Physiological Effects of Stretching

Stretching:

- Lengthens the sarcomeres

As a muscle stretches, the actin-myosin overlap decreases (increasing the overall sarcomere length) allowing the muscle fibre to elongate.

- Stretches the collagen within the tendons (via plastic deformation)

Once the fibre has reached it maximum length, additional stretching places force on the surrounding connective tissue. As the tension increases, collagen fibres align themselves along the same line of force as the tension (helps realign any disorganised fibres in the direction of the tension). The realignment is what helps to rehabilitate scarred tissue back to their previous length.

- Can help to train the stretch reflex (muscle spindles)

Muscle spindles are sensorimotor organs located within skeletal muscle. Each muscle spindle is made up of three to five specialized muscle cells known as intrafusal fibres. These cells, bundled together by a sheath of connective tissue, lay alongside the rest of the skeletal muscle fibres. When intrafusal fibres detect a change in muscle length, they reflexively stimulate a muscle contraction to prevent over-stretching and muscle fibre damage (stretch reflex).

It is important to hold a stretch for prolonged period of time because as you hold the muscle in a stretched position, the muscle spindle habituates (becomes accustomed to the new length) and reduces its signaling.

 

Physiological Effects of Strengthening

Neural factors which may increase muscle strength:

·         Motor units acting synchronously

·         More motor units activated during a muscular contraction

·         A reducing or counteracting inhibitory impulses (e.g. from golgi tendon organs)

Motor unit = A single motor neurone and all the muscle fibres that it stimulates.

Muscle hypertrophy:

• Transient: oedema in the interstitial and intracellular spaces of the muscle (fluid returns to blood within hours)
• Chronic: fibre hypertrophy or fibre hyperplasia

Fibre Hypertropy –

-          More myofibrils

-          More actin and myosin filaments

-          More sarcoplasm

-          More connective tissue

During exercise, protein synthesis decreases while protein degradation increases. The reverse is true in the post-exercise recovery period.

When the muscle is damaged during exercise (e.g. microtrauma) mononucleated cells in the muscle are activated by the injury, providing the chemical signal to circulating inflammatory cells. Neutrophils invade the injury site and release cytokines (immunoregulatory substances), which then attract and activate additional inflammatory cells. Neutophils possibly also release oxygen free radicals that can damage cell membranes. Macrophages then invade the damaged muscle fibres, removing debris through the process of phagocytosis. Last, a second phase of macrophage invasion occurs, which is associated with muscle regeneration (which might be the cause of muscle hypertrophy).

Fibre Hyperplasia -  

It is postulated that individual muscle fibres have the capacity to divide and split into two daughter cells, each of which can then develop into a functional muscle fibre. It has more recently been established that satellite cells (myogenic stem cells involved in skeletal muscle regeneration) are likely involved in the generation of new muscle fibres. Satellite cells are typically activated by muscle stretching and injury. Muscle injury can lead to a cascade of responses, in which satellite cells become activated and proliferate, migrate to the damaged region, and fuse to existing myofibres (hypertrophy) or combine and fuse to produce new myofibres (hyperplasia).

Wilmore, J., Costill, D. and Kenney, W. Physiology of sport and exercise. 4^th ed. (2008)

Muscle Contraction - Sliding Filament Theory

Myofibrils contain myofilaments:
Thick myofilaments - myosin
Thin myofilaments - actin
Myosin and actin filaments slide over one another to make the sarcomeres (short units of the myofibril) contract.

Muscle Contraction

1. Depolarisation of the sarcoplasmic reticulum releases Ca2+ into the sarcoplasm.
2. Ca2+ binds to troponin (changing its shape) pulling tropomyosin out of the actin-myosin binding site.
3. Myosin head binds to actin (actin-myosin cross bridge).
4. Ca2+ also activates ATPase (breaking down ATP) to move the myosin head which pulls the actin myofilament along.
5. ATP also required for the removal of the myosin head from the binding site.
6. Cycle repeats - progressively shortening the sarcomere.

Muscle Relaxation

1. Ca2+ ions are actively transported back to the sarcoplasmic reticulum.
2. Troponin molecules change back to their original shape - binding sites blocked by tropomyosin.
3. No actin-myosin cross bridges.
4. Actin filaments slide back to their relaxed position - lengthening the sarcomere.

Accessory Mobilisations (Maitland)

Maitland's Grades of Oscillatory Mobilisations

• Grade I Small amplitude movement performed at the beginning of the range.
• Grade II Large-amplitude movement performed within the range but not reaching the limit of the range. It can occupy any part of the range that is free of any stiffness or muscle spasm.
• Grade III Large amplitude movement performed  up to the limit of the range.
• Grade IV Small amplitude movement performed at the limit of the range.

Therapeutic Effects

- Activates the pain gate (grades 1/2)

- Stretches tissues (grades 3/4):

• Collagen fibres have a slight wavy appearance under a microscope (crimping)
• 1st line of response to loading: fibres line up in the direction of the applied force during movement taking up the slack (uncrimping)
• 2nd line of response to loading: when force is applied the tissue can stretch, but when the force is removed the tissue returns to its resting length (elastic deformation)
• 3rd line of response to loading: the deformation of a tissue in response to a maintained or constant load. The excessive load causes the collagen fibres to 'give' (collagen cross-links begin to fail) and the tissue begins to tear (creep)

Loading affects the length of connective tissues through a process of internal microfailure mechanisms that result in a change in the resting length of connective tissue through plastic deformation.

Process: stretching the connective tissue causes minor ruptures of the collagen fibres leaving free 'end points'. This initiates an inflammatory response, in which the fibroblasts deposit more collagen fibres. These reunite with the 'end points' to elongate the fibres increasing the length of the connective tissues.

- Activates trans-synovial pump
- Provides temporary muscle relaxation
- Improves neurodynamics
- Facilitates healing

Complete Contraindications:
Rhematoid collagen necrosis
Fracture - recent or unhealed
Joint ankylosis
Vertebrobasilar insufficiency
Active inflammatory or infective arthritis
Malignancy

Relative Contraindications:
Pregnancy
History of malignancy
Hypermobility
Osteoporosis
Neurological signs
Spondylolisthesis
Dizziness

Phases of Healing - Summary

The inflammatory response is stimulated by the release of chemical mediators from the cells damaged at the injury. There is a vascular response and a cellular response.

-          Vascular: vasodilation and vasopermeability causing hyperaemia and the production of oedema within the tissues (via increased hydrostatic pressure and decreased osmotic pressure). WBCs marginate, platelets adhere to the vessels walls and endothelial cells swell. The exudate dilutes irritant substances, forms a fibrin clot around the intact tissues, and the fibrin also develops into a meshwork to trap foreign particles and debris.

-          Cellular: chemotaxis (by chemical mediators), phagocytosis and site clearance. Lactic acid is the end product of phagocytosis and this is a stimulant of the proliferative phase of healing.

Macrophages and lactate stimulate the proliferative stage. Fibroblasts and endothelial cells are attracted to the damaged area from neighbouring tissues. Fibroblasts are responsible for secreting collagen and an amorphous ground substance. The ground substance provides a linking mechanism for the collagen fibres (primarily type III at this stage). The collagen fibres are deposited in a haphazard manner and are relatively weak and not specialised to the parent tissue at this time. Angiogenesis also occurs which is the growth of new blood vessels within the damaged tissue to provide more oxygen and remove debris/co2. The revascularisation is what makes the tissues look red around the scar caused by an injury. Myofibroblasts are responsible for drawing the edges of the wound together (from contraction) reducing the size of the final scar. When the damage is healed these cells die from a process called apoptosis. As the granulation tissue matures there is a process of devascularisation with obliteration of the lumen of the vessels.

The remodelling stage can begin as early as the first 1/2 weeks post injury and last upto 2 years. This is the stage in which the collagen fibres align in the direction of stress (from movement). It is also made stronger by the deposition of stronger type I collagen fibres and the reabsorption of the original type III collagen. It never becomes as strong as the parent tissue.

Healing of Muscle Strains: 

Muscle can regenerate. Satellite cells are ‘stem cells’ that have the ability to differentiate into myoblasts and to form new muscle fibres. However if a patient suffers a third degree strain and the muscle is completely severed, the two segments heal by dense scar tissue formation. Muscle does not regenerate across the scar and functional continuity is not restored.



Passive Mobilisations: Primary Therapeutic Effects

Elongates contracted connective tissues: Movement encourages the normal turnover of collagen and its alignment along the lines of mechanical stress. This adaptive reorganisation provides the tissue with better tensile properties. Movement improves the balance of glycosaminoglycans and water content within the tissue which helps maintain the interfibril distance and lubrication. This reduces the potential for abnormal cross-links formation and adhesion.    

   

Pain gate: Nociceptors (small diameter fibres) block the inhibitory neurone and excite the projection neurones. Therefore the inhibitory interneurone cannot block the output of the projection neurone that connects with the brain - gate is open. Large diameter fibres excite the inhibitory interneurone and also the projection neurone, therefore the inhibitory interneurone can block the output of the projection neurone - gate is closed.

Passive mobilisations stimulate mechanoreceptors located within joint capsules and ligaments. Information travels faster via large-diameter fibres (mechanorecptors), their stimulation causes them to arrive faster at the spinal cord, thereby inhibiting the pain messages from small-diameter fibres (nociceptors).

Speed of Conduction

Nociceptors:

C fibres - travels at a rate of 0.5 - 2 metres per second (unmyelinated)

A delta fibres - travel at a rate of 5 - 15 metres per second (thinly myelinated)

Mechanoreceptor:

A beta - travels at a rate of 30 - 70 metres per second (myelinated)

Myelin - an insulated sheath around an axon; consists of multiple layers neuroglial membrane; significantly increases the impulse propagation rate along the axon (saltatory conduction).

*Also action potentials are conducted quicker along axons with bigger diameters because there is less resistance to the flow of ions than in the cytoplasm of a smaller axon.*

 

Facilitates the trans-synovial pump:

Movement (active or passive) activates the trans-synovial pump which facilitates the formation and drainage of synovial fluid in the joint. On one end of the pump movement causes increased blood flow around the synovium (which is important for the formation of synovial fluid) and on the other end of the system, it stimulates drainage into the interstitial spaces (lymphatic system). Movement also alters the intra-articular pressures within a joint; an increase in the intra-articular pressure produces an outflow, while a decrease in the intra-articular pressure increases the influx into the joint cavity.

Joint swelling is the primary cause for stiffness and reduced range of motion post-injury. Early mobilisation will help reduce joint swelling by activating the trans-synovial pump and draining the oedamatous peri-articular structures.


Other therapeutic effects include...

• Facilitation of the healing process
• An improvement in neurodynamics
• Temporary muscle inhibition