Muscle physiology 3 Flashcards

1
Q

Describe summation

A

Whereby the Ca2+ that is released from the SR, due to multiple AP, is not removed as quickly as it is released so cross bridge cycling continues building the contraction force.

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2
Q

What are the different types of muscle contraction

A

Isometric and isotonic

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3
Q

Describe isometric

A

A contraction where no external shortening takes place. I.e. the force of the weight equals the force developed by the muscles

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4
Q

Describe isotonic

A

A contraction where there is movement in the muscle. There is a mismatch between the tension generated by the contracting muscle and the load on the muscle.

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5
Q

What are the two forms of isotonic contraction

A

Concentric (where the muscle is actively shortening e.g. upward motion of bicep curl) and eccentric (where the muscle is actively lengthening e.g. downward motion of bicep curl)

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6
Q

What kind of muscle contraction is delayed onset muscle soreness typically associated with

A

Isotonic, eccentric contractions.

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7
Q

What is the optimal muscle length in relation to maximum force and why

A

Around 2 micrometers. This is the length where there is maximum crossbirdge connections. As muscles lengthens the actin is stretched away from myosin. As the muscle shorten there is interaction between filaments (overlapping) preventing cross bridge formation

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8
Q

Describe the current theory relating to delayed onset muscle soreness

A

During eccentric (isotonic) contraction the sarcomeres lengthen unevenly. The weakest sarcomeres lengthen first and are stretched till they give way damaging them.

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9
Q

Describe ATP usage in skeletal muscle

A

High usage. Big variation between relaxed cell and contracting cell. Three sources creatinine phosphate, glycolysis, oxidative phosphorylation.

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10
Q

Timeline of ATP sources

A

Immediate- CP, short term- glycolysis, long term- oxidative phosphorylation

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11
Q

Three fiber types in skeletal muscle including description.

A

Type 1 fibers- slow twitch, red in colour, lots of mitochondria, resistant to fatigue, abundant in postural muscles and endurance athletes.

Type 2a fibers-mix of above and below: fast oxidative also red and lots of mitochondria. Utilise both aerobic and anaerobic metabolism. More prone to fatigue

Type 2 b- fast glycolytic. White. Produce ATP slowly by anaerobic metabolism. Capable of short, fast burst of power, fatigue rapidly.

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12
Q

Aetiologies of muscle fatigue

A

Not clearly established. Think of the potential sites between brain and contractile protein interaction.

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13
Q

Categories of muscle fatigue

A

Central fatigue- decreased CNS activity. Decreased number of motor units recruited.
Peripheral fatigue- Things that affects the cellular mechanisms e.g. smaller Ca2+ transient, reduced Ca2+ sensitivity of myofilaments (reduced affinity of Ca2+ to binding sites), slower cross bridge cycling. Causes include accumulation of metabolites, depletion of energy supplies.

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14
Q

Describe the accumulation theory of fatigue

A

Build up of lactic acid decreases Ca2+ affinity for TnC, obstructs glycolysis and slows relaxation. Increased K+ decreases membrane excitability.
Increased Pi decreases Ca2+ release, uptake and sensitivity. Reactive oxidative species increase protein damage.

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15
Q

Describe Duchennes muscular dystrophy

A

Genetic mutation of dystrophin. Muscles normal at birth with increasing skeletal muscle weakness and degeneration. Wheel chair by 10 respiratory failure by 20. Diagnosis around 4. Dystrophin helps with force transduction across the cell membrane and in Ca2+ channel regulation, leaky membranes.

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16
Q

Describe sarcopenia

A

Whereby raging causes a decrease in muscle mass/ body mass. Significant loss of strength.