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PHYSIOTHERAPY > HUMAN FUNCTIONING MSK > Flashcards

HUMAN FUNCTIONING MSK Flashcards

1
Q

What are the main features of the vertebrae?

A

Vertebral body
Vertebral Foramen
Pedicle
Laminae
Spinous process
Transverse process
Articular process

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2
Q

What is the intervertebral vertebral foramen?

A

An opening between vertebrae through which nerves leave the spine and extend to other parts of the body. It lies between the pedicles of neighbouring vertebrae.

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3
Q

What is the sagittal plane?

A

(also known as the longitudinal plane)
It is perpendicular to the ground and divides the body into left and right.

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4
Q

What is the coronal plane?

A

(also known as the frontal plane)
It is perpendicular to the ground and divides the body into posterior (back) and anterior (front) portions.

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5
Q

What is the transverse plane?

A

(also known as an axial plane)
It divides the body into head and tail portions. It is parallel to the ground, which in humans, separates the head from the feet.

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6
Q

What is the sagittal axis?

A

Passes horizontally from the posterior to anterior and is formed by the intersection of the sagittal and transverse planes.

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7
Q

What is the frontal axis?

A

Passes horizontally from left to right and is formed by the intersection of the frontal and transverse planes.

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8
Q

What is the vertical axis?

A

PAsses vertically from inferior to superior and is formed by the intersection of the sagittal and frontal planes.

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9
Q

What plane and axis does extension and flexion occur in?

A

The sagittal plane
The frontal axis

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10
Q

What plane and axis does abduction and adduction occur in?

A

The frontal plane
The sagittal axis

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11
Q

What plane and axis does rotation occur in?

A

The transverse plane
The vertical axis

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12
Q

Give an example of a movement that occurs in the sagittal plane and frontal axis?

A

Walking
Squat

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13
Q

Give an example of a movement that occurs in the frontal plane and sagittal axis?

A

Jumping backs
Cartwheel

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14
Q

Give an example of a movement that occurs in the transverse plane through the vertical axis?

A

Shaking your head
Twisting your upper body whilst your feet remained planted on the floor.

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15
Q

Define pain

A

IASP 2020 - an unpleasant sensory and emotional experience associated with, or resembling that associated with actual or potential tissue damage.

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16
Q

What is pain perception?

A

The understanding of physiological pain, which is generally invoked by stimulus that elicit or threaten to elicit tissue injury. It involves a combination of sensory, emotional, cognitive and behavioural components that collectively contribute to an individual’s experience of pain.

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17
Q

What is somatogenic pain?

A

Pain with a cause (usually known) localized in body tissue

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18
Q

What is psychogenic pain?

A

A pain for which there is no known physical cause but the processing of sensitive information in CNS is disturbed

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19
Q

Explain the multidimensional nature of pain?

A

The sensory dimension - the physical sensations associated with pain
The emotional dimension - pain is often associated with negative emotions, such as fear, anxiety and depression
The cognitive dimension of pain - dimension of pain that refers to the thoughts and beliefs associated with pain
The behavioural dimension - the observable response to pain such as facial expressions, body posture and activity level
The sociocultural dimension of pain - the impact of social and cultural factors on pain percepton eg gender, ethnicity, socioeconoic status and is affected by all of the above factors.
These factors account for differences in pain tolerance among humans.

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20
Q

What is the timeline fr pain?

A

Acute - 0-6 weeks
Sub-acute - 6 weeks to 3 months
Persistant (chronic) - 3+ months

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21
Q

What is the organisation of the nervous system?

A

Central nervous system - brain and spinal cord
Peripheral nervous system - cranial nerves and spinal nerves
Autonomic nervous system - heart muscle, smooth muscle, glands
Somatic nervous system - voluntary skeletal muscles
Parasympathetic division - rest and digest
Sympathetic division - active and alert

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22
Q

What are the 5 steps in the perception of pain by the peripheral nervous system?

A
  1. Transduction of noxious stimuli by sensory receptors
  2. Conduction
  3. Transmission of nocioceptive information
  4. Modulation of the incoming noxious information
  5. Perception of noxious information
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23
Q

What regions of the brain are involved in pain processing?

A

Somatosensory cortex
Limbic system
Prefrontal cortex

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24
Q

Explain the role of the somatosensory cortex?

A

Sensory processing of pain
The primary somatosensory cortex processes the physical characteristics of pain, such as location, intensity and quality
The secondary somatosensory cortex integrates sensory inputs and contributes to the perception of pain’s spatial and temporal aspects

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25
Q

What is the role of the anterior cingulte cortex?

A

Emotional and affective aspects
Integrates sensory, emotional and cognitive aspects of pain, playing a role in the subjective experience of pain intensity and emotional response. Contributes to the distressing and motivational aspects of pain perception.

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26
Q

What is the role of the insular cortex?

A

Emotional and affective aspects
Integrates sensory, emotional and cognitive aspects of pain, playing a role in the subjective experience of pain intensity and emotional responses.

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27
Q

What is the role of the prefrontal cortex?

A

Cognitive and evaluation attention
Assesses the significance of pain, incorporates evaluations and influences the decision to engage with or disengage from pain-related stimuli.

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28
Q

Explain the role of the prefrontal and anterior cingulate cortex?

A

Cognitive and evaluation of attention
Regulate attention, cognitive control, and coping strategies related to pain perception.
INFLUENCESDECISION TO ENGAGE WITH PAIN

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29
Q

Explain the role of the periaqueductal gray (PAG)?

A

Modulation of pain perception
Initiates descending pain modulation pathways, influencing pain transmission and perception through the endogenous pain control mechanisms

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30
Q

Explain the role of the restroventral medulla?

A

Modulation of pain perception
Contributes to pain modulation by inhibiting or facilitating pain signal as they travel up the spinal cord.

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31
Q

Explain the role of the somatosensory cortex, ACC and Insula?

A

Integration and pain matrix
Form the core of the pain matrix, integrating sensory, emotional, and cognitive aspects to create the overall pain experience.

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32
Q

Explain the role of the thalamus?

A

Integration and pain matris
Acts as a relay station, directing pain signals to relevant brain regions for processing.

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33
Q

What are the individual variables in pain perception?

A

Genetic factors
Cultural factors
Experiential factors
Individuals differences
Psychological factors

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34
Q

Define anterior

A

Forward, in front of of

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35
Q

Define posterior

A

Behind, further back

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36
Q

What is the axial body?

A

Head, neck and trunk

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37
Q

What is the appendicular body

A

The limbs

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38
Q

Define proximal

A

Closer to the axial body (toward the trunk)

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39
Q

Define distal

A

Further from the axial body (further away from the trunk) eg the foot is distal to the thigh

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40
Q

What is an isotonic muscle contraction?

A

Characterised by a change in length of muscle during contraction without a change in load or resistance
Concentric contraction and eccentric contraction are both types of isotonic muscle contraction
Concentric contraction - muscles shortening under load eg flexion phase of bicep curl
Eccentric - muscle is lengthened under load eg extension phase of a bicep curl

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41
Q

What is isometric muscle contraction?

A

There is no change in muscle length during contraction eg rectus adbominus during the plank. It is a static muscle contraction, eg holding a bicep curl at one point.

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42
Q

What is isokinetic contraction?

A

The muscle changes length during contraction. They produce movement at a constant speed. Eg breastroke when swimming when the water provides a constant, even resistance to at adduction movement. To provide this type of contraction you would need to be using an isokinetic dynamoeter system

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43
Q

What are antagonistic muscle pairs?

A

When muscles work in pairs to produce a movement. Eg flexion at the elbow the bicep contracts and shortens and the tricep lengthens. The bicep is called the agonist and is the main muscle (the prime mover doing the work) and the tricep is the antagonist relaxing and lengthening.
Kicking a football the hamstrings are the antagonists

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44
Q

What are some differential diagnosise for lower back pain?

A

Alternative conditions that may present with low back pain include:
Neurological - sciatica, higher cord lesion, peroneal palsy, deep gluteal syndrome, spinal stenosis
Systemic - vascular claudication, ankylosing spondylitis
Other - abdominal aortic aneurysm, facet joint arthropathy, osteoporosis, osteoarthisitis, rheumatoid arthisitis, shingles

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45
Q

What is nocioception?

A

The neural process of encoding and processing noxious stimuli. (a stimulus strong enough to threaten the body’s integrity). Nocioception refers to a signal arriving at the CNS as a result of the stimulation of specialised sensory receptors in the peripheral nervous system.
Nocioceptors can be activated by three types of stimulus: temperature, mechanical and chemical.
The cell bodies of nociceptors are located in the dorsal root ganglia. Their axons extend into the peripheral nervous system.

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46
Q

How are nocioceptors divided?

A

A delta fibres - large, myelinated, fast conducting fibres, concerned with localized, sharp and fast sensation of pain
Type I As: mechanically sensitive afferants
Type II As: lower heat thresholds but higher mechanical thresholds
C fibres - are small, unmyleinated, slow conducting nerve fibres, concerned with dull, and slow pain sensation.
A-beta are myelinated, large diameter, and have the fastest conduction velocity. These fibrs respond to non-painful stimuli such as: touch sensation, mild pressura and vibration.

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47
Q

What is the gate control theory of pain?

A

A mechanism, in the spinal cord, whwhich pain signals can be sent up to the brain to be processed to accentuate the possible percieved pain, or attenuate it at the spinal cord itself.
The gate is the mechanism where pain signals can be let through or restricted. If the gate is open, pain signals can pass through and will be sent to the brain to percieve the pain. If the gate is closed, pain signals will be restricted from travelling up to the brain, and the sensation of the pain won’t be percieved.

If someone experiences a painful stimulus, the application of a non-noxious stimulus can help to activate the gate control machanism.

It is located in the dorsal horn of the spinal cord.

48
Q

What are pain descending pathways?

A

Once a pain signal from the ascending pathway reaches the somatosensory cortex, it triggers descending pain modulatory system. The goal of this system is to allow the organism to function enough to respond t the pain source by reducing the pain signal through neural inhibition in the top down modulation of pain.

49
Q

How do endogenous opoids work?

A

When endogenous opoids act on these receptors it reduces neurotransmitter release from the first order neurone, and causes hyperpolarisation of the second order neurone. Together, this reduces the firing of action potentials in the second order neurone, blocking the transmission of pain signals.

50
Q

What muscles are involved in forced inhalation?

A

Sternocleidomastoideus
Scalene
Serratus anterior
Pectoralis minor
Intercostals
Rectus abdominus
Internal oblique
External oblique
Transverse abdominus

51
Q

What is the pleura?

A

Each lung is sitting in its own sealed chamber, both the lung and its outer chamber have a very smooth lining called the pleura.
Each of the lung is covered by a visceral pleura. They sit in their space which is covered by the parietal pleura. The space between the two pleura is very thin in life.
The visceral pleura lines the lungs an the parietal pleura lines the cavity. It is filled with fluid called pleural fluid.
A liquid between the surfaces of such a thin space creates significant capillary forces, which hold the two surfaces together - it pulls the lungs surface with the cavity’s surface because the lung is flexible.
At the bottom of the lung there is the parietal pleura which is just cavity, which is a reserve space for the full expansion of the lung at maximal inhalation.

52
Q

What are the airways in the lungs?

A

Tubes that bring air in and out of the alveoli. They have larger air spaces than the alveoli and thicker walls. Smaller airways have thicker walls because thee have a small muscle layer. This layer contracts during asthma, which impairs air flow to the alveoli which leads to shortness of breath.

53
Q

What is the diaphragm?

A

The main muscle involved in respiration.
It has a tough connective tissue sheet in its middle, called the central tendon. The fibres form a dome shaped structure which pulls the central tendon downwards when they contract.
They insert into the margain of the lowest ribs and the sides of the lowest thoracic vertebrae.
During relaxed breathing, the diaphragm contracts, which pulls the central tendon down and creates more space. As the lung is tethered to the wall of its cavity by capillary forces, it expands and the elastic fibres get stretched, which causes air to flow in.
Exhalation is mostly achieved by the recoil of the elastic fibres in the lung. The lung is pulled back to its original size.

54
Q

What happens during forced inhalation?

A

The auxillary muscles pull the thorax upward and outward. The intercostal muscles contract and bring the ribs closer to each other. The scalenes anterior and posterior, serratus anterior, sternocleidomastoideus, intercostals and pectoralis minor pull the thorax upwards, and this extends the thorax.

55
Q

What are the functions of bones?

A

Mechanical: support, protection, assists movement, shape and form
Chemical: homeostasis of minerals, energy store for metabolism
Haematological: blood cell production

56
Q

What are the properties of bone?

A

Dynamic
Metabolically active
Highly vascular
Capacity for self repair

Microscopic make up: 65% minerals (calcium and phosphorus), 30% organic matrix (90% collagen fibres and 10% protein) 5% water

70-80% of bone strength is accounted for by bone density (calcium and phosphorus)
20% strength comes from bone architecture.

57
Q

What are osteocytes?

A

Mature osteoblasts, connected and surrounded by bone matrix

Their function is to regukate bone metabolism and they are pivotol in bone turnover and adaption of bone

58
Q

What are osteoclasts?

A

Originate from haemopoietic stem cells

Their function is bone resportion, regulated by the thyroid gland. Activated low blood calcium levels, bone repair and remodelling

Predominantly found on the endosteal and periosteal surfaces.

59
Q

What is cortical/compact bone?

A

80% of the skeleton
Hollow tube of long bone
Lamellae form concentric rings around central longitdinal canals

60
Q

Explain the formation of bone structure?

A

Osteoblast percursor cells arise from stems cells in the bone marrow
Osteoblasts take up calcium compounds from the blood to make more bone matrix
Further addition of calcium phosphate to the bone matrix leads to calcification. The mature cells become embedded and stuck.
Eventually become embedded in the matrix forming uncalcified bone matrix.

61
Q

What are the 4 stages of bone healing?

A

Haemotoma 0-48 hours: ruptured blood vessels leak blood into the fracture site which fills the gap. Clotted blood allows nutrophils into the site and get rid of nexrotic tissue. New blood vessels are laid down.
Soft callus stage - 0-2 weeks: white blood cells and platelets relaese growth factors. Osteoblasts lay down woken tissue
Bony callus stage
Bony callus stage - 2-12 weeks
Remodelling: pressure through bone takes weight tissue which causes tissue thickening, reducing size of bony callus.

62
Q

What is wolf’s law?

A

Remodelling of bone is a cyclical process which happens throughout life
Takes between 4 to 8 months

Reabsorption (10 days)
Matrix formation (10-20 days)
Mineralisation (3-4 months)

Bone is laid down where it is needed and re absorbed where it is not
Bone has the ability to adapt by changing size shape and structure to the mechanical demands placed on it.

Those that are inactive ir immobile are at greater risk of the balance of remodelling shifting towards greater reabsorption.

63
Q

What are the stages of bone remodelling?

A

Reabsorption: pre-osteoclasts and active osteoclasts
Reversal: pre-osteoblasts
Bone formation: osteoblasts
Mineralisation: osteocytes

For a healthy skeletal system, there needs to be a balance between reabsorption and deposition of cells.

64
Q

What is the link between bone mass density and physical activity?

A

More physical activity increases bone mass in early teen years
Normal forces in daily activities in older adults is not enough to sustain critical bone mass

65
Q

What factors influence the reabsorption of bone?

A

Smoking
Age
Alcoholism
Eating disorder
Drug - steroid use
Reduced weight bearing
Causes more bone to be reabsorbed than is laid down, which results in structural fragility.

66
Q

What most important factors negatively effect bone mass density?

A

Mechanical loading, ageing, menopause, achieving peak bone mass in childhood.

67
Q

What is osteoporosis?

A

Characterised by low bone mass and structural deterioration of bone tissue.
Consequences increases bone fragility and susceptibility to fracture
1 in 3 women and 1 in 5 men over 50 will experience osteoporosis

The lattice (honeycomb) structure becomes more porous, weaker and gaps widen. Even a low level fall would be sufficient trauma to cause a fracture.

68
Q

What are some risk factors for osteoporosis?

A

All women over 65, all men over 75

Or below this age with the following risks:
- previous fragility fracture
- current or frequent use of oral glucocorticoids
- a history of falls
- a family history of hip fracture
- low body mass index
- smoking
- alcohol intake of more than 14/21 units per week for women/men

69
Q

Why do bones fracture?

A

Disease: structurally weak
Over stress or strain: sudden injury
Over stress or strain: repeated microtrauma

70
Q

How are fractures classified?

A

Aetiology: injury, fatigue or stress, pathological
Type: closed/simple, compound/open
Pattern: intra (inside joint)/extra (outside joint) articular, deformity of fragments

71
Q

What are some fracture examples?

A

Compression
Comminuted: combined loading
Undetected

Classifications:
unloaded
avulsion (pulled apart)
compression
transverse bending
oblique shear
spiral torsion
combined loading

72
Q

What is needed for fracture healing?

A

Vascular supply
Stability/immobilisation

73
Q

What is haemotoma in response to fractures?

A

Disruption to the vascular supply
Cells form a clot
Ischaemia (cells death) occurs due to compromised blood supply
Vasoconstriction leading to local cell death

74
Q

What is the inflammatory response to fractures?

A

Production of serotonin and histamine stimulate the inflammatory response

The haemotoma is converted into connective tissue ‘granulation (new connective tissue)
The granulation tissue takes the place of haemotoma (acts like a weak splint, surrounding the fracture where immune cells and growth factors can collect)

75
Q

What s the cellular callus stage is response to fractures?

A

Growth of capillary buds at fracture site

Precursor cells differentiate into chondroblasts (produce collagen) and osteoblasts
New matrix is laid down made from sticky type 2 collagen

Not detectable on X ray.

76
Q

What is the mineralised callus stage in response to fractures?

A

Cellular matrix mineralised
Chondrocyctes mature and synthesise minerals (calcium)

Osteoblasts lay down woven bone amongst hyaine cartilidge.

Partial strength is restored.

Eventually the fracture gap is bridged by the hyaline cartilidge and woven bone, restoring some of its original strength. Therefore some pressure can begin to be put through the bone. (union is the partial repair of bone)

77
Q

What is the consolidation phase of fracture healing?

A

Woven bone and hyaline cartilidge are replaced by lamellar bone (trabecular)

No movement at site

Fracture is no longer visible on an x ray, with no pain on palpation and full strength. Can increase the loading and activity.

78
Q

What is the remodelling stage in fracture healing?

A

Begins where there is no movement at site. Remodelling of trabecular bone to compact bone.

Osteoclasts - dissolve trabecular bone
Osteoblasts - lay down compact bone

Reshaping of bone along line of stress
Can take years.

79
Q

What are some local anatomical factors and systemic factors that influence fracture healing?

A

Anatomical:
Soft tissue injury
Interruption of local blood supply
Interposition of soft tissue at fracture site
Bone death caused by radiation, thermal, chemical burns or infection.

Systemuc:
Mulnutrition (causes reduced activity and decreased callus formation)
Smoking (cigarette smoke inhibits osteoblasts, nicotine causes vasoconstriction diminishing blood flow to fracture site)
Diabetes Mellitus (associated with collagen defects)

80
Q

What are the 5 main principles of treatment?

A

Reduction
Achieve Union
Maintain stability
Prevent deformity
Optimise function-rehabiliate.

81
Q

What is reduction?

A

The manipulation of the fracture ends back into correct anatomical alignment.

Open: surgically invasive
Traction: requires bed rest, higher associated risks, mulitple injuries/unstable for surgery
Closed: no surgical intervention, confirmation of alignment checked with x-ray.

82
Q

What is the mechanism of healing?

A

Bleeding, inflammation, proliferation and remodelling/maturation

83
Q

What is the bleeding phase in the mechanism of healing?

A

Local bleeding into area
Transient vasoconstriction (oxygen and cell necrosis)
Release of enzymes (breakdown cells and stimulate inflammation)
Fibrinogen released and converted into fibrin (meshwork barrier blood clotting mechanism)

Generally short lived 6-8 hours but up to 24

84
Q

What is the inflammation phase in the mechanism of healing?

A

Cardinal signs of inflammation: heat, odema (swelling), pain, erythema (redness), disturbance of function

Vasodilation of microcirculation with increased blood flow
- permeability of small vessels
Allows water, electrolytes and small proteins to leak from the vessels into the surrounding tissue
Results in swelling

Therapy: manual therapy, exercise, electro-physical modalities, may influence chemistry of inflammation

85
Q

What is the POLICE acronym for early management of msk injuries?

A

Protect the injured part from further damage eg crutches
OL - optimal loading, rest can inhibit recovery
Ice
Compression
Elevation and possibly administration of anti-inflammatory medication

86
Q

What is the proliferation phase in the mechanism of healing?

A

Beginning of healing
Generation of repair material ‘granulation tissue’
Rapid onset 24-48 hours
Reaches a peak 10-14 days

Angiogenesis - production and development of capillary buds
Fibroplasia - production fibroblasts synthesis of type 3 collagen.

87
Q

What is the remodelling phase in the mechanism of healing?

A

Increase in number of fibroblasts
Increase in activity type 3 collagen synthesis
Conversion of type 3 collagen to type 1 (tissue gradually becomes stronger by being subjected to controlled stress)

Growth of capillary buds, creating a capillary network link around the injured area
Neutrophils continue to remove cellular debris, erythrocytes and the fibrin clot
Inflammatory cells gradually disappear

88
Q

What is the Maturation phase in the mechanism of healing?

A

Major slow down in collagen turnover (mostly type 1)
Response to loading is now poor.
Stretching and loading along the direction of stress will have little impact on collagen fibrils.

89
Q

What might soft tissue injury lead to?

A

Pain
Inflammation
Swelling
Sensitivity (hyper)
Erythema
Disturbance of function

90
Q

What is a sprain?

A

Overstretched/tear beyond normal anatomical limit. Usually refers to ligaments/capsule.

Ligaments

91
Q

What is a strain?

A

Over stretch, over exertion, overuse. Usually musculo-tendinous injuries.

Muscles

92
Q

What are the three main types of injury that can affect muscles?

A

Strain (tear)
Contusion (bruise)
Haematoma

93
Q

What are the different grades for muscle strains?

A

Grade 1 - small number of muscle fibres affected. Localised pain with no loss of strength.
Grade 2 - significant number of muscle fibres affected. Associated pain on contraction with swelling, strength and function reduced
Grade 3 - Complete muscle tear, commonly at musculo-tendinous junction

94
Q

What are haemotomas?

A

Intra-muscular haematoma - contained within muscle fascia, high intramuscuar pressure

Inter-muscular haematoma - spreads into the interfascial spaces, normal muscle pressure.

95
Q

What are different collagen types?

A

Type 1 - Bone, ligaments and tendon. Resists tension.
Type 2 - Hyaline cartilidge. Withstands pressure.
Type 3 - Smooth muscle, structure.
Type 4 - Epithelial. Support and Filtration.

96
Q

What are the different grades of

A
97
Q

What is the role of ligaments?

A

Joint stabilisers
Provide proprioceptive input into the brain that allows a person to known what position the joints are in.

Aids performance of complex coordinated activities needed for functional movement.

They sense tension and transfer this information to the brain. Brain responds by signalling muscles to contract or relax.

98
Q

What are some functions of skeletal muscles?

A

Locomotion
Heat generation
Respiration
Communication
Maintaining posture
Storing and moving substances within the body (eg glycogen)
Protects vital organs
Source of mechanical tension for the skeleton

99
Q

What is sarcopenia?

A

Loss of muscle mass due to ageing

100
Q

What is disuse muscle atrophy?

A

Disuse muscle atrophy can occur after a few days of immobilisation
Intemittent episodes of acute DMA linked to development of sarcopenia

Triceps surae and quadriceps muscle groups appear to be more susceptible to disue. Atrophy at 3 times the rate of ankle dorsiflexors.

101
Q

What are some adaptations to endurance training?

A

Centrally
Increased VO2 max
Increased blood plasma
Increased cardiac output

Peripherally
Increased capillary density
Increased % of type 1 fibres
Increased oxidative enzymes
Increased mitochondrial volume

102
Q

Describe the mechanisms of VO2 max

A

Improvements in VO2 max:
- 50% due to increased stroke volume
- 50% due to increase in a-VO2.

Increased a-VO2 due to:
- increased capillary density (25%)

Increased stroke volume due to:
- increased preload
- decreased afterload.

103
Q

HITT vs SIT training?

A

HITT: repeated short 45 seconds to long 2-4 minutes bouts of rather high but not maximal intensity exercise interpred by periods of rest (85-90% max HR)

SIT: 10-30seconds sprint intervals sessions with recovery periods (90-95% maxHR)

MICT: 50 minutes at 70% max HR

104
Q

Describe the mechanisms of muscle hypertrophy?

A

Results from increase of sarcomeres and myofibrils added in parallel
The synthesis and accretion of contractile proteins that account for the hypertrophy
Type 2 a fibres display the greatest growth, then type 2x, then type 1

105
Q

What is concurrent training?

A

Combining aerobic and resistance exercise within the same training programme.

Recommendations:
Any high intensity endurance training should be performed early in the day, then a period of 3 hours recovery should be given
Resistance exercise supported by readily digestible, leucine rich protein as soon as possible after training
Fully refueld between morning endurance and afternoon strength training

Consider performing strength training immeditaly after low intensity non depleting endurance sessions (to improve endurance response and provide a strong strength stimulus).

106
Q

Describe the action of muscle fibres during contraction

A

The sarcomeres shorten as myosin heads pull on the actin filaments.
Sliding filament theory.
Shortening of the muscle fibre length.

107
Q

Describe skeletal muscle?

A

Attached to bones by tendons
Voluntary control
Long cylindrical fibers
Multinucleated cells
Striated appearance

Rapid conractions that occur involuntarily in response to stimuli
Under conscious control through neral stimulation.

108
Q

Describe smooth muscle

A

Walls of internal organs
Involuntary control
Spindle shaped cells
Single nucleus per cell
Nonstriated

Involuntary contractions are sustained and slow
Capable of contracting for an extensive variety of lengths.

109
Q

What are the 5 health related components of physical fitness?

A

Body composition
Muscular strength
Muscular endurance
Flexibility
Cardiorespiratory fitness

110
Q

What are the different types of muscle fibres?

A

Slow Oxidative (type 1) - marathon
Fast Oxidative (type 2 a)
Fast Glycolytic (type 2x) - sprint

111
Q

What is the difference between physial activity and exercise?

A

Physical Activity is any bodily movement induced by skeletal muscles that increases energy expenditure
Exercise is any type of physical activity consisting of planned, structured and repetitive bodily movement done to improve or maintain compjents of physical fitness

112
Q

What are slow oxidative muscle fibres (type 1)

A

Large amounts of mitochondria
Large supply of capillaries
Fatigue resistance
Active during ambulation (walking)

113
Q

What are fast oxidative muscle fibres (type 2a)?

A

Can hydrolyse ATP 3-5x faster than Type 1
Moderate mitochondria content
Somewhat fatigue resistant
Active during 400-800m races

114
Q

What are fast glycolytic muscle fibres (type 2x)?

A

Heavily recruited during activities requiring max rate or force development
large capacity for hypertrophy
Fatigue rapidly.

115
Q
A

PHYSIOTHERAPY (14 decks)

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