Structure Of Muscle
The Physical Body: The Anatomy of Asana.
When we begin to study our practice of yoga we meet a paradox. First, we are aiming to describe an holistic system, yet our traditional method of understanding the body and movement is based on reductionist and mechanical thinking. Equally, we struggle to truly describe movement, challenged by the subjective and uniquely personal nature of the experience and the experiencer.
Indeed, in practice we are aiming for a state both where we are totally aware of the processes involved in our experience, yet simultaneously feel no desire to be drawn into any. We aim to experience a self where language and understanding do not matter, for we are anchored in something deeper and older and more truly connected than human inventions of grammar and order. An increasing understanding of the living, and extra-cellular matrix alongside fascial mappings of the body is helping to bridge this gap between reductionism and integration.
It is vital that even as we describe the components in the next section we must never lose sight of that whole.
Voluntary muscle is what we most often think of when we consider ‘muscle’ and is also referred to as skeletal, or striated muscle.
Each individual muscle fibre is multilnucleated, and surrounded by an electrically polarized membrane (the sarcolemma). Each bundle of muscle fibres is referred to as a fasiculi with each fibre separated by the endomysium (a delicate connective tissue) that also fills in the spaces between individual fibres.
Each fasciculus is then defined by a stronger layer of connective tissue, the perimysium (that is continuous with the endomysium), which itself is continuous to an even thicker layer of connective tissue the epimysium which defines the ‘muscle’. NB// we use the word define to be clear that there is no true separation, rather perhaps functional and variable compartmentalisation.
Subcutaneous adipose tissue and superficial fascia then covers the whole muscle trunk, whilst connecting in various arrangements to the deep fascia and through it other body structures.
The contractile component of the muscle fibre are the myofibrils, and are formed of thick and thin protein myofilaments which create a sarcomere.
The thick myofilament is largely composed of myosin and makes up the dark ‘A’ band, and the thin myofilaments of actin (primarily) but also tropomysoin and troponin, and make up the light ‘I’ band. Notably, we also have the ‘Z’ line (a narrow band in the central regions of the ‘I’ band which the thin filaments connect to. The area between two adjacent ‘Z’ lines is called a sarcomere, and it is the sarcomeres in varying concentrations that shorten to create overall muscle contraction.
Myofibrils are surrounded by structures made from membranes in the form of vesicles and tubules, the sacroplasmic reticulum and the transverse tubules which create a triad structure. The close association of these two system enables the transverse tubules to function as a conduit for the transmission of electrical impulses (from the motor unit) to the sarcoplasmic reticulum, which releases calcium thus triggering muscle contraction. Here on the micro and the macro level, we see separate systems operating cumulatively around the same axis. We see an electrical impulse moving through the system and we see a fascial and living matrix that encapsulates, creates, and joins all these systems.
A single nerve fibre innervates a multitude of muscle fibres, which then forms a motor unit as the fibres are excited in unison from the single stimulus. These muscles fibres are often widely distributed through the muscle belly which means stimulation of a single motor unit causes a weak activation in a broad area of a muscle - not a strong contraction in one point. Muscles that control fine movements are characterised by small amounts of fibres in each motor unity, for example the ocular unit contains as little as ten fibres to a unit, whereas the quadriceps can have hundreds. With a stimulus, it is either all or nothing. Each motor unit will have a threshold which must be reached for the action to occur, however sub-threshold stimuli may cause a response if they are applied in succession (summation of stimuli).
The motor response then depends upon; the strength of the stimulus, the speed of application of a stimulus, the number of stimulations but also, the initial length of the muscle and the temperature of the muscle. Muscle typically functions optimally at 37degrees with maximum force generated when the muscle begins at its maximum resting length (provided this stays within the realms of normal movement). Rate of contraction varies throughout the body, and is usually predictable by assessing normal use of the area.
As a muscle is subjected to successive stimuli of increasing strength, nerve fibres with higher thresholds will respond and activate the fibres of their respective motor units and the force of the muscle contraction will increase progressively as increasing numbers of motor units are recruited.
A repeated series of stimuli at low frequency will produce a succession of rising peaks of contraction, a response known as clonus or incomplete tetanus. Whilst repeated stimulation at a high frequency will cause the fusion of summated twitches, resulting in a sustained contraction called tetanus.
Ultimately, continued contractions will be weakened as the nutrients and oxygen are used up and metabolic wastes (notably lactic acid) build up in the system, eventually leading to a complete cessation of contraction. At this point, the muscle is also unable to relax completely after each subsequent contraction, known as contracture.
Categories of Muscle Fibres
Red, slow-twitch or type I are slow to contract, and slow to fatigue. They have a small diameter, a rich network of capillaries, many mitochondria and small glycogen stores. This profile underpins the rate of fatigue as they have a high aerobic capacity.
White, fast-twitch or types IIa and IIx are respectively fast and super-fast to contract, intermediate and fast to fatigue. They have a large diameter, few capillaries and mitochondria, and contain an abundance of glycogen which favours a dependence upon anaerobic glycolysis. Large-diameter fibres also have an extensive sarcoplasmic reticulum facilitating rapid release and re-uptake of large amounts of calcium ions.
The fibres of a third group of motor units, described as fast-contracting and fatigue- resistant, are of variable diameter and liberally supplied with capillaries. Their glycogen and mitochondrial levels promotes utilisation of both aerobic and anaerobic pathways.*
All three types are present throughout the body, but their relative percentage varies both on the requirement of the area and genetics. There is evidence to suggest that it is possible to change the relative amounts of the two fast twitch fibres within a muscle however it is not possible to change from type I to type II or III, this may account for certain individuals inherent abilities and limitations.
Muscles make up around 40-50% of our structure but unlike many other cells in the body they do not replicate by dividing, rather they recruit nearby myosatellite cells to reproduce and specialise to become myoblasts which then merge with existing muscle cells forming the dual function of repair, and growth. Only when we are very young can myoblasts become separate muscles.
There are two ways to add sarcomeres to meet the demands of the muscle fibre: in series in which case they add length, or in parallel increasing mass and contractile power, or 'force'. If a muscle fibre is then no longer used then the body quickly reabsorbs the sarcomeres, known as atrophy, or autophagy.
Practical applications of gender differences in muscle structure.
Women on average are able to produce two-thirds the total strength and applied force that men are capable of. Women’s structures are also such that their build can carry approximately two-thirds the muscle mass that a male structure can. Regardless of gender differences in quantity and distribution, muscle tissue responds to stimulation in the same way however there are some functional differences. Muscles are essential in the flexibility equation and this means that men and women have muscular advantages in different areas. While men are taller and broader, built to carry, lift and press, women have an advantage using muscular strength for flexibility, coordination and balance related tasks. In the absence of external-weighted load, women also appear to have a greater ability to use rhythmic co-ordination of their musculature, however, this advantage switches when external weight is added.*
Testosterone is the primary anabolic (muscle building) hormone. Women will not usually produce more than ten percent of the circulating testosterone that men do*. This means that muscle and strength building will occur at a faster rate in men. Flexibility will also vary throughout the course of a female practitioners monthly cycle as progesterone & oestrogen have a loosening effect on ligaments (necessary of course ultimately for pregnancy and birth) with most flexibility seen in high progesterone periods.*
The effect of intramuscular fat on skeletal muscle mechanics
Skeletal muscle accumulates intramuscular fat for various reasons, but most notably through the ageing process and obesity. It is not clear exactly why, but the measure of muscle strength decreases as the level of intramuscular fat increases*. An increase in stiffness is also noted within the fascia and muscle tissue with greater fatty tissue inclusions*. Women generally have a greater amount of intramuscular fat.*
There are also significant metabolic changes within affected areas of muscle; a decreased sensitivity to insulin, an increased level of pro inflammatory cytokines, and an increase in citrate synthase activity which causes a reduction in the Krebs cycle (the chemical cycle that allows cells to generate energy).*
Involuntary muscle is composed of fusiform (diamond shaped) cells with a single nucleus, arranged in sheets of three filaments types. Actin filaments (5-8 times more than skeletal muscle but no troponin or tropomyosin), myosin, and a series of other filaments that are not involved in contraction. Because there are no myofibrils or sarcomeres, the muscle appears ‘smooth’ under the microscope rather than striated.
Because of their size, the cells have no t-tubules, and a basic sarcoplasmic reticulum, and actin filaments are mostly anchored to the internal surface of the plasma membrane, or onto irregularly placed bodies (unlike the organised Z-lines in voluntary muscle). The contractile units run diagonally across the cell (as opposed to parallel in voluntary muscle) resulting in the characteristic bulging that occurs with contraction where the actin is attached. Functionally, involuntary muscle is usually categorised as either multi- or single-unit.
In multi-unit involuntary muscle the muscle consists of discrete units that function independently of each other, and require individual activation through the autonomic nervous system. Single-unit involuntary muscle is more common, and is alternately referred to as visceral muscle. In this instance sheets of muscle fibres contract as a single unit, electrically linked through gap junctions, permitting coordinated contraction of an entire organ.
Involuntary muscle contraction usually starts much more slowly, and lasts for significantly longer than voluntary muscle, and is constantly in a state of partial contraction to maintain for example, blood pressure, or movement in the gastrointestinal tract. Additionally, involuntary muscle is able to shorten and stretch to a much greater degree without loosing their contractile function.