CYCLING PERFORMANCE TIPS
The amount of energy produced by oxidation reactions is limited by the availability of either oxygen or the "fuel" being oxidized (carbohydrates, fats, and protein). Carbohydrates are the primary source of energy for short, maximum performance events (sprints at or near 100% VO2 max). Both fats and carbohydrates provide the energy for endurance events (generally performed at less than 50 - 80% VO2 max). Proteins are used to maintain and repair body tissues and are only rarely (with starvation or malnutrition) used for energy to power muscle activity.
The cardiovascular system delivers the oxygen for ATP production. Oxygen is extracted by the lungs and transported via the circulatory system (bound to hemoglobin) to the individual cells. One of the byproducts of energy production, carbon dioxide, is transported from the cell back to the lungs by the circulating blood after the oxygen is delivered and then expired.
The limiting factors in cellular energy production are:
The controlled oxidation, which takes place in a cell's mitochondria (small structures or organelles in a cell, found in the fluid that surrounds the cell nucleus) of all three basic food compounds (carbohydrates, fats, and proteins) results in the formation of a single common chemical molecule, adenosine triphosphate or ATP). It is ATP that then transfers the energy that has been released by oxidation into muscle activity.
The ATP molecule consists of the organic molecule adenosine, the sugar ribose, and three phosphate groups. The chemical bonds with the three phosphate groups contain the energy stored in the molecule. When a phosphate bond is broken in the metabolic cycle, the energy released is used to power muscle contractions and other cellular functions. In this process, the Adenosine Triphosphate (ATP) is converted into Adenosine Diphosphate (ADP).
There are three pathways for ATP synthesis depending on the degree and duration of the physical activity.
At one time it was taught that lactic acid was THE acidic compound responsible for muscle pain and impaired muscle cell function. Recent work has shown that to be untrue. Although lactic acid is produced in the cell during energy production, it is protective in preventing excessive intracellular acidity and other acidic compounds are actually responsible for the impairment of muscle cell function.
ATP production occurs in a cell's mitochondria and is most efficient when adequate oxygen is available. (For those interested in evolutionary biology, the theory on the development of the mitochondrial energy pathway - presented below ** - is fascinating).
The carbohydrates come from muscle stores (glycogen) and glucose extracted directly from the bloodstream. Blood glucose is a combination of diet sugars absorbed in the small intestine supplemented by glucose released from non-muscle glycogen storage in the liver. A small amount of fat is stored in the muscle cells as triglycerides (the equivalent of 2000 - 3000 Calories) but the bulk is transported to the muscle cell in the form of free fatty acids (FFA) from fat cells throughout the body.
At moderate levels of exertion (~50% VO2 max) both glucose and fats are utilized to produce ATP but as exertion increases the ratio shifts towards glucose as preferred fuel and at >100% VO2max only glycogen can be utilized for ATP production. There are several several theories on the reason for this shift.
This graph (from (from Romjin et al) graphically presents the relative energy contributions of glycogen and triglycerides stored in the muscle cell compared to that available from circulating glucose and FFAs as the level of exertion increases. The ability of the muscle cell to extract FFA to support exercise is limited and the absolute number of fat Calories utilized by the exercising muscle plateaus as exertion (% VO2max) increases. As a result the percent to total energy needs supplied by fats falls as exertion increases above 50% VO2max.
Training will modify the ratio of triglyceride/glycogen utilized. To quote: "As discussed by Terjung (Sports Science Exchange, 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 can you use to improve cycling performance?
Lynn Margulis made her debut in March 1967 with a long paper in the Journal of Theoretical Biology, the same journal that had carried Zuckerkandl and Pauling's influential 1965 article on the molecular clock. This paper was much different. Its author was no canonized scientist 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 evolutionary history. It included some cartoonish illustrative figures, funny little pencil-line drawings of cellular shapes, and virtually no quantitative data. According to one account, it had been rejected 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 another their 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 eukaryotic cell [cells that contain a nucleus and organelles] is the result of the evolution of ancient symbioses. (Symbiosis: the living together of two dissimilar organisms.) She gave her theory the more specific name endosymbiosis, connoting one organism resident inside the cells 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 within stomachs, 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 compound individuals 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 occurred during the early eras of life, but it must have been very rare that the resultant amalgams survived 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 become organelles - 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 are tiny bodies, of various shapes and sizes but found in all complex cells, that use oxygen and nutrients to produce the energy packets (molecules known as adenosine triphosphate, or ATP) for fueling metabolism. ATP molecules are carriers of usable energy, like rechargeable AA batteries; when the ATP breaks into smaller pieces, that energy is released for use. Mitochondria are factories that build (or recharge) ATP molecules. To drive the production, mitochondria respire, like aerobic bacteria. Chloroplasts are little particles -- green, brown, or red -- found in plant cells and some algae, that absorb solar energy and package it as sugars. They photosynthesize, like cyanobacteria. Centrioles are crucial too, but for now, I'll skip the matter of how. All these components, Sagan wrote, resemble bacteria by no coincidence but rather for a very good reason: 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 hosts for 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 or disgorged, took up residence and made themselves useful. The resulting compound individuals were eukaryotic cells.
Never mind that 'compound individuals' is oxymoronic. The whole process, as Sagan described it, was oxymoron brought to life - paradoxical and counter-intuitive, though supported throughout the paper by her detailed arguments.
FATmax - OPTIMIZING USE OF FAT CALORIES FOR ENDURANCE PERFORMANCE
Fat and carbohydrates provide the energy for our muscle cells. The relative
contribution of each of them varies with the level of exertion. The specifics are
article and presented in this illustration.
The number of fat calories utilized per hour is a bit higher at approximately 60% VO2 max,
but are essentially stable (per hour) at all levels of exertion up to 85% VO2max.
This graph from
article in RoadBikeRider.com is the same data presented in a way that more clearly
demonstrates the absolute number of fat and carbohydrate calories expended as the
level of exertion increases and again highlights the fact that fat provides a relatively
flat and stable amount of calories per minute across all levels of exertion while the
carbohydrate contribution continues to increase with greater exertion.
This graph from My Coach Cycling shows the relationship a third way. The only problem I have with this graph is the implication that the abolute number of fat calories per hour falls off rapidly above moderate levels of exertion which misrepresents the original findings from 1993 of a stable hourly fat calorie utilization up to at least to 85% VO2max. It is only as exercise approaches 100% VO2max (with metabolism largely anaerobic) that fat is no longer a significant energy source for the muscle cell.
The term FATmax, an exercise intensity at which peak fat oxidation occurs, was coined by Jeukendrup and Achten in 2001. As the contribution of carbohydrate calories continues to increase with exercise intensity, it is also the exercise intensity (%VO2max) at which the ratio of carbohydrate calories to fat calories shifts to carbohydrates as the predominant fuel for the muscle.
Why is FATmax important? In endurance sports using the maximum amount of as a fuel delays depletion of stored glycogen and the onset of performance limiting fatigue (the bonk) which occurs when stored glycogen calories have been depleted.
FATmax varies from individual to individual but is approximately 63%VO2max which is equivalent to Zone 2 (of a 7 zone training program) or a a perceived exertion of 3 to 4 (10 point scale) or 60-70% MHR.
It was originally suggested that exercising at FATmax would maximize the fat loss benefits of exercise when minimal exercise time was available. But as you can see from this table (also from the RoadBikeRider.com article) this is not the case. Let’s say you had 2 hours to exercise and chose to exercise at a FATmax 65%VO2max. You would use 850 fat calories in the two hours. If you instead pushed up to 85%VO2max, you would increase total calories used in the two hours but the number of fat calories used over the two hours would remain unchanged. The extra calories are all from glycogen storage. If you were on a calorically stable diet, the increased exertion would cause a daily caloric deficit and you would ultimately use fat to resynthesize glycogen stores. BUT it was not the rate of exertion that made a difference, rather it was the total calories used for the two hours of exercise. If your goal is to actually burn fat calories at the time of exercising, any moderate level of activity will get you the same per hour result. But if the goal is weight loss, a higher level of activity gets you more weight loss per hour of exercise time.
The concept of FATmax explains why slowing down extends riding time (assuming no snacks or energy drinks) for long distance and multi hour events. These calculations use assumptions on power output from ChatGPT (it is a time saver) and calculations from BikeCalculator.com. Both assume no oral glucose or caloric supplements.
From Chat GPT:
Now from bike calculator:
At low levels of production, lactic acid is metabolized by liver and muscle cells as another source of ATP. It is only as cell energy needs increase (a sprint, for example) with a shift to anaerobic metabolism that lactic acid levels begin to rise (paralleling the rise in other intracellular acidic compounds).
Aerobic pathways are the dominant pathway for energy production (using both fats and carbohydrates as an energy source) up to approximately 50% VO2 max. At that point (the "crossover point"), energy production remains mainly aerobic but 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 continue aerobic ATP production, the phosphocreatine system and anaerobic metabolism 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 again shifts away from anaerobic pathways with excess oxygen now available to regenerate phosphocreatine and metabolize (clear) the excess acids produced during the anaerobic sprint type activity.
With training, the cardiovascular system and muscle cells adapt to support higher levels and longer durations of physical activity to reach the crossover point and clear lactic acid more quickly leading to faster recovery from anaerobic sprints.
In a well fed and rested cyclist, oxygen is the limiting factor in the rate of production of ATP - the molecule that powers the muscle cell. More ATP is produced per oxygen molecule from glucose than from fat, which makes glucose a more efficient fuel for the muscle cell than fat. It is why you bonk when glycogen stores are depleted. Fat just can't produced as many ATP per oxygen molecule and you have to slow down.
For any specific level of exertion (%VO2max), the more ATP that is being produced from glycogen (and less from fat) the more "efficient" the cyclist will be in using the oxygen supplied by the lungs and circulatory system. This is the basis for the improvement in performance seen with interval training - shifting the balance toward glycogen (and away from fat) as the fuel for the watts to be delivered at any level of %VO2max.
But there is more to efficiency in exercise (and cycling) than optimizing the use of glycogen for ATP production. There is what we will call the "economy of motion". What factors impact this economy of motion? This summary is adapted form a well written article on training and endurance.
How can you improve your overall cycling exercise economy? The simplest is being certain you are positioned on the bike for optimal mechanical advantage - a good bike fit. Then an optimized training program - high Intensity intervals, more hours of training (volume of training) per week or month. And finally attention to technique (cadence, smooth efficient pedal stroke). Years of dedicated training make a difference as well. One study documented an 8% improved cycling efficiency over 7 years in elite cyclists.
LACTIC ACID - AND THE "SECOND WIND" PHENOMENA
As you exercise, a series of chemical reactions metabolize glucose in a step wise
fashion, releasing ATP at each step. When adequate oxygen is available, the glucose
is completely converted into carbon dioxide and water. However, exercising intensely,
when your are anaerobic, there is not enough oxygen and the series of reactions stops
at the production of lactic acid which then accumulates in the muscles and the bloodstream.
When adequate oxygen is again available, this lactic acid is once again metabolized (like
any other carbohydrate) with the release of additional ATP. In fact, cells require less
oxygen (are more efficient) metabolizing lactic acid than other carbohydrate.
Why do we slow down when lactic acid accumulates? At one time it was postulated the acidity of the lactic "acid" impaired muscle cell contractions. But further studies on isolated muscle cells suggest lactic acidosis "...has little detrimental effect or may even improve muscle performance during high-intensity exercise." It is more likely the bloodstream acidosis from associated acidic byproducts of anaerobic metabolism that impairs exercise performance by reducing our CNS drive (the central governor theory).
It appears that rather than being a negative for performance, lactate (the Na+ or K+ salt of lactic acid) is a positive by fueling the exercising muscle with glycogen sparing effects. And in fact may be the basis of the "second wind" phenomena.
First, two relevant articles:
The muscle burning and shortness of breath caused by the accumulation of lactic acid (note: Dr. Mirkin's contention – I disagree) 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:
This article reviews the literature and concludes: "... the results in the literature are very inconsistent and difficult to compare as different disciplines and varying exercise protocols were applied in the included studies. In addition, results differed even if the same exercise and supplementation protocols were applied."
When you find conflicting results in the scientific literature - even more so when using similar protocols - the odds are high that there is really no effect. Statistical analysis allows a 1 of 10 to 1 of 20 chance that random variation may show a positive result when none exists. And many negative studies never get published and included in these literature reviews, making the odds of "no benefit" are even higher. My take away - oral alkaline supplements are of no benefit in improving athletic performance.
Carbohydrate metabolism is much more efficient than fat metabolism when adequate oxygen is available. But once VO2max has been reached, and anaerobic metabolism takes over, the efficiency of carbohydrate metabolism drops off significantly. Carbohydrates produce 19 times as many units of ATP per gram when metabolized in the presence of adequate cell oxygen supplies (aerobic) compared to 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 another 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% VO2max) for days.
With exercise, the muscle cells use their internal glycogen reserves for fuel first, then continue to extract blood glucose released from liver glycogen stores, and finally, when there is no more glucose available, switch to less efficient fat metabolism. This is the onset of "the bonk".
Oral supplements can delay the depletion of muscle and liver glucose and need to switch to fat to support muscle contractions. On a long ride, the rider that has been snacking will have more glucose remaining to fuel that final anaerobic sprint than one who cuts corners on their nutrition.
Two other strategies will help maintain the body's glycogen stores:
The disease of diabetes is either a lack of insulin (type I or juvenile diabetes) or an insensitivity to circulating insulin (type II or adult onset diabetes). This results in too little glucose inside the cells to power their metabolic machinery.
Mitochondria are the powerhouses of the muscle cell. 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 which then increases ATP production per minute (assuming there are sufficient carbohydrates and oxygen available.)
This article suggests the physiologic changes from training are more complex, also involving a gut - muscle cell/mitochondria interaction of some type. It makes the argument that it the mitochondria in some way impact the colon bacterial composition. The bacteria in turn produce molecules positively influencing mitochondrial metabolism and growth. A positive feedback loop which magnifies the benefits of aerobic training.
We know that regular aerobic training changes both the types and numbers of colon bacteria( the microbiome). 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 of the microbiome?
This study suggests it may be lactic acid, the byproduct of high level aerobic activity, which stimulates the growth of a specific colon bacteria, Veillonella, (whose only energy source is lactic acid) that then improves athletic performance. Did the bacteria work as a metabolic sink to remove lactate from the blood, and it was lactate build-up in the muscles that created fatigue and impaired performance? Unlikely as it is generally accepted that lactate build-up is not the reasons for post exercise fatigue. Perhaps it was the generation of a byproduct of Veillonella metabolism of lactic acid, the short chain fatty acid propionate, that provided the performance boost. To investigate further, the researchers introduced propionate into mice [via enema] and tested running ability. Their performance improved!
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 if we can identify specific bacteria that metabolize lactic acid, it may be possible to take an oral probiotic that gives the athlete an extra boost from their own lactic acid. And as we know our diet can directly affect the microbiome, perhaps we will find helpful (or harmful) diets to be included/avoided in a training program.
So no recommendations yet. Just a nice example demonstrating how complex physiology can be, and illustrate how science might give us clues to provide a competitive edge.