4/ /2019


Energy to power muscle contractions is released when oxygen combines with carbohydrates, fats, and proteins in the cell to produce Adenosine Triphosphate or ATP. These are termed oxidationreactions (literally "a combination with oxygen") and are only a few of the manyreactions (metabolism) within the cell that maintain cell viability. The amount of energy produced in oxidation reactions is limited by either theamount of oxygen available to the cell for oxidation, or limited fuel(carbohydrates, fats, and protein) to be oxidized.

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:


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 in an UNCONTROLLED fashion as heat and light. In the cell, this same energy from carbohydrates and fats in food is released more slowly and in a CONTROLLED fashion that makes itavailable to power basic cell functions and mechanical movement by muscle cells.

Controlled oxidation in the cell converts the three basic food compounds (carbohydrates, fats, and proteins) into a single common chemical compound adenosine triphosphate (ATP). It is the ATP, this intermediate synthesized fromthe three basic compounds, that transfers the energy content of food into muscle activity.

ATP is a molecule consisting of a base (adenosine), a sugar (ribose) and three phosphate groups. The chemical bonds between the phosphate groups contain the stored energy in this molecule, and it is the breaking of these bonds (as ATP is converted into ADP or adenosine diphosphate) that in turn provides the energy to power muscle contractions and other cellular functions.


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.


Almost all ATP is produced from the oxidation of carbohydrates and fat. Only in starvation does protein become a significant source of energy.

ATP production occurs in our mitochondria is most efficient when adequate oxygen is available.(For those interested in evolutionary biology, the theory on the development of the mitochondrialenergy pathway - presented below** - is fascinating.).

The carbohydrate for muscle ATP production is provided from muscle stores (glycogen) as wellas by glucose extracted directly from the blood. Blood glucose, in turn, comes from dietary sugarabsorbed from the small intestine supplemented by glucose released from non-muscle storage, mainlyliver glycogen.

Fat is stored in the muscle cells as triglycerides as well as transported to the muscle cellfrom fat cells throughout the body as free fatty acids (FFA).

Muscle cell triglycerides contain 2,000 - 3,000 kcal of potential energy, making thema larger source of energy than muscle glycogen (about 1,500 kcalof energy). Even though both carbohydrates and fats could provide significant amounts of ATPto the exercising muscle, glycogen is used preferentially at higher levels of exertion. There are a number of suggestions as to why this might be the case.

This graph(from Romjin et al shows therelative energy contributions of glycogen and triglycerides stored in the muscle cell compared tothat available from circulating glucose and FFAs as the level of exertion increases.

What I found most interesting was the plateau in fat Calories utilized as exertion (% VO2max)increased, resulting in a fall in the percent of total expended Calories. The ability of the muscle cell toextract FFA to support exercise appears limited and total fat Calories may actually go down at higherlevels of exertion.

Trainingcan 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 should we take away?

  1. If you want to maximize the number of triglycerides Calories being used to fuel exercise(thus maintaining glycogen stores for later, high VO2 sprint activity), theideal rate of exertion is ~65% VO2 max.

  2. Training will modify the fat/carbohydrate energy ratio so that for any specific %VO2max the metabolism of intracellular fat (triglycerides) relative to intracellular glycogen will increase. This is the result of an increase in the number of mitochondria (where carbohydrate and fat metabolism take place) and changes in the enzyme makeup facilitating triglyceride metabolism.

  3. You can graphically appreciate the reason for "the Bonk". Once glycogen stores have been depleted, no matterhow hard you try, you can only produce ~ 50 - 60 % of the total Calories possible if glycogen is still available.


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.


As you exercise, a series of chemical reactions metabolizes glucose in a stepwise fashion, releasing ATP at each step. When adequate oxygen is available, theglucose is completely converted into carbon dioxide and water. However, when youare exercising intensely, are anaerobic, there is not enough oxygen you need, theprocess stops at the production of lactic acid. It then accumulates in the musclesand the bloodstream. When adequate oxygen is again available, lactic acid is once again metablized (like any other carbohydrate) to CO2 and water with the release of additional ATP. In fact, cells require less oxygen (are more efficient) metabolizing lacticacid than other carbohydrate.

Why do we slow down when lactic acid accumulates? At one time it was postulated theacidity of the lactic "acid" impaired muscle cell contractiopns. But further studies on isolated muscle cells suggest lactic acidosis"...has little detrimental effect or may even improve muscle performance duringhigh-intensity exercise." And it is the bloodstream acidosis from associated acidicbyproducts of anaerobic metabolism that impair exercise performance by reducing the CNSdrive to muscle (the central governor).

Lactic acid accumulation, an important intermediate in glycogen/glucosemetabolism in the muscle, which may help to protect the cell fromthe excess acidity of anaerobic metabolism is often blamed for the "burn" experienced withanaerobic metabolism. However other productsof ATP metabolism (free H+ ions) also increase in the anaerobic environment and aremore 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 exercisingmuscle with glycogen sparing effects.

Two relevant articles:

These 2 studies support the contention of Dr. Mirkinthat the second wind phenomena is a result of this increased lactic acid metabolism with a slightslowing 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 burncarbohydrates, fat and protein for energy.... However, if you run so fast that your musclesdo not get all the oxygen that they need, you develop an oxygen debt that slows down thesuccessive reactions of the Krebs cycle. This causes lactic acid to accumulate in yourmuscles to make them acidic. It is the acidity that makes muscles burn, and you gaspfor air, trying to get more oxygen.

The muscle burning and shortness of breath caused by the accumulation of lactic acidforces 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 yousuddenly got your "second wind", but actually:

Of course when you keep on pushing the pace, you can again accumulate large amounts of lacticacid in muscles, which will make them burn and hurt again."

For those of you interested, hereis another link to a Dr. Mirkin blog on lactic acid.


The energy contained in equal weights of carbohydrate, fat, and protein is not the same. Energy content is measured in Calories (note the capital C). Carbohydrates and protein both contain 4.1 Calories per gram (120 Calories per ounce) while the energy "density" of fat is more than double at 9 Calories per gram. The disadvantage of fat as a fuel for exercise is that it is metabolized through pathways that differ from carbohydrates and can only support an exercise level equivalent to 50% VO2 max. It is an ideal fuel for endurance events, but unacceptable for high level aerobic (or sprint) type activities.

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.


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 is the stress (of aerobic training) stimulates adaptive changes within the muscle cell, very likelywithin the mitochondria, and improved performance is the result.

Mitochondria are the powerhouses of our muscle cells. They contain the enzymesthat convert glycogen and fats into the ATP needed to power muscle contraction.With aerobic training, we know the mitochondria increase in both size and numberwhich then translates into more ATP produced per minute (assuming thereis sufficient carbohydrates and oxygen delivered to the exercising cell.)

This articlesuggests that the physiologic chnages behind training improvement is more complex thanjust adaptive changes within the muscle cell and involves gut - muscle cell/mitochondriainteraction of some type.

The article makes the argument that it is our mitochondria that affectcolon bacterial composition which in return produces molecules that will positivelyinfluence mitochondrial metabolism and growth. A positive feedback loop whichmagnifies the benefits of aerobic training.

We know that regular aerobic trainingchanges both the types and numbers of bacteria(the microbiome) in the colon. It is not clear which came first, "the chicken or the egg". Do athletes eat healthier with a diet higher in fiber and vegetables(which we know changes the composition of the microbiome)?Or does exercise itself alter the composition ofthe microbiome?

This study suggests it may be lactic acid, a byproduct of high levelaerobic activity, that stimulates the growth of a colon bacteria whose only carbonenergy source is lactic acid - Veillonella.

And it appears that this bacteria does improve athletic performance. The researchersconfirmed the link to improved exercise capacity in mouse models, where they sawa marked increase in running ability after supplementation with Veillonella.

Did the bacteria work as a metabolic sink to remove lactate from the system, the ideabeing that lactate build-up in the muscles creates fatigue? Probably not as the idea thatlactate build-up causes fatigue is not accepted to be true.

Perhaps it wasn't the removal of lactic acid, but the generation of a product ofViillonella metabolism, the short chain fatty acod propionate, that provided a performance boost.

To investigate further, the researchers introduced propionate into mice [via enema]to test whether that was sufficient for an increased running ability. And it was.

A great example of a positive feedback loop. The athlete is producing somethingthat this particular microbe favors, and in return, the microbe is creatingsomething that benefits the athlete.

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 ifwe can identify specific bacteria that metabolize lactic acid, it may be possibleto take an oral probiotic that gives the athlete an extra boost from theirown lactic acid. And as we know our diet can directly affect the microbiome, perhaps we willfind helpful (or harmful) diets that to be included/avoided to provide a training benefit.

So no recommendations yet. Just a nice example demonstrating how complexphysiology can be, and illustrate how a clear understanding could give usclues to provide a competitive edge.


A theory on the development of mitochondria and other cell organelles - from The Tangled Tree by David Quammen.

In 1967, a young, little-known scientist named Lynn Margulis made a daring scientificproposal that was immediately and widely rejected: namely that the small organellesinside of cells had originally been separate bacteria that had taken up residence insidelarger cells, which then became useful, symbiotic partners with that cell, and eventuallysimply part of the cell. It was a theory that radically rewrote evolutionary theory.Today, that theory is widely accepted.

Lynn Margulis made her debut in March 1967 with a long paper in the Jour­nal of TheoreticalBiology, the same journal that had carried Zuckerkandl and Pauling's influential 1965article on the molecular clock. This paper was much different. Its author was no canonizedscientist like Pauling, and its assertions were peculiar, to say the least. Put more bluntly:it was radical, startling, and ambitious, proposing to rewrite two billion years of evolutionaryhistory. It included some cartoonish illustrative figures, funny little pencil-line drawingsof cellular shapes, and virtually no quantitative data. According to one account, it had beenrejected by 'fifteen or so' other journals before a daring editor at JTB accepted it. Once published,though, the Margulis paper provoked a robust response. Requests for reprints (a measure of interest,back in those slow-moving days before online access to journals, when scientists mailed one anothertheir articles) poured in. It was titled "On the Origin of Mitosing [Dividing] Cells.

This paper presents a theory, [Lynn] Sagan [nee Margulis] wrote - a theory proposing that 'the eukaryoticcell [cells that contain a nucleus and organelles] is the result of the evolution of ancientsymbi­oses. (Symbiosis: the living together of two dissimilar organisms.) She gave hertheory the more specific name endosymbiosis, connoting one organism resident inside thecells of another and having become, over generations, a requisite part of the larger whole.Single-celled creatures had entered into other single-celled creatures, like food withinstomachs, or like infections within hosts, and by happenstance and overlapping interests,at least a few such pairings had achieved lasting compatibility. So she proposed, anyway.The nested partners had grown to be mutually dependent, staying together as compoundindividuals and supplying each other with certain necessities. They had replicated -independently but still conjoined - passing that compoundment down as a hereditary condition.Eventually they were more than partners. They were a single new being. A new kind of cell.

No one could say, not in 1967, how many times such a fateful combining had occurredduring the early eras of life, but it must have been very rare that the resultant amalgamssurvived for the long term. Later, there would be ways of addressing that question.Sagan left it open. Microscopy, which was her primary observational mode of research,couldn't answer it.

The little entities on the inside of such cells had begun as bacteria, she argued. They had becomeorganelles - working components of a new, composite whole, like the liver or spleen inside a human -with fancy names and distinct functions: mitochondria, chloroplasts, centri­oles. Mitochondria aretiny bodies, of various shapes and sizes but found in all complex cells, that use oxygen and nutrientsto produce the energy packets (molecules known as adenosine triphosphate, or ATP) for fuelingmetabolism. ATP molecules are carriers of usable energy, like rechargeable AA batteries; when theATP breaks into smaller pieces, that energy is released for use. Mitochondria are factories thatbuild (or recharge) ATP molecules. To drive the production, mitochondria respire, like aerobicbacteria. Chloroplasts are little particles -- green, brown, or red -- found in plant cells andsome algae, that absorb solar energy and package it as sugars. They photosynthesize, likecyanobacteria. Centrioles are crucial too, but for now, I'll skip the matter of how. Allthese components, Sagan wrote, resemble bacteria by no coincidence but rather for a very goodreason: because they evolved from bacteria.

The bigger cells, within which the littler cells were subsumed, had been bacteria too(or possibly archaea, though that distinction didn't exist at the time). They were the hostsfor these endosymbioses. They had done the swallowing, the getting infected, the encompassing,and had offered their innards as habitat. The littler cells, instead of being digested ordis­gorged, took up residence and made themselves useful. The resulting compound individualswere eukaryotic cells.

Never mind that 'compound individuals' is oxymoronic. The whole process, as Sagan described it,was oxymoron brought to life - paradoxi­cal and counterintuitive, though supportedthroughout the paper by her detailed arguments.

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