Basic Skeletal Muscle Physiology

[GFR]

http://home.hia.no/~stephens/musfacts.htm

This is intended to be a bare-bones review of physiology of muscle function. There are numerous sources on the internet for those who are interested in a more in-depth exploration of skeletal muscle physiology. The concepts here have direct application to understanding how specific training improves (or decreases) endurance performance capacity. Basic Architecture

A single muscle fiber is a cyclindrical, elongated cell. Muscle cells can be extremely short, or long. The sartorious muscle contains single fibers that are at least 30 cm long. Each fiber is surrounded by a thin layer of connective tissue called endomysium. Organizationally, thousands of muscle fibers are wrapped by a thin layer of connective tissue called the perimysium to form a muscle bundle. Groups of muscle bundles that join into a tendon at each end are called muscle groups, or simply muscles. The biceps muscle is an example. The entire muscle is surrounded by a protective sheath called the epimysium. Between and within the muscle cells is a complex latticework of connective tissue, resembling struts and crossbeams that help to maintain the integrity of the muscle during contraction and strain. It is an amazing cellular system even before it contracts!
Interior Components

Every muscle cell contains a series of common components that are directly associated with contraction in some way, and influenced by training. I will briefly describe these. For now we will not worry about the rest (like the nucleus, ribosomes etc.).

1. The Cell Membrane - Controls what enters and leaves the cell. Contains regulatory proteins that are influenced by hormones like epinephrine (adrenalin) and insulin. The blood concentration of these hormones greatly influences fuel utilization by the muscle cell.
3. Contractile Proteins - The contractile machinery of a muscle fiber is organized into structural units called sarcomeres. Muscle length is determined by how many sarcomeres are lined up in series, one next to the other. Muscle thickness ultimately depends on how many sarcomeres line up in parallel (one on top of the other). The sarcomere structures consist of two important proteins, actin and myosin (about 85% by volume). Several other important proteins called troponin and tropomyosin, and proteins with cool names like titin, nebulin, and desmin help to hold these units together. The sarcomeres are organized as many thin myofibrils. A single muscle fiber will contain 5 to 10,000 myofibrils. Each myofibril in turn contains about 4500 sarcomeres. Multiply the number of muscles in the body by the number of muscle fibers per muscle by the number of myofibrils per fiber by the number of sarcomeres per myofibril and well, the numbers become pretty staggering. It is the individual myofibrils, long chains of sarcomeres, which actually produce force in the muscle cell. All of the rest of the machinery plays a supporting or repair function.
5. The Cytosol. This is the aqueous fluid of the cell. It provides a medium for diffusion and movement of oxygen, new proteins, and ATP within the cell???s interior. The cytoplasm also contains glycogen, lipid droplets, phosphocreatine, various chemical ions like magnesium, potassium and chloride, and numerous enzymes.
7. Mitochondria - 1. The organelles in each muscle cell that contain oxidative enzymes consume oxygen during exercise. Recent research suggests that mitochondria may look more like an interconnected network than little isolated oval ???powerhouses??? shown in most old textbooks. Mitochondria convert the chemical energy contained in fat and carbohydrate to ATP, the only energy source that can be used directly by the cell to support contraction. Ultimately, glucose and fat molecules (and certain amino acids) break down and combine with oxygen to form ATP, carbon dioxide, water, and heat energy. This occurs via enzymatic processes occurring first in the cytosol and then the mitochondria. The carbon dioxide and excess water leave the body through our breath. The ATP generated provides a usable energy source for muscle contraction and other cell functions. Heat removal occurs by sweating and as radiant heat transfer from the skin to the surrounding air. Clearly, each by-product of energy metabolism has significance to the exercising athlete.
9. Capillaries - 1. These microscopic size blood vessels are not actually part of the muscle cell. Instead, capillaries physically link the muscle with the cardiovascular system. Each muscle cell may have from 3 to as many as 8 capillaries directly in contact with it, depending on fiber-type and training. One square inch of muscle cross-section contains 125,000 to 250,000 capillaries! The volume of blood forced through the heart???s aorta (about the diameter of a heavy duty garden hose) is spread so thin among the billions of capillaries that red blood cells must squeeze through in single file like soldiers marching along a path. Distributing the blood flow through such an immense network of vessels is critical so every individual cell maintains a supply line and waste removal system. This and other ???infrastructural challenges??? are the price multi-celled organisms (we humans) pay for our complex organization. Endurance exercise increases the demands on nutrient supply and waste removal, but also stimulates the growth of more capillaries. Endurance training improves the delivery and removal function of this fantastic network of vessels. The total number of capillaries per muscle in endurance-trained athletes is about 40% higher than in untrained persons. Interestingly, this is about the same as the difference in VO2max between well-trained and untrained people. In contrast, strength training tends to decrease the capillary to muscle fiber diameter ratio. This occurs because muscle fibers grow in diameter, but the number of capillaries essentially remains unaltered.

The Motor Unit

A motor unit is the name given to a single alpha motor neuron and all the muscle fibers it activates (neurophysiologists use the term innervates). With 250 million skeletal muscle fibers in the body (give or take a few million), and about 420,000 motor neurons, the average motor neuron branches out to stimulate about 600 muscle fibers. Interestingly, large muscles may have as many as 2000 fibers per motor unit, while the tiny eye muscles may have only 10 or so fibers per motor unit. The size of a motor unit varies considerably according to the muscle???s function. Muscles with high force demands but low fine control demands (like a quadriceps muscle) are organized into larger motor units. Muscles controlling high precision movements like those required in the fingers or the eyes are organized into smaller motor units. The motor neuron branches into many terminals, and each terminal innervates a specific muscle fiber. The motor unit is the brain???s smallest functional unit of force development control; if a motor unit comprising 600 muscle fibers in the left biceps is stimulated, than all 600 of those fibers will contract simultaneously and contribute to the total force produced by the biceps. The brain cannot stimulate individual fibers one at a time. Even for our sophisticated nervous system, that would require far too much wiring.

Regulation of Muscular Force

The brain combines two control mechanisms to regulate the force a single muscle produces. The first is RECRUITMENT. The motor units that make up a muscle are not recruited in a random fashion. Motor units are recruited according to the Size Principle. Smaller motor units (fewer muscle fibers) have a small motor neuron and a low threshold for activation. These units are recruited first. As more force is demanded by an activity, progressively larger motor units are recruited. This has great functional significance. When requirements for force are low, but control demands are high (writing, playing the piano) the ability to recruit only a few muscle fibers gives the possibility of fine control. As more force is needed the impact of each new motor unit on total force production becomes greater. It is also important to know that the smaller motor units are generally slow units, while the larger motor units are composed of fast twitch fibers. The second method of force regulation is called RATE CODING. Within a given motor unit there is a range of firing frequencies. Slow units operate at a lower frequency range than faster units. Within that range, the force generated by a motor unit increases with increasing firing frequency. If an action potential reaches a muscle fiber before it has completely relaxed from a previous impulse, then force summation will occur. By this method, firing frequency affects muscular force generated by each motor unit.

Firing Pattern

If we try and relate firing pattern to exercise intensity, we see this pattern. At low exercise intensities, like walking or slow running, slow twitch fibers are selectively utilized because they have the lowest threshold for recruitment. If we suddenly increase the pace to a sprint, the larger fast units will be recruited. In general, as the intensity of exercise increases in any muscle, the contribution of the fast fibers will increase. For the muscle, intensity translates to force per contraction and contraction frequency/minute. Motor unit recruitment is regulated by required force. In the unfatigued muscle, a sufficient number of motor units will be recruited to supply the desired force. Initially desired force may be accomplished with little or no involvement of fast motor units. However, as slow units become fatigued and fail to produce force, fast units will be recruited as the brain attempts to maintain desired force production by recruiting more motor units. Consequently, the same force production in fatigued muscle will require a greater number of motor units. This additional recruitment brings in fast, fatiguable motor units. Consequently, fatigue will be accelerated toward the end of long or severe bouts due to the increased lactate produced by the late recruitment of fast units.


Specific athletic groups may differ in the control of the motor units. Top athletes in the explosive sports like Olympic weightlifting or the high jump appear to have the ability to recruit nearly all of their motor units in a simultaneous or synchronous fashion. In contrast, the firing pattern of endurance athletes becomes more asynchronous. During continuous contractions, some units are firing while others recover, providing a built in recovery period. Inital gains in strength associated with a weight training program are due to improved recruitment, not muscle hypertrophy.

 

[GFR]

http://muscle.ucsd.edu/musintro/hypertrophy.shtml

Hypertrophy
Hypertrophy, an increase in mass or girth, of a muscle can be induced by a number of stimuli. The most familiar of these is exercise. What happens to a muscle undergoing an exercise program?
Neural Response
The first measurable effect is an increase in the neural drive stimulating muscle contraction. Within just a few days, an untrained individual can achieve measurable strength gains resulting from "learning" to use the muscle.
Genetic Response
As the muscle continues to receive increased demands, the synthetic machinery is upregulated. Although all the steps are not yet clear, this upregulation appears to begin with the ubiquitous second messenger system (including phospholipases, protein kinase C, tyrosine kinase, and others). These, in turn, activate the family of immediate-early genes, including c-fos, c-jun and myc. These genes appear to dictate the contractile protein gene response.
Protein Synthesis
Finally, the message filters down to alter the pattern of protein expression. It can take as long as two months for actual hypertrophy to begin. The additional contractile proteins appear to be incorporated into existing myofibrils (the chains of sarcomeres within a muscle cell). There appears to be some limit to how large a myofibril can become: at some point, they split. These events appear to occur within each muscle fiber. That is, hypertrophy results primarily from the growth of each muscle cell, rather than an increase in the number of cells.

 

[topolo]

The prose were a tad bit pedestrian but overall it was an article of high quality.

 

[GFR]

Muscle Fiber Hypertrophy vs. Hyperplasia:

WHAT IS HYPERPLASIA? Hypertrophy refers to an increase in the size of the cell while hyperplasia refers to an increase in the number of cells or fibers. A single muscle cell is usually called a fiber.
HOW DO MUSCLE FIBERS ADAPT TO DIFFERENT TYPES OF EXERCISE?
If you look at a good marathon runner's physique and compared him/her to a bodybuilder it becomes obvious that training specificity has a profound effect. We know that aerobic training results in an increase in mitochondrial volume/density, oxidative enzymes, and capillary density (27). Also, in some elite endurance athletes the trained muscle fibers may actually be smaller than those of a completely untrained person. Bodybuilders and other strength-power athletes, on the other hand, have much larger muscles (14,40). That's their primary adaptation, their muscles get bigger! All the cellular machinery related to aerobic metabolism (i.e., mitochondria, oxidative enzymes, etc.) is not necessary for maximal gains in muscle force producing power, just more contractile protein. We know that this muscle mass increase is due primarily to fiber hypertrophy; that is the growth of individual fibers, but are their situations where muscles also respond by increasing fiber number?
EVIDENCE FOR HYPERPLASIA
Scientists have come up with all sorts of methods to study muscle growth in laboratory animals. You might wonder what relevance this has to humans. Keep in mind that some of the procedures which scientists perform on animals simply cannot be done on humans due to ethical and logistical reasons. So the more convincing data supporting hyperplasia emerges from animal studies. Some human studies have also suggested the occurence of muscle fiber hyperplasia. I'll address those studies later.
DOES STRETCH INDUCE FIBER HYPERPLASIA?
This animal model was first used by Sola et al. (38) in 1973. In essence, you put a weight on one wing of a bird (usually a chicken or quail) and leave the other wing alone. By putting a weight on one wing (usually equal to 10% of the bird's weight), a weight-induced stretch is imposed on the back muscles. The muscle which is usually examined is the anterior latissimus dorsi or ALD (unlike humans, birds have an anterior and posterior latissimus dorsi). Besides the expected observation that the individual fibers grew under this stress, Sola et al. found that this method of overload resulted in a 16% increase in ALD muscle fiber number. Since the work of Sola, numerous investigators have used this model (1,2,4-8,10,19,26,28,32,43,44). For example, Alway et al. (1) showed that 30 days of chronic stretch (i.e., 30 days with the weight on with NO REST) resulted in a 172% increase in ALD muscle mass and a 52-75% increase in muscle fiber number! Imagine if humans could grow that fast!
More recently, I performed a study using the same stretch model. In addition, I used a progressive overload scheme whereby the bird was initally loaded with a weight equal to 10% of the its weight followed by increments of 15%, 20%, 25%, and 35% of its weight (5). Each weight increment was interspersed with a 2 day rest. The total number of stretch days was 28. Using this approach produced the greatest gains in muscle mass EVER recorded in an animal or human model of tension-induced overload, up to a 334% increase in muscle mass with up to a 90% increase in fiber number (5,8)! That is pretty impressive training responsiveness for our feathered descendants of dinosaurs.
But you might ask yourself, what does hanging a weight on a bird have to do with humans who lift weights? So who cares if birds can increase muscle mass by over 300% and fiber number by 90%. Well, you've got a good point. Certainly, nobody out there (that I know of), hangs weights on their arms for 30 days straight or even 30 minutes for that matter. Maybe you should try it and see what happens. This could be a different albeit painful way to "train." But actually the physiologically interesting point is that if presented with an appropriate stimulus, a muscle can produce more fibers! What is an appropriate stimulus? I think it is one that involves subjecting muscle fibers to high tension overload (enough to induce injury) followed by a regenerative period.
WHAT ABOUT EXERCISE?
The stretch induced method is a rather artificial stimulus compared to normal muscle activity. What about "normal" muscular exercise? Several scientists have used either rats or cats performing "strength training" to study the role of muscle fiber hyperplasia in muscular growth (9,13,17,18,20-22,25,33,34,39,41,42). Dr. William Gonyea of UT Southwestern Medical Center in Dallas was the first to demonstrate exercised-induced muscle fiber hyperplasia using weight-lifting cats as the model (20,21,22). Cats were trained to perform a wrist flexion exercise with one forelimb against resistance in order to receive a food reward. The non-trained forelimb thus served as a control for comparison. Resistance was increased as the training period progressed. He found that in addition to hypertrophy, the forearm muscle (flexor carpi radialis) of these cats increased fiber number from 9-20%. After examining the training variables that predicted muscle hypertrophy the best, scientists from Dr. Gonyea's laboratory found that lifting speed had the highest correlation to changes in muscle mass (i.e., cats which lifted the weight in a slow and deliberate manner made greater muscle mass gains than cats that lifted ballistically) (33).
Rats have also been used to study muscle growth (25,39,47). In a model developed by Japanese researchers (39), rats performed a squat exercise in response to an electrical stimulation. They found that fiber number in the plantaris muscle (a plantar flexor muscle on the posterior side of the leg) increased by 14%. Moreover, an interesting observation has been made in hypertrophied muscle which suggests the occurrence of muscle fiber hyperplasia (13, 17, 28, 47). Individual small fibers have been seen frequently in enlarged muscle. Initially, some researchers believed this to be a sign of muscle fiber atrophy. However, it doesn't make any sense for muscle fibers to atrophy while the muscle as a whole hypertrophies. Instead, it seems more sensible to attribute this phenomenon to de novo formation of muscle fibers (i.e., these are newly made fibers). I believe this is another piece of evidence, albeit indirect, which supports the occurrence of muscle fiber hyperplasia.
EXERCISE-INDUCED GROWTH IN HUMANS
The main problem with human studies to determine if muscle fiber hyperplasia contributes to muscle hypertrophy is the inability to make direct counts of human muscle fibers. Just the mere chore of counting hundreds of thousands of muscle fibers is enough to make one forget hopes of graduating! For instance, one study determined that the tibialis anterior muscle (on the front of the leg) contains approximately 160,000 fibers! Imagine counting 160,000 fibers (37), for just one muscle! The biceps brachii muscle likely contains 3 or 4 times that number!
So how do human studies come up with evidence for hyperplasia? Well, it's arrived at in an indirect fashion. For instance, one study showed that elite bodybuilders and powerlifters had arm circumferences 27% greater than normal sedentary controls yet the size (i.e., cross-sectional area) of athlete's muscle fibers (in the triceps brachii muscle) were not different than the control group (47). Nygaard and Neilsen (35) did a cross-sectional study in which they found that swimmers had smaller Type I and IIa fibers in the deltoid muscle when compared to controls despite the fact that the overall size of the deltoid muscle was greater. Larsson and Tesch (29) found that bodybuilders possessed thigh circumference measurements 19% greater than controls yet the average size of their muscle fibers were not different from the controls. Furthermore, Alway et al. (3) compared the biceps brachii muscle in elite male and female bodybuilders. These investigators showed that the cross-sectional area of the biceps muscle was correlated to both fiber area and number. Other studies, on the other hand, have demonstrated that bodybuilders have larger fibers instead of a greater number of fibers when compared to a control population (23,30,36). Some scientists have suggested that the reason many bodybuilders or other athletes have muscle fibers which are the same size (or smaller) versus untrained controls is due to a greater genetic endowment of muscle fibers. That is, they were born with more fibers. If that was true, then the intense training over years and decades performed by elite bodybuilders has produced at best average size fibers. That means, some bodybuilders were born with a bunch of below average size fibers and training enlarged them to average size. I don't know about you, but I'd find that explanation rather tenuous. It would seem more plausible (and scientifically defensible) that the larger muscle mass seen in bodybuilders is due primarily to muscle fiber hypertrophy but also to fiber hyperplasia. So the question that needs to be asked is not whether muscle fiber hyperplasia occurs, but rather under what conditions does it occur. I believe the the scientific evidence shows clearly in animals, and indirectly in humans, that fiber number can increase. Does it occur in every situation where a muscle is enlarging? No. But can it contribute to muscle mass increases? Yes.
HOW DOES MUCLE FIBER HYPERPLASIA OCCUR?
There are two primary mechanism in which new fibers can be formed. First, large fibers can split into two or more smaller fibers (i.e., fiber splitting) (6,25,39). Second satellite cells can be activated (11,16,17,43,44).
Satellite cells are myogenic stem cells which are involved in skeletal muscle regeneration. When you injure, stretch, or severely exercise a muscle fiber, satellite cells are activated (16,43,44). Satellite cells proliferate (i.e., undergo mitosis or cell division) and give rise to new myoblastic cells (i.e., immature muscle cells). These new myoblastic cells can either fuse with an existing muscle fiber causing that fiber to get bigger (i.e., hypertrophy) or these myoblastic cells can fuse with each other to form a new fiber (i.e., hyperplasia).
ROLE OF MUSCLE FIBER DAMAGE
There is now convincing evidence which has shown the importance of eccentric contractions in producing muscle hypertrophy (15,24,45,46). It is known that eccentric contractions produces greater injury than concentric or isometric contractions. We also know that if you can induce muscle fiber injury, satellite cells are activated. Both animal and human studies point to the superiority of eccentric contractions in increasing muscle mass (24,45,46). However, in the real world, we don't do pure eccentric, concentric, or isometric contractions. We do a combination of all three. So the main thing to keep in mind when performing an exercise is to allow a controlled descent of the weight being lifted. And on occasion, one could have his/her training partner load more weight than can be lifted concentrically and spot him/her while he/she performs a pure eccentric contraction. This will really put your muscle fibers under a great deal of tension causing microtears and severe delayed-onset muscle soreness. But you need that damage to induce growth. Thus, the repeated process of injuring your fibers (via weight training) followed by a recuperation or regeneration may result in an overcompensation of protein synthesis resulting in a net anabolic effect (12,31).
HAS THE DEBATE BEEN SETTLED?
In my scientific opinion, this issue has already been settled. Muscle fiber hyperplasia can contribute to whole muscle hypertrophy. There is human as well as rat, cat, and bird data which support this proposition (1-3,5-8,13,17,20-22,25,29,35,37,47), a veritable wild kingdom of evidence. Does muscle fiber hyperplasia occur under all circumstances? No. There are several studies which show no change in fiber number despite significant increases in muscle mass (4,18,19,23,26,30,36,41). Is it possible that certain muscles can increase fiber number more so than others? Maybe. Can any Joe Schmoe off the street who lifts weights to get in better shape increase the number of fibers for instance in their biceps? Probably not. What about the elite bodybuilder who at 5'8" tall is ripped at a body weight of 250 lbs.? Are his large muscles purely the result of muscle fiber hypertrophy? I think it would be extremely naive to think that the massive size attained by elite bodybuilders is due solely to fiber hypertrophy! There is nothing mystical about forming new muscle fibers. Despite the contention that fiber number is constant once you're born (18,19), we now have an abundance of evidence which shows that muscle fiber number can increase. Besides, there is nothing magical at birth which says that now that you're out of the womb, you can no longer make more muscle fibers! A mechanism exists for muscle fiber hyperplasia and there is plenty of reason to believe that it occurs. Of course, the issue is not whether fiber number increases after every training program, stress, or perturbation is imposed upon an animal (or human). The issue is again, under which circumstances is it most likely to occur. For humans, it is my speculation that the average person who lifts weights and increases their muscle mass moderately probably does not induce fiber hyperplasia in their exercised muscle(s). However, the elite bodybuilder who attains the massive muscular development now seen may be the more likely candidate for exercise-induce muscle fiber hyperplasia. If you are interested in a comprehensive scientific treatise on this subject, read a scientific review article that I wrote a few years ago (7).






http://home.hia.no/~stephens/hypplas.htm

 

[assassin]

i'm too lazy to read all this but i'll save it and readed later .... thnx foreman for those nice posts

 

[GFR]

i'm too lazy to read all this but i'll save it and readed later .... thnx foreman for those nice posts