This post originally appeared on the Flexibility Research Forum on November 30, 2021.
The requirements of joint moments determine the outcome of all voluntary movements. A moment is force multiplied by the distance from the fulcrum (the axis of rotation), which is illustrated in the image below.
In simpler terms, a moment of force is a turning or rotational force; a joint moment, therefore, is the force that occurs at an articulation as it rotates around its axis. (I will use the preferred term 'joint moment' because that is the convention of the biomechanics literature, and it is good practice for you to get used to it.)
Joint moments are caused almost exclusively by muscles, but forces arising in other passive structures, such as tensile loading of ligaments and bony contact forces, may also contribute to the gross joint moment.
Therefore, it is necessary to know how a single muscle produces and controls force and how multiple muscles crossing a particular joint interact with each other to understand how a person controls movement.
Isolated muscle force is not the only consideration, and other factors that contribute to voluntary movement control include such things as the control of multiple joints rather than a single joint (many muscles are multi-articular, and so a muscle crossing one joint may also affect actions at other joints) and the level of skill required to perform a movement.
However, this article will exclusively cover the fundamental aspects of just one factor related to movement control: muscle activation.
One way to think about muscle activation is like a lightbulb controlled by a dimmer switch; rather than being an on/off mechanism in which the light produced by the bulb is constant (a common misconception), a variable switch or knob controls the brightness by altering the voltage waveform delivered to the bulb.
This is analogous to the strength of the signals sent by the central nervous system to muscles (since nerve signals activate muscles).
Those commands from the CNS arrive at the target muscle via alpha motoneurons, which are also known as motor neurons and motor nerves.
Alpha motoneurons are nerve cells that exit the spinal cord through the ventral (front of the body) roots and finish at specialised sites on the muscle fibres called neuromuscular junctions (see image below).
When a distinct type of nerve signal called an action potential reaches the end of the axon (called the presynaptic terminal), a number of biochemical reactions will commence that end with the release of acetylcholine (abbreviated to ACh).
ACh is a type of chemical called a neurotransmitter, a substance that nerves use to communicate with one another.
ACh is released from synaptic vesicles (structures within cells that serve a defined function), and it diffuses (moves from one region to another) across the gap between the presynaptic and postsynaptic membranes called the synaptic cleft.
Once ACh crosses the synaptic cleft, it binds to receptor molecules located on the postsynaptic membrane, thereby causing an increase in permeability of the muscle cell's membrane so that sodium ions pass through more easily.
The absorption of sodium into the muscle cell causes its membrane to depolarise (changes the electrical charge), generating an action potential that travels along the affected muscle fibre.
The action of ACh is terminated by Acetylcholinesterase (ACHE), an enzyme located in the basement membrane of the muscle cell, which splits ACh into acetic acid and choline.
The action potential arrives at the interior of the muscle fibre at extensions of the cell membrane that penetrate inwards called T-tubules.
Within the T-tubules, depolarization of the cell membrane releases calcium ions from the sarcoplasmic reticulum, into the sarcoplasm and throughout the myofibrils (the part of the muscle containing sarcomeres, i.e., the 'functional units' that generate force).
Calcium subsequently binds to sites on the actin (thin) protein filaments containing Troponin-C.
Troponin-C is a derivative of troponin, which contains calcium-binding sites that essentially "hold" the calcium ions, thus removing the inhibitory effect of the troponin-tropomyosin complex.
The removal of this inhibitory influence allows cross-bridges to form and cross-bridge cycling to occur, enabling force to be produced by the myofilaments.
The (current) consensus hypothesis for how cross-bridges produce force is by rotation and a sliding of the actin (thin) filaments past the myosin (thick) filaments, much like how one would pull a rope hand-over-hand.
This process requires energy, namely chemical, and it is provided by the breakdown of adenosine triphosphate (ATP) into adenosine diphosphate (ADP), plus a phosphate ion.
The energy provided by ATP is used to actively pump calcium back into the sarcoplasmic reticulum, stopping the cross-bridge cycling and ceasing force production in the myofibril.
A single action potential from a motoneuron will create a single force response, colloquially known as a 'twitch.'
When the frequency of this stimulation from motoneurons increases, the force in a muscle fibre also increases.
It is important to note that it is impossible to activate single muscle fibres during voluntary contractions.
Muscles are organised into motor units, which are simply motor neurons and all of the individual fibres that they innervate.
When a motor unit is activated, it will cause all of its associated fibres to produce force; therefore, the smallest unit for controlling force in a muscle is the motor unit, not single fibres.
In small muscles, like those found in the eye, motor units tend to contain only a few muscle fibres owing to the need for high levels of precision, whereas in the large muscles of the legs, motor units innervate thousands of muscle fibres.
The amount of force that a motor unit can produce is determined by the frequency of stimulation from the central nervous system and the physiological cross-sectional area (PCSA) of the motor unit, i.e., the number of fibres it contains, and the PCSA can vary widely from one motor unit to another within the same muscle.
The total magnitude (size) of the force produced by a whole muscle depends on the number of motor units activated at any given moment in time, the frequency of stimulation from the CNS, and the PCSA of each activated motor unit.
According to Henneman's size principle, small motor units are activated ("recruited") first when the demand for force is low, with larger motor units being progressively activated as the demand for force increases.
Generally, small motor units consist of slow-twitch fibres and large motor units are comprised of fast-twitch fibres.
Slow-twitch fibres have a higher resistance to fatigue than fast-twitch fibres, and so they are used for everyday tasks like standing, walking, dressing, eating, etc.
Fast-twitch fibres are utilised only when the muscle must meet high demands for force or speed.
Keep in mind that no muscle is made up exclusively of one fibre type or another, or even two well-defined fibre types with sharply contrasting functional properties.
Instead, muscle fibre types and their functional properties tend to be continuous, and the border between one fibre type and the other is often blurred.
Henneman's size principle is generally accepted as being accurate as far as isometric and slow concentric contractions are concerned, but the recruitment order may be reversed for high speed and eccentric muscle contractions.
Also, consider that Henneman's size principle has primarily been evidenced in single muscles, and more research is needed to elucidate whether it can be applied with confidence across entire muscle groups.