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Lactic acid has been unfairly demonized for everything from delayed onset muscle soreness to cramping to robbing banks. In this article we will dispel all myths about lactic acid, and cover physiologic explanations for the phenomena supposedly associated with lactic acid. The inflammatory response itself may be responsible for aggravating afferent sensory neurons which would “cause” the pain associated with soreness.
Lactic acid is a metabolite not involved with any of the factors in delayed onset muscle soreness. In fact, lactic acid is removed almost totally from the muscles within 30 minutes of cessation of exercise. Apparently, loss of electrolytes does not cause cramps, especially from sweating during physical exertion. 2 NADH from Glycolysis + 1 (*2) NADH from Acetyl-CoA generation + 3 (*2) NADH from citric acid cycle generate 10 H+ per glucose molecule. Hydrogen ions are buffered by microchondria through H+ ion gradients which drive the ATP synthase enzyme (this has very important implications which will be discussed later). There are a large number of reasons for decline and failure of contraction and peak tension in muscles.
Muscular acidosis is indeed one cause of fatigue; however, as we already examined lactic acid is not involved in “creating” muscular acidosis. Metabolically, the accumulation of lactic acid does usually signal that the body is fatiguing; however, it is not directly involved and may only be used as a measuring stick especially in anaerobic exhaustion.
Some “recent” articles in the media here and here have given the public an image that lactic acid is a fuel. The alternative reaction that lactate can undergo within the muscle if exercise intensity decreases is that it can be reformed to pyruvate with NAD+ and then remetabolized into the citric acid cycle normally. The Cori Cycle is only one of the important “alternate” metabolic pathways in the body for resynthesis of glucose in the liver.
If oxidative metabolism is limited by the number of mitochondria, then excess pyruvate is converted into alanine from pyruvate and another amino acid. This leads to a dual interplay between the Cori Cycle (CC) and Glucose-Alanine cycle (GAC) which shifts the metabolic “debt” over to the liver. So basically we have both pathways playing off each other to send off substrates to the liver to help resupply glycogen to the muscles. During exercise, excess lactate within the blood stream can be uptaken by the brain, heart, and slow twitch muscles as a source of energy besides being used by existing muscles. Most laypeople and even medical and exercise physiology texts still follow “conventional wisdom” without fact checking their sources. Steven Low, author of Overcoming Gravity: A Systematic Approach to Gymnastics and Bodyweight Strength, is a former gymnast who, in recent years, has been heavily involved in the gymnastics performance troupe, Gymkana. You are correct that the conversion of pyruvate to lactate (not pyruvic acid to lactic acid) will not contribute to acidosis. We see lactic acidosis contributing to metabolic acidosis frequently in the hospital due to most commonly diabetic ketoacidosis and drugs that cause toxicity to mitochondria.
All I am trying to say is that the presence of high levels of lactate are indicative of metabolic acidosis within the body and also in such instances as anion gap. In anion gap, the increasing acid levels depress bicarbonate ion levels (via Le Chatelier’s equilibrium principle), and the body compensates by increasing breathing to rid itself of extra CO2. If lactic acid does not cause cramps, why does it in rigor mortis wich is somewhat similar to anaerobic-glycolysis.
This is why you can also get cramps when you are heavily exerting yourself because of depletion of ATP stores. The point at which oxygen consumption plateaus defines the VO2 max or an individual's maximal aerobic capacity. Aerobic power, aerobic capacity and maximal oxygen uptake are all terms used interchangeably with VO2 max. VO2 max is usually expressed relative to bodyweight because oxygen and energy needs differ relative to size. One study followed a group of 12-year-old boys through to the age of 20 - half of which were trained, the other half untrained but active.
VO2 max varies greatly between individuals and even between elite athletes that compete in the same sport. Genetics plays a major role in a persons VO2 max (11) and heredity can account for up to 25-50% of the variance seen between individuals. Untrained girls and women typically have a maximal oxygen uptake 20-25% lower than untrained men.
In previously sedentary people, training at 75% of aerobic power, for 30 minutes, 3 times a week over 6 months increases VO2 max an average of 15-20% (6).
Amongst groups of people following the same training protocol there will be responders - those who make large gains, and non-responders - those who make little or no gains (14,9). Crucially, once a plateau in VO2 max has been reached further improvements in performance are still seen with training. Resistance training and intense 'burst-type' anaerobic training have little effect on VO2 max.
Perhaps more significant than VO2 max is the speed at which an athlete can run, bike or swim at VO2 max. While a high VO2 max may be a prerequisite for performance in endurance events at the highest level, other markers such as lactate threshold are more predictive of performance (3). Think of VO2 max as an athletes aerobic potential and the lactate threshold as the marker for how much of that potential they are tapping.


There are many physiological factors that combine to determine VO2 max but which of these are most important? This theory maintains that aerobic capacity is limited by lack of sufficient oxidative enzymes within the cell's mitochondria (3). Presentation theory suggests that aerobic capacity is limited not predominantly by utilization, but by the ability of the cardiovascular system to deliver oxygen to active tissues. So what plays the greater role in determining an athlete's VO2 max - their body's ability to utilize oxygen or supply oxygen to the active tissues? In a review of the literature, Saltin and Rowell (7) concluded that it is oxygen supply that is the major limiter to endurance performance. One of the most common is the Bruce protocol often used for testing VO2 max in athletes or for signs of coronary heart disease in high risk individuals. Indirect testing is much more widely used by coaches as it requires little or no expensive equipment. VO2 max decreases as altitude increases above 1600m (5249ft) or about the altitude of Denver, Colorado. Usually, the decline in age-related VO2 max can be accounted for by a reduction in maximum heart rate, maximal stoke volume and maximal a-vO2 difference i.e. Vigorous training at a younger age does not seem to prevent the fall in VO2 max if training is ceased altogether. It seems that training can slow the rate of decline in VO2 max but becomes less effective after the age of about 50 (3).
13) Bouchard C, Shephard RJ, Stephens T, Sutton JR and McPherson BD (Eds.), Exercise Fitness and Health (pp. 33) Kraemer WJ, Patton JF, Gordon SE, Harman EA, Deschenes MR, Reynolds K, Newton RU, Triplett NT, Dziados JE. References allow you to track sources for this article, as well as articles that were written in response to this article.
It is the process in which there is the oxidation of one molecule and the reduction of another molecule, but with oxygen present.
If you have one that I have not covered please comment at the bottom of the article, and I will integrate it in later.
How it could even begin to explain delayed onset muscle soreness which comes 24-72 hours later is beyond me. What this means is if there is trauma to an area of the body, the body will generally tighten up to protect the area which thusly may cause cramping. Similarly to the low blood flow, we have a case where the muscle cannot keep up metabolically supplying the sarcoplasmic reticulum transporters with ATP to pump Ca2+. When muscles are moved into a short range of motion and contracted, they are likely to cramp. High quantities of it may be detected in severely oxygen limited muscle cells with diminished amounts of ATP.
This frees up blood flow for healing and ATP production as well as breaks up scar tissue and reintroduces inflammation to heal the prolonged damaged and contracted areas of muscle. ATP synthase is responsible for production of all ATP in the body by combining ADP + P and literally “smashing” them together to form ATP. These are transported as you can see in the image to the liver which metabolizes the lactate to glucose. But saying it is a “fuel” itself is an stretch at best, and calling it new is certainly absurd. Since the GAC conserves NADH as opposed to the CC due to the pyruvate-lactate reaction (pyruvic acid + NADH -> NAD+ + lactic acid), the GAC allows more energy to be produced within the muscle because the NADH can be used to create 3 ATP in electron transport. I’ll let you decide for yourself if you consider it a fuel, or a network of vast metabolic interactions taking place on a grand scale. The fact that it correlates fairly well with the above symptoms and ailments does not mean it is a causative factor. Lactate and other negative anions pick up the slack to buffer the extra H+, but they don’t contribute to the increases in acidosis itself. However, a point is reached where exercise intensity can continue to increase without the associated rise in oxygen consumption. It is generally considered the best indicator of cardiorespiratory endurance and aerobic fitness. It can also be expressed relative to body surface area and this may be a more accurate when comparing children and oxygen uptake between sexes. Relative to bodyweight no differences in VO2 max were found between the groups suggesting that training had no influence on maximal oxygen uptake. However, this is an average and there are large individual variations with increases as wide ranging as 4% to 93% reported (6).
This was originally put down to a simple issue of compliance but more recent research suggests that genetics plays a role in how well any one individual responds to an endurance training program (13). The fitter an individual is to begin with, the less potential there is for an increase and most elite athletes hit this peak early in their career. This is because the athlete is able to perform at a higher percentage of their VO2 max for prolonged periods (2).
Any improvements that do occur are usually small and in subjects who had a low level of fitness to begin with (17). The winner of a marathon race for example, cannot be predicted from maximal oxygen uptake (15). Proponents of this theory maintain that an increase in blood volume, maximal cardiac output (due to increased stroke volume) and better perfusion of blood into the muscles account for the changes in VO2max with training. Studies have shown only a weak relationship between an increase in oxidative enzymes and an increase in VO2 max (8,9,10).


For every 1000m (3281ft) above that, maximal oxygen uptake decreases further by approximately 8-11% (3). The average rate of decline is generally accepted to be about 1% per year or 10% per decade after the age of 25.
In some cases the decease may be purely a reflection of increased body weight with no change in absolute values for ventilation of oxygen. When they maintain the same relative intensity of training, a decrease of only 3.6% over 25 years has been reported (28) and most of that was attributable to a small increase in bodyweight. Oxygen uptake during running as related to body mass in circumpubertal boys: a longitudinal study.
The nature of the training response; peripheral and central adaptations of one-legged exercise. Distance running performance and metabolic responses to running in men and women with excess weight experimentally equated.
Compatibility of high-intensity strength and endurance training on hormonal and skeletal muscle adaptations. During this process, the cell uses carbon dioxide and water, releasing the oxygen which we breath. For example, neurons activate by firing action potentials which may be more easily set off by accumulated ion concentrations from the tears in the muscles. For example, the quads are likely to cramp if you try to do an L-sit or V-sit the first time you try. If the pH of the blood drops, this tells the body that there is too much CO2 in the blood making it too acidic. Hence lactic acidosis is a misnomer and untrue because the pyruvate’s carboxylic acid group already has the hydrogen ion dissociated from it. This assumes, of course, that the intensity is not high enough that the extra NAD+ is needed for glycolysis.
If the intensity is lower but above lactate threshold, the Glucose-Alanine Cycle is more prevalent.
However, as well discuss in a moment, it is more useful as an indicator of a person's aerobic potential or upper limit than as a predictor of success in endurance events. However, when VO2 max was expressed relative to body surface area, there was a significant difference between groups and maximal oxygen uptake did indeed increase in proportion to training (4). Taking it step further, if VO2 max is adjusted to account for fat free mass in elite male and female athletes, the differences disappear in some studies. There also seems to be a genetic upper limit beyond which, further increases in either intensity or volume have no effect on aerobic power (5). Resistance training alone does not increase VO2 max (30,31,32) even when short rest intervals are used between sets and exercises (33). In fact peak aerobic power can be maintained even when training is decreased by two thirds (18). Proponents of this theory point to numerous studies that show oxidative enzymes and the number and size of mitochondria increase with training. One of these studies measured the effects of a 6-month swim training program on aerobic function.
Direct testing requires sophisticated equipment to measure the volume and gas concentrations of inspired and expired air. Some are more reliable and accurate than others but none are as accurate as direct testing. In some cases, the relative decline is greater than for the average population - as much as 15% per decade or 1.5% per year (27,28). This goes back the poor blood flow scenario where a sustained contraction cuts off oxygen availability and the muscles cramp due to lack of ATP. Once that ATP is used up, the muscles are unable to relax and will seize up causing rigor mortis. Cureton and Collins (29) suggest that sex-specific essential fat stores account for the majority of metabolic differences in running between men and women.
Runners and swimmers have reduced training volume by 60% for a period of 15-21 days prior to competition (a technique known as tapering) with no loss in VO2 max (19,20,21).
This is coupled with increased differences between arterial and venous blood oxygen concentrations (a-vO2 difference) accounting for improved oxygen utilization and hence improved VO2max.
There are many protocols used on treadmills, cycle ergometers and other exercise equipment to measure VO2 max directly. Examples include the multistage shuttle run (bleep test), 12 minute walk test and 1.5 mile run. Maximal heart rate may also decrease and the net effect is that less oxygen is "pushed" from the blood into the muscles (2). The organelles called chloroplast holds the nutrients from the suns energy and the rest is used to remove electrons from other substances. If there is not enough oxygen to facilitate production of ATP, pumping of Ca2+ back into the sarcoplasmic reticulum cannot occur. People that are inflexible usually have tight musculature and lots of scar tissue already and are thus “predisposed” to poorer blood flow and easier cramping.
He has also spent thousands of hours independently researching the scientific foundations of health, fitness and nutrition and is able to provide many insights into practical care for injuries.
This whole process is Photosynthesis and is what plant cells use to transform sunlight to energy.



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