1

Neuromuscular Physiology

Opening screen: There are three types of muscles. Skeletal

muscles are attached to the bones of the skeleton – thus the name –

muscles provide the force that move the bones. You will also hear

them referred to as voluntary muscles meaning that the athlete has

control over them.

While we will not talk about smooth muscle these muscles are

found in many internal organs in the body including blood vessels.

Smooth muscles are classified and involuntary muscles because

they are not under conscious control.

The third type of muscle is cardiac muscle that is found only in the

heart and has characteristics of both skeletal and smooth muscle.

All three muscle types are important to an athlete. The focus of this module is skeletal muscle, how they are structured,

how they are stimulated to move, and how you can train them to adapt to a higher workload.

Click the start presentation button: Neuromuscular

physiology examines the interaction between muscle and the

nervous system. In this animation you will see an overview of all

the steps involved in a muscle contraction. Watch as the signal

moves down the nerve in the arm to the muscle. When the muscle

receives the signal the smallest functioning unit of the muscle

called the sarcomere will contract. The sarcomere consists of

overlapping protein filaments that slide past each other.

Focus now on the video clip on the right. The numbers on the

diagram correspond to the events that are going to appear in the

video clip. We’ll come back in a little bit and discuss the anatomy

of a muscle in more depth – for now just aim to get the general

idea of what’s going on.

We begin with the muscle – it could be any muscle the athlete is using. Now let’s travel deeper into the muscle structure

– number 2 is the muscle fiber itself. Note its stripped appearance. The purple structure is one of the muscle fiber’s many

nuclei.

Each muscle fiber has its own nerve – indicated as number 3 - that sends the electrical signal that stimulates the muscle

fiber to contract. The muscle fiber is packed with hundreds of banded rod-like elements called myofibrils that contain the

fiber’s contractile machinery – and is shown as number 4.

Now let’s travel deeper into the myofibril – the nerve’s electrical stimulus sets off a number of processes within the

sarcomere. Now we are closing in on the smallest functional unit of the myofibril called the sarcomere. As we zoom in

closer you will notice a bluish network of tube-like structure surrounding the myofibril that is an important container for

calcium and plays an important role in the activation of muscle contraction. In number 5 we are entering the sarcomere

and number 6 is showing a working sarcomere. We are now zooming deeper into the sarcomere and the very small protein

structures become visible – these are numbers 7 and 8 on the diagram.

When you are done with this module you will understand everything that is going on here.

2

Go to the next screen: Once again, remember that while we

are about to talk about the neuromuscular system, this system

works in conjunction with the energy, cardiovascular and

respiratory systems. Movement cannot occur without energy, and

energy production requires oxygen and fuel. We can see muscle

activity by watching its electrical pattern. An electrical signal

means that the muscle is contracting. When there is no electrical

signal then the muscle is relaxed. When muscle contraction and

relaxation occurs hundreds of chemical processes are taking place

and the structures involved require maintenance, rebuilding and

strengthening in order to perform the work demands placed on

them.

Go to the next screen: This is the index screen.

Click the Goals Button: These are your learning goals for

this module.

Click the Home Menu Button

Click the Blood and Nerve Supply Button: The

mitochondria require a steady and nearly instantaneous

supply of oxygen: every minute 1 ml of mitochondria

consumes about 5 ml of oxygen when the athlete is working

at VO2max. The blood flows past the muscle cells in a

network of capillaries that run predominantly parallel to the

muscle fiber. Capillary volume is related to the number of

mitochondria in the muscle – a muscle doing a lot of aerobic

work will have a lot of mitochondria and network of

capillaries surrounding that muscle will reflect the number of

mitochondria that must be supplied with oxygen. For this

reason athletes have a larger capillary network than non

athletes.

However, the number of capillaries supplying a muscle is not

directly proportional to the number of mitochondria in the muscle. But, when you look at both the capillary network and

the number of erythrocytes or red blood cells the two together are proportional to mitochondrial volume.

3

So, athletes will not only have an increased network of capillaries around their working muscles, their hematocrit is also

larger. It turns out that it is more efficient for the body to split the structural adjustments to higher work output between

the capillary network and red blood cells. Capillaries that are expensive to build and difficult to maintain so the body will

try to economize. In male and female athletes around 5-7 capillaries surround each muscle fiber and their red blood cell

volume increases with training .

The problem is that a higher hematocrit increases viscosity of the blood making it more difficult for the heart to pump the

blood throughout the body. This is not normally a problem, though, because in athletes plasma volume also increases and

their blood is actually less viscous than a sedentary individual so long as the red blood cell volume was not artificially

enhanced.

Go to the next screen: Oxygen and fuel delivery for

energy to muscles is just part of the story. Muscles will not

work unless the brain tells them to work – and that requires

some way of communicating between the brain and the

muscle. A lightening fast electrical system accomplishes this

task. The cables along which the electrical signal travels

linking the brain to the rest of the body are called nerves.

Let’s very quickly overview the structure of the nervous

system. The first division we can make is the brain and

spinal cord. This portion of the nervous system is the central

nervous system or CNS where all the cell bodies of the

nerves are located. Think of this as the central

communication control center.

The communication control center sends out processes, or you can think of these as the cables, that extend out into the

periphery of the body. These cables are called axons and collectively we refer to all the cables linking the body to the

central nervous system as the peripheral nervous system or PNS.

The peripheral nervous system is in turn split into the somatic nervous system and the autonomic nervous system. The

autonomic branch services all the organs of the body function without any conscious control – such as the heart and

kidneys and blood vessels just to name a few. The somatic branch serves the voluntary skeletal muscle or those muscle

you can consciously control. The somatic branch is what is of interest to us in this module.

two branches of somatic nerves serve skeletal muscle - an efferent branch – think E for exit – that relays information from

the CNS to the muscle. The afferent branch relays information from muscle to the CNS. These afferent fibers here

monitor the stretch of the muscle fiber and then stimulates the fiber to provide more tension so that the arm will not

collapse due to the added weight.

Click the Home Menu Button

Click the structure of the muscle cell and how

it works Button: Skeletal muscle attach to bone with a

connective tissue called a tendon. Muscle is composed of

bundles of muscle fibers called faciculi separated by

connective tissue known as the perimysium. Each fasiculus

is made up of muscle fibers that are separated by

connective tissue called the endomysium. Skeletal muscle

cells are composed of subunits called myofibrils and each

myofibril is made up of several myofilaments. The large

myofilaments shown in red here are composed of the

protein myosin and the thin myofilaments shown in blue

are composed of the protein actin. The repeating

arrangement of thick and thin myofilaments are called

sarcomeres. The sarcomere shortens because the thin

filament slides past the thick filament as you see right here. In 3-D each thick myofilament is surrounded by 6 thin

4

myofilaments arranged in a hexagonal pattern. The 3-D arrangement of sliding myofilaments is the microscopic basis of

muscle contraction.

Go to the next screen: Here’s a summary of muscle

structure. The muscle is divided into fascicles that are

clusters of muscle fiber cells surrounded by a connective

tissue called the perimysium. The endomysium is the

connective tissue that surrounds the muscle cell itself. The

muscle cell membrane itself is called the sarcolemma and

is just inside and attached to the endomysium. All the

connective tissues surrounding the various portions of the

muscle converge in the tendon that is attached to the bone.

The smallest functional unit of the muscle is the sarcomere

that consists of overlapping protein strands called actin and

myosin. It is these overlapping protein myofilaments that

give muscle its stripped appearance. The sarcomere is

bordered on either end by Z lines. This is where the actin

myofilaments attach. The other structure I want to point out

is the sarcoplasmic reticulum. This is a netlike system of tubules and vesicles surrounding each myofibril that is important

in the transmission of the neural impulse. The sarcoplasmic reticulum serves as a storage site for calcium that is important

to the action of the sarcomere. We’ll come back to this structure in a little bit.

Go to the next screen: Let’s take a closer look at the

sarcomere. As we have already discussed each sarcomere

contains many thick and thin protein filaments arranged side-

by-side in parallel array. Thick filaments are composed of

myosin. As we zoom into the structure of myosin you will

see a long tail and double head. The heads are called cross

bridges and act to pull the actin towards the center of the

sarcomere. The actin are like two strands of pearls twisted

together. Two other protein structures are important –

troponin and tropomyisin. Note how the tropomosin is

covering the myosin binding sites on the actin that are

represented by black dots.

Go to the next screen. Now, let’s take a look at how

the actin and myosin interact to cause contraction.

Remember that the somatic division of the nervous system

only controls skeletal muscle and has a one type of efferent

neuron called the motor nerve. Because the somatic

nervous system is under voluntary control it is also referred

to as the voluntary nervous system. The motor nerve

originates in the CNS and synapses with a skeletal muscle

at a highly specialized central region of the muscle fiber

called the neuronmuscular junction.

5

Go to the next screen. The motor nerve axon

terminals are called terminal boutons and they store and

release acetylcholine. Opposite these terminal boutons is a

specialized region of the muscle fiber’s plasma membrane

called the motor end plate, which has invaginations

containing a large number of special acetyl choline

receptors. An enzyme called acetylcholineesterase is

responsible for terminating the effect of the acetyl choline

allowing the muscle fiber to relax

When a motor nerve is activated the action potentials are

propagated to the terminal boutons at the neuromuscular

junction. This causes calcium channels in the boutons to

open allowing calcium to enter into the bouton. The calcium triggers the vesicle containing the acetylcholine to empty

their contents into the synaptic cleft. The acetyl choline bind to protein channels the motor end plate of the skeletal muscle

cell causing them to open and allow sodium to enter. It is the sodium entering the muscle cell that generates the action

potential in muscle cell. In this way the motor neuron transmits an electrical impulse to the muscle cell

Go to the next screen: This is where the sarcoplasmic

reticulum comes into play. Recall that the sarcoplasmic

reticulum is a saclike membranous network that surrounds

each of the myofibrils. The other important structure here is

the Transverse or T-tubules. The Transverse or T-tubules are

connected to the sarcolemma – remember the sarcolemma is

the name for the muscle cell membrane - and penetrate into

the cell’s interior.

Here’s a closer view of the sarcoplasmic reticulum. It is the

blue network surrounding the myofibrils. The T-Tubules are

the yellow stripes extending from the sarcolemma.

And here’s another view – this view clearly shows the t-

tubules as extension of the sarcolemma. The sarcoplasmic reticulum is show in yellow here.

Go to the next screen: When the muscle cell membrane

receives the impulse it travels down the T-tubules. of the

sarcoplasmic reticulum. This causes calcium channels in the

sarcoplasmic reticulum to open and calcium ions leave the

sarcoplasmic reticulum and enter the myofibril.

Now let’s see what happens as we move in closer to the actin

and myosin. The green balls represent calcium. Remember

that myosin is a protein with a head and a long tail. The

myosin head is also referred to as a crossbridge. Tropomyosin

covers the hot spots for myosin that are located on the actin.

The troponin is attached to the tropomyosin and this is where

the calcium is heading.

The calcium attaches to the troponin and activates the tropomyosin so that it moves away from the myosin binding sites

on the actin. As soon as these sites are exposed the myosin head will pop up and attach to the actin. Once the myosin is

bound to the actin the myosin head pivots towards the middle of the sarcomere, pulling the thin filament along with it. At

the stage the myosin head is stuck to the actin – it’s called rigor mortis and the stiffening of the body that occurs after

death is due to the crossbridges getting stuck on the actin.

6

Go to the next screen: This is where ATP comes into

play. An ATP attaches to the myosin head on a special site

called the ATPase site. ATP is split into ADP plus Pi plus

energy. It is this energy that is used to release the myosin

head from the actin and cock it back into it’s high energy

position.

There are hundreds of myosin heads all working out of

phase of each other. It’s like pulling a rope towards you

hand over hand – some myosin heads are pulling while

others are resetting themselves into the high energy

position.

Each myosin head can flex 5 times per second in a rowing

like action. When the nerve impulses stop the calcium ions

return to storage in the sarcoplasmic reticulum and the muscle cell relaxes.

Click the Home Menu Button

Click the Muscle Fiber Type button: At this point we

need to briefly discuss the different fiber types that are found within

a muscle. When different muscles are stimulated to contract some

take longer to reach peak tension than others and are slower to relax.

When we stimulate muscle A reaches its peak tension quickly and

relaxes very quickly. Muscle B takes a bit longer to reach its peak

tension and a bit longer to relax. Muscle C takes longer still.

The reason for this is that muscles contain different populations of

fibers – some contract very slowly while others contract very fast.

We basically divide the muscle fibers into 2 groups – fast twitch

fibers and slow twitch fibers. The slow acting fibers are called slow-

twitch and all the others are called fast twitch fibers. The velocity of muscle contraction depends on the rate of cross-

bridge cycling –the fast twitch fibers are able to split ATP very quickly. This allows the sarcomere to shorten at a much

faster rate. Although we’ve shown the amount of tension being produced as the same here slow twitch have a lower rate

of force production.

There are other significant differences between the fiber types. Slow twitch fibers are generally thinner and have a more

dense capillary network surrounding them. They appear red because of a large amount of oxygen binding protein called

myoglobin within their cytoplasm. This rich capillary network facilitates oxygen transport to the fibers which rely mostly

on the mitochondria to produce ATP. Slow twitch fibers have a large number of mitochondria but have have a low

glycogen content and low glycolytic enzyme activity – in other words they are not good at producing ATP anaerobically –

but are excellent at producing ATP aerobically.

Fast twitch appear white and have a high glycogen content – for this reason they are called glyolytic fibers. They are

really good at producing ATP anaerobically. Both fast twitch and slow twitch fibers are found in all muscles of the body,

but their proportions vary among the different muscles.

7

Go to the next screen Of course, things are a bit more

complicated than simply classifying muscle fibers as fast twitch

and slow twitch. Fast twitch fibers are themselves divided into

two important types that are particularly relevant to coaches

and athletes. But, before we discuss the two classifications let’s

first take at this electron micrograph of a muscle cell.

Here is the mitochondria and these are the myofibrils that are

composed of actin and myosin. Around the periphery of the

mitochondria are glycogen granules and what you have here are

a couple of lipid droplets. Recall that glycogen and lipids or

fatty acids are important fuels for ATP production. The

glycogen is broken down into pyruvate that can then enter into

the krebs cycle in the mitochondria or it can be converted to

lactic acid if there is not enough oxygen to meet the needs of

the mitochondria. The lipid droplets are broken into fatty acids that are then broken down so that they can enter the Krebs

cycle but lipids are only used under aerobic conditions.

Here we’ve zoomed in a bit closer to the lipid droplets. Note how they are wedged in between mitochondria. Here’s the

glycogen. This is a t-tubule and here is the sarcoplasmic reticulum. Recall that the sarcoplasmic reticulum is where the

calcium is stored.

The reason I am pointing the glycogen and lipid structures out is because they are relevant to your understanding of the

two types fast twitch fibers important to athletic performance.

Go to the next screen: Now you should have enough

information to understand the two important fast twitch fiber

types. Some fast twitch fibers are fatigue resistant and this is

because they have a high proportion of mitochondria and

therefore they can produce ATP aerobically. They also have a

high glycogen content. But, they appear similar to slow

twitch fibers with respect to their myoglobin content and

metabolic machinery. For this reason they are referred to as

fast oxidative glycolytic or FOG. You’ll also see them

referred to as Fast twitch IIA fibers. One important difference

between FOG fibers and slow twitch fibers is their high

glycogen content.

The other cluster of fast twitch fibers don’t have a lot of

mitochondria, but have a lot of glycogen. For this reason they

are called fast glycolytic or FG fibers. You will also see them referred to as Fast Twitch IIB fibers. From a coaching and

training perspective I prefer the terms FOG and FG rather that IIA and IIB. The FG fibers have a very low myoglobin

content and relatively few enzymes for aerobic energy production. But they are very rich in glycolytic enzymes which

makes them capable of producing a lot ATP anaerobically. Another important feature of the FG fiber is its elasticity. Slow

twitch fibers have more collagen or connective tissue than the fast twitch fiber and is therefore less elastic and stiffer than

fast twitch fibers.

When glycolytic fibers are active and producing ATP at a high rate, lactic acid is produced as a byproduct. This is one

reason why glycolytic fibers fatigue more quickly than slow oxidative fibers that produce little lactic acid so long as they

are supplied with adequate amounts of oxygen. The FOG fibers have a better capacity to clear lactic acid than the FG

fibers because of their high mitochondrial content. Lactic acid does not normally accumulated slow twitch fibers because

of their high oxidative capacity that enables them to convert pyruvate to acetyl CoA as fast as it is produced.

The FG fibers are capable of high force and are generally the largest of all the fiber types.

8

Go to the next screen: One more feature I want to

quickly talk about – and this is the timing for recruitment of

these fibers. Slow twitch fibers are always recruited first

regardless of the exercise intensity. Fast twitch fibers are

recruited during higher intensity exercise or during prolonged

activity leading to fatigue.

FG fibers are considered high threshold fibers and untrained

muscles cannot fully activate high threshold fibers. Repetitive

stimulation activates high threshold fibers enhancing the

athlete’s ability to produce a maximal force.

Set the cursor at the left hand end of the red bar. Now slide

the cursor along the red bar to see the order of muscle

recruitment.

Go to the next screen: This is all we will say about

the fiber types. On this screen you can test your knowledge

and learn a bit more about fiber types on your own.

Click the Home Menu Button

Click the Motor Unit button: Here’s the motor

neuron or nerve. Notice how this one motor neuron splits

near the muscle fibers and actually innervates several muscle

fibers. A single motor nerve and the muscle fibers it supplies

is called a motor unit. This is what we are now going to talk

about.

9

Go to the next screen: Single motor nerves may

innervate from 5 to 150 or more muscle fibers. A high fiber

to nerve ratio is associated with gross movement requiring

considerable force such as when this athlete is lifting a

heavy weight. A low fiber to nerve ratio exists when very

precise, low force demands are required of muscle. The

eye is an example of this.

Click the One Motor Unit Button. When a muscle

contracts, only rarely do all of its fibers actively generate

force. Some motor units are active, but the fibers in the

other motor units simply go along for the ride passively

shortening in response to forces generated by the fibers

that are actively contracting.

Click on the Two Motor Unit Button: When larger

forces are needed, the nervous system can activate some of

the extra fibers and this increases the total number of active

fibers. The nervous system exerts most of its control over

muscular force by varying the number of active motor units.

It can also increase the frequency of stimulation of individual

fibers but this plays a secondary role. An increase in the

number of active fibers is called recruitment.

10

Go to the next screen: The larger the muscle, the

greater the potential force development. But, muscle strength

is not only related to cross-sectional muscle size, it also

relates to the ability of the central nervous system to activate

those muscles. For a muscle to produce the greatest force

possible, all available motor units must be recruited. High

muscle force production requires the recruitment of high

force and fast motor units.

Go to the next screen: During the first few sessions

of training an athlete will be able to life heavier weights

and produce more force. This is due to the adaptation of

the CNS and its ability to recruit motor units more

effectively. This is referred to as the neurological

adaptation phase. Gradually, over time improved strength

comes about as the result of an increase in muscle fiber

size or hypertrophy. The graph here shows this effect. In

week 2 of training the neural factors such as the CNS

becoming more efficient in recruiting motor units

contributes to 80 percent of the strength gains over that 2

week period. Gradually the CNS reaches its maximum

efficiency. Note how muscle growth is gradually

contributing a higher and higher proportion of the strength

gains. By week 8 the hypertropic effect contribute to most

of the strength gains. In the early phases of training the

athlete will not notice any muscle growth even through more weight is being handled or more force is being produced. All

the improvement is due to neural factors. It takes a couple of months to see any muscle adaptation in terms of growth.

Go to the next screen: Here’s a graph that looks at

the relative contribution of neural factors and hypertrophy

to strength gains. Total strength is shown in red. Keep in

mind that most training studies reported in the research are

of a very short duration – 6 – 12 weeks whereas athletes

are training for a much longer period of time. By the end of

12 weeks neural adaptation flattens off but note how

hypertrophy of the muscle fiber continues. However, even

that will plateau and as a result total strength will plateau –

this will be the athlete’s natural genetic potential. The

influence of steroids is shown here as well which is the

reason why athletes will resort to this strategy to keep

building muscle and thus strength.

11

Go to the next screen: Just a couple more comments.

The faster the motor units are recruited, the quicker muscle

force production occurs. But, the ability of the CNS to

stimulate quickly takes specific training and a long time to

develop.

As well, increase in muscle size results from and increase

in size of the fibers – referred to as hypertrophy – rather

that to an increase in the number of fibers due to splitting –

or hyperplasia, although some scientist claim hyperplasia

does occur. However, for the most part it is presently

generally believed that muscle fiber numbers are fixed

early in life and any increase or decrease in muscle weight

is predominantly attributable to hypertrophy or atrophy of

existing fibers.

Click the Home Menu Button

Click the Stretch shortening cycle button: Muscles contract more forcefully when they are stretched

immediately prior to the contraction. We refer to this as the

prestretching the muscle and the enhanced contraction due

to the prestretching is called the stretch shortening cycle.

The muscle’s reaction to this pre-stretch is called the elastic

response.

I have a small experiment set up that will demonstrate the

stretch shortening concept but first I need to introduce you

to titin. Titn forms an elastic connection between the end of

the myosin and the Z-line. Titin does not actively generate

force – as it stretches though it stores energy.

Here’s the muscle at its resting length. Now as we stretch it

out note how the titin is being stretch as the actin and

myosin are being pulled apart.

Here the muscle is well stretched out but there is still some overlap of the actin and myosin. At this stretch level the

myosin cannot produce much force on the actin but the energy in the titin will cause a reflex type action and begin

shortening the muscle.

At this point there is a reasonable level of actin and myosin that they can now begin producing a force to shorten the

muscle and energy in the titin diminishes.

Go to the next screen: On the screen you now see an experimental setup that will illustrate the influence of pre-

stretching a muscle on its ultimate ability to produce a force. There are 6 different lengths set up here. The muscle length

for the first experiment is 50 mm. When we stimulate this muscle at this length it produces an active force of 0.11 – don’t

worry about the units. Active force is simply the force due to the muscle fiber itself. In this very shortened situation the

actin and myosin are not in the best position to created a pulling motion on the sarcomeres. Note that there is no passive

force. The passive force is the force due to the stretching effect on the titin fibers. Clearly at 50 mm this muscle is not

stretched at all and there is no energy stored within the titin fibers.

12

Now let’s stretch the muscle out to 62 mm. We’ve stimulated it and recorded the force produced. The active force has

now increased dramatically. The actin and myosin are in a much better position to work. Note that the passive force is still

zero – there is still no stretch on the titin fibers.

Let’s continue our experiment and stretch the muscle out to 70 mm. After stimulation we now see that it has produced

more force still. There is still no response from the titin fibers though.

Now we’ve stretched the muscle out to 80 mm. The muscle has not produced any more force – at this point the actin and

myosin fibers have reached their optimum overlap. Note, though that we are beginning to reach the titin fibers.

Now we have stretched the muscle out to 90 mm. Note that the muscle force has actually dropped from 1.75 to 1.20. The

actin and myosin are no longer in a very effective position to produce a sarcomere shortening. The energy stored in the

titin fibers is not yet sufficient to make up fot the loss in muscle force and so total force produced has dropped.

Let’s stretch the muscle a bit more – out to 100 mm. Active force by the muscle fiber has dropped significantly – down to

0.11. But passive force – or the energy stored in the titin fibers has now produced a dramatic increase in passive force –

up to 1.75 for the highest total force.

This little experiment shows you how complicated force production is. It involves the perfect timing between reclaiming

the energy stored in the titin fibers with the position of the actin and myosin. The titin stretch causes a reflex response.

There are other sensory organs found in muscle that also contribute to the stretch reflex action but the titin fibers play

quite a significant role.

Go to the next screen: There are many times an athlete

uses the stretch shortening cycle to produce an optimum

performance. One example is shown here on the screen.

Another example is the sweep of the free arm and turning of

the chest during delivery in the throwing events. This creates

stretches across the chest musculature in order to accelerate

the throwing arm. Another is the slight give in the takeoff leg

as it contacts the board in a long jump, prestretching the

extensor muscles of the leg in order to set up a more powerful

takeoff.

Running itself employs many stretch reflex situations, such as

the successive stretching of the gluteals and hamstrings when

the knee is lifted in each stride, the stretching of the hip flexors at push-off from each stride, and matching stretches in the

arms and shoulders.

While pre-stretching a muscle does contribute to elastic energy production, more is not always better. Excessive give in

the joints of the take-off leg, excessive torque, etc., are associated with weakness, collapse and causes loss of these elastic

benefits. As you saw in the experiments, timing between the recovery of the elastic energy of the titin with muscle action

will provide the greatest overall energy. Pre-stretch situations must be optimized.

Click the Home Menu Button

13

Click the Fatigue button: The precise causes of muscle

fatigue are not fully understood. Competitive cyclists can ride

all day, covering well over 100 miles. By comparison,

Olympic-class weight lifters cannot lift at or near their

maximum capacity for more than a few seconds. The difference

is due to the fact that muscles differ in their ability to resist

fatigue. Although fatigue eventually sets in after any kind of

muscular activity, it generally occurs more quickly when a

muscle is stimulated at higher frequencies and when larger

forces are generated.

Go to the next screen: Fatigue can occur at two levels –

the CNS and the PNS. Central fatigue mechanisms refer to

poor motivation through altered central nervous system

transmission or recruitment. Peripheral fatigue involves

impaired functional transmission, muscle electrical activity,

and activation. The failure of a muscle to contract voluntarily

could be due to fatigue of the following:

1. the motor nerve

2. the neuromuscular junction

3. contractile mechanism

4. the central nervous system

Fatigue is a very complex issue and this is all well will say

about it in this module. I’ve listed some of the reasons for

fatigue here just to alert you to its complexity. But, remember, this is still a fairly mysterious area and we don’t

understand a lot about it.

Click the Home Menu Button

You have now completed this module