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

by Casey Butt

Neuromuscular Physiology

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

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.

the neuron

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.

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').

the myelin sheath the myelin sheath

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).

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).


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. What I have 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. If you're interested, the links below provide more information along these lines.

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

Nicholas Institute of Sports Medicine and Athletic Trauma A Primer on Muscle Physiology

Muscle Physiology Lab at the University of California, San Diego

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