Muscles Flashcards

1
Q

Hennemans’s size principle

A

small motor units within a pool are recruited first

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2
Q

Specific tension

A

the maximum amount of force exerted by the fibers per unit pf PCSA (capacity of muscle fiber to produce force). Influenced by muscle fiber type (type 2 have higher specific tension.

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3
Q

Effects of velocity on contractile force

A

Decreased contraction speed can increase the force produced by the muscle as the filaments move past each other at a slower speed meaning there is an increased chance for a cross bridge to be formed.

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4
Q

Factors that contribute to muscle force

A

PCSA (greatest predictor of muscle force generating capacity) + pennation angle

Specific tension

Neural drive

Type and speed of contraction

Active and passive force

Neuromuscular fatigue

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5
Q

Function of titin

A

Titin attaches myosin to the z line. Titin contributes to muscle force by storing passive energy and also protects the sarcomere form over stretch.

Passive elastic force

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6
Q

How does PCSA and pennation angle contribute to muscle force

A
  • PCSA = muscle volume/fibre length
  • Fibre pennation angle is important as it relates to how much force is being transferred to the tendon. Increases pennation angle = decreased force onto tendon
  • Both PSCA and pennation angle will change with contraction
  • Fibre length is normally very different to muscle length
  • optimal fibre length and sarcomere length occur at same point (greatest force generating capacity)
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7
Q

How does specific tension contribute to muscle force

A

Specific tension is the maximum number of force exerted by the fibers per unit of PCSA (capacity of muscle fibres to produce force)

  • ST depends on muscle fiber makeup, higher specific tension in type 2B muscle fibers
  • Postural muscle have more type 1 muscle fibres therefore lower specific tension
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8
Q

Effects that neural drive has on muscle force

A

Each muscle innervated by motor neuron, they receive input from descending pathways, when enough excitatory input is received they send down an AP. Every AP generated in Mu will generate and AP in muscle fibre resulting in active force production.

Force can be alter by number and discharge rate of single motor units

Smaller motor units are recruited first (type 1), this is because they reach AP threshold first (greater change in membrane potential in smaller units). With greater excitatory input the number of motor units increases and the size of the MU recruited increases. Hennemans size principle.

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9
Q

Effects that type and speed of contraction have on muscle force

A

Eccentric → isometric → isotonic

Each motor unit discharge produces more torque in eccentric. Therefore eccentric achieves same torque with least amount of MU achieve.

Actin and myosin hold on longer for each AP in eccentric + more stretch of elastic component (titin) when lengthening

With increasing rate of change of muscle length, the less force produced.

Force producing capacity depends on total number of attached cross bridges, as filaments slide past each other at faster rates fewer cross bridges are able to attach.

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10
Q

Hill mechanical models and how active and passive structures contribute to force

A

Hills mechanical model of the muscle tendon unit

Contractile component CC - muscle fibers, actin and myosin cross bridges

Series elastic component SEC - intracellular titin, tendon

Parallel elastic component PEC - connective tissue (epi, peri and endo + titin)

The stretch shortening cycle occurs due to both active and passive reasons

When a muscle tendon unit is stretched just prior to contraction the resulting contraction is more forceful than in absence of pre stretch

  • Elastic recoil of SEC
  • Stretch reflex of lengthened muscle
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11
Q

Concept of neuromuscular fatigue

A

Has components in the peripheral (muscle) and central (brain, spinal cord). Most common with eccentric exercises. Some sarcomeres resist the stretch more than others causing some overstretch and disrupted → membrane damage.

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12
Q

Peripheral neuromuscular fatigue

A

Peripheral = failure to produce force appropriate to drive:

  • Neuromuscular junction, reduce relase of Ach (AP not initiated along muscle)
  • Muscle cell membrane potential changes
  • Reduce Ca release for excitation contraction coupling
  • Accumulation of metabolites (lactate and H will change pH= alter cell membrane)
  • Depletion of fuels such as ATP which allows for CB cycle
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13
Q

Central neuromuscular fatigue

A

Central = failure to drive motoneurons adequately (cant get them to AP threshold):

  • Lower excitatory drive from cortex (motivation, pain ect)
  • Increased inhibitory input
  • Decreased muscle spindle input
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14
Q

2 main factors that can calculate total muscle force

A

Total muscle force = PCSA x specific tension

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15
Q

Maturation in embryo

A

0-8 weeks = embryo

week 3 = trilaminar (3 layers germ disc) ectoderm (neural), mesoderm (muscles + connective tissues), endoderm (epithelia)

9-38 weeks = fetus, period of functional maturation

Somites, adjacent to the neural tube differentiate to form dermatome (skin), myotome (muscles) and sclerotome (connective tissue)

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16
Q

Tone maturation

A

At birth muscle tone is considered rather than muscle size. Tone is combination of both neural and non neural input:

  • Neural
    • Faciliatory input (EPSPs) + proprioceptive inputs + highetne central drive
    • Prolonged high excitatory drive (spasticity)
    • Prolonged low excitatory drive (hypotonia)
  • Non neural - degree of muscle tone remains without muscle activation by neural
    • Muscle cell properties (changes in titin)
    • Muscle tissue properties
    • Connective tissue (abnormal collagen formation in down syndrome = low tone) (fibrosis = thickening of connective tissue → high tone)

Tone increases with age

17
Q

Sarcopenia (7)

A

Loss of lean body mass and muscle weakness associated with advancing age

  • Muscle fibers decrease in number and size (mostly type 2, 1 mostly uneffected)
  • Fiber transformation (denervation of type 2 with reinnervation of type 1)
  • Satellite cells reduce in number and activation (injury)
  • Increase intermuscular adipose tissue (muscle mass → fat)
  • Reduced number and efficiency of mitochondria (notable in type 1 muscle fibers as they have more)
  • Reduction in number of receptors in T tubule meaning less calcium release
  • Altered titin properties

Exercise is the primary strategy to prevent sarcopenia