Neuromuscular Physiology

There are two different kinds of neurons involved in the neuromuscular physiology: sensory and motor neurons.  Sensory neurons are afferent, meaning they carry information to the brain.  Muscle spindles and golgi tendon organs (GTO) are proprioceptors, which are specialized sensory receptors that give the CNS information necessary to maintain muscle tone and perform complex, coordinated movements.  We'll go into deeper detail about them a little later in the section. Motor neurons are efferent, meaning they carry information to the muscles.  There are alpha motorneurons that send info to skeletal muscles, and gamma motorneurons that send info to the muscle spindle fibers. 

Steps of the Activation of Muscles

  1. Neuron action potential at the motor neuron

    • Electrical current flows along a motor neuron

  2. Chemical transmission

    • The motor neuron releases Acetylcholine, which crosses the neuromuscular junction to excite the sarcolemma, which is the cell membrane of the muscle fiber.

  3. Muscle action potential

    • An action potential occurs when the Ach threshold is reached, causing Calcium to release form the sarcoplasmic reticulum and the muscle to contract.  The all or none principle comes into play here: either all of the fibers in a motor unit contract and develop force at the same time, or none of them do.  Like an average light switch with no dimming feature, muscle cells cannot partially contract.

    • The action potential results in either a twitch or a tetanus.  A twitch is a brief contraction that only has low force development because calcium was remove before the contraction could reach maximum force.  A tetanus is like continuous twitches when calcium isn't removed and the maximum amount of force is generated.  Tetanus happens when there's an increased frequency of stimuli.

  4. Sliding filament theory

    The sliding filament theory explains how myosin and actin interact to cause a muscle contraction.  There are 5 stages: resting, excitement-contraction, contraction, recharge, and relaxation.

  1. The resting phase is before there is any tension in the muscle, pretty self explanatory.

  2. The excitement-contraction phase occurs once the sarcoplasmic reticulum (SR) releases calcium, that binds to troponin, which causes tropomyosin to shift, allowing the myosin cross-bridge to attach to actin. The muscle force is determined by the number of cross bridges involved.  When there's an increase in the number of cross-bridges, myofibril and sarcoplasmic reticulum hypertrophy, which result in more actin + myosin and more fuel for the muscle respectively.  To increase the power generated in a contraction, there needs to be an increase in the speed of cross bridges.  Also make note: at this point, the muscle still hasn't quite contracted.

  3. The contraction phase is where the power stroke occurs.  ATP undergoes hydrolysis via the enzyme myosin ATPase, and loses a phosphate to become ADP.  This allows the myosin head to change shape and pull on the actin, which is referred to as the power stroke.  Myosin pulling on actin causes the muscle fiber to shorten.

  4. The recharge phase is when the contraction continues and can only occur when calcium, ATP, and myosin ATPase are all still available.

  5. The relaxation phase occurs when nerve stimulation stops and those components are no longer available.  The calcium returns to the sarcoplasmic reticulum and myosin lets go of actin.

Muscle Fiber Types

We talked about the different muscle fiber types in the muscle physiology section, so we'll keep this part here brief.  You already know of the three different types of muscle fibers: Type 1, Type 2a, and Type 2x (formerly known as Type 2b). Also below are two tables that clearly show the differences in the muscle fiber characteristics between the three types, as well as their relative involvement in different sports.

Type 1 is slow twitch, and has a lower Ach threshold but also produces a lower amount of force.  These muscle fibers also have nerves with smaller diameters, smaller capillaries, and smaller mitochondria compared to the other two types.  This all results in a muscle fiber with the least force-producing capability.

Type 2a is fast twitch, has a higher Ach threshold and can produce more force than Type 1.  It's nerve diameter, capillaries, and mitochondria are all intermediately sized, making this the "middle" muscle fiber.

Type 2x is also fast twitch, but has the largest nerve diameter, capillaries, and mitochondria, allowing it to generate the greatest amount of force out of all of the muscle fiber types.  It also has more myosin ATPase, which is the enzyme that catalyzes the reaction that allows the myosin head to attach to actin, and is necessary in abundance for tetanus, or continuous contraction.

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Force Production

The variations in the amount of force produced depend on neuromuscular activation and cross sectional area of the muscle fiber.  Unless (maybe) you're a super elite athlete, there's no way to increase the number of muscle fibers you have.  You get what you get, but you can do a better job using them by increasing the number of motor units recruited, the frequency of activation, and synchronize the recruitment. This can all be done by staying hydrated and properly nourished so that the body has enough fuel for the work you're going to put it through.  You can also increase the cross sectional area of the muscle fiber by increasing the diameter of actin and myosin.

Motor unit recruitment is based on a size principle: the smallest muscle fibers with the lowest threshold are recruited first.  If you don't remember, check back to the text or table above and you'll see that this is describing Type 1 fibers.  Although recruitment is dependent on the physiological demands of the activity, recruitment typically starts with Type 1, to Type 2a, to Type 2x.  It's possible to train to lower the threshold to activate Type 2 muscle fibers and to produce greater force.  It's proven that trained individuals activate Type 2 muscle fibers more quickly during exercise.  This is similar to the onset of sweating and is another way that the body becomes more efficient with more and better training.

Preloading helps with strength development early on in a movement because max force production doesn't occur early in a range of motion.  When you preload a muscle, the sarcomeres are stretched and create an optimum length-tension relationship and adds elastic recoil force.  This provides passive tension across the muscle which increases force, length, and tension.   


Proprioceptors are specialized sensory receptors located within the muscles, tendons, and joints that share information with the central nervous system (CNS) to help maintain muscle tone, prevent overstretching, and perform complex, coordinated movements.  The two skeletal muscle proprioceptors are muscle spindles and golgi tendon organs (GTO), and they have opposite functions.  To put it very plainly, when the muscle spindles are activated, they cause a contraction, but the golgi tendon organs cause relaxation when activated.

Muscle spindles provide information about muscle length and the rate of change in length.   When they sense that a muscle is being stretched too far or too fast, they activate and result in a stretch reflex to limit the range of motion.  A powerful and rapid stretch results in a powerful and rapid response by the muscle spindles to prevent that stretch from going too far.  Muscle spindles are also involved in reciprocal inhibition, which is the relaxation of a muscle being stretched when its antagonist is contracting.  So think of a dumbbell curl: on the concentric (raising) phase of the motion, the biceps brachii are contracting and the triceps brachii need to stay relaxed so that they're not adding any extra load for the biceps to overcome. 

Golgi tendon organs (GTOs) provide information about any changes in tension on a tendon.  When GTOs are activated, it inhibits the motor unit and causes the muscle that's under tension to relax; this is called autogenic inhibition.  GTOs protects the muscle from excessive force production.