Week 1 - Principles Flashcards
What do ligaments do
Connect bones
Stabilise joint by limiting excessive movement
Provides proprioception – contain sensory receptors that provide feedback, eg golgi tendon organs, stretch spindles
Made up of collagen fibres collagen fibres
Types of ligament damage
Grade 1 – few fibres
Grade 2 - >50% increased laxity, with end feel
Grade 3 – Complete no end feel
What do muscles do
Made up of muscle fibres, which are composed of proteins called actin and myosin.
Provide movement. When muscle fibre receives and electrical signal from nervous system the actin and mysin filaments slide past each other causing contraction, which generates force and allows movement
Provides stability. This is done via passive stability (provided by ligaments and other connective tissues surrounding joints), active stability (provided by the muscles themselves by pulling on bones to stabilise joints).
Concentric movement: when a muscle contracts as it shortens eg a bicep curl
Eccentric movement: when a muscle lengthens as it contracts eg a squat
Types of muscle damage
Muscles tears (pain, strength, flexibility). Tend to heal quickly because of good blood supply.
* Grade 1 – few fibres (few days)
* Grade 2 >50% pain and swelling – pain on contraction, reduced strength, reduced ROM (6-8 weeks)
* Grade 3 – Complete tear. Full loss of function (minimum 3 months recovery time) (3 months)
Contusion/haematoma eg dead leg
* Intermuscular/bruising
* Intramuscular/compartment syndrome
What do tendons do
- Muscle to bone
- Transfers force from muscles to bone, allowing movement of joint
Structure of tendons
- Collagen fibres organised in a parallel manner (mostly type 1 collagen).
- Therefore, tendon is the lever made of collagen and elastin, muscle is the power made of muscle fibres
- Layers of the tendon – epitenon, endotenon, fascicles, collagen fibres, tenocytes
Types of tendon damage
- Tendonitis,
- Tendonopathy/tendinosis,
- Tenosynovitis (inflammation of membrane surrounding tendon),
- Rupture,
- Tenoperiositis/ethesopathy,
- Bursitis
o Stiffness - “relation between the force exerted on the tendon and its change in length”
Improves running economy (releases energy quickly) so can improve performance
Can be protective against tendinopathy
Can be improved with plyometric, isometric/eccentric exercise - Tendinopathy stage 1 – reactive
- Tendinopathy stage 2 – Dysrepair
- Tendinopathy stage 3 – Degenerative
What does fascia do
- Thin connective tissue covering, supports and reduces friction
- Superficial – conveys blood vessels and nerves to and from skin, promotes movement between skn and underlying structures
- Deep – surrounds skeletal muscle fibres, dense connective tissue sheets of large numbers of closely packed collagen fibres, helps to promote movement and provide stability
- Eg ITB – iliac crest lateral condyle of tibia. Stabalises the hip and knee joint during movement. Works with glutes to control hip movement.
Types of fascial damage
- Excessive or prolonged loading leads to damage from chonic inflammatory response, leading to cyclotoxic levels opf cytokines, increase macrophages, release of substance P
- Fibrosis and pain – impacts on tissue dynamics, impact on force generation capacity
- Eg ITB – poor control of hip rotation, weak glutes, tight hip flexors, overpronating feet, training errors
Types of cartilage
- Hyaline eg articular – most common found in nose/trachea/long bones. Smooth and glassy, provides cushioning to support joints and allow smooth movement
- Fibrocartilage eg meniscus (joint capsules) – tough and dense type of cartilage, eg intervertebral discs and pubic symphysis. Provides support and stability and distributes shock evenly across joints
- Elastic (external ear, epiglottis) – flexible and elastic tupe of cartilage that provides support and shape to structures.
Cartilage change in osteoarthritis
- Metabolic – metabolic deposition (eg cholesterol, iron), crystals (hydroxyapatite)
- Inflammatory – enthesitis, underlying inflammatory arthritis, systemtic low grade inflammation
- Structural – impaired lymphatic transport, age
- Mechanical – overuse, trauma, frictional forces by osteophytes, osteochondral lesion
Traumatic injury linked with increased risk of OA, sport not necessarily linked and has a healthy relationship with cartilage (no difference in cartilage volume). COMP (cartilage oligometric matrix protein) increases immediately after running but then settles (1-2hours) eg don’t run on consecutive days if arthritic problems. Ultimately promotes nutrition of cartilage.
Types of bone and what does it do
Cortical and trabeular
Provide protection for underlying organs, a supply of Ca, production of blood cells, lever in locomotion
Types of pain
- Nociceptive – injured or irritated somatic or visceral structure
- Neuropathic – injury to the neural structure
- Nociceptive and neuropathic components
Why do injuries occur
Imbalance between training/load management and conditioning. Consider impact of recovery, sleep, environment, REDS etc.
Describe the healing process
Acute inflammatory phase:
In the initial stage there is inflammation with aim to protect the site from further damage and remove dead or damaged tissue.
Haemostasis, capillary rupture, infiltrative bleeding, oedema and inflammation (plasma exudation) -> haematoma
Neutrophils infiltrate the area within 1 hour of injury (peak @ 24-48 hours), magnifying the inflammatory process. Macrophages further assist the inflammatory process and also release growth-related mediators
Proliferative phase:
Angiogenesis occurs (growth of new capillaries) allowing the rebuilding and repair of dead tissues. There is an accumulation of endothelial cells and fibroblasts which helps to lay down granulation tissue, allowing gradual repair and remodelling.
Remodelling stage
In this stage the granulation tissue remodelled and strengthened. There is significant reduction of macrophages and a mature blood supply is established.
Thicker collagen fibers are formed in direction of tissue tension and network of cross bridges established
Form and function of scar tissue depends on the degree to which the tissue is subjected to loading during this stage.
