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Hypertrophy
Refers to an increase in muscle size due to enlargement of individual muscle cells typically caused by progressive overload.
There are three types of hypertrophy which contribute to increased muscle size including, myofibrillar, connective tissue and sarcoplasmic hypertrophy.
The most common form is myofibrillar hypertrophy which refers to an increase in the number of sarcomeres.
When muscles are put under load, damage to the muscle fibres causes an increase in growth hormones facilitating repair.
While it enhances force production, excess hypertrophy can cause restricted ROM and alter posture and gait.
E.g. Hypertrophy in the triceps brachii may cause increased forelimb retraction due to increased elbow extension.
Atrophy
Refers to a decrease in muscle size and strength due to disuse, immobilsation, systemic illness or neurological deficit.
Atrophy can be localised or generalised. Localised atrophy is usually caused by offloading due to injury or peripheral nerve injury whereas generalised atrophy tends to be a result of systemic illness.
At a cellular level there is a loss of sarcomeres, reduced muscle fibre size and an increase in connective tissue which can lead to stiffness.
Functionally this leads to reduced force production, joint stability and visible asymmetry.
E.g. Atrophy of the quadriceps reduces protraction and force production.
Hypertonicity
Refers to an increase in muscle tone at rest where there is resistance to passive ROM. This is often caused by overuse, adaptive shortening or neurological dysfunction. It can occur when muscles are often used or held in the shortened position. At a cellular level this leads to increased neural input and sustained sarcomere contraction.
E.g. hypertonicity in triceps brachii muscle may cause reduced elbow flexion due to its role in elbow extension.
Hypotonicity
Refers to a decrease in muscle tone at rest resulting in decreased resistance to passive ROM.
It is commonly caused by neurological dysfunction, and lack of muscle activation due to offloading and compensation.
At a cellular level there is a lack of neural input at the neuromuscular junction causing reduced muscle contraction.
This causes a weakness and a lack of stability at the joints affecting performance and coordination.
E.g. Hypotonicity in the triceps brachii muscle may cause reduced elbow stability.
Fibrosis/adhesions
Hyper-irritable spot within a taut band of muscle that produce local pain.
They are often caused by overuse, strain or motor end-plate dysfunction.
At a cellular level, there is a sustained release of acetylcholine causing sustained sarcomere contraction. This creates local ischaemia and hypoxia.
Functionally this reduces muscle activation and restricts movement, globally they contribute to pain and reduced performance.
During palpation, these often show as fasciculations. Commonly found along the back in muscles such as the Longissimus dorsi
Inflammation
The bodys acute response to injury or infection. Involves vascular changes and immune cell influx to promote healing.
The main signs of inflammation include pain and heat. This causes hypersensitivity and hyperalgesia.
Reducing inflammation is an important part of pain management. acute inflammation is an essential stage of healing but chronic inflammation is not useful and should be minimised. In horses this is common in the lumbar region of the back and in the distal limbs
Odeoma
Accumulation of excess fluid in the interstitial space surrounding the tissues. This is often caused by disruption of normal capillary filtration or lymphatic drainage following injury, inflammation or infection. Fluid buildup increases pressure on the tissues reducing oxygen diffusion and impairing cellular metabolism. Locally, oedema presents as swelling and pain. Functionally, it can limit joint mobility, alter gait and reduce performance due to discomfort. Often found surrounding the caudal vertebrae and in the distal limbs following excessive loading.
Trigger points
Forms following injury as part of the healing process. Fibrosis occurs within a tissue whereas adhesions bind separate tissues. scar tissue is elastic, less organised and lacks normal tissue function such as contractility. At a cellular level, collagen is laid down in a disorganised manner. Functionally, this restricts movement and reduces tissue extensibility. Globally it can cause stiffness reduced ROM, and increased risk of reinjury.