It may very well be true that you don't need to know much (if any) of muscle and nervous system 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.
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 nutritional supplements. I'll keep it as simple and brief as possible, without leaving any information relevant to weight training out.
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.
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.
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.
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 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.
Striated skeletal muscle - the kind we're concerned with - comes in three basic fiber types (you may see references to further types of muscle fibers but they are really only a continuation of the continuum that the three basic types represent). They are:
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:
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.
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 (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, however, it does serve to illustrate the basic process.
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.
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, it occurs when most of the cells in the muscle are at their optimal lengths for producing maximum tension. This usually corresponds to the length of the muscle when it is elongated slightly 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.