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Exercise Physiology > 5L skeletal muscles and adaptiation to exercise training > Flashcards

5L skeletal muscles and adaptiation to exercise training Flashcards

1
Q

What is skeletal muscle?

A

40-50% of total body mass
major site of metabolic activity
largest protein reservoir

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2
Q

What are the 3 main functions of skeletal muscle?

A

1) locomotor activity
2) postural behaviour
3) breathing
4) other

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3
Q

What is the structure of skeletal muscle?

A

muscle consists a number of muscle fibres lying parallel to one another and held together by CT

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4
Q

What is a muscle fibre? (myofibre)

A

a single skeletal muscle cell
multinucleated
large, elongated, and cylindrically shaped
fibres can extend entire length of muscles

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5
Q

What is myofibril?

A
  • contractile elements of muscle fibre
    regular arrangement of thick and thin filaments (myosin and actin)
  • alternating dark (the A bands) and light bands (I bands) giving appearance of striations
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6
Q

What is the difference between a myofibre and myofibril?

A

Myofibers are the muscle cells itself.

Myofibrils are long protein cords in the sarcoplasm

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7
Q

NWhat is a nerve?

A

a enclosed cable-like bundle of nerve fibres or axons

provides a common pathway for the electrochemical nerve impulses transmitted along each fo the axons

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8
Q

What is the strength of contraction determined by?

A

number of fibre stimulated

frequency of stimulation

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9
Q

what is a motor unit?

A

a motor neuron (nerve cell) and all of the fibres that it innervates
all fibres are of the SAME fibre type
group of fibres activated via the same neuron
all muscle fibres of one particular motor unit are always the Same fibre type

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10
Q

precise (fine) movements

A

consists of a large number of motor units and few muscle fibres

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11
Q

less precise movements (gross)

A

carried out by muscles composed of fewer motor units with many fibres per unit

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12
Q

What is intra-muscle cooordination?

A

how much do you need?
mainly highly trained power athletes are able to activate up to 85% of their available muscle fibres simultaneously
(untrained)
trained athletes have not only a large = muscle mass than untrained individuals, but can also exploit a large number of muscle fibres
trained individuals can further increase strength only by increasing muscle diameter

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13
Q

What is summation?

A

two successive ap if the twitch tension resulting form the first AP does not declines to zero before second twitch arrives, the twitch forces summate

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14
Q

What is tetanus?

A

a frequncy of APs - a rise in the contractile force of a single muscle (fibre) until force reaches a plateau called the tetanic tension. This is the maximum tension that can be produced by a fibre.

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15
Q

Slow twitch Fibres

A

swuited for repeated contractiosn durign activities requireing a force output of < 20-25% of max force output
- smaller motor units
first activated
examples: lower power activities, endurance events

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16
Q

Muscle fibres Type:

the greater the slow twitch fibre content of a muscle…

A

the lower the force producing capactiy
the slower the contraction speed
the greater the endurance characteristics of the muscle
*based on typical size

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17
Q

Fast twitch fibres

A

significant greater “force” and speed generating capability than slow twitch fibres (size and speed)
well suited for activities involved high power
activated after ST
larger motor units

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18
Q

Muscle Fibre type:

the greater the fast twitch fibre content of a muscle..

A

1) greater the force output capacity
2) the greater the overall speed of contraction
3) the greater the fatigability will be when the muscle has been maximally activated
* based on typical size

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19
Q

Properties of type 1 muscle fibres

A

red
slow oxidative (SO)
type I myosin
contractile: slow

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20
Q

properities of type 2B

A

White
fast glycolytic
fastest contractile

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21
Q

structural aspects of SO

A

muscle fibre diameter: dmall
mito density: High
capillary density: high
myoglibin content: high

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22
Q

structural aspects of FG

A

Muscle fibre diameter: large
mito density: low
capillary density: low
myglobin content: low

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23
Q

functional aspects of SO

A

twitch time: slow
relaxation time: slow
force production: low
fatigability: resistant

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24
Q

Functional aspects of FG

A

twitch time: fast
relaxation time: fast
force production: high
fatigability: most fatigable

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25
Q

metabolic aspects of SO

A 
pc stores: low
glycogen stores: low
TG stores: high 
myosin ATPase activity: low
glycolytic enzyme activity: low
oxidative enzyme activity: high
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26
Q

metabolic aspects of FG

A 
pc stores: high
glycogen stores: high
TG stores: low
myosin ATPase activity: high
glycolytic enzyme activity: high
oxidative enzyme activity: low
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27
Q

Testosterone

A

directly effects muscle growth by binding to receptors on the surface of muscle cells and amplifying the biochemical signals in muscle tissue that result in protein synthesis.
overall increase in muscular size, strength and recovery from exercise.
more muscle but does not change the fibre type

28
Q

thyroid hormone

A

key hormoen wrt fibre type

increases mitos; mosin heavy change switch (type one decresases type 2 increases

29
Q

hyperthyroid

A

atrophy and muscle weakness

30
Q

can exercise training change muscles fibre types in humans?

A

it depends upon how one defines fibre types

31
Q

increased neuromuscular activity/overloadinging

A

endurance exercise
repeated stimulation stretch
move from fast to slow
easier

32
Q

decrease neuromuscular activity, unloading

A

detraining, immobilization, microgravity
harder to do but more inconveniences
moving from slow to fast

33
Q

What is muscular strength?

A

the ability of a muscle or muclr group to exert focrce against a resitance
commonly measured as a maximal value
force and strength are synonymous

34
Q

factors influencing the force of muscle contractions:

A
  1. the individuals state of health
  2. the individuals training status
  3. joint angles
  4. muscle cross-sectional area
  5. speed of movement (myosin heavy chain composition)
  6. muscle fibre type (influences forces)
  7. age
  8. sex
35
Q

Force-velocity curve

A

at any given velocity the trained can apply more forces

against any given load the trained can move (an object) faster

36
Q

How do we get stronger?

A

myostatin, alpha actinin3
neural - motor unit recruitment
hypertrophy - PS pathways, testosterone, IGH - 1 insulin

37
Q

Genes that define “skeletal muscle phenotype”

A

include:
AMPK
Calcineurin
Peroxisome proliferator - activated receptor gamma
(PPAR gamma) coactivator 1 alpha(PGC-1alpha)

38
Q

Type of contractions

A

in response to physiological demands, intracellular calcium concentration is elevated, activating
calcineurin/nuclear factor of activated T cells (NFAT_ and MEF2/HDAC signaling pathways.
In response to workload, ATP is depleted activated AMPK

39
Q

AMPK

A

sustained depression of energy change
[atp] decrease < – > {ADP] increase [AMP] increases –> AMPK –> mitochondiral biogensesis, Glut 4, HK (increased oxidative metabolism, not MHC)

has many roles

40
Q

Calcineurin

A

a ca2+/calmodulin activate phosphatase
- implicated in enrve activity - dependent fibre type specification in skeletal muscle
controls the phopshyrlation state of transcription factor NFAT

alow for its translocation to the nucelus
- leading to the activation of slow type msucle proteins in cooperation with myocyte enhancer factor 2 (MEF2)

causes a change from fast to slow muscles

41
Q

PGC -1 aplha

A

transcriptional co-activator PGC-1 alpha drives the formation of slow-twitch muscle fibres
regulates the genes involved in energy metabolism
regulator of mitochondrial biogenesis and function
activated in endurance exercise in human skeletal muschle
major factor that regulated muscle fibre type determination
serves as a target for calcineurin singling

42
Q

PGC-1alpha + nuclear receptor PPAR-gamma

A

permits the interaction of this protein with multiple trnasciption factors

43
Q

Neural response

A

the first measurable effect is an increase in the neural drive stimulating muscle contraction.
within just a few days, an untrained individual can achieve measurable strength gains (without hypertrophy) resulting from learning to use the muscle

44
Q

increased strength with NO hypertrophy

A

development of maximal strength through increased intra-muscular coordination (the abiltiy to recruit more motor units)

45
Q

Hypertrophy

A

is the increase of the size of an organ or in a select area of the tissue

46
Q

how you get bigger =
rate of protein synthesis vs. rate of protein degradation

MPS = muscle protein synthesis
factional synthetic rate
protein accretion

A

PS = PD = Mass
PS > PD increase mass
increase PS = increase mass
decrease degration = increase mass

47
Q

hormonal responses

A

controls myofibre size and maturation by idnirect and direct actions
does not directly affect the proliferation and differentiation of hte cells that make the muscle in the first place

testoersterone
insulin
growth hormone (IGF-1)

48
Q

insulin and myofibres

A

myofibres have more insulin receptors tahn type 1 IGF receptors, thus insulin is nexessary for myofiber hypertrophy. (nexessary to store protein in muscle)

49
Q

resting muscle and insulin

A

the resting muscle needs insulin to increase in size, thus following a meal, when insulin is secreted, excess nutrients can be stored in muscle. If insulin is low, protein stores are mobilized (protein degradation increases)

50
Q

myofibres and contracting muscle

A

contracting msucles DO NOT need insulin for glucose uptake; thus nutrietns in the cirulation can enter muscle to supply energy for contraction without eating a meal and getting the subsequent rise in circuatling insulin

51
Q

insulin

A

eating keeps insulin high and therefore keeps protein synthesis high

52
Q

insulin and GH

A

in response to IGF, the AKt/mTOR signalling pathway is activated. Activation of mTOR by AKT promotes protein synthesis and increases muscle mass –> hypertrophy

Foxo is an inhibiting pathway

53
Q

hypertophy (presynthetic/anabolic) pathways

A

GH - IGF signalling
AKT - mTOR pathway
P13k - Akt-GSK3beta pathway
ca2+

54
Q

Growth hormone (IGF-1)

A

stimualtes igf-1
gorwht factor with a configuration which closely resembles insulin –> increase protein synthesis
produced in the liver and skeletal muscles by GH
many of the actions fo the GH are through IGF-1

55
Q

p70s6 kinase

A

targets s6 ribosomal protein –> phosphoraltyion –> protein synthesis in the ribosome –> increase type II area after training

56
Q

training for strength

A

low reps with high loads

57
Q

training for endurance

A

high reps low loads

58
Q

repeated muscle contraction

A

PGC-1 activates that does not activate fox O therefore causes protein degration inhibition and then pgf also icnrease slow fibres in the mito –> aerobic cpaacity increases
local IGF-2 inhibits fox O and activates AKT–> MTOR which increase protein synthess _->icnrease fibre size

59
Q

Satelitte cells

A

a distinct sub-population of myoblasts that fail to differentiate and remain associated with the surface of the developing fibre as quiescent “muscle cells”
are precursors to primary myoblasts
muscle stem cells
surrounded by basal lamina
join existing fibre or replace a damged cell

60
Q

types of muscle contraction: static

isometic strength training

A

limitations:
- strengethens muscle at a specific pt in ROm
time consuming

61
Q

Tpyes of muscle contraction: dynamic

plyometric training

A

uses explosive humps to mobilize the stretch-recoil properties of msucle
ballistic resistance

62
Q

Muscle soreness and stiffness

A

delyed onset msucel soresness (DOMS)

lengthening contractiosn produce muscle soreness

63
Q

hyperplasia

A

increase the nubmers of cells

64
Q

Hyperplasia or hypertrophy

A

mostly hypertrophy

65
Q

physiological effects of strength training

A

increased muscle mass and size of muscle fibres
increased utilization and coordination of motor units
incrased strength of tendons, ligaments and bones
increased storage of fuel in and blood supply to muscles
improvmenets in blood - fat levels and biochemical processes.

Exercise Physiology (9 decks)

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