Muslce Metabolism Flashcards

1
Q

What are the three types of muscle fibres?

A

Slow oxidative type 1 fibers
Fast oxidative type 11 a fibers
Fast glycolitic 11x fibers.

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2
Q

How are they classified and what are the main differences between the three types?

A

By their biological capacity.
Differentiated by Their- speed of contraction (slow/fast)
- Type of enzymatic machinery they primarily use for ATP formation (oxidative or glycolysis)

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3
Q

What are the Characteristrics of slow oxidative type 1 fibers?

A

Has low myosin-at pause activity
Slow speed of contraction
High resistance to fatigue
High OXP capacity
Low enzymes for Anaerobic Glycolysis
Many mitochondria
Many capillaries
HIGH myoglobin contents
Red colour of Fiber
Low glycogen content

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4
Q

What are the characteristics if fast oxidative type 11a fibers?

A

High myosin-at pause activity
Fast speed of contraction
Intermediate resistance to fatigue
High OXP capacity
Intermediate enzymes for glycolysis
Many mitochondria and capillaries
High myoglobin content
Red fibers colour
Intermediate Glycogen Content

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5
Q

What are the characteristics of type 11x fibers?

A

High Myosin-Atpase activity
Fast speed if contraction
Low resistance to fatigue
Low OXP capacity
High enzymes for glycolysis
Few mitochondria and capillaries
Low myoglobin content
White colour of Fiber
High glycogen content

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6
Q

Fast versus Slow fibers.

A

Fast fibers have higher myosin atpase than slow fibers
The higher ATPASE ACTIVITY, THE MORE RAPPIDLY atp is split
Faster at which energy is made available for CB CYCLING.
Resulting in faster twitch compared to slow fibers which split atp more slowly.

+

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7
Q

What are the peak twitch tensions for slow and fast fibers?

A

Fast fibers= 15-40 ms
Slow = 50-100ms

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8
Q

What two factors determine the speed with which muscle contracts?

A

1- the load( velocity relationship)
2- myosin atpase activity of contacting fibres (fast/ slow) twitch

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9
Q

FIBERS ATP synthesis differentiation

A

Fibers also differentiate in atp- synthesising capability.
Those with greater capacity to forM atp = more resistant to fatigue.
Some are better equips FOR OXP but some primarily for AG
Because OXp yields more atp from each molecule processed- it does not readily deplete stores- thus does not result in lactate accumulation.
Therefore OXp is more resistant to fatigue than Glycolytic fibers

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10
Q

Fast fibres specaileid for glycolysis characteristics

A

Few mitcohodria but high content of glycolytic enzymes instead
Has lots of stored glycogen - glucose for optimum glycolysis
Has few capillaries- because doesn’t need as much 02 to function (compared to oxp)
Has little myoglobi- white
Dark white meat visible observation between fibers.
Muscles of leg- red
Breaststroke white

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11
Q

Glyocolytic fibers have little myoglobin?

A
  • are pale in colour
    Myoglobin - red
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12
Q

What do humans have ?

A

Mixture of all three fibers
% of each type is largely determined by type of activity flow which the muscle is specialised for. And varies among individuals

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13
Q

Where are high proportions of slow- oxidative found?

A
  • in muscles specialising for maintaining low intensity contractions for long periods- without fatigue.
    Ie- muscles of back+ legs- supporters body’s weight against force if gravity
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14
Q

Where are high proportions of fast- glycolytic fibers are found?

A

In arm muscles- which are adapted for performing rapid, forceful movements such as lifting heavy objects

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15
Q

Advantages of having more fast/ slow glycolytic fibers?

A

Greater % of Fast- best for power/ sprint events
Slow- endurance activities ie- marathon races

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16
Q

Muscle fibres adapt in response to demands placed on them

A

Different types of muscles produce different patterns if neuronal discharge to muscle involved.
Depending on the pattern of neural activity, long term adaptive changes occur in muscle fibres - which enables them to respond efficiently to the types of demands placed on the muscle

17
Q

What two types of changes can be induced in muscle fibres?

A

Changes in their oxidative capacity and changes in their diameter

18
Q

Improvement in oxidative capacity

A

Regular aerobic endurance exercise (long distance jogging|) promotes metabolic changes within oxidative fibers - which are the ones primarily recruited during AE
IE- NUMBER OF MITCOHONDRRIA- NUMBER OF CAPLILLARIES- SUPPLYING BLOOD TO FIBERS INCREASE.
Muscles adapt so taht they can use o2 more efficiently- to better endure prolonged activity without fatiguing.
But do not change in size.

19
Q

What us Muscle Hypertrophy?

A

Whereby Size of muscle can be increased by regular bouts of anaerobic short duration, high intensity resistance training. Ie- weight lifting.
Resulting muscle enhancement- comes from primarily increase in diameter- hypertrophy of fast glycolytic fibers that are called into play during powerful contractions.
Fiber thickening

20
Q

What causes Fiber thickening?

A

Results from increased synthesis of myosin and actin filaments which permits greater opportunity for cross bridge interactions + consequently increases muscle contractile strength.
The mechanical streets that resistance training exerts on muscle fibers triggers signaling proteins to turn on genes that direct synthesis of m/a
Vigorous training = bulging muscles better adapted to activities that require immense strength for short periods of time- endurance not improved,

21
Q

Why are mens muscles thicker/ stronger/larger? What does the influence of testosterone do?

A

TESTOSTERONE- is more in men
Muscles stronger even without weight training
Due to actions of testosterone- steroid hormone secreted primarily in males which promotes synthesis + assembly of myosin/actin.
Stimulates protein synthesis (anabolic effect) and inhibits protein degradation ( anti-catabolic effectt) - combines promotes muscle hypertrophisches by Tester one.

22
Q

What is the Role of testosterone?

A

To stimulate protein synthesis- by anabolic effect- process which builds organs and tissues
+ inhibits protein degrading- anti-catabolic affect
Combined these effects account for the promotion of muscle hpertophy by testosterone

23
Q

What is the % rate of using anabolic - androgenic steroids?

A

Males 6.4
Females 1.6
To improve apprentice and performance in combo with resistance exercise
Aas increases muscle protein synthesis resulting in MH.

24
Q

How do Aas increases muscle protein synthesis resulting in MH?

A

Primarily by binding to androgen receptor. Aas exert their hypertrophic affect via genomic and non genomic and non catabolic mechanisms.
But using ass has drastic effect of metabolism - increases rick of cardiovascular disease. Which increases risk of developing atherosclerosis with increases risk of heart attacks and strokes

25
Q

How does aas affect male reproductive system?

A

Testosterone secretion/sperm production by testes- controlled by hormones in anterior pituitary gland.
By negative feedback as testosterone inhibits secretion of these controlling hormones so that the level of testosterone is maintained. THE AP IS inhibited by ANDROGENIC steroids taken as a drug- resulting in testes not receiving normal stimulate input from ap - testosterone secretion- sperm production decreases- testes shrink
Increased risk from testicular and prostate cancer .

26
Q

How DO AAS AFFECT female reproductive system?

A

Females normally lack potent and androgenic hormones, the use of anabolic steroids promotes male type muscle mass, strength and masculisation of features . Ie facial hair, deepinoing voice
Inhibition of anterior pituitary glands by androgenic drugs suppresses hormonal output that controls ovarian function- failure to ovulate, Menstruationen irregularities, decreased secretion of feminising female sex hormones- diminished breast size

27
Q

What is i nconversion between fast muscle types? Explain

A

All muscle fibres which in a single motor unit are of the same Fiber type.
Pattern is established in early life but 2 types of fast twitch fibres are in inconvertible ( depending on training efforts)
1- fast glycolytic fibres that can be converted to fast glycolytic fibers. Vice versa
Adaptive changes in sm gradually reverse to Orginal state over period of months if regular exercise is dismissed.

28
Q

What fibres aren’t inconvertible ?

A

Slow and fast.
But all training can induce changes in MF METABOLIC support systems no matter the Fiber. It depends on the fibres nerve supply.
Slow twitch fibers- are supplied by motor Neurons- which exhibit low frequency patternn of electrical activity
Fast- are innovated by motor Neurons exhibiting intermittent rapid bursts of EA

29
Q

What is muscle ATROPHY?

A

Whereby if as mucle is not used- its actin and myosin levels decreases- fibers become smaller.
And muscle accordingly decreases ins size - atrophy- becomes weaker

30
Q

WHAT ARE THE THREE WAYS OF WHICH ma can occur?

A

1- DISEASE ATROPHY
2- DENERVATION ATROPHY
3- age related atrophy or sarcopenia

31
Q

What is disease atrophy?

A

It occurs when a muscle is not used for a long period of time even though nerve supply is intact .
Ie in a cast or brace- during long bed confinement.

32
Q

What is denervation atrophy?

A

Occurs after nerve supply to muscle is lost
If muscle is stimulated electrically until innervation can be reestablished then atrophy can be dismissed but not entirely prevented( restoration of severed peripheral nerve)
Contractile activity plays important role in preventing atrophy.

33
Q

What is Age related A or Sarcopenia?

A

Occurs naturally with ageing- begins around 40yrs
As people loose motor Neurons progressively, particularly ones that innervate fast glycolytic fibre types
Results in loss of muscle mass, strength, speed of muscle contraction.
Reduced rate of p synthesis and lowered hormone levels (growth hormone, testosterone, insulin like growth factor 1) contributes to loss of muscle mass
Average person looses 1/4 pound of muscle mass per year 40+
It’s inventible.
Resistance training and proper diet can slow rate of development of s.

34
Q

What is meant by limited repair of muscle?

A

Whereby muscle damage has limited repair possibilities even though muscle cells cannot divide mitotically to replace lost cells.
Satellite cells- small population of inactive muscle specific stem cells are located close to muscle surface.
When muscle fibres damage occurs- locally released factors activate the cells- gives rise to my oblasts (same undifferentiated cells that form muscle in embryonic development)
Group of m,oblasts fuse = large multi nucleated cell- immediately begins to synthesise + assemble intracellular characteristics of muscle0- matures into muscle fibre
Extensive injury- this limed mechanism is not adequate to completely replace lost fibers.
Remaining ones often hypertrophy to compensate.

35
Q

Clinical correlation?

A

Transplantation of satellite cells or my oblasts provides hope for condition MUSCULAR DYSTROPHY
Hereditary pathological condition - which progressively degenerates contractile elements which are replaced by fibrous tissue.