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The Science of Energy Expenditure
Question/Answer #373 in 2004.
In looking at recovery on both an intra and inter-game basis, do we have a good picture of how much energy a pitcher expends in a theoretical average inning?
It's stuck in my mind that it's equivalent to running a 400m race.  But, I honestly have no idea where that comes from.  In addition to the things that most pitching coaches don't know, they seem to completely lack any understanding of rest and recovery.
To calculate energy expenditure, researchers determine the energy system that the athletes use to resynthesize adenosine-triphosphate (ATP).  While I am sure that readers want some simple, quick answer, such as it is equivalent to running a 400 yard dash, I prefer to show the complexity of the question and, hence, the wide variety of answers I could provide.
When compared with resting levels, heavy exercise increases the total energy expenditure of the body fifteen to twenty-five times and energy utilization two hundred times.
When athletes go from resting levels to moderate exercise, within one to four minutes, they increase their oxygen consumption to a steady state.
To do this, athletes activate their adenosine-triphosphate-phosopho-creatine (ATP-PC) system,  Then, almost immediately, they activate their Glycolysis system.  Lastly, after athletes reach their steady state, they activate their Oxidative Phosphorylation system.
When athletes move from resting to exerciseing, their oxygen uptake does not keep up with their oxygen requirement.  Therefore, they create an oxygen deficit.  However, because well-trained athletes activate their aerobic system earlier than not well-trained athletes, they create lower oxygen deficits and produce less lactic acid.
After athletes stop exercising, for several minutes, their metabolic rate remains elevated.  The greater the intensity at which athletes exercise, the longer that their metabolic rate will remain elevated.
To determine fitness, researchers relate elevated metabolic rates to oxygen consumption.  When athletes train intensely for two to three minutes, they consumed high levels of oxygen.  However, when athletes train at lower intensity for thirty or more minutes thereafter, they consumed lower steady-state amounts of oxygen.
Until about twenty years ago, when, after athletes stopped exercising and still consumed elevated levels of oxygen, researchers though athletes paid an ‘oxygen debt’.  However, recent research shows that that the elevated oxygen consumption following exercise is not entirely related to borrowing oxygen from oxygen stores in the body.  Therefore, researchers now call the process, ‘Excess Post-Exercise Oxygen Consumption’ (EPOC).
Researchers estimate that fast-twitch muscle cells convert seventy percent of lactic acid to pyruvic acid, twenty percent to glucose and ten percent to amino acids.  The slow-twitch muscle cells in the heart and skeletal muscle metabolize the pyruvic acid and store the glucose and amino acids.
Because only twenty percent of the elevated oxygen consumption following exercise converts lactic acid to glucose, researchers speculate that athletes use the other eighty percent to resynthesize phospho-creatine and restore blood, tissues oxygen, body temperature and epinephrine and norepinephrine.
When high-intensity exercise produces lactic acid, athletes need to use low-intensity exercise to increase their lactic acid removal process.  During recovery from high-intensity exercise, researchers recommend that athletes continue to train at thirty to forty percent of their high-intensity level.
The length of time that athletes exercise determines the degree to which the ATP-PC system, the Glycolysis and the Aerobic system require to resynthesize the ATP to pre-exercise levels.
For the first five seconds, the ATP-PC system resynthesizes the ATP.  After five seconds, glycolysis starts to resynthesizes the ATP.  After forty-five seconds, the Aerobic system starts helping the glycolysis system to resynthesize the required ATP.
With two exceptions, during sub-maximal exercise of moderate duration, athletes can generally maintain their steady-state oxygen uptake.
01.  Hot/humid environments gradually increase body temperature, which causes oxygen uptake to ‘drift’ upward.
02.  Exercise intensities greater than seventy-five percent of maximum oxygen volume also causes oxygen uptake to ‘drift’ upward.
To determine cardiovascular fitness, researchers measure the maximal capacity of athletes to transport and utilize oxygen during exercise.
After a brief warm-up, researchers have athletes exercise at incremental or graded levels.  By varying the speed and/or incline of treadmills until athletes can no longer linearly increase their oxygen uptake, researchers increase the work rate.
VO2 max is the ‘physiological ceiling’ of the ability of the cardiovascular system to deliver oxygen and the ability of muscles to utilize the oxygen to aerobically resynthesize ATP.
Where blood levels of lactic acid begin to rise in untrained subjects at about fifty to sixty percent of their 'physiological ceiling,' in trained athletes, blood levels of lactic acid do not begin to rise until sixty-five to eighty percent of their 'physiological levels.'      Researchers argue that an increasing reliance on anaerobic metabolism causes the sudden increase in blood lactic acid levels.  Whether the end product of glycolysis is pyruvic or lactic acid depends on a variety of factor other than hypoxia.  Therefore, researchers call this either 'Lactate Threshold' or 'Anaerobic Threshold.'
During glycolysis, for NADH production, muscle cells have a shuttle system with which to transport hydrogen molecules from their sarcoplasm to their mitochondria.  However, at rapid rates of glycolysis, pyruvic acid uses some ‘unshuttled’ hydrogen molecules to produce lactic acid.
In four situations, athletes can form lactic acid even when their muscle cells have sufficient oxygen for aerobic ATP production.
01.  At fifty to sixty-five percent of VO2 max, blood levels of epinephrine and norepinephrine begin to rise.  Epinephrine and norepinephrine can increase the rate of glycolysis.
02.  The fast-twitch muscle fiber Lactate dehydrogenase (LDH) isozyme readily attaches to pyruvic acid molecules.  Therefore, (LDH) catalyzes the conversion of pyruvic acid to lactic acid.
03.  At low exercise intensities, slow-twitch muscle fibers contract.  At higher exercise intensities, fast-twitch muscle fibers start contracting.  Therefore, the onset of fast-twitch muscle fiber involvement increases lactic acid production.
04.  The liver, heart, skeletal muscle and other slow-twitch muscle cell organs remove lactic acid from the blood for resynthesizing ATP.  Therefore, the blood lactic acid level depends not only on the production rate, but also the removal rate.  At some point, the lactic acid production rate exceeds the capacity of these tissues to remove lactic acid.
Athletes with lactate thresholds at higher percentages of their maximum oxygen uptake level perform better in anaerobic events.  Therefore, to design specific interval-training programs, coaches need to know the lactate thresholds of each of their athletes.
How many oxygen (O2) molecules does palmitic acid (C16H32O2) need to produce carbon dioxide (CO2) and water (H2O)?
Sixteen carbon molecules need sixteen oxygen (O2) molecules to form sixteen carbon dioxide (CO2) molecules.  Thirty-two hydrogen (H) molecules need eight oxygen (O2) molecules to form water.  Therefore, because palmitic acid already has one oxygen (O2) molecule, it requires twenty-three more oxygen (O2) molecules to form carbon-dioxide and water.  This means that, for fat metabolism, sixteen (CO2) molecules divided by twenty-three (O2) molecules equals 0.6956 or .70.  Consequently, the Respiratory Exchange Ratio for fat is .70.
How many oxygen (O2) molecules does glucose (C6H12O6) need to produce carbon dioxide (CO2) and water (H2O)?
Six carbon molecules need six oxygen (O2) molecules to form six carbon dioxide (CO2) molecules.  Twelve hydrogen (H) molecules need six oxygen (O2) molecules to form water.  Therefore, because glucose already has six oxygen (O2) molecules, it requires six more oxygen (O2) molecules to form water.  This means that, for carbohydrate metabolism, six (CO2) molecules divided by six (O2) molecules equals 1.0.  Consequently, the Respiratory Exchange Ratio for carbohydrates is 1.0.
Respiratory Exchange Ratios between 0.70 and 1.0 indicate combinations of fat and carbohydrate metabolism.  The closer the number to 0.70, the more fat contributed to metabolism.  The closer the number to 1.0, the more carbohydrates contributed to metabolism.  At 0.85, fat and carbohydrates contribute equally to metabolism.
For exercise that less than one hour, proteins contribute less than two percent to metabolism.  For three to five hours of exercise, proteins contribute five to fifteen percent of the fuel for metabolism.
Diet and exercise duration determine which substrate contributes to metabolism.  Where high-fat, low-carbohydrate diets promote fat metabolism, low-fat, high-carbohydrate diets promote carbohydrate metabolism.  Where low-intensity exercise promotes fat metabolism, high-intensity exercise promotes carbohydrate metabolism.  During low-intensity prolonged exercise, the percent of fat metabolized progressively increases as the exercise continues.
As the intensity of exercises increases to higher percentages of maximal oxygen utilization, the proportions that fat and carbohydrates that contribute to metabolism changes.  At low-intensity, fat contributes much more than carbohydrates.  At high-intensity, carbohydrates contribute much more than fat.  As exercise intensity moves from low to high, fat contributes less and less and carbohydrates contribute more and more.  The cross-over point occurs at about thirty-five percent of maximal oxygen utilization.
Fast-twitch muscle fibers and epinephrine cause the shift from fat to carbohydrate metabolism.  Because fast-twitch muscle fibers have abundant glycolytic enzymes, but few mitochondria and lypolytic enzymes, they metabolize carbohydrates.  Blood epinephrine levels increase as intensity increases.  High blood epinephrine levels increase muscle glycogen breakdown.  High lactate levels reduce the availability of fat as a substrate, which inhibits fat metabolism.
When low-intensity exercise lasts longer than thirty minutes, the contribution of carbohydrates to metabolism gradually shifts to a reliance on fat as the substrate.  Lipases break down triglycerides into free fatty acids (FFA).
Lipolysis is a slow process that takes several minutes of exercise to start.  During prolonged low-intensity exercise, blood epinephrine levels increase.  Epinephrine, norepinephrine and glucogen stimulate lipase activity.  However, insulin and high blood lactic acid levels inhibit fatty acid mobilization.
When athletes eat high-carbohydrate meals within thirty minutes of exercise, they increase their blood glucose levels, which because high blood glucose levels increase blood insulin levels, they inhibit fatty acid mobilization.
Fat oxidation is greater at higher exercise intensities that are below the anaerobic (lactate) threshold.  At twenty percent of maximal oxygen utilization, fat contributes to sixty percent of metabolism.  At fifty percent, fat contributes only forty percent.  However, because the total energy expenditure is two and one-half times greater at fifty percent, the absolute amount of fat that the body metabolizes is thirty-three percent greater.  Therefore, to reduce fat stores, athletes have to consider both the rate of energy expenditure and the percentage of energy metabolism to which fat contributes.
If athletes exercise for more than two hours, they can reduce their muscle and liver glycogen stores to very low levels.  Glycolysis converts glycogen to pyruvic acid.  Pyruvic acid is a precursor for Krebs Cycle intermediates such as oxaloacetate amd malate.  Through a series of actions, low muscle and liver stores causes muscle fatigue.
Low muscle and liver carbohydrate levels reduce the rate of glycolysis, which reduces pyruvic acid concentration in muscle, which reduces the Krebs Cycle intermediates, which reduce the rate of Krebs Cycle activity.
In muscle with adequate glycogen stores, exercising at seventy percent of maximal oxygen utilization increases the amount of Krebs Cycle intermediates nine-fold.  Elevated levels of Krebs Cycle intermediates speeds up the ATP production by Krebs Cycle activity.
When low amounts of Krebs Cycle intermediates reduces Krebs Cycle activity, the Krebs Cycle cannot metabolize fat.  This means that, when the Krebs Cycle has plenty of carbohydrate intermediates already metabolizing, the Krebs Cycle can only metabolize fat.  Therefore, for athletes to perform prolonged low-intensity exercise, they must have high levels of carbohydrate intermediates.  Thirty to sixty grams of carbohydrates per hour enhance prolonged exercise performances.
Where muscle glycogen directly contributes to muscle energy metabolism, liver glycogen only indirectly contributes.  During prolonged exercise, low blood glucose levels stimulate liver glycogenolyis to release glucose into the blood.  Muscle uses this glucose as fuel for metabolism to resynthesize ATP.  Therefore, both muscle glycogen and blood glucose contribute to exercise.
How much muscle glycogen and blood glucose contribute to ATP resynthesis depends on the intensity and duration of the exercise.  Where, during low-intensity exercise, blood glucose contributes more, during high-intensity exercise, muscle glycogen contributes more.  During the first hour of prolonged low-intensity exercise, muscle glycogen contributes more.  However, as muscle glycogen levels decrease, blood glucose gradually increases its contribution.
One pound of fat contains 3,500 kilocalories.
When athletes consume more fat than they expend, they store fat in adipocytes.  The availability to muscle cells determines the role of fat as a substrate for exercise.  Triglycerides must degrade to free fatty acids and glycerol.  To enter the Krebs Cycle, free fatty acids must convert to acetyl-CoA.
Where plasma free fatty acids contribute to low-intensity exercise, muscle triglycerides contribute to high-intensity exercise.  Between sixty-five and eighty-five percent of maximal oxygen utilization, plasma free fatty acids and muscle triglycerides equally contribute to ATP resynthesis.  As the duration of exercise increases, plasma free fatty acids gradually increases its contribution.
Muscle protein metabolism depends on the presence of branch-chained amino acids such as valine, leucine, isoleucine and alanine.  The liver converts alanine to glucose.  Amino acid pools in muscle and in blood provide these amino acids.  Two or more hours of exercise activate proteases that degrade proteins to useable amino acids.  Increased muscle and liver amino acid pools enhance protein metabolism.
Via gluconeogensis, the liver converts lactate to glucose.  This glucose moves to fast-twitch muscle fibers for fuel.  Slow-twitch muscle fibers and the heart converts lactate to pyruvate, which transforms to acetyl-CoA and enters the Krebs Cycle.  The ‘lactate shuttle’ refers to fast-twitch muscle fibers producing lactate, blood transporting lactate to slow-twitch muscle fibers and the heart and slow-twitch muscle fibers and the heart using lactate as a fuel.