Simple Science – sportsgeek

Performance Benefits of Training

Exercise taxes the various physiological systems of the body beyond their normal resting level of performance. Two of the most important purposes of training are to increase the rate of energy release during races and to delay fatigue.

Training the ATP-CP System

The energy for muscular contraction comes from ATP, which is the only chemical stored in muscles that can provide that energy. The primary purpose for all other phases of metabolism is to replace the energy in ATP so that contraction can continue. The ATP-CP system can provide energy for muscular contraction more rapidly than any other phase of metabolism, but it can do so for only 4 to 6 seconds.

After ensuring that technique is good, an athlete can improve maximum speed most significantly by 1) increasing the size and strength of the fibres in particular muscle groups so that the fibres can generate more power and 2) improving the rate and pattern of fibre recruitment by the central nervous system so they can be brought into play quickly and in the proper sequence for a particular skill without involving unneeded fibres.

Increasing the quantities of ATP and CP stored in muscle fibres represents another possible training effect that might increase athletic speed. Increases could extend the maximum rate of ATP recycling for an additional few seconds, which in turn may allow athletes to maintain their sprint speed slightly longer. Training has been reported to increase the storage of both ATP and CP by 18% and 35%, respectively (MacDougall et al. 1977).

Besides training, athletes have tried to improve the creatine phosphate supply in their muscles by supplementing their diets with creatine. This procedure has been reported to increase the free creatine in muscle fibres by about the same amount as training does, 20% (Hultman et al. 1996). The results have been equivocal about whether creatine loading can improve the performances of sprint athletes. Some have reported improved performances, but others have not.

Training Anaerobic Metabolism

The anaerobic breakdown of muscle glycogen supplies approximately half the energy for ATP-CP recycling during the first 5 to 6 seconds of a race. Thereafter, the proportion will increase considerably until anaerobic metabolism will be supplying by far the greatest amount of energy for sprinting within 10 to 15 seconds after the race begins.

Because anaerobic glycolysis involves 11 steps, the power available for speed will decline somewhat after the first few seconds of a race. An athlete’s ability to generate muscular power will decrease by approximately 10% after the first 4 to 6 seconds of effort when the muscle’s creatine phosphate supply is partially depleted and anaerobic glycolysis becomes the primary source of energy for ATP recycling. For this reason the rate of anaerobic glycolysis has a greater influence than the ATP-CP system does on how fast athletes can perform in sprint events.

Training appears to increase both the quantity and activity of many of the enzymes of anaerobic glycolysis. Sprints are particularly good for bringing about these increases, whereas endurance training tends to suppress their quantity and rate of activity. In general, training-induced increases of anaerobic enzymes have not been as great as those reported for the enzymes of aerobic metabolism. Most of the increases in anaerobic enzymes have ranged between 2% and 22%.

The major obstacle to increasing the quantities of anaerobic enzymes is the endurance training that athletes must engage in. Endurance training suppresses the activity of most anaerobic enzymes.

The dilemma most athletes face is that they must improve both endurance and speed to improve their performance in many events. But athletes typically do so much endurance training that the best they can do is maintain their innate ability to recycle ATP rapidly through anaerobic metabolism. More often, their rates of muscle contraction and anaerobic metabolism decline during most of the season because of the large volume of endurance training they perform. Lucky athletes manage to regain their speed during the taper. When the loss of speed has been extreme, however, the taper may not be long enough and speed will not return to inherited levels until several weeks after endurance training has been terminated or considerably curtailed.

Training to Delay Acidosis – Training Aerobic Metabolism

The desired training effect is to reduce the rate and severity of acidosis during races. That effect is the result of two factors – reducing the rate of lactic acid production within muscles and increasing the rate of lactate removal from them.

1. Many training adaptations reduce the rate of lactic acid production:

Increased diffusion of oxygen from the lungs, which results from improved volume of air exchanged each minute and an increase in the capillaries around the alveoli of the lungs
An increase in blood volume that permits blood to circulate through the body faster
An increase in red blood cells so that the blood can carry more oxygen
An increase in cardiac output so that the blood makes a quicker round-trip from the lungs to the muscles
An increase in capillaries around the muscles so that more oxygen can be made available for diffusion
Improved blood shunting so that more of the blood supply and its oxygen can reach the working muscles during each minute of exercise
An increase in myoglobin so that more oxygen can be transported to the mitochondria of the muscles each minute
An increase in the size and number of mitochondria in muscles so that the receptacles for aerobic metabolism will be larger and more numerous
An increase in the activity of the aerobic enzymes so that aerobic metabolism can proceed at a faster rate
An increase in the rate of the glucose-alanine shuttle so that more pyruvate can be removed before it combines with hydrogen ions to form lactic acid

2. Several training adaptations increase the late of lactate removal from working muscle fibres:

Increased activity of the lactate transporter in working muscle fibres and receptor fibres
Increased blood volume and improved cardiac output so that more blood can make the trip to and from working muscle fibres in a shorter time, thus transferring more lactate from the working muscle fibres to the blood and then to areas where it is removed during each minute of exercise
An increase in capillaries around the working and receptor muscle fibres so that more lactate can be transferred into and out of the blood during each minute of exercise
Improved blood shunting so that more lactate can be carried away from the working muscle fibres with each minute of exercise

Training Effects that improve the Ability to Train

An increase in the amount of glycogen stored in working muscle fibres so that athletes can train more intensely more often.
An increase in the rate of fat metabolism so that the muscles use more of this compound for energy and less glycogen, leaving more glycogen for a greater number of intense training sessions.

Energy Metabolism and Athletic Performance

Energy Metabolism

Energy is stored in our bodies in combination with the following chemical compounds: adenosine triphosphate (ATP), creatine phosphate (CP), carbohydrates fats and proteins.

ATP

ATP is the only source of energy that our bodies can use for muscular contraction. All the other energy containing chemicals are used to recycle ATP after its energy has been used for muscular work. The energy from ATP becomes available for muscular contraction in the following manner: When muscle fibers contract, they activate an enzyme, (ATPase), that causes one of the phosphate molecules to split away from the ATP molecule and in the process release the energy that bound it to that molecule. What is left is adenosine diphosphate (ADP). ATP cannot be transported to working muscle fibres from other parts of the body. Therefore, when the amount in a particular muscle fibre loses some of its energy and phosphate, other sources of energy within the same fibre must replace it almost immediately or the fibre will not be able to release enough energy to continue contracting. This recycling of ADP back to ATP requires that another phosphate molecule and energy be made available. The donors are the remaining 4 chemicals in muscles: CP, carbohydrates, fats and proteins.

Creatine Phosphate

Good stuff this creatine phosphate! It is what provides the most rapid source of energy and phosphate for ATP recycling. It is composed of one molecule of creatine and one molecule of phosphate. Energy binds the two molecules together. The enzyme creatine kinase (CK) catalyzes the splitting of the phosphate molecule from creatine, which also releases the energy that bound these two molecules together. That energy and the phosphate then combine with ADP to reform ATP. The process of replacing ATP with phosphate and energy from CP requires only two steps: the splitting of CP and the combination of is phosphate and energy with ADP. These two steps occur so rapidly that no delay will occur in the process of releasing energy from ATP. The upshot of this is that athletes can maintain a maximum rate of muscular contraction as long as sufficient CP is available to restore the energy provided by ATP. Fast-twitch muscle fibres have a higher concentration of CP than do slow-twitch muscle fibres.

Unfortunately, the amount of CP that can be stored in either type of muscle fibre is quite small, small enough in fact that humans can only use CP to recycle ATP for approximately 4 to 5 seconds of an all-out effort. This means that humans can only maintain a maximum rate of muscular contraction for 4 to 6 seconds. Now athletes must rely on the metabolism of carbohydrates, fats, and proteins for the energy and phosphate they need to recycle ATP. This circumstance will slow the rate of muscular contraction because several additional steps are needed to release energy from these foods. In the absence of sufficient CP, the next most rapidly available source of energy and phosphate is carbohydrates in the form of glycogen stored in the muscles.

Carbohydrates

Carbohydrates are made up of simple sugars and starches, which supply the energy for all body functions. Glucose is the simple sugar used for ATP recycling. Glucose, after being taken in as food, can be used immediately or stored for later use. The storage form of glucose is termed glycogen. Glycogen is stored in the muscles and in the liver. Glucose therefore provides 3 forms of energy: blood glucose (used immediately), muscle glycogen and liver glycogen.

Muscle glycogen is the primary source of energy from carbohydrate. When combined with phosphate, it results in the rapid recycling of ATP in all but the shortest of events. When exercise begins, the glycogen stored in muscles is converted back to glucose by glycolysis. Energy and phosphate for ATP recycling is released at several points during the glycolysis process. The energy and phosphate released most quickly come from anaerobic glycolysis, which does not require oxygen for release to take place. The longer, slower process, aerobic glycolysis, requires oxygen.

The liver and blood also contain supplies of glucose that can be mobilized and transported to the muscles when they are needed for energy. The glucose that previously entered the liver was stored there as glycogen. It must be converted back to glucose before it can be transported to the muscles and used to supplement their glycogen supply. The reconversion process occurs whenever the blood glucose supply drops below normal. So when muscles are contracting and glucose is diffusing into them from the blood, liver glycogen will be converted to glucose and poured into the bloodstream to replenish the supply of glucose in the blood.

Blood glucose is more commonly known as blood sugar. When an athlete is training, glucose that was circulating in the blood can diffuse into the muscle cells and enter the metabolic process without first being converted to glycogen. So glucose from the blood helps athletes maintain a high level of glucose in the muscles during exercise. Blood glucose may supply 30 to 40% of the total amount of energy used during training. But both liver glycogen and blood glucose can supply only small amounts of energy during racing. The process of converting liver glycogen to blood glucose is too slow to provide energy for recycling ATP. Similarly, the diffusion of blood glucose into muscle cells requires too much time to sustain the high intensity of racing. Blood glucose and liver glycogen play important roles in replacing the glycogen supplies of muscles during the recovery period following exercise.

Fats

Fats are also an important source of energy for ATP recycling during exercise. More ATP can be replaced with fat than with carbohydrate. However, the process of metabolizing fats is entirely aerobic, which means that energy can only be released slowly. Although a small amount of fat is stored in muscles, most is stored under the skin as adipose tissue.

Adipose tissue supplies about one-half of the fat that is metabolized for energy during exercise. The fat stored in the muscle cells supplies the other half. Slow-twitch fibres are better suited for fat metabolism than fast-twitch fibres because slow-twitch fibres have more fat stored within them, have a greater blood supply, and can transport additional fat from adipose tissue more rapidly. Slow-twitch muscle fibres also have more mitochondria, where fat from both the circulation and muscles can be metabolized. The rate of fat metabolism in slow-twitch fibres has been estimated to be 10 times greater than the same rate in their fast-twitch friends. Consequently, distance athletes, who generally have a higher percentage of slow-twitch fibres, burn more fat (and less muscle glycogen) for energy during training. Thus distance athletes should deplete their muscle glycogen supply more slowly. This may be one of the reasons why they seem to tolerate successive days and weeks of hard training better than sprinters do.

The major role that fat metabolism plays in replacing the ATP of athletes occurs during training. Fat metabolism can provide a significant amount of energy during long repeat sets at moderate speeds, thus reducing the rate of muscle glycogen use and delaying fatigue. Fat metabolism probably supplies between 30% and 50% of the total energy used during typical 2 hour training sessions that includes a significant amount of endurance training. The energy supply for sprinting and fast endurance repeats is another matter. The process of fat metabolism is simply too slow to supply any but a small amount of the energy needed to support fast speeds. Thus, the contribution of fats to ATP recycling falls dramatically when athletes train at speeds that approach and exceed their anaerobic thresholds. Therefore, most of the energy for these sets must come from glycogen and glucose.

Proteins

Often people will think of strength when they think of proteins because proteins are the basic structural elements of muscles and are intimately involved in the repair and rebuilding of those tissues. What is less known is the role they play in endurance. Many of the structural components of muscles (principally, mitochondria) that are involved in aerobic metabolism are built from protein. Proteins are made up of carbon, hydrogen, oxygen and nitrogen arranged in a way to form a large combination of amino acids.

Besides other functions, proteins can donate small amounts of energy for recycling ATP during exercise. This occurs when some of the nitrogen in certain amino acids is removed and passed to other proteins to form new amino acids. The carbon portions that remain from the old amino acids can then be converted to acetyl-CoA so that they can enter the Krebs cycle and be metabolized for energy in the same manner that glucose is.

Like fat, the recycling of ATP from protein is a slow, aerobic process that requires many steps. Protein metabolism is the slowest and least economical method for recycling ATP. Why use protein to recycle ATP if fat is available? The muscles must contain a certain amount of glucose to metabolize fat for energy. So if an athlete’s glucose supply is very low, he or she has no choice but to rely more heavily on the muscles’ own protein to recycle ATP.

Because it is an extremely slow process, protein metabolism does not contribute any substantial amount of energy during competition, but it does contribute to the energy supply for training, around 10 to 15% during a 2 hour session. Athletes should maintain adequate supplies of glycogen and glucose in their muscles during training so that they do not use excessive amounts of protein for energy. Doing so will cause muscles to lose some of their protein content and therefore some of their strength and endurance.

The small amount commonly used can generally be replaced overnight, so training adaptations should not be adversely affected. But when athletes train when muscle glycogen supplies are low, negative effects can become significant. For example, if an athlete’s muscle glycogen is low from days of previous training, the amount of energy derived from protein could increase from 15 to 45%. The energy for ATP recycling donated by protein will also increase significantly during long continuous training sessions if the glycogen supplies in muscles and the liver become depleted. When the amount of protein metabolized for energy becomes so great that the athletes cannot replace it on a regular basis, they may literally cannibalize the structural components of the contractile proteins, mitochondria, myoglobin, and metabolic enzymes within their muscles. Over time, the loss may become so severe that they lose strength and endurance.

V02MAX

Here is the long promised posting on V02max.

V02Max and Work Intensity

Scientists frequently use V02max measurements to equate the intensity of exercise within and between groups of subjects. They speak in terms of work being performed, for example, at a speed that elicits oxygen consumption that is 70% of a person’s V02max. By doing so they can quantify the level of effort relative to each person’s individual maximum oxygen consumption and provide a more accurate representation of the work intensity. This method is great for scientists but not so good for coaches as coaches will often not know the V02max of their athletes. Coaches prefer to refer to efforts subjectively as a percentage of maximum. To help equate the two, information from studies in which work intensity has been reported as a percentage of V02max can be translated to percent efforts as follows:

efforts of 50% to 60% of V02max are probably equivalent to subjective feelings that the effort is 30% to 40% of maximum
efforts of 70% to 90% of V02max are probably equivalent to subjective feelings that the effort is 60% to 80% of maximum
efforts of 100% of V02max are probably equivalent to subjective feelings that the effort is 80% to 90% of maximum
efforts of 90% to 100% of maximum are probably equivalent to values that are between 110% and 130% of V02max

The distance of swimming repeats has a considerable effect on these crude estimates. During short repeats the athlete may sense a lower percentage of maximum effort than the actual percentage of V02max at which he or she is swimming because the duration of the swimming will not cause intense fatigue. Subjective feelings of percent effort will correspond more closely to the percentage of V02max indicated earlier when the repeats are longer.

Heart rates, if counted correctly and interpreted properly, can provide a more accurate method than subjective percentages of maximum effort for estimating the percentage of V02max during work.

V02Max and Performance

Although a person can improve V02max by training, research shows that heredity sets limits on the amount of improvement. Generally, athletes can improve their absolute maximum oxygen consumption by 15 to 20%.

For many years, the capacity to consume oxygen maximally was considered the most valid measure of an athlete’s ability to perform in endurance events. It was believed that a large V02max would provide an athlete with a distinct advantage in endurance events and, for that reason, endurance training emphasized improving this measure. However, persons who are able to consume large quantities of oxygen during races do not always defeat those with smaller maximum consumption rates. Other factors are involved.

Percentage Utilization of V02max

More predictive of performance in endurance events is fractional percentage of maximum oxygen consumption (%v V02max). It refers to the highest rate of work that a person can perform for a long period, say 20 to 40 minutes, without becoming fatigued. It is determined by measuring an athlete’s oxygen consumption during a maximum effort swim of 20 to 40 minutes and then determining what fraction of the athlete’s maximum oxygen consumption rate it represents. For example, let us assume an athlete has the ability to consume oxygen at a maximum rate of 70ml/kg/min. If the highest rate of oxygen consumption that the person can maintain for a long time with becoming fatigued is 60ml/kg/min, then the person is able to work at 85% of V02max.

As with V02max, heredity seems to play a role in determining the highest percentage of maximum that athletes can reach (about 20% trainable). A more common term used to identify the highest fractional utilization of V02max that can be maintained for a long period is anaerobic threshold. The anaerobic threshold does not indicate the rate of work at which anaerobic metabolism begins. It represents a manageable level of anaerobic metabolism that a person can sustain for a long period without experiencing severe fatigue.

Advantages of Increasing %VO2Max

Most athletes can only maintain speeds that require them to consume oxygen maximally for 1 to 3 minutes of continuous effort before they are forced to slow their pace because of fatigue. In long races and long training sets, athletes must select speeds that require less than a maximum rate of oxygen consumption so that they do not accumulate too much lactic acid in their muscles too early. For example, most runners can complete a marathon at an average pace that requires them to use 75% to 80% of their maximal oxygen consumption capacity. You should be able to understand now why the ability to use a larger fraction of V02max in these races would be a decided advantage. Athletes who can train themselves to use 85% to 90% of V02max without becoming fatigued should be able to run their long races at a faster average pace.

The ability to compete at a higher percentage of V02max should also be advantageous in shorter events. In middle distance and distance swimming races, the pace at which athletes must compete always exceeds the pace that would produce maximum oxygen consumption. Let us assume that two athletes with identical maximum oxygen consumption ability are swimming a race that requires each of them to work at a rate equivalent to 130% of V02max. Let’s assume also that one athlete is able to work at 85%of V02max without becoming fatigued whereas the other can work at only 80% of V02max without becoming fatigued. It should be easy to see that the athlete who can swim closer to 100% of V02max will be producing less lactic acid at race pace and should therefore be able to maintain that pace longer.

Athletes with a smaller V02max can sometimes excel over competitors who have larger values through their ability to compete at a higher percentage of maximum. For example, Alberto Salazar, former world record holder in the marathon, had a V02max of 70ml/kg/min, which was lower than that of many of his competitors. But he was able to run the marathon at a pace that used 86% of his maximum, a much higher percentage utilization of V02max.

Respiratory System

Respiratory System

The 2 primary purposes of respiration are to provide our bodies with oxygen and to remove carbon dioxide. This process makes life possible (along with a few other things). We could not live more than a few minutes without oxygen. A lesser-known but almost equally important function of respiration is to regulate the acid-base balance of the blood (this becomes important later when we learn the role acidosis plays in fatiguing).

The respiratory system consists of the lungs and a set of branching tubes that transport air and oxygen from outside the body to the bloodstream. During inhalation we take air from the outside into the mouth and nose, down the pharynx or throat, and into each lung by means of two large tubes called the bronchi. Within the lungs air travels through an ever smaller system of branching tubes called bronchioles until these finally end as small sacs called alveoli. Capillaries surround the alveoli.

The inhalation phase of respiration allows us to take in oxygen as a component of the air that comes into our bodies. Some of that oxygen remains in our bodies when we exhale the air. With the air we expel during the exhalation phase, we also expel carbon dioxide and some water vapor that our bodies produced.

We take in air through the nose and mouth. It travels down the pharynx through the bronchi, the bronchioles, and lastly to the alveoli, where it inflates these small elastic sacs. From there, some of the oxygen in that air diffuses from the alveoli into the bloodstream by way of the pulmonary capillaries. At the same time, carbon dioxide produced in the muscles diffuses in the opposite direction, that is, out of the capillaries and into the alveoli. The carbon dioxide is then transported through the bronchioles and finally exhaled into the air from the nose and mouth.

The term for the amount of air exchanged per breath is the tidal volume. The amount of air exchanged per minute is termed the minute volume. Average tidal volume is between 500 and 700 ml of air per breath, and we breath 12 to 15 times per minute. The average minute volume is thus 6 to 10 L of air.

Oxygen Consumption and Athletic Performance

Oxygen consumption refers to the amount of oxygen used during exercise. That amount is equal to the amount of oxygen taken in during exercise minus the amount exhaled, usually expressed as litres per minute.

The amount of oxygen used by the muscles each minute will be directly related to the intensity of the exercise until a maximum rate is reached. That maximum rate will be between 2 and 3L per minute for average nonathletic females and males, respectively. The rate can be as high as 4 to 6 L per minute for female and male endurance athletes. The term for the maximum amount of oxygen that a person can take in during 1 min of exercise is maximal oxygen consumption, more commonly referred to as VO2max. Values for VO2max are a direct expression of a person’s ability to supply energy for muscular contraction through aerobic metabolism.

Maximal Oxygen Consumption

We calculate maximal oxygen consumption, VO2max, by measuring oxygen consumption during repeated intervals of exercise at progressively faster speeds until the athlete reaches a plateau where a further increase of speed does not cause an increase in oxygen consumption. When that happens, the athlete has reached his or her maximum ability to consume oxygen.

One aspect of VO2max difficult for many people to understand is that athletes will reach it when they are exercising slower than their maximum speed. Athletes can continue to increase their speed even after they have reached their maximum ability to consume oxygen because of their capacity for anaerobic metabolism. Anaerobic capacity makes it possible for them to continue supplying energy to their muscles even though not enough oxygen is available to metabolize the chemical sources of that energy. They will only be able to this for a short time however because the chemicals that were not completely metabolized, principally lactic acid and more specifically the hydrogen ions in that compound, will accumulate in the muscles and change their pH from neutral to acidic, which will slow the speed and force of muscular contraction and in the process slow the swimming (running/cycling etc) speed.

During submaximal exercise, oxygen consumption will increase from its resting rate of around 0.25 L per min to some level that will sustain the contractile energy needed by the muscles. It will usually take between 1 and 3 minutes to reach this level of increased oxygen consumption. An oxygen deficit occurs during this period of adjustment. The oxygen deficit represents the oxygen that was needed but not available during the first few minutes of exercise. The athlete can repay the deficit during the remainder of the exercise if the intensity of work is low. To repay the deficit, the body can make available for a short time more oxygen than it needs to provide energy for work. The amount of oxygen consumed during the exercise period plus the oxygen deficit is termed the oxygen requirement for the task at hand.

If the demand for oxygen exceeds the amount that the athlete can repay during exercise, it will continue to build. The athlete will repay it after exercise by maintaining a high level of oxygen consumption for a short period. This period of additional oxygen consumption after exercise has become known as the oxygen debt. Although this term is in common use by members of the sporting community, it has become obsolete in the scientific community because sophisticated evaluation techniques have shown that the increased consumption of oxygen after exercise does not correspond directly to the oxygen deficit that occurred in the first few minutes of exercise.

New thoughts on oxygen debt

We now understand that the extra oxygen consumed after exercise does not entirely represent the repayment of a debt incurred during the exercise (we tend to take in more extra oxygen than what we owe). For this reason, scientists have suggested other terms for the additional oxygen consumed during recovery. One of these terms is excess post-exercise oxygen consumption (EPOC).

Typically, recovery oxygen uptake has fast and slow components. About half of the total amount of excess oxygen consumed during recovery will take place within 30 sec to 3 min after completion of the exercise, depending on the length and intensity of the exercise. This portion is termed the fast component for obvious reasons. The slow portion of recovery oxygen uptake refers to the slightly elevated breathing rate that can continue for several minutes or even several hours after exercise. One explanation is that the additional oxygen is probably used to metabolize the lactic acid produced during exercise. Another is that an increase of body temperature keeps the respiration rate elevated.

Circulatory System

This post will be longish seeing as there is nothing difficult in it, pretty much a refresher for most.

Circulatory System

The circulatory system is essentially like the filtering system of a swimming pool. The pool is like the tissues of the body, principally the muscles. The heart is the pump. The arteries and veins are the pipes going to and from the pool. The blood is like the water that is pushed out to the pool after being cleaned and then pulled back from the pool for subsequent cleaning. The left side of the heart pumps blood out to the muscles and other tissues of the body through the arteries and arterioles which are like branching sets of pipes that become smaller in diameter until they reach their destinations in the tissues. Arterioles end in capillaries which are the smallest vessel units and surround individual muscle fibres.

The blood delivers oxygen, glucose, and other substances to the capillaries. At that point, blood is at its greatest proximity to muscles, and some of these substances diffuse out of the capillaries and into the muscle fibres they surround. At the same time the carbon dioxide, lactate, and hydrogen ions produced in the muscles during exercise diffuse and are transported out of them into the capillaries. Blood then leaves the tissues through the same capillaries and travel through another set of progressively larger tubes, the venules and veins, back to the right side of the heart. The heart pumps the blood out to the lungs through pulmonary arteries and arterioles, ending in pulmonary capillaries that surround small sacs in the lungs called alveoli. Here, carbon dioxide diffuses out of the blood and into the alveoli when it reaches the lungs, where it is exhaled. At the same time, oxygen inhaled into the lungs diffuses into the capillaries, and blood transports it back to the left side of the heart through venules and veins. Once it reaches the heart, the process begins again.

The lactic acid picked up from the muscles will be dropped off at several locations as the blood makes its way back to the heart. Some of it will be dropped off at other muscle fibres and the liver, where it will be converted back to glycogen for use later as a source of energy. Some of the remaining amount will be picked up by the heart muscles and used as fuel or converted to glycogen and stored for later use.

Heart Rate

The number of times your heart contracts during each minute is your heart rate (right and left sides contracting simultaneously counting as one beat). Resting heart rates are in the neighbourhood of 60 to 80 beats per minute (bpm) for most untrained persons and 30 to 50 bpm for trained athletes. Cardiac muscles of the heart become larger and stronger from training, and they can push more blood out with each beat so the heart requires fewer beats to supply the usual quantity of blood the athlete needs at rest.

Stroke Volume

The amount of blood pushed out of the ventricles of the heart with each beat is termed stroke volume. A normal range of values at rest is between 60 and 130ml per beat. These amounts can increase to between 150 and 180 ml per beat during exercise. These values refer only to blood pumped out of the left ventricle. Stroke volume increases with endurance training. Many factors contribute to the increase, including increased strength of the cardiac muscle fibres, an increase in ventricle size, and a decrease in the thickness of the blood. The stroke volumes of athletes are usually greater after training than before, which explains why they have a lower resting heart rate.

Cardiac Output

The amount of blood ejected from the heart during each minute is referred to as cardiac output. Again, we consider only the amount ejected from the left ventricle when citing values for the cardiac output (right ventricle will eject an equal amount).

Cardiac output is calculated by multiplying the heart rate by the stroke volume. Normal cardiac output for a person at rest is between 5 and 6 L per minute (L/min). The bodies of females and males contain between 4 and 6 L of blood; therefore, each red blood cell usually makes one round-trip from the lungs to the muscles and back again in approximately 1 min when athlete’s bodies are resting. Resting cardiac output does not increase with training, but the heart becomes more efficient in the way it supplies the blood. Stroke volume increases and heart rate decreases. So when a person is resting the heart does not have to work as hard to push the same 5 L of blood out to the body each minute. Training does not increase an athlete’s cardiac output during similar submaximal efforts because there is no need for it.

Athletes can increase their maximum cardiac output by training. Maximum cardiac output values of 30 and 35 L/min are not unusual for trained endurance athletes.

Blood Pressure

Blood flowing through vessels exerts pressure on the walls of those vessels. This pressure is measured by the number of millimeters that the blood causes a column of mercury (Hg) to rise. Two measurements of pressure are needed to identify the force of blood flow: (1) the pressure when the heart beats, known as systolic pressure, and (2) the pressure when it is resting between beats, diastolic pressure. Typical resting systolic and diastolic blood pressures are 120 and 80 mm Hg, respectively.

Systolic blood pressure increases in proportion to the intensity of work because a larger amount of blood is present in the vessels at any one time.

Endurance training reduces both systolic and diastolic blood pressure by 6 to 10 mm Hg at rest and by an equal amount during submaximal exercise. This reduction in pressure probably occurs because the elasticity of blood vessels increases through constant expansion and constriction that occurs in training.

Ok, so nothing hard there. We’re up to the respiratory system. I’m going to leave that to another post because this goes a bit into what we do with the oxygen we take in and measuring VO2max, oxygen debt and some other stuff so is probably worthy of its own post. Then we get into energy metabolism (that we use up our creatine phosphate in the first few seconds of exercise is a bit of a downer isn’t it but hey, we’ve got glycogen so why did we even get given CP in the first place I don’t know – actually, because it can be utilized really really quickly), how we produce and clear lactate. Then there is a section on metabolic training. Finally we get to the info on the energy zones – EN1, EN2, EN3, SP1, SP2, SP3.

A Little Bit On Fast Twitch and Slow Twitch Fibres

Much of the info that will end up in this ‘Simple Science’ section will come from a magnificent book I have (all 2.5kg!!! of it) called Swimming Fastest by Ernest Maglischo. But don’t let the word ‘swimming’ put you off if you aren’t a swimmer. For most of this you can take out the word swimming and just plop in running, rowing, cycling, tennis, bob-sled, tiddly winks, whatever you are into. Only the middle section of the book is on physiology and energy systems, so don’t worry, if you print out the posts you won’t end up lying in bed for your nighttime reading with 2.5kg of pages scattered about. Besides which, although I make no apology for lifting info straight out of the book, in the interests of keeping everything nice and simple it has all been and will be radically condensed, hopefully without changing the meaning.

Ok, so this first bit is on fast twitch and slow twitch fibres:

Slow twitch (ST) fibres (red) contract 10 to 15 times per second (still sounds quite fast to me). Fast twitch (FT) fibres (white) contract 30 to 50 times per second. FT fibres also shorten more rapidly, and can shorten up to 6 fibre lengths per second. ST fibres have more endurance and they have more capacity for aerobic work, but their capacity for anaerobic metabolism is limited. ST fibres have more myoblobin, which is the substance that transports oxygen across the muscle cell. ST fibres also contain more mitochondria, the protein structures within muscle cells where aerobic metabolism occurs and ST fibres also have a greater concentration of the aerobic enzymes that catalyze the release of energy during aerobic metabolism. On the other hand FT fibres have a lower capacity for aerobic metabolism as they have less myoglobin, fewer mitochondria and a lower concentration of enzymes. FT fibres produce more lactic acid than ST fibres at equivalent workloads and so fatigue more quickly. They also use glycogen more quickly.

Now I thought this bit on endurance training was interesting and a bit unfair. Endurance training will increase the aerobic capacity of slow twitch and fast twitch fibres. Trained fast twitch fibres never reach the level of aerobic capacity of trained slow twitch fibres. An athlete can increase the aerobic capacity of fast twitch fibres, however, to a level that surpasses that of untrained slow twitch fibres. Conversely, strength and sprint training will increase the size and contractile speed of fast twitch and slow twitch fibres as well as their potential for rapid energy release. Fast twitch fibres however, possess a greater potential than slow twitch fibres for such increases. Although an athlete can increase contractile speed and force in slow twitch fibres that have been sprint trained, they never reach the level of even untrained fast twitch fibres. Sounds like sprinters get the best deal. I wish I was a sprinter!

There are 3 subgroups of FT fibres. Fta, FTb and FTc. We’re going to forget FTc as they, and what they do, are controversial and make up only about 3% of our fibres anyway. Fta fibres contract faster and with greater force than ST fibres and make up about 33% of our fibres. FTb fibres contract with about twice the force of Fta fibres and make up about 14% of our fibres. Roughly 50% of fibres are ST.

It’s not true that we only use ST fibres when we go slow and FT fibres when we go fast. ST are the first to contract. When the resistance increases, both the ST and FT fibres will contract to overcome it whether the movement is slow or fast.

It seems that although you can’t change an ST fibre into a FT fibre you can change the proportion of FTb’s and Fta’s. Most notably, FTb’s becoming Fta’s by an increase in the amount of myoglobin etc.

So that was ok wasn’t it? About 10 pages of the mighty tome condensed into one manageble post. The next section/s are some really easy back-to-basic stuff on the circulatory and respiratory systems.