ARTICLES: Physiology Related by Casey Butt

  1. Post ARTICLES: Physiology Related Articles by Casey Butt

    Casey Butt was a scientific-minded bodybuilder/researcher and for several years wrote for bodybuilding and strength training magazines such as HARDGAINER and MILO. He was different than many in that he seriously scrutinized medical, physiological and metabolism journals biochemistry, kinesiology, biomechanics and medical texts and books for anything relevant to weight training. He started his own now defunct publication "The WeighTrainer" from which the following articles are taken. They are physiology related and are a prelude to his training articles, with the original images reconstructed as only the text was cached by The Internet Wayback Machine.

    The articles posted here are Physiology Related:

    1. The Neuromuscular System Part I: What A Weight Trainer Needs To Know About Muscle
    2. The Neuromuscular System Part II: What A Weight Trainer Needs To Know About Muscle
    3. The Neuromuscular System Part III: What A Weight Trainer Needs To Know About The Nervous System
    4. Failure: Muscular Fatigue During Weight Training
    5. Muscular Growth: How Does A Muscle Grow?
    6. Muscular Growth Part II: How Does A Muscle Grow?

    In addition seven Basic Training Related articles (as well as a FAQ) were meant to be read after these are posted here at:

    Also practical training routines built from the application of the physiology knowledge related in the articles contained herein and upon concepts discussed in the Basic Training Related articles are conveyed in Casey's Training Related - Making A Strength/Size Routine series posted at:

  2. Post The Neuromuscular System Part I

    The WeighTrainer
    The Neuromuscular System Part I:
    What A Weight Trainer Needs To Know About Muscle

    First off, let me say that you don't need to know much (if any) of muscle physiology in order to get bigger and stronger. In fact, most people who have succeeded at weight training did so completely ignorant of these things. When you're dealing with the nitty-gritty of science there often comes a point where people get bogged down in the details and ignore what's really important - they can't see the forest for the trees as they say. After all, what matters is results. And while I believe that there sometimes is a lot to be said for 'just doing it', you can't make intelligent decisions based upon ignorance of the facts. There's an old saying that goes, "know thine enemy". Well, that applies here. Maybe you don't see the weights themselves as the enemy, but stagnation and frustration certainly are - as are the people out there who are peddling unsound weight training theories and useless supplements. Remember - as Mike Mentzer is fond of pointing out - too many people get caught up in mysticism when it comes to weight training.

    Before you can really identify the necessary training elements to produce muscle growth and strengthening you need to understand at least some basics of how muscles are structured and how they work. I realize that for a lot of you this constitutes boring stuff, but it really is useful and necessary knowledge for analyzing the merits (or lack thereof) of training theories and certain nutritional supplements. I'll keep it as simple and brief as possible, without leaving any information relevant to weight training out.

    Muscle Physiology and Contraction - The Sliding Filament Theory

    Muscle cells are arranged in bundles, running lengthwise in the muscle, called fasciculi. Each fasciculus is surrounded by a sheath of connective tissue called a perimysium. It is the function of the perimysium to keep all the muscle cells 'in place' as such. Groups of fasciculi are what make up the muscle itself, which is in turn contained by a sheath of connective tissue called the fascia (or epimysium). Each muscle is surrounded by its own fascia, this keeps each muscle distinct within its own 'bag' (as the fascia is commonly referred to as). The fascia also acts as a 'girdle' for the muscle, causing it to assume its shape. This can all be seen in the illustration below.

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    Image of the Structure of Skeletal Muscle
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    Within each muscle cell (also referred to as a muscle fiber) are structures called myofibrils. Myofibrils are, among other things, made up of tiny units called sarcomeres. These sarcomeres are the smallest structures in a muscle that can contract; they are long filament-like structures, arranged in series - end to end - which run lengthwise in the myofibril. Within the sarcomeres are two types of protein filaments - actin and myosin - running lengthwise, parallel to each other. The myosin filaments have 'cross-bridges' across to the actin filaments which, during contraction, allow them to bond with the actin filaments. The source of energy for this bonding is the molecule adenosine triphosphate (ATP). During the bonding, energy is released by the breaking down of ATP into adenosine diphosphate (ADP) and Pi at another site - the ATPase site - on the myosin cross-bridge (by the action of the enzyme ATPase). This provides the energy which produces a swiveling action, pulling the actin filaments closer to the centre of the sarcomere - overall, making the muscle shorten. The ATPase site on the myosin cross-bridge must pick up another ATP molecule if it is to repeat the swiveling action further. A full muscular contraction requires many repeated such picking up and 'splitting' of ATP throughout the sarcomeres. A simple animation depicting the sliding filament theory can be seen below.

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    The Sliding Filament Theory of Muscular Contraction
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    For some degree of completeness, it should be mentioned that this cross-bridge swiveling takes place at different times along the same sarcomere - if all cross-bridges were released at the same time the actin filaments would slide back to their original, uncontracted positions. It is also worthy of note that contractile machinery comprises about 80% of muscle fibre volume. The rest of the volume is accounted for by tissue that supplies energy to the muscle or is involved with the neural drive.

    Some Basic Neuromuscular Physiology

    Muscle fibers are stimulated by the nervous system by way of alpha motor neurons. Each neuron may control only several muscle fibers or as many as a thousand or more. Each muscle fiber, however, is innervated by only one neuron. A neuron and the fibers it innervates are referred to as a motor unit. All of the muscle fibers in a motor unit (stimulated by the same neuron) tend to be of the same fiber type (more on fiber types later). You may have heard of the 'all-or-none' theory in regards to this subject. It states that all of the fibers in a motor unit must fire or none of them, although this may not be 100% true in certain cases (such as fatigue).

    How does the neuron 'innervate' it's associated muscle fibers? Well, the neuron 'connects' to the fibers at their center (their length-wise center). To innervate them they transmit an electric current to the fibers, which travels out from the center of the fibers to their ends, thus setting off a contraction. This process will be covered in more detail in Part III of this series.

    Muscle Firing Patterns

    Muscle Fibers have two recruitment patterns. In the first pattern, units that innervate the same types of fibers are recruited at different times, so that some units are resting (recovering) while others are firing. Obviously, at high loads this pattern isn't possible because all available motor units will have to be fired at the same time to lift the load. In the second pattern, motor units that are more fatigue resistant are recruited before fibers that are more rapidly fatigued.

    Muscle Fiber Types

    Striated skeletal muscle - the kind we're concerned with - comes in three basic fiber types (some experts will refer to further types of muscle fibers but they are really only a continuation of the continuum that the three basic types represent). They are:

    Type I: slow twitch (ST), slow oxidative (also called red fibers)

    Type IIA: fast twitch (FT), fast oxidative (also called white fibers)

    Type IIB: fast-glycolytic (a kind of white FT fibers)

    FT fibers have higher myosin ATPase activity rates than ST fibers. This allows them to release energy more quickly and deliver more power than ST fibers (even if the ST fibers were the same size as the FT ones). FT fibers are also larger in diameter because of higher concentrations of actin and myosin filaments within them as compared to ST fibers. This further allows them to develop more force. ST fibers have greater intramuscular triglyceride stores (for sustained energy), more aerobic enzyme activity, more of a substance called myoglobin (which is instrumental in the process of using oxygen to create energy), greater mitochondrial density (mitochondria manufacture about 95% of the ATP that exists in muscle tissue) and greater capillary density.

    For the above reasons:

    FT fibers are best suited to generating large amounts of force over a short period and are very sensitive to fatigue.
    ST fibers are best suited to low-load, long duration activities.

    Of the FT fibers, type IIAs have both good anaerobic and aerobic qualities. They have high ATPase activity like fast-glycolytic (IIB) fibers, but also a high oxidative capacity like type I fibers. Because of this, they can maintain a contraction longer than type IIBs, but contract faster (thus developing more power) than type Is. Type IIBs do not exhibit this duality and are poor performers aerobically but very well equiped for anaerobic activities. They can,consequently, develop even more short-burst power than the IIAs. Both types of FT fibers have significantly larger innervating neurons than STs and, therefore, have higher activation thresholds than STs. They are activated only after the STs have been fired, but they can twitch faster and more often. FT fibers are brought into play by either the effort to more a heavy load or by the need to move an object faster than is possible with ST fibers. Type IIB fibers can twitch three times faster (and therefore, more often) than ST fibers. Type IIAs can also twitch faster and more often than ST fibers. Because of this, and the recruitment pattern, a FT fiber may begin its contraction after a ST fiber but actually finish at the same time or before. This leads to another contributor to the FT fibers abilities to produce greater force - their enhanced frequency of firing. Because they complete the firing sequence more quickly they can fire more often than ST fibers, thus developing more tension.

    NOTE: Because of the differing activation thresholds of the different types of fibers, type II fibers may be referred to as 'high-threshold' fibers and type I fibers as 'low-threshold' fibers in future references on this site.

    The force developed by a muscle is largely determined by the number of fibers that are forced to contract. The more units contracting, the more force developed. In addition, as effort fractionally increases, so does the frequency of firing of each motor unit. A sudden increase in force requirement is met by the recruitment of more motor units. So, on a very fundamental level, lifting heavy weights recruits more muscle fibers than lifting light weights. And as the weight then gets progressively heavier these fibers will fire more frequently to meet the force requirements.

    To clarify things, let's look at a typical Bodybuilding-type strength training set - let's say we do 8-12 reps (it doesn't really matter about the exact number). During the first rep only a proportion of the IIA fibers are recruited, and none of the IIBs. During the second rep other IIA fibers are recruited while the ones used during the first rep rest. After a few reps, continuing in this pattern, all the IIAs start to fatigue (they don't get quite long enough rest periods between recruitments). When this happens some of the IIBs are called in to meet the force requirements. The IIBs don't twitch at maximum frequency, however - they don't have to in order to generate the forces necessary. Eventually, all the available IIBs (and IIAs) are recruited but they still don't have to twitch at their maximum frequency. By the end of the set all available fibers in the muscle are being fired as fast as possible - the problem is the IIBs and IIAs are not capable of firing at their maximum frequencies now because they are fatigued (and so is the nervous system from having to control all of this muscular activity). Think about it - that's why you're weaker at the end of a set than you were when you started - no matter how hard you try. NOTE: This example isn't entirely accurate because typical Bodybuilding sets, in the 8-12 rep range, usually result in all of the available fibers (IIAs and IIBs) being recruited right from the first rep, with the IIBs not firing at maximum frequency - it does serve to illustrate the basic process, however.

    Muscle Size

    Overall muscle size is determined primarily by the size of the individual fibers within the muscle. It's also true that the genetically set number of muscle cells within a muscle also affect the overall size of a muscle, but this is to a much lesser extent. It is only under extreme circumstances does the body increase the actual number of fibers within a muscle (hyperplasia) - not the kind of circumstances that you would want to replicate in your regular weight training. Muscle biopsies of serious weight trainers have shown that it was the size of the individual fibers within their muscles that was responsible for the abnormal muscle size and not the actual number of muscle fibers present.

    Muscle's Optimal Length for Generating Force

    Particularly relevant to muscle building is the fact that each muscle fiber has an ideal length at which it generates maximum force when contracting. The force generated is directly influenced by the amount of elogation (contraction or extension) that the fiber is under at the start of the contraction. Going back to the sliding filament theory, this optimum length is the point at which the actin and myosin filaments line up in such a way that allows maximum cross-bridge formation. When the muscle cell is extended more than this the actin filaments cannot make contact with as many myosin cross-bridges - they have slid past each other, so to speak. (Take another look at the The Sliding Filament Theory of Muscular Contraction animation above - the "% Tension Developed" meter gives you an idea of what's going on.) When the muscle cell is contracted to a shorter length than optimal, less force can be developed for a few reasons (the animation doesn't "contract" far enough to show this). For one, the normal chemical processes taking place within the fiber become altered so that fewer actin cross-bridge attachment sites are uncovered and available for cross-bridging (the reason this happens is unknown at present). In addition, filaments from the opposite ends of the sarcomere overlap and cover some actin cross-bridge attachment sites, further reducing the number of possible cross-bridges. Still further, the myosin filaments come up against the ends of each individual sarcomere (what's referred to as the z-lines), impeding any further shortening.

    So what is a muscle's optimum length for generating force? Well, generally, it's the length of the overall muscle when most of the cells are at their optimal lengths for producing maximum tension. This usually corresponds to the length of the muscle when it is elongated a little bit past it's natural, relaxed state. How much strength is lost when the muscle contracts at some other length than optimum? Well, at the extreme points of a muscle's extension or contraction (extended ~30% longer and contracted ~30% shorter than optimal) a muscle has the ability to contract only ~50% as forcefully as it can at the optimal length. Keep in mind, though, that you may still demonstrate more strength in these positions (usually in the contracted position) than at the position of optimal muscular force because of mechanical factors such as leverage. The muscle itself, however, will be contracting with less force.

    In Part II of this series we'll take a closer look at the structure and differences between the muscle fiber types and look at some of the basic biochemistry involved in producing muscular energy. Stick with me.

  3. Post The Neuromuscular System Part II

    The WeighTrainer
    The Neuromuscular System Part II:
    What A Weight Trainer Needs To Know About Muscle

    The Energy for Muscular Contractions

    There is only one source of energy for muscular contractions: ATP. Energy, to power muscular contraction, is released when ATP is broken down to adenosine diphosphate (ADP) and phosphate (Pi). The body has several different paths by which it produces ATP; and it is vitally important for the body to have these ATP production mechanisms because only a very small amount of ATP can be stored in the muscle (enough for only a few seconds of maximum muscular effort). For this reason, ATP must be supplied to the muscles on a continuous basis during muscular exertion. There are three ways by which the body produces ATP, all of which take place predominantly at the mitochondria.
    They are:

    by the phosphagen system - the chemical breakdown of phosphocreatine (PC) - an anaerobic mechansim

    by anaerobic glycolysis - an anaerobic mechanism

    by oxidative phosphorylation (Kreb's cycle and electron transport) - an aerobic mechanism

    The phosphagen system: PC is stored in the muscle. A rested muscle contains ~5 times as much PC as it does actual ATP. When PC is broken down, the energy released is used to recombine Pi and ADP to form ATP again. This process can happen in merely a fraction of a second, and so provides a source of quickly replenishable energy. Because of the nature of this mechanism, ATP stores remain fairly constant during the early stages of muscular contraction, but PC stores get depleted. As contraction continues, there is not enough PC left to continue fueling the ADP -> ATP conversion and ATP stores get depleted also. This, along with the influence of some other occurances, brings a cease to muscular contraction. In total, within 30 seconds or less of maximum muscular contraction the ATP and PC stores in the muscle are exhausted. It should be noted that the phosphagen system provides the largest power source of any muscular energy mechanism.

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    As you can probably figure out, the phosphagen system is the primary energy source for short-term, high-intensity work, such as heavy weight training.
    NOTE: PC stores cannot be used to provide energy for long-term, low-intensity work.

    Anaerobic glycolysis: Glycogen (the form of glucose that is stored in muscle) is broken down to provide the energy for ATP formation and and also the formation of pyruvic acid. Additionally, some blood glucose may be used in this process, along with the intramuscular glycogen. One of the end products of this mechanism is lactic acid, which is made by the eventual conversion of pyruvic acid.

    This mechanism can provide more total energy than the phosphagen system, but not as quickly. This being the case, anaerobic glycolysis is the major energy pathway for muscular contractions lasting from ~30 to ~60 seconds.

    The effects that the lactic acid (which is produced during this process) has on muscular contraction must be considered here. Lactic acid build-up in the muscle cells makes the interior of the muscle more acidic. This acidic environment interferes with the chemical processes that expose actin cross-bridging sites and permit cross-bridging. It also interferes with ATP formation. So, these factors, along with depleted energy stores, cause the muscle fibers to become fatigued and contraction to cease. Contrary to what was once believed, lactic acid does not cause delayed onset muscle soreness (the soreness that you feel in an exercised muscle the next day or so). High lactic acid concentration does, however, cause pain in motor nerve endings during muscular contraction.

    Oxidative phosphorylation: In this mechanism the body metabolizes carbohydrates and fats (and protein when under starvation conditions or during very long duration exercise sessions) to create energy. Carbohydrates are used more extensively during intense aerobic work (at near 100% capacity levels carbohydrates are used almost exclusively as the energy source) and fats become the primary energy source during low-intensity, long duration exercise sessions. The process of energy release from these substrates is much more complex than we need to get into, and as this process is the least crucial for most weight training activities, it will suffice to say that they require oxygen. Hence, your breathing rate increases during aerobics.

    This mechanism provides virtually endless amounts of energy (well, until you collapse) as your body will actually begin to cannibalize itself in order to keep the process going. It does, however, require time and so is not a major player in supplying energy for intense muscular contractions.

    As was mentioned above, certain fiber types are optimized to utilize each of these energy production mechanisms.

    Type Is (slow twitch (ST), slow oxidative - called red fibers) utilize primarily the oxidative phosphorylation mechanism.
    Type IIAs (fast twitch (FT), fast oxidative - called white fibers) utilize both the phosphagen system and the anaerobic glycolysis mechanisms primarily.
    Type IIBs (fast-glycolytic - a kind of white FT fiber) utilize primarily the phosphagen system.

    It should also be noted that all three of these mechanisms begin at the start of muscular contraction, but because of their natures, and the natures of the muscle fibers being used for the activity, they only become prominent during the time frames given above. This is illustrated in the graph below.

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    Time Course of Contributions from Different Energy Sources
    Taken from Gleim, Anaerobic Testing and Evaluation, Med Exerc Nutr Health 1993;2:27-35
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    ATP Replenishment

    Oxygen is not only used during the processes of oxidative phosphorylation. It is also required in mechanisms which replenish ATP, PC and glycogen. This is one of the reasons why, even if you only do lows reps, you breath heavy between sets of Squats (or any other exercise that utilizes a lot of muscle mass). ATP replenishment occurs roughly in the time frames presented below.

    ATP replenishment times
    time since activity ended - percentage of ATP replenished
    20 sec 50.00 %
    40 sec 75.00 %
    1 min 87.50 %
    80 sec 93.75 %
    100 sec 96.88 %
    2 mins 98.44 %
    140 sec 99.22 %
    160 sec 99.61 %
    3 min 99.81 %

    These times assume that the fibers recovering are at rest. If you do anything during this period that depletes ATP then the process would be impaired and the time needed for replenishment lengthened.

    If the activity that the muscles were doing generated a lot of lactic acid (anaerobic glycolysis mechanism) - such as intense weight training in the 12 rep and above range - then light activity of the muscles during the replenishment period may actually be of benefit. This is because some of the lactic acid would be used to fuel the light activity and, hence, the activity would help clear lactic acid from the muscle. Care must be taken, though, to ensure that this light activity is not intense enough to require the use of the phosphagen or anaerobic glycolysis mechanisms for energy - this would deplete ATP as warned of above.

    Once glycogen stores in the muscle are depleted (from prolonged anaerobic glycolysis) they may take several days to be restored. As this is getting into the realm of nurition, the subtleties of the practice of replenishing glycogen between weight training sessions will be covered in an article on the 'Nutrition And Supplementation Articles' page.

    In Part III of this series we'll take a look at the nervous system and the processes that occur to 'set off' a muscular contraction.
  4. Post The Neuromuscular System Part III

    The WeighTrainer
    The Neuromuscular System Part III:
    What A Weight Trainer Needs To Know About The Nervous System

    Neuromuscular Physiology

    Starting with a section from the Part I of this series:

    Muscle fibers are stimulated by the nervous system by way of alpha motor neurons. Each neuron may control only several muscle fibers or as many as a thousand or more. Each muscle fiber, however, is innervated by only one neuron. A neuron and the fibers it innervates are referred to as a motor unit. All of the muscle fibers in a motor unit (stimulated by the same neuron) tend to be of the same fiber type (more on fiber types later). You may have heard of the 'all-or-none' theory in regards to this subject. It states that all of the fibers in a motor unit must fire or none of them, although this may not be 100% true in certain cases (such as fatigue).

    How does the neuron 'innervate' it's associated muscle fibers? Well, the neuron 'connects' to the fibers at their center (their length-wise center). To innervate them they transmit an electric current - called the 'action potential' - to the fibers, which travels out from the center of the fibers to their ends, thus setting off a contraction...

    So how does all this happen? Let's take a closer look.

    Anatomy of a Neuron

    All nerve cells (called 'neurons') outside the central nervous system (the brain and spinal cord) are made up of large cell bodies and single, elongated extensions (called 'axons'), for sending messages. Many neurons within the central nervous system also have this configuration. At the end of these axons are 'axon terminals' which are the point of release of chemicals that transmit impulses across to other cells (i.e. other neurons or muscle cells). Motor neurons connect your spinal cord to your muscles and can, therefore, have very long axons (as much as 1 m long and only a few micrometers in diameter). There is a steady transport of materials (e.g. vesicles, mitochondria, etc) from the 'cell body' (which houses the nucleus as well as other organelles) along the entire length of the axon to the axon terminals.

    In many neurons, nerve impulses are generated in short branched fibers called 'dendrites' and also in the cell body. These impulses are then conducted along the axon, which usually branches several times close to its end for the purpose of innervating several other cells.

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    The Resting Potential

    All cells (not just the neurons) have a resting potential - an electrical charge across their surface membranes (called the 'plasma membrane'). To produce this the interior of the cell is maintained with a negative charge with respect to the exterior. The size of this resting potential varies with cell type, but in neurons it is about -70 milliVolts (mV) and about -95 mV in muscle cells.

    The resting potential is generated and maintained in two ways:

    1. The Sodium/Potassium ATPase Pump: There is, typically, a 20 times higher concentration of positively charged potassium ions (K+) inside the cell than outside the cell (in the extracellular fluid). Conversely, the extracellular fluid contains a concentration of positively charged sodium ions (Na+) as much as 10 times greater than that within the cell. These concentration gradients are maintained by the active transport of both ions back and forth across the plasma membrane by the Na+/K+ ATPase transporter system. It transports 3 Na+ ions out of the cell for each 2 K+ ions pumped in (using energy produced from the breakdown of ATP to fuel the process).

    As an aside: Besides just maintaining the cell's resting potential, this Na+/K+ balance has another function - of interest primarily to Bodybuilders. The accumulation of sodium ions outside of the cell draws water out of the cell and thus enables it to maintain osmotic balance. This is why excessively high sodium levels in the blood make you hold water and look 'smooth'. Potassium has the opposite effect, so the two are often manipulated by Bodybuilders prior to physique competitions.

    2. Facilitated diffusion of K+ out of the cell: Some potassium channels in the plasma membrane are 'leaky', allowing a slow diffusion of K+ out of the cell.

    Depolarization and the Action Potential

    Certain stimuli can cause the Na+/K+ balance across the plasma membrane to change. By far, the most significant of these stimuli are 'neurotransmitters' (chemicals which transmit neural stimulation across the gap between neurons and other excitable cells) such as acetylcholine (ACh). These neurotransmitters cause Na+ channels on the plasma membrane to open and Na+ to 'rush' into the cell. This, in turn, causes the electric potential across the plasma membrane to decrease, and if it decreases enough (i.e. reaches the 'threshold voltage') an 'action potential' is generated in the cell. Electrically, this changing of the cell's resting potential is called 'depolarization'.

    It should be mentioned that certain mechanical stimuli, such as stretching, can also cause Na+ channels to open, thereby setting off an action potential. This helps form the basis (along with some other factors) of what is often called the 'stretch reflex' or 'myotatic reflex' in muscular contraction. Some strength training authors recommend exploiting this reflex to recruit 'more muscle fibers' - this will be examined in an article on the 'Training Related Articles' page of The WeighTrainer.

    The Action Potential: If depolarization at a spot on the cell reaches the threshold voltage hundreds of sodium channels open in that portion of the plasma membrane. And, even though the channels only remain open for a millisecond (the enzyme acetylcholinesterase quickly breaks down the ACh in the neuromuscular junction, thus allowing the Na+ channels to close again), thousands of Na+ ions rush into the cell. This sudden complete depolarization of the plasma membrane opens up the voltage-gated sodium channels in adjacent portions of the membrane and a 'wave' of depolarization sweeps along the cell. This, in fact, is what is called the 'action potential' (in neurons it may also be called the 'nerve impulse').

    The Refractory Period: Another stimulus applied to a neuron (or muscle fiber) cannot trigger another impulse until a sufficient time has passed so that the resting potential can be restored in the plasma membrane. During that 'refractory' period the membrane is depolarized and the Na+/K+ ATPase Pump works to restore the Na+/K+ charge balance. This repolarization processes is initiated by the facilitated diffusion of K+ ions out of the cell. Then, when the neuron is fully rested, the sodium ions that came in during the impulse are actively transported back out of the cell.

    As was eluded to in Part I of this series, this process of depolarization and repolarization can occur much more rapidly in type II fibers than in type I fibers - leading to a much faster twitch rate in the former. In essence, this is why type II fibers are often referred to as 'fast twitch' and type Is as 'slow twitch'.

    Each cell type has only one 'strength' of action potential. This means that as long as the threshold potential of the cell is reached, 'strong' stimuli will produce no stronger action potentials than 'weak' ones. This is what is referred to as the 'all-or-none' principle (and, no, I don't believe Weider has grabbed that one yet). The difference in stimuli strength is reflected by the frequency of the action potentials that it generates. This explains why fractional increases in muscular tension requirements are met by the muscles twitching faster (as was covered in Part I of this series).

    Skeletal Muscle Motor Neurons Are 'Myelinated'

    The axons of skeletal muscle motor neurons are encased in a fatty sheath called the 'myelin sheath' (it is actually the greatly expanded plasma membrane of an accessory cell called the 'Schwann cell'). Where the sheath of one Schwann cell meets the next, the axon is unprotected. The voltage-gated sodium channels of myelinated neurons are confined to these spots (called 'nodes of Ranvier').

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    The inrush of sodium ions at one node creates just enough depolarization to reach the threshold of the next. In this way, the action potential jumps from one node to the next. This results in much faster propagation of the nerve impulse than is possible in nonmyelinated neurons.

    Other Factors

    There are other ions that can influence plasma membrane charge balance (most notably chloride - Cl-) and, therefore, affect resting and action potential. Certain neurotransmitters actually inhibit the transmission of nerve impulses by opening chloride ion channels that allow these negatively charged ions to enter the cell. These neurotransmitters may also open K+ channels, allowing potassium ions to 'leak' out. The overall result is a state of enhanced plasma polarization called 'hyperpolarization'. In this state the action potential is 'further away' from the resting potential because the resting potential has increased, thus a stronger stimulus is needed to reach the threshold.

    The Synapse

    Since the junction between the axon terminals of a neuron and other receiving cells (i.e. muscle cells or other nerve cells) is of such importance for transmission of impulses, let's take a closer look at that junction - called the 'synapse'. For future possible reference, synapses at muscle fibers are called 'neuromuscular junctions' or 'myoneural junctions'.

    Each axon terminal is swollen into a knob containing membrane-bounded 'vesicles' which store neurotransmitters. When an action potential arrives calcium ion (Ca++) channels open in the plasma membrane and trigger some of the vesicles to fuse with the outer cell wall and release their neurotransmitter into the synaptic cleft. These neurotransmitter molecules then bind to receptors on the postsynaptic membrane (which could be the plasma membrane of a muscle cell, for instance), thereby setting of a process of Na+/K+ diffusion and depolarization of the postsynaptic membrane. For a muscle cell this would result in contraction. It should also be mentioned here that the terminal vesicles of motor neurons always cantain the neurotransmitter acetylcholine (ACh).

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    Ship to Shore: From Excitation to Contraction

    In resting muscle fibers, an intracellular organelle called the 'sarcoplasmic reticulum' stores calcium ions (Ca++). Spaced along the plasma membrane of the muscle fiber (called the 'sarcolemma') are depressions in the membrane that 'plunge' into the muscle cell called 'T-tubules'. These T-tubules (collectively called the 'T System') terminate near the calcium-filled sacs of the sarcoplasmic reticulum. Each action potential created at the neuromuscular junction travels along the sarcolemma, down into the T-tubules and innervates the sarcoplasmic reticuli - thus triggering them to release their Ca++ into the interior of the cell. The Ca++ then diffuses among the actin and myosin filaments of the sarcomeres where it binds to the protein troponin. This is of extreme importance in creating a muscular contraction because, under resting conditions, there is a troponin-tropomyosin (a special protein complex) barrier that 'covers' the cross-bridge sites (by binding to actin) thus preventing contraction from taking place. Ca++ changes the shape of this troponin-tropomyosin barrier, thereby allowing for cross-bridges to be formed. Without this action the myosin cross-bridges would not be able to make binding contact on the actin filaments. In this way, Ca++ plays the active role in muscle contraction because it 'turns on' the interaction between actin and myosin.

    Because of the speed of the action potential (milliseconds), the action potential arrives virtually simultaneously at the ends of all the tubules of the T system, ensuring that all sarcomeres contract in unison. When the process is over, the calcium is taken back into the sarcoplasmic reticulum by way of what is called the Ca++/ATPase Pump (or the Ca-Pump).

    The Wrap-Up

    So there you have it. Just about everything you need to know about neuromuscular physiology. If you made it through you've probably learned a few things that you can put in the context of your own training already (unless you already knew this stuff). If not, then this stuff will be referenced heavily in other articles on the 'Training Related Articles' and 'Nutrition And Supplementation Articles' pages. If you really don't take to the scientific side of weight training don't worry, you didn't read all that scientific mumbo-jumbo for nothing - it'll be used in other articles to put together, and make sense of, weight training and nutrition and supplementation practices.

    NOTE: The information that has been presented here is by no means extensive. Believe me, you can go a lot deeper into this stuff than I have. What I tried to do is present what is relevant to weight training from a weight training perspective. Also, it should be realized that the sum of our knowledge today is hopefully smaller than what the sum of our knowledge will be tomorrow, so new facts and understandings may come along that shed a whole new light on things.
  5. Muscular Fatigue During Weight Training

    The WeighTrainer
    Muscular Fatigue During Weight Training

    In this article we're going to take an in-depth look at the physiological reasons why a muscle fatigues. Why is this important? Because, if we understand what causes a muscle to fail we can understand whether or not training to failure is actually an effective training 'technique'. We can also gain a perspective on how intensely we should, in fact, be training. Maybe we can even gain a small glimpse into such things as ideal training volume and frequency. So, like other articles on the 'Physiology Related Articles' page, this stuff can be pretty dull (for some) but it can also be very useful.

    Our focus here will be on the muscular and neural fatigue that occurs when training in the strength training rep range (1-20). Fatigue may occur in the higher rep ranges for reasons other than those that will be dealt with in this article.

    Lactic Acid Accumulation

    As was covered in the The Neuromuscular System Part II: What A Weight Trainer Needs To Know About Muscle article, lactic acid build-up in the muscle cell (due to repeated muscular contractions) causes a reduced intracellular pH that affects force development. This occurs largely because lactic acid accumulation leads to increased intracellular hydrogen ion (H+) concentrations (most of the lactic acid dissociates into H+ and lactate) - and H+ is thought to be a competitive inhibitor of Ca++ binding to troponin. When this happens, fewer actin molecules are 'exposed' to the myosin heads for cross-bridging. Of course, this leads to a weaker contraction. Note that this appears to affect Type II fibers more than Type I. As was also mentioned, lactic acid (actually the H+ produced from lactic acid) also interferes with ATP formation (inteferes with the glycolysis process). This means that less ATP will be around to actually 'fuel' contractions - potentially leading to further weakening.

    For you biochemistry buffs, increased H+ interferes with glycolysis by decreasing the transformation of 'phosphorylase b' to the active 'a' form, and also inhibits phosphofructokinase (PFK).

    All this would be a strong factor in work that utilizes the anaerobic glycolysis mechanism of energy production - especially work in the 8 - 15 rep range. So that 'burn' you get when doing higher reps and pushing close to failure may actually be the reason that you're failing and not just a side effect.

    Shortage of ATP

    Declining intramuscular ATP is thought to be a major cause of fatigue during high intensity exercise. However, numerous studies have demonstrated that ATP concentrations fall to no less than ~70% of pre-exercise levels during high-intensity exercise. This would seem to imply that ATP shortage is not a major cause of muscle fatigue.

    The rebuttal to this argument lies in the speculation that 70-80% of the sarcoplasmic ATP is restricted to the mitochondria and is, in fact, unavailable for cross-bridging. This would mean that while sufficient ATP is actually inside the cell, it is not located where it could be used to 'fuel' muscle contraction. So high intensity exercise may cease due to ATP depletion in the specific areas of cross-bridging, but total sarcoplasmic ATP concentrations may still remain relatively high (at ~70%). This is the 'ATP compartmentalization' hypothesis of muscle fiber fatigue.

    There are, of course, worthy arguments against this hypothesis, though. So, let's just say the jury's still out on whether declining ATP levels, themselves, are significant contributors to muscular fatigue during 'normal' conditions. I make the qualification of 'normal' conditions because low intramuscular ATP and/or glycogen levels at the onset of exercise will result in a loss of strength due to low or declining ATP concentrations. In this case there just isn't enough 'gas in the tank' to begin with. This condition can be brought on by overtraining (too much volume or too frequent training) or by insufficient carbohydrates in the diet or impairment of their utilization (such as in insulin resistance).

    Shortage of Creatine Phosphate

    As was explained in the The Neuromuscular System Part II: What A Weight Trainer Needs To Know About Muscle article, creatine phosphate (CP) is used to replenish intramuscular ATP levels during contraction. CP concentrations quickly decrease within the first few seconds of exercise and eventually decreasing to 5-10% of the pre-exercise concentration within 30 seconds. When this happens there is insufficient CP levels to replenish ATP stores at an optimal rate. Does this, in fact, cause muscular fatigue? One would intuitively think so, but there are reasons to question this. It has been established that CP levels, during the initial seconds of exercise, deplete more rapidly than the decline in muscle force occurs. And, because intracellular ATP concentrations rarely fall more than 30% during high intensity exercise, it seems that fatigue caused by CP depletion does not occur. If one believes the ATP compartmentalization theory, though (which I do), then this becomes easily explained and fatigue due to CP depletion seems very likely.

    As an aside: Creatine supplementation has been speculated to result in more rapid CP resynthesis between sets and, therefore, increase endurance across multiple sets. It is also well known to produce strength gains in low-rep maximum sets - I consider this as evidence for the ATP compartmentalization theory.

    Lactic Acid, The Sarcoplasmic Reticulum and the T-tubules

    It was explained in the article The Neuromuscular System Part III: What A Weight Trainer Needs To Know About The Nervous System that, during muscle contraction, calcium ions (Ca++) are released from the sarcoplasmic reticulum by way of the T System and then returned to that organelle by way of the Ca-Pump. What would happen then, if all this didn't go as smoothly as anticipated?

    Studies on isolated muscle fibers have, indeed, linked reduced sarcoplasmic Ca++ concentrations to fatigue. Specifically, repetitive 'tetanic' contractions of isolated muscles caused a gradual decline of force that was closely associated with a decline in sarcoplasmic Ca++ concentrations (Westerblad & Allen, 1991). After only 10-20 such contractions, sarcoplasmic calcium concentrations became insufficient for forceful contraction (Westerblad et al., 1991). The reason for this is simply because decreased Ca++ release for binding to troponin reduces the number of actin/myosin cross-bridges that can be formed.

    Forceful contraction could be reestablished with extremely high doses of caffeine (which stimulates greater Ca++ release from the sarcoplasmic reticulum), but this required caffeine doses at physiologically dangerous levels. This does show, however, that the problem appears not to be with the Ca++ concentrations in the sarcoplasmic reticulum, or their release channels, but probably as a consequence of impaired T-tubule signaling. During repeated contractions of a muscle fiber, K+ begins 'pooling' in the T-tubules. This results from an inability of the Na+/K+ ATPase Pump to maintain the proper Na+/K+ balance on the sarcolemma (at the T-tubules). This disturbance of the membrane potential in the T-tubules inhibits the conduction of the action potential to the sarcoplasmic reticulum and Ca++ is not optimally released - and, thus, forceful contraction is not achieved.

    In addition, lactic acid build-up factors in here also. Increased intracellular H+ concentrations (caused by lactic acid accumulation) slows the uptake of Ca++ by the sarcoplasmic reticulum. This occurs because H+ interferes with the operation of the Ca++/ATPase Pump. This reduces muscle contraction force by interfering with intracellular and sarcoplasmic reticulum Ca++ concentrations.

    Incidently, the Ca-Pump is, itself, a major ATP consumer. During isometric contractions (when it's relative ATP consumption is greatest) it is estimated to consume ~30% of the total ATP produced in the muscle cell. This could, theoretically, contribute to declining ATP stores available for cross-bridge formation.

    Accumulation of Inorganic Phosphate (Pi)

    As ATP is broken down to provide energy for muscular contraction inorganic phosphate (Pi) accumulates in the cell. On the one hand this is 'good' because phosphate (Pi) is known to be an important stimulator of glycolysis (the breakdown of glucose to produce ATP) and glycogenolysis (the breakdown of glycogen to produce ATP) - thus stimulating the production of more ATP by these pathways. But the increased Pi levels also inhibit further cross-bridges from being formed between actin and myosin filaments. When ATP is used to fuel contraction Pi must be released from the myosin head. Elevated intracellular Pi concentrations impairs this process, resulting in reduced tension development - meaning that as Pi builds up, muscular force production goes down. This may be another contributing factor to muscle fatigue.

    Peripheral Nervous System Fatigue

    It is a well-established fact that as a maximum muscular contraction continues, the frequency of motor units firing decreases. In fact, one study showed that by the end of a 30 second maximum voluntary contraction the firing frequency decreased by 80%. Eventually the frequency of twitching of the high threshold fibers becomes insufficient to sustain the effort.

    Neurons transmit impulses down the length of their axons by way of Sodium/Potassium transport and the Sodium/Potassium ATPase Pump. The signal is carried across the membrane of the muscle cell in the same manner. The process also relies heavily on calcium concentrations and enzymes that are involved in the synthesis and breakdown of acetylcholine and numerous other substances. The frequency, of motor unit firing decreases, therefore, as these substrates are exhausted, potentially lowering force production.

    There is also evidence that fatigue during fast and powerful activities (such as some forms of weight training) occurs first at the neuromuscular junction. Precisely, the motor neurons cannot manufacture and release acetylcholine (ACh) fast enough to maintain transmission of the action potential from the motor neurons to the muscles.

    Central Nervous System Fatigue

    In order for a muscle fiber to twitch the central nervous system (CNS) must send a nerve impulse to the controlling motor unit. The innervating nerve cannot maintain its capacity to transmit this signal, with optimum frequency, speed and power for extended periods of time. Eventually concentrations of substrates such as sodium, potassium, calcium, neurotransmitters, enzymes, etc. decreases to the point where muscle contraction becomes markedly slower and weaker. If high discharge rates are continued the nerve cell will assume a state of inhibition to protect itself from further stimuli. The force of contraction, therefore, is directly related to the frequency, speed and power of the electrical 'signal' sent by the CNS.

    Interestingly, though far from understood, is the fact that a trainee's motivation and emotional state can profoundly affect the discharge characteristics of the central nervous system.

    Clearly, the central nervous system can play a pivotal role in the perception and reality of fatigue.


    It is currently believed that, although muscle fatigue can be traced to fewer attached cross-bridges, the major portion of the force decline is attributable to reduced force output of the individual cross-bridges. If this is true, it would point to accumulation of Pi and H+ as the likely dominant mechanisms of causing fatigue. However, failure of the sarcoplasmic reticulum to release sufficient Ca++ due to signaling problems from the T-tubules is also a probable contributor - if the reps or set volume is high enough. And, also depending on the number of reps performed and the weight used, the nervous system's inability to maximally recruit and fire muscle fibers may factor heavily.

    All of this is under the assumption that the lifter can muster a sufficient level of effort to train intensely enough to bring these factors into prominence (i.e. the central nervous system is not in a state of inhibition and the lifter's 'psyche' is sufficient).

    The Wrap-Up

    So, after all that, you may have a different perspective on what's actually going on when your muscles hit failure. As with all of the articles in this physiology section of the site the information presented here will be used to examine how a muscle should actually be trained - not from the basis of "Mr. 'So and So' does this" or "a guy at my gym said..." but from the perspective of what is actually going on in your body. The next time somebody voices some crazy "your body does this when you train to failure" theory you'll know exactly how the real story goes.


    Bigland-Ritchie B, Johansson R, Lippold OCJ and Woods JJ: Contractile speed and EMG changes during fatigue of sustained maximal voluntary contractions. Journal of Neurophysiology, 1983; 50: 313-324.

    Bompa TO: Theory and methodology of training: The key to athletic performance. (2nd ed.) Dubuque: Kendall/Hunt Publishing Company, 1990.

    Brooks, G.A., T.D. Fahey, T.P. White, and K.M. Baldwin. (2000). Exercise Physiology: Human Bioenergetics and Its Applications. Mountain View, CA: Mayfield Publishing.

    Marsden CD, Meadows JC and Merton PA: Isolated single motor units in human muscle and their rate of discharge during maximal voluntary effort. Journal of Physiology (London), 1971; 217: 12-13.

  6. Muscular Growth: How Does A Muscle Grow?

    The WeighTrainer
    Muscular Growth: How Does A Muscle Grow?

    Let's get right into this and start with a segment from the Neuromuscular System series:

    Muscle biopsies of serious weight trainers have shown that it was the size of the individual fibers within their muscles that was responsible for the abnormal muscle size and not the actual number of muscle fibers present.

    ...although extreme conditions may result in modest hyperplasia. This tells us that the formation of new muscle cells (hyperplasia) is, at most, likely to be only a minor factor in increasing muscle size. The mechanism responsible for supercompensation is hypertrophy - the increase in size of existing muscle fibers.

    Taking another segment from the Neuromuscular System series:

    It is also worthy of note that contractile machinery comprises about 80% of muscle fiber volume. The rest of the volume is accounted for by tissue that supplies energy to the muscle or is involved with the neural drive.

    This tells us that there are a couple of ways to increase muscle size.

    Increase the volume of the tissue that supplies energy to the muscle or is involved with the neural drive - called sarcoplasmic hypertrophy.
    Increase the volume of contractile machinery - called sarcomere hypertrophy.

    Let's take a look at both routes.

    Sarcoplasmic Hypertrophy

    Increasing the volume of the tissue that supplies energy to the muscle or is involved with the neural drive: Intimately involved in the production of ATP are intracellular bodies called "mitochondria". Muscle fibers will adapt to high volume (and higher rep) training sessions by increasing the number of mitochondria in the cells. They will also increase the concentrations of the enzymes involved in the oxidative phosphorylation and anaerobic glycolysis mechanisms of energy production and increase the volume of sarcoplasmic fluid inside the cell (including glycogen) and also the fluid between the actual cells. This type of hypertrophy produces very little in the way of added strength but has profound effects on increasing strength-endurance (the ability to do reps with a certain weight) because it dramatically increases the muscles' ability to produce ATP. Adaptations of this sort are characteristic of Bodybuilders' muscles.

    It should also be obvious that as the volume of the tissue that supplies energy to the muscle represents only around 20% of the total muscle cell volume in untrained individuals, this isn't where the real size potential lies.

    Sarcoplasmic hypertrophy of muscle cells does directly produce moderate increases in size . But also, as you'll know from the Neuromuscular System series, ATP is the source of energy for all muscular contraction - type II fibers included. Wouldn't having more of this in the muscle, and having the ability to produce greater intramuscular quantities at any one time, be an asset? The answer is, cleary, "yes". That's where a major portion of the importance of sarcoplasmic hypertrophy comes into Bodybuilding. (We'll deal with training to produce this type of adaptation in an article on the 'Training Related Articles' page.)

    As for increasing the tissue that is involved with the neural drive, this would theoretically occur in response to the need for contracting cells with hypertrophied contractile machinery. Directly, it would produce very little in the way of added size.

    In addition, there are other intracellular bodies who's growth and/or proliferation would fall under the category of sarcoplasmic hypertrophy. These would be organelles such as the "ribosomes", which are involved in protein synthesis. As in the case of neural drive machinery, in most cases they would increase in size or number only to support sarcomere hypertrophy. They would have little direct impact on overall muscle size.

    Sarcomere Hypertrophy

    Increasing the volume of contractile machinery: The vast majority of the volume of each muscle cell (~80%) is made up of contractile machinery. Therefore, there lies the greatest potential for increasing muscle cell size. Trained muscle responds by increasing the number of actin/myosin filaments (sarcomeres) that it contains - this is what is responsible for increased strength and size. But before a muscle will grow like this it has to be "broken down". Let's take a look at both the "breaking down" and "building up" processes:

    The Process Of Exercise-Induced Muscle Cell Damage

    Actin/myosin filaments sustain "damage" during high-tension contractions. In addition, breaches in plasma membrane integrity allow calcium to leak into the muscle cells after training (there is much more calcium in the blood than in the muscle cells). This intracellular increase in calcium levels activates enzymes called "calpains" which "break off" pieces of the damaged contractile filaments (called "easily releasable myofilaments"). Following this, a protein called "ubiquitin" (which is present in all muscle cells) binds to the removed pieces of filaments thus "identifying" them for destructive purposes. At this time, neutrophils (a type of granular white blood cell that is highly destructive) are chemically attracted to the area and rapidly increase in number. They release toxins, including oxygen radicals, which increase membrane permeability and phagocytize (ingest and "destroy") the tissue debris that the calcium-mediated pathways released. Neutrophils don't remain around more than a day or two, but are complimented by the appearance of monocytes also attracted to the damaged area. Monocytes (a type of phagocytic cell) enter the damaged muscle and form into macrophages (another phagocytic cell) that also release toxins and phagocytize damaged tissue. Once the phagocytic stage commences, the damaged fibers are rapidly broken down by lysosomal proteases, free O2 radicals, and other substances produced by macrophages. As you can tell, the muscle is now in a weaker state than before it was trained. Incidently, macrophages have an essential role in initiating tissue repair. Unless damaged muscle is invaded by macrophages, activation of satellite cells and muscle repair does not occur.

    Also, increased intracellular Ca++ concentrations are known to activate an enzyme called phospholipase A2. This enzyme releases arachidonic acid from the plasma membrane which is then formed into prostaglandins (primarily PGE2) and other eicosanoids that contribute to the degradative processes.

    So, now that we've seen how the muscle gets damaged, how does it grow?

    The Process Of Exercise-Induced Muscle Growth

    It was mentioned in the The Neuromuscular System Part I: What A Weight Trainer Needs To Know About Muscle article that muscle cells have many nuclei and other intracellular organelles. This is because nuclei are intimately involved in the protein synthesis process (don't forget, actin and myosin are proteins), and a single nuclei can only support so much protein. If muscle cells didn't have multiple nuclei they would be very small muscle cells indeed. So if a muscle is to grow beyond its current size (i.e. synthesize contractile proteins - actin and myosin) it has to increase the number of nuclei that it has (called the "myonuclei number"). How does it do this? Well, around the muscle cells are "myogenic stem cells" called "satellite cells" (or "myoblasts"). Under the right conditions these cells become more "like" muscle cells and actually donate their nuclei to the muscle fibers (very nice of them). For this to happen, to any degree, several things need to take place. One, the number of satellite cells has to increase (called "proliferation"). Two, they have to become more "like" muscle cells (called "differentiation"). And three, they have to fuse with the needy muscle cells.

    When the sarcolemma (the muscle cell wall) is "damaged" by tension (as in weight training or even stretching) growth factors are produced and released in the cell. There are several different types of growth factors. The most significant are:

    Insulin-like Growth Factor 1 (IGF-1)
    Fibroblast Growth Factor (FGF)
    Transforming Growth Factor -Beta Superfamily (TGF-beta)

    These growth factors can then leave the cell and go out into the surrounding area because sarcolemma permeabilty has been increased due to the "damage" done during contraction. Once outside the muscle cell these growth factors cause the satellite cells to proliferate (mainly FGF does this) and differentiate (mainly IGF-1 does this). TGF-beta actually inhibits growth - but everything can't be perfect. After this process the satellite cells then fuse with the muscle cells and donate their nuclei. The muscle cell can now grow.

    So now factors that promote protein synthesis such as IGF-1, growth hormone (GH), testosterone and some prostaglandins can go to work. How does that all happen? Read on...

    Protein synthesis occurs because a genetically-coded subtsance called "messenger RNA" (mRNA) is sent out from the nucleus and goes to organelles called "ribosomes". The mRNA contains the "instructions" for the ribosomes to synthesize proteins, and so the process of constructing contractile (actin and myosin) and structural proteins (for the other components of the cell) from the amino acids taken into the cell from the bloodstream is set off. Several substances can influence this process. A short overview of the major ones are found below:

    IGF-1: IGF-1 comes in two varieties - actually, they are both the same molecule but come from different places. paracrine IGF-1 (also called "systemic" IGF-1) is made primarily in the liver and autocrine IGF-1 (also called "local" IGF-1) is made locally in other cells (it's called "local" IGF-1 because it isn't released in large quantities into the bloodstream - it stays in the area in which it was made). Cells don't let systemic IGF-1 in unless they want to (there are "picky" receptors on the cell wall) but the IGF-1 that was manufactured and released in the muscle cell as a response to the high tension contractions can do it's thing because it's already inside. So, once in the cell, IGF-1 interacts with calcium-activated enzymes and sets off a process that results in protein synthesis (and the calcium ions that were released during muscle contraction and also the ones that leak into the muscle after the sarcolemma is damaged by training ensure that the necessary enzymes are activated). A large part of this increase in protein synthesis rate is due to the fact that the IGF-1/calcium/enzyme complexes make protein synthesis at the ribosomes more efficient.
    By the way, insulin works at the ribosome in a similar manner, hence the name insulin-like growth factor-1 (IGF-1). So get some quick digesting carbs in after your workout to raise insulin levels.

    GH is thought to work, primarily, by causing the cells (muscle cells included) to release IGF-1.

    Certain prostaglandins are released during contraction (and stretch); two of the most significant to growth being PGE2 and PGF2-alpha. PGE2 increases protein degradation, whereas PGF2-alpha increases protein synthesis. But PGE2 isn't all bad because it also powerfully induces satellite cell proliferation and infusion. The mechanism of PGF2-alpha's action is much less clear but is suspected to be connected to increasing protein synthesis 'efficiency' at the ribosomes also.

    And the Granddaddy of them all: testosterone. "Free" testosterone (the kind that isn't bound to some other substance) travels freely across the muscle cell membrane and, once inside, activates what's called the "androgen receptor". "Bound" testosterone must first activate receptors on the cell surface before it can enter (the number of receptors on the surface is what controls this pathway). Once the androgen receptor is activated by testosterone it travels to the nucleus and sets off the protein synthesis process. In this way, testosterone directly causes protein synthesis and is, by far, the most powerful anabolic agent found naturally in the human body. Testosterone also increases the satellite cells' sensitivity to IGF-1 and FGF, thereby promoting satellite cell proliferation and differentiation. It also increases the body's systemic output of GH and IGF-1.

    And, guess what, after a workout the muscle cells are more "receptive" to testosterone, systemic IGF-1 and GH - it's almost as if the muscle "knows" that it needs to grow.

    In addition, there have also been some studies showing that the build-up of phosphates and hydrogen ions, that occurs as a muscle fatigues (see the Failure Muscular Fatigue During Weight Training article), may also contribute (directly or indirectly) to the growth process. The reasons, as of yet, are unknown.

    The whole process of cellular damage and subsequent overcompensation (the cells grow back a little bigger than they were before) can take anywhere in the neighbourhood of 24 hours to several days - depending on the severity and type of training.

    And You Though It Was Magic

    Learn anything useful? Even if you don't realize it you probably did. Knowing the process can be an extremely useful tool when designing training programs.


    Adams GR, McCue SA, Local infusion of IGF-1 results in skeletal muscle hypertrophy in rats. J. Appl. Physiol., 1998; 84(5): 1716-1722

    Brooks, G.A., T.D. Fahey, T.P. White, and K.M. Baldwin. (2000). Exercise Physiology: Human Bioenergetics and Its Applications. Mountain View, CA: Mayfield Publishing.

    Dunn SE, Burns JL, Michel RN. Calcineurin is required for skeletal muscle hypertrophy. J. Biol. Chem., 1999; 274(31):21908-21912.

    Palmer RM. Prostaglandins and the control of muscle protein synthesis and degradation. Prostaglandins Leukot Essent Fatty Acids, 1990 Feb; 39(2):95-104

    Robert K., Md Murray, et al. (1999). Harper's Biochemistry. McGraw-Hill Professional Publishing

    Rooney KJ, Herbert RD, Balnave RJ. Fatigue contributes to the strength training stimulus. Med Sci Sports Exerc, 1994 Sep; 26(9):1160-4.

    Rosenblatt JD, Yong D, Parry DJ, Satellite cell activity is required for hypertrophy of overloaded adult rat muscle. Muscle Nerve, 1994; 17:608-613.

    Rosner W, Hryb DJ, Khan MS, et al. Androgens, estrogens, and second messengers. Steroids, 1998; 63:278-281.

    Schott J. McCully K. Rutherford O.M. The role of metabolites in strength training. Eur-J-Appl-Physiol., 1995 71(4) P 337.

    Spagnoli A, Rosenfeld RG. The mechanisms by which growth hormone brings about growth. The relative contributions of growth hormone and insulin-like growth factors. Endocrinol Metab Clin North Am, 1996 Sep; 25(3):615-31.

    Thompson MG, Palmer RM. Signaling pathways regulating protein turnover in skeletal muscle. Cell Signal. 1998 Jan; 10(1):1-11.

    Thompson SH, Boxhorn LK, Kong W, and Allen RE. Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor-I. Endocrinology, 1989, 124:2110-2117.

    Vandenburgh HH, Shansky J, Solerssi R, Chromiak J. Mechanical stimulation of skeletal muscle increases prostaglandin F2 alpha production, cyclooxygenase activity, and cell growth by a pertussis toxin sensitive mechanism. J Cell Physiol, 1995 May; 163(2):285-94

    The WeighTrainer
    Muscular Growth Part II: How Does A Muscle Grow?

    Rational and Irrational Hypertrophy

    In part one of this series I said that sarcoplasmic hypertrophy produces moderate increases in size but that there were other important reasons why you'd desire such adaptations. This is part of the reason I said that:

    Metabolic processes within the cell require ATP to "fuel" them (remember, ATP is the body's primary source for all of its energy). If enough ATP isn't present then a host of cellular processes slow down (including protein synthesis) resulting in the operations of the cell being compromised. That means, among other things, slower removal of waste products, slower recovery from training and slower or less protein synthesis. Research done in the former Soviet Union by Zalessky and Burkhanov has shown that if the contractile components of the cell continue to grow (sarcomere hypertrophy) without a concurrent increase in the energy supplying systems of the cell (i.e. the mitochondria, etc. - sarcoplasmic hypertrophy) then such a situation will develop. Essentially the motor has become too big for the fuel injection system. In addition, fellow Soviet researchers, Nikituk and Samoilov have demonstrated that such a condition can be brought about through poorly planned training.

    Once such a situation is achieved progess, as far as metabolic processes in the muscle is concerned, will come to a halt. Training may stimulate growth and strengthening but the cell simply lacks the means to support any additional hypertrophy. It can't produce the ATP necessary to fuel the synthesis and maintenance of new protein (muscle protein is constantly being broken down and rebuilt - a process of "maintenance"). In layman's terms, you hit one helluva plateau.

    Such a condition is called irrational hypertrophy because the situation just doesn't make any sense from an adaptative standpoint. The defining characteristic of this kind of growth is cells that contain much larger mitochondria than before, but much fewer of them. The net result is an ATP shortage in the cell.

    On the other hand, if training results in proportionate vascular improvements within the cell (mitochondrial density increases - the total number of mitochondria also increases as the existing mitochondria get bigger), such a plateau will not be encountered and training-invoked hypertrophy can continue as normal. This is called rational hypertrophy, for obvious reasons.

    As this article isn't intended to get into the nitty-gritty of training procedures I'm just going to leave this subject by saying that for continued progress sarcoplasmic hypertrophy is, indeed, needed (especially when increased muscle mass and/or endurance is desired) and must be trained for. How to achieve rational hypertrophy, while avoiding the irrational kind, will be dealt with in other articles on this site.

    "But Why Aren't Olympic Lifters Bigger Than Bodybuilders?"

    It wouldn't be right not to address the fact, though, that training with weights ~90% of your 1RM and above seems to favor the development of strength and power more so than muscular size. But, in light of the information presented in Part I of this series, how is that possible? Well, it appears that an intense set of several reps may consistently recruit and train more fibers than an intense set of only 1 rep (this may also vary from muscle to muscle). It is also theorized that when using loads of ~90% of 1RM and above muscular failure may occur because of signaling problems at the neuromuscular junction, and that this occurs before a significant growth stimulus has been delivered to the cells.

    Think of it like this: The total time that the muscle fibers are required to produce force is shorter in low-rep sets than in higher-rep sets and this may result in exhaustion of fewer muscle fibers and a lesser growth stimulus. Simply put, a hard set of 8 reps may deliver more growth stimulus to the muscle cells than a hard set of 3 reps because in a 3-rep set (or any low number of reps) failure may occur before a significant growth stimulus has been achieved.

    In addition, when higher reps are performed substrates such as phosphate and hydrogen ions build up in the muscles - some researchers theorize that the presence of these substrates may further stimulate the muscular growth process. It is also widely believed that lifting heavy weights (~90% of 1RM and above) stimulates the nervous system to "improve" its firing pattern, frequency and efficiency to produce peak strength, making you stronger without actually increasing muscle size.

    These reasons are why bodybuilders, as a group, have bigger muscles than Olympic lifters - they train with lighter weights, and perform higher reps. It also explains why Olympic lifters, as a group, are much stonger than bodybuilders, but not nearly as heavily muscled.

    It also needs to be pointed out that any type of repetitive weight training (regardless of rep range) will result in the type IIB fibers having endurance-type adaptations. This occurs most quickly and profoundly at lighter loads (8-15 rep maximums) because, with these loads, the type IIBs do not twitch with maximum frequency and, therefore, start adapting to twitch at lower frequencies but for longer periods. When this happens the IIB fibers will be able to produce tension for long enough periods to incur substantial muscular damage and build up high concentrations of fatigue products. This gives the Bodybuilder more more material to work with in terms of muscle growth (in addition to the type IIA fibers themselves).

    If you look closer at fiber recruitment patterns during sets in the higher rep ranges you'll see exactly how this happens: initially the IIAs are recruited and, perhaps, the IIBs also. As the IIAs fatigue more and more IIBs are recruited, gradually, to meet the force requirments. These IIBs are called upon to produce force for longer periods than they are biologically suited for. Training of this sort is actually endurance training for the IIB fibers, so they begin to adapt so that they have better endurance characteristics (i.e. higher mitochondrial densities and greater abilities to sustain enzyme concentrations).

    Don't do as others have, and use these observations to argue that bigger muscles are not stronger muscles. As was eluded to above, muscles adapt very specifically to specific tasks. If you train using three rep sets then they get good at doing three rep sets. If you train using 8 rep sets then they get good at doing 8 rep sets. It just happens to be that years of empirical evidence has indicated that 8 rep sets stimulate more muscle growth than 3 rep sets (assuming of course, you are training with sufficient intensity). Make no mistake about it though, your legs will be bigger when you're squatting 405 for 8 than they were when you were squatting 275 for 8. For the case of 3 rep sets, you may not be much bigger when you're cleaning 315 for 3 than you were when you were cleaning 185 for 3, but you will have a much more efficient nervous system for the task.

    Train for strength!

    I don't mean to sound like a broken Mike Mentzer seminar record here, but if you want to get stronger OR bigger you MUST train for strength. If strength is your main concern you should train predominantly with lower reps - with ~85% of your 1RM and more. If it's muscular size you're after you should train with higher reps - with ~70% to ~85% of your 1RM. But getting stronger in the rep range that you're using should be your first and foremost goal.

    If the above physiological arguments didn't convince you that you can't significantly increase the size of a muscle without it getting stronger ask yourself this question: Do you really believe that when you add 50 pounds to your barbell curls your biceps won't be bigger?

  7. Awesome! That's a sticky right there.

  8. Very nice. Some light reading for this evening.

  9. This is a great post, awesome read for sure. However, as i was browsing through and i noticed at the end about the 50lbs to your BB curl=being bigger, i cant help but to think about Franco's deadlift at a very light body weight considering his body size vs some of today's mass monster's whom(some) do not even do what franco did on the deadlift in his day. But, i am definitely not saying that you can not get somewhat bigger by training for strength; it'll be interesting to read the whole article.
    ---The internet is the father of the electronic lynch-mob---


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