Final Support and Movement

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Last updated 10:28 PM on 10/9/26
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136 Terms

1
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What is Vm?

electric potential inside cell relative to outside cell

2
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What is resting membrane potential?

Vm when cell is at rest, when electric and chemical gradient forces balance each other out so there is no net movement of ions across the membrane

3
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How can equilibrium potetial be calculated?

nernst equation for 1 ion, goldman-hodgkin-katz equation for multiple ions involved

4
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For a cell with resting potential of -70mV and Ek is -94mV, which direction will a K+ ion travel?

chemical force is outward to get to -94mV, but electrical force is inward for any positive ion, net outward force because -94mV is where the forces balance, but it will never get there because there are other factors at play

5
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Why are chemical and electrical forces on Na+ stronger than forces on K+?

resting membrane potential of -70mV is closer to Ek of -94mV than Ena of 60mV

6
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What are some functions of ions and their fluctuations?

intracellular pH balance, excitability of muscle and nerves, secretion and exocytosis, gene transcription and differentiation, water balance and volume regulation, adhesion and motility

7
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What are the different ways an ion channel can be opened?

voltage gated, ligand gated, stretch gated

8
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What is a promiscuous ion channel?

allows multiple different ions through, non-selective

9
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What are graded potentials?

small changes in membrane potential that can sum to cause depolarization, get smaller as they travel to axon hillock, can be excitatory or inhibitory

10
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What are action potentials?

large depolarizations, do not decrease in strength over time, stronger than normal stimulus is needed to trigger another one during refractory period

11
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How does hyperpolarization occur?

K+ channels open and close slightly after Na+ channels, so when Na+ channels open, Na+ enters, Na+ channels close while K+ channels are half open at peak of action potential, no more Na+ enters while K+ begins to leave, K+ channels fully open at bottom of action potential, K+ continues to leave, making inside very negative

12
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What is the Z line?

anchors thin filaments, borders sarcomeres

13
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What is the M line?

middle of thick filaments

14
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What is the H zone?

area of only thick filaments, shrinks when muscle contracts

15
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What is the I band?

area of only thin filaments, shrinks when muscle contracts

16
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What is the A band?

area of thick and thin filaments, does not change size when muscle contracts

17
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Describe the structure of actin

monomeric G actin molecules made of 1 peptide chain join together to make polarized F actin with positive barbed ends and negative pointed ends

18
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What are the steps in skeletal muscle contraction?

synaptic transmission, action potential, excitation-contraction coupling

19
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Describe the neuromuscular junction

nicotinic cholinergic receptors on motor end plate of muscle cell, always strong enough to activate action potential in muscle

20
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How is an action potential propagated in a muscle cell?

voltage gated Na+ channels open along sarcolemma and into t tubules

21
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What is excitation-contraction coupling?

electric stimuli converted to mechanical action, due to calcium release and increase in intracellular calcium concentration

22
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How is calcium released in muscle cells?

dihydropiridine receptor on t tubule membrane linked to ryanodine receptor on sarcoplasmic reticulum membrane, action potential opens both and calcium is released into intracellular space

23
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How do muscles relax?

acetylcholine is removed from neuromuscular junction by acetylcholinesterase, Ca is transported back into sarcoplasmic reticulum via sarco/endoplasmic reticulum Ca2+ ATPase pump, calsequstrin binds Ca to concentrate ions, Ca2+ pumped out of cell by active transport channels on sarcolemma

24
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What is a first order lever?

fulcrum in the middle, weight on one side, muscle on opposite side, muscle and weight move in opposite directions

25
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What is a second order lever?

gravity in the middle, fulcrum off to the side, muscle lifts weight on same side as weight, like a wheelbarrow, input lever longer than output lever

26
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What is a third order lever?

muscle in the middle, fulcrum off to the side, muscle lifts weight on same side as weight, like tongs, input lever shorter than output lever

27
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What is the advantage of third order levers?

it takes much more effort to lift weight at the end of a lever, but a short movement of the muscle makes a large movement of the weight on the far end, making the output movement very fast

28
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What is a DMPLO projection?

dorsomedial to palmolateral projection

29
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What is a DLPMO projection?

dosolateral palmomedial projection

30
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Where is the tuber sacrale?

next to sacrum on medial side

31
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Where is the tuber coxae?

lateral side of pelvis

32
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Where is the tuber ischii?

most caudal projection of pelvis

33
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What muscle tendons contribute to the calcaneal tendon?

biceps femoris, semitendinosis, gracilis, superficial digital flexor, gastrocnemius

34
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What are fabellae?

small sesamoid bones above femoral condyles in dogs and cats

35
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Where are 1st order somatic afferent neurons?

PNS

36
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Where are 2nd order somatic afferent neurons?

spinal cord to thalamus

37
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Where are 3rd order somatic afferent neurons?

thalamus to cortex

38
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Where are 1st order somatic efferent neurons?

cortex to spinal cord

39
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Where are 2nd order somatic efferent neurons?

spinal cord to effector organ skeletal muscle

40
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What order neurons are in the PNS?

1st order afferent and 2nd order efferent

41
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What is somatotopic organization?

point to point correspondence of area of body to specific point in CNS

42
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What are the areas of gray matter?

dorsal horn, intermediate gray, ventral horn

43
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What does the dorsal horn contain?

afferent cell bodies, somatic and visceral

44
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What does the intermediate grey matter contain?

visceral efferent cell bodies, pre-ganglionic neurons

45
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What does the ventral horn contain?

somatic efferent cell bodies

46
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What does the dorsal funiculus contain?

ascending sensory tracts

47
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What does the lateral funiculus contain?

ascending sensory tracts and descending motor tracts for fine control of distal muscles

48
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What does the ventral funiculus contain?

descending motor tracts for posture control and gait maintenance of proximal and axial muscles

49
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What is the resting tone for upper motor neurons?

inhibitory signals to prevent extensors from over contracting

50
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What is the resting tone for lower motor neurons?

constantly firing to stay standing, be able to run

51
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What occurs if upper motor neurons were damaged?

nothing to inhibit lower motor neurons from firing, so rigidity of extensor muscles

52
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What occurs if lower motor neurons were damaged?

no signals reaching muscles, so paralysis or weakness

53
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What are reflexes?

stereotypical response from specific stimulus, repeatable until fatigue, brain not involved, present at birth in both autonomic and somatic nervous systems, mostly polysynaptic

54
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What is rigor mortis?

no more oxygen, so no more ATP generated, so no ATP to make myosin unbind actin, so muscles stay rigid

55
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What is myasthenia gravis?

autoimmune disease that attacks nicotinic-cholinergic Na+/K+ ion channels on sarcolemma, causing muscle weakness, treated with edrophonium that inhibits acetylcholinesterase enzyme that breaks down ACh, instant improvement

56
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What is hyperkalemic periodic paralysis?

mutation of ion channel that lets Na+ leak in, preventing repolarization, K+ keeps leaving and entering bloodstream trying to repolarize, causing hyperkalemia, treated with low K+ diet

57
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What is a muscle twitch?

mechanical response to a single action potential

58
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What is an isometric contraction?

muscle contracts but does not change length, load is more than muscle can move

59
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What is an isotonic contraction?

muscle contracts and changes length, can be eccentric or concentric

60
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What is an eccentric contraction?

type of isotonic contraction, muscle shortens during contraction

61
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What is a concentric contraction?

type of isotonic contraction, muscle lengthens during contraction

62
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How is calcium related to force generation in skeletal muscle?

higher concentration of calcium means more exposed myosin binding sites and therefore more active crossbridges

63
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How does muscle fiber diameter contribute to force generation in skeletal muscle?

larger diameter fibers have more fibrils in them, meaning more crossbridges, hypertrophy is induced via training

64
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What is the length-tension relationship?

the closer a muscle is to neutral, the more crossbridges that can be made, if its already too stretched out or too compressed, the myosin and actin are physically too far away or too overlapped to contract

65
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What is the advantage of a long muscle fiber, many sarcomeres in series?

each sarcomere only has to shorten a little bit to produce the same total distance as a short fiber with its sarcomeres shortening a lot, so the long fiber is capable of accommodating another action potential, shortening more, and generating more force, while the short fiber can’t shorten any more

66
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What is the disadvantage of a long muscle fiber?

requires more energy than short muscle fibers

67
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How does magnitude of load contribute to velocity of contraction?

larger load means slower contraction and faster to run out of energy

68
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How does muscle fiber length, number of sarcomeres in series, contribute to velocity of contraction?

loner fibers contract faster because each sarcomere only has to shorten a little bit, while sarcomeres in a short fiber have to shorten a lot, which takes more time

69
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How does muscle fiber type contribute to velocity of contraction?

depends on myosin ATPase activity, which is an inherent property of the enzyme present in the fiber type and cannot change with training, fast twitch muscles also remove Ca2+ from sarcoplasm quicker and have energy more readily available

70
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What are the sources of ATP in skeletal muscle in order?

small pool of ATP, creatine phosphate, carbohydrates, fats

71
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What role does creatine phosphate play in skeletal muscle ATP generation?

first source of energy after small pool of ATP depleted, makes ADP into ATP

72
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What role does glycogen play in skeletal muscle ATP generation?

muscle cells store it, converted to glucose-6-phosphate then pyruvate to generate ATP, lack of glucose-6-phosphatase means it can only be used for energy production in skeletal muscle, can’t be converted to glucose to fix hypoglycemia, so its a reliable source of energy even when animal is hungry

73
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How is glucose absorbed into skeletal muscle cells?

typical insulin dependent hexokinase pathway, but also GLUT4 transporters in vesicles that move to cell membrane during muscle contraction, grabbing glucose from blood independently of insulin

74
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What is oxygen debt?

pools of creatine phosphate and glycogen need to be replenished, accumulated lactate needs to be metabolized, interstitial oxygen needs to be rebalanced which all require oxygen, which is why you still breath heavily for a while after completing exercise

75
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What are some causes of skeletal muscle fatigue?

energy reserve depletion, metabolic waste accumulation, reduced blood flow during strong contractions, neuromuscular fatigue

76
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What are the major skeletal muscle fiber types?

slow oxidative I, fast oxidative-glycolytic IIA, fast glycolytic IIB

77
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What are the properties of fast glycolytic muscle fibers?

ATP production via glycolysis, wider for more glycogen stores, therefore stronger

78
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What are the properties of slow oxidative muscle fibers?

ATP production via oxidative phosphorylation, more mitochondria, narrower fibers for more surface area exposure to blood supply for oxygen, more myoglobin, darker on histology

79
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What will aerobic training yield?

increased oxidative capacity via growth of mitochondria and capillaries

80
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What will anaerobic training yield?

increased glycogen storage and fiber diameter, satellite cells will create more myofibrils in parallel

81
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Describe what occurs in a muscle fiber during training, atrophy, and retraining

training will increase number of nuclei in muscle cell, when muscle atrophies, nuclei will remain, and trained muscle will regrow faster than a muscle that has never been trained

82
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What is recruitment?

when a load is too heavy for a motor unit, more motor units are activated

83
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What are the properties of a large motor unit?

more muscle cells innervated by same neuron, less excitable, meaning more difficult for graded potentials to reach axon hillock and trigger an action potential, recruited last, fast glycolytic fibers

84
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What are the properties of a small motor unit?

fewer muscle cells innervated by same neuron, more excitable, recruited first, slow oxidative fibers

85
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What are muscle spindles?

in muscles, sense muscle stretch, tell brain about muscle length, gamma motor neuron tells them to contract to maintain spindle sensitivity by following surrounding tension so it doesn’t get floppy when rest of muscle contracts, patellar reflex activates these

86
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What are golgi tendon organs?

in tendons, respond to tension, activation causes inhibitory signals to motor neuron of muscle its associated with, like if you try to catch a bag of bricks, withdrawal reflex activates these

87
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What are the characteristics of pharmacological neuromuscular blockers?

used during surgery to prevent animal from moving, not used alone, don’t provide anesthesia or analgesia, need ventilation because will stop diaphragm

88
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How do non-depolarizing competitive neuromuscular blocks work?

bind to nicotinic ACh receptors and inhibits them, preventing depolarization, receptor antagonist, short acting, counteragent with ACh-ase inhibitor, same as myasthenia gravis treatment

89
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How do depolarizing neuromuscular blocks work?

bind to nicotinic ACh receptors and activates them, receptor agonist, phase1 has extended refractory period and twitching, phase 2 membrane finally repolarizes but channel still inhibited so depolarization can’t occur, takes longer to work but lasts longer, no counteragent

90
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What is elastic potential?

type 1 collagen can uniformly crimp like a spring, making less effort to pick up foot, but dangerous because risk of overstretching and rupture, narrow safety range

91
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What is myotonia congentia?

defective chloride channels in t tubules, preventing repolarization, causing muscle rigidity when startled

92
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What is malignant hyperthermia?

mutation in ryanodine receptor causing uncontrolled release of calcium from SR, uncontrolled muscle contractions, high body temp, heartrate, carbon dioxide

93
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What is masticatory myositis

autoimmune destruction of specific myosin type in jaw muscles only, causing inflammation and pain, early treatment with steroids is important because fibrosis is permanent

94
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What are sore muscles?

mechanical damage, z line streaming, soreness occurs day after exercise due to immune system response, myoglobin can cause kidney damage after extreme exercise, test creatine kinase in blood

95
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What is muscular dystrophy?

genetic disease that weakens dystrophin protein that distributes force from muscle to tendon, causing weakness, atrophy, bunny hopping, dysphagia, sialorrhea, high mortality in first days of life

96
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What is exertional myopathy?

mutation in cytochrome oxidase enzyme in ETC in old english sheepdogs, causing exercise intolerance, lactic acidosis, weakness, can still use glycolysis and creatine phosphate, can’t do oxidative phosphorylation

97
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What determines muscle mass?

balance between protein synthesis and degradation

98
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What stimulates protein synthesis?

mTOR, sensitive to nutrients, hormones, growth factors, mechanical load, oxygen levels

99
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What is myostatin?

inhibits mTOR, stimulated by injury, negative energy balance, infection, myostatin inhibitors under therapeutic investigation, but would have consequence of not degrading damaged cells

100
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What stimulates protein degradation?

disuse, aging, starvation, certain disease trigger different proteolytic pathways