2Nd Physiology Midterm

Front 1

Types of Muscle

Back 1

Skeletal, Cardiac and Smooth

Front 2

Skeletal Muscle

Back 2

Voluntary, innervated by somatic motor nerve, and no hormonal influence.

Front 3

Cardiac Muscle

Back 3

Involuntary, innervated by autonomi nervous system, under hormonal influence, can initiate own contraction, and is a rhythmic contraction.

Front 4

Smooth Muscle

Back 4

Involuntary, innervated by autonomic nervous system, under hormonal influence, and static (tonal) contraction.

Front 5

Types of Connective Tissue

Back 5

Epimysium, Perimysium, Endomysium, and Tendon

Front 6

Epimysium

Back 6

Surrounds entire muscle

Front 7

Perimysium

Back 7

Divides muscle into sections called fascicles

Front 8

Endomysium

Back 8

Surrounds individual muscle fibres

Front 9

Tendon

Back 9

Attaches muscle to bone

Front 10

Myofibril

Back 10

Contractile Protein

Front 11

Sarcomere

Back 11

Sections that myofibril is divided into

Front 12

Actin and Myosin

Back 12

Actin - thin filament.
Myosin - Thick Filament
Make up the contractile machinery of muscle

Front 13

Myosin

Back 13

The motor of the muscle, has a tail and two heads. Responsible for the actual movement of muscles. Myosin head is an ATPase enzyme

Front 14

Actin

Back 14

Small globular proteins, each molecule has an active site that the myosin head can bind to. Forms long chains of actin.

Front 15

The "Other" Size Principle

Back 15

Larger fibres generate more force

Front 16

Sarcolemma

Back 16

A membrane that encloses the contractile machinery

Front 17

ECC - The Triad

Back 17

1. T-Tubules
2. Sarcoplasmic Reticulum
3. Feet

Front 18

T-Tubules

Back 18

Carry action potential into muscle

Front 19

Sarcoplasmic Reticulum

Back 19

Stores, releases, and uptakes Ca++

Front 20

Feet

Back 20

Dihydropyridine Receptor (DHPR) - located in membrane of T-Tubule, and is voltage sensitive.
Ryanodine Receptor (RYR) - located in membrane of SR, and controls the release of Ca++.
The depolarization of T-Tubules causes change in DHPR, then RYR and Ca++ is released.

Front 21

Control of Voluntary Movement

Back 21

1. Limbic System
2. Motor Cortex
3. Cerebellum
4. Basal Ganglia
5. Brain Steam and Spinal Cord

Front 22

Nerve Impulses

Back 22

Contraction initiated by a motor nerve, this one motor nerve innervates a group of muscle fibres called a motor unit.

Front 23

Motor Unit

Back 23

Is triggered by a motor nerve and then controls a group of fibres

Front 24

Neuromuscular Junction

Back 24

Where nerve meets the muscle.
When nerve impulse reaches end of neuron ACh is released into the neuromuscular junction.
ACh binds with receptors on the sarcolemma and initiates an action potential.

Front 25

Botulinum Toxin

Back 25

Powerful neurotoxin, causes muscle paralysis, reduces muscle spasms and stiffness, functions by reducing ACh release from motor neuron.

Front 26

Troponin Complex

Back 26

T - attaches to Tropomyosin
I - inhibits active site on actin
C - active binding site for Ca++
Regulates muscle contaction in combination with tropomyosin

Front 27

Troponin and Calcium

Back 27

When calcium binds to troponin C tropomyosin is moved away from actin active site. Which allows myosin heads to bind to actin. Forms a "cross-bridge".

Front 28

Cross-Bridges

Back 28

Where the myosin head binds to actin

Front 29

Contraction Cycle

Back 29

1. Rigor State
2. Myosin Release
3. ATP Hydrolysis
4. Myosin Reattaches
5. Power Stroke
6. ADP Release

Front 30

Rigor State

Back 30

Myosin head is bounded to actin and no ATP is there

Front 31

Myosin Release

Back 31

ATP binds to myosin head and myosin releases from actin

Front 32

ATP Hydrolysis

Back 32

ATP is broken down the energy released allows myosin to move forward

Front 33

Myosin Reattaches

Back 33

Myosin head binds weakly to the actin site and myosin is in cocked position

Front 34

Power Stroke

Back 34

Pi is released from myosin head this strengthens the bond between myosin and actin and then myosin pulls actin filament forward

Front 35

ADP Release

Back 35

During power stroke ADP is released, and goes back to rigor state

Front 36

End of Contraction

Back 36

When nerve impulse stops RYR closes, Ca++ is removed from cytosol and back to SR, it is accomplished by active transport via SERCA or SR pump.

Front 37

Muscle Fibre Types

Back 37

1. Slow twitch (oxidative, type I)
2. Fast twitch (glycolytic, type II)
- type IIa fast oxidative glycolytic
- type IIb fast glycolytic

Front 38

Type I

Back 38

Red and Smaller. Slow myosin ATPase. Generate force slowly. Fatigue resistant. Aerobic.

Front 39

Type IIa

Back 39

Fast myosin ATPase. Generates force quickly. Moderately fatigable. Mix of aerobic and substrate level phosphorylation.

Front 40

Type IIb

Back 40

Very fast myosin ATPase. Generates force very quickly. Very fatigable. Substrate level phosphorylation.

Front 41

Henneman's Size Principle

Back 41

Small neuron recruited first, and large later.

Front 42

VO2 Max

Back 42

Sets maximum aerobic capacity, important for events less than 10 minutes.

Front 43

Lactate Threshold

Back 43

Determines speed that can be sustained for prolonged periods.

Front 44

Fatigue

Back 44

With exercise membrane can become depolarized which slows action potential

Front 45

Why does depolarization occur

Back 45

Depolarization can occur for several reasons. 1. Na++ channels become dysfunctional over time. 2. K+ channels remain open.

Front 46

What causes Fatiuge

Back 46

Pi
ATP/ADP
Glycogen
Reactive oxygen species

Front 47

Pi

Back 47

1. Decrease cross bridge force production
2. Decrease tropomyosin Ca++ sensitivity
3. Decrease in Ca++ concentration

Front 48

ATP and ADP

Back 48

Need them for contraction

Front 49

Glycogen

Back 49

You generate energy from glycogen through the main pathways

Front 50

Reactive Oxygen Species (ROS)

Back 50

When high can damage many areas of the cell such as, DNA, protein, and inactivation of enzymes. Could be related to altered Ca++ sensitivity of Ca++ release

Front 51

Fatigue during different intensities of exercise

Back 51

During intense exercise we rely on substrate level phosphorylation, so you get Pi, ATP and lactate very quickly. During moderate exercise the reasons for fatigue are, glycogen depletion, decreased substrate provision, altered Ca++ sensitivity and ROS.

Front 52

What is Healthy Muscle

Back 52

Healthy muscle should allow for movement and high quality of life. Ability to take up glucose.

Front 53

Muscle Strength

Back 53

Closely tied to muscle size

Front 54

Fitness

Back 54

Ability of muscle to generate ATP. More ATP muscle is able to generate the greater the intensity of duration of sustained physical activity.

Front 55

Age Associated Sarcopenia

Back 55

Age related to decrease in muscle mass.
Reasons Why.
1. Loss of enervation
2. Imbalance between protein degradation and synthesis.
3. Genetic Mutation
4. Stem cell loss of function

Front 56

Obesity and Type II Diabetes

Back 56

Decrease in strength, fitness, and ability to take up glucose.

Front 57

What does Exercise do?

Back 57

Increases muscles mass and strength, improves mitochondrion content, and improves insulin sensitivity. Can decrease the rate at which your muscles deteriorate at.

Front 58

Endergonic Reactions

Back 58

Mechanical work - muscle action
Chemical work - synthesis of cellular molecules
Transport work - active transport

Front 59

PCr System

Back 59

10-15 seconds
Weight lifting
Sprinting
Uses high energy bond to turn ADP to ATP

Front 60

Glycolysis

Back 60

Breaking down glucose or glycogen
Anaerobic
Glycogen stored in muscle
Glucose must be transported into muscle from blood
Uses ATP at the beginning

Front 61

Nets of Glycolysis

Back 61

2 ATP
2 NADH
3 ATP from glucose

Front 62

Pyruvate Dehydrogenase

Back 62

Pyruvate is turned into Acetyl CoA, gain NAHD

Front 63

FA oxidation

Back 63

Breaks down of free fatty acid to form acetyl CoA. CPT1 is the rate limiting enzyme.

Front 64

Beta - Oxidation

Back 64

Break of two carbon atoms. 2 C units form acetyl CoA. Produces reducing equivalents.

Front 65

Net of FA metabolism (beta-oxidization)

Back 65

9 ATP
35 NADH
17 FADH2
Total ATP 148

Front 66

Aerobic Metabolism

Back 66

TCA cycle
Electron Transport Chain
Oxidative Phosphorylation

Front 67

TCA Cycle

Back 67

Break down acetyl CoA, produces CO2, ATP, and reducing equivalents.

Front 68

Net for TCA Cycle for glycogen or glucose

Back 68

6 NADH
2 FADH2
4 CO2
2/3 ATP (glucose/glycogen)
Total ATP 38/39 (glucose/glycogen)

Front 69

Important Enzymes

Back 69

Citrate Synthase
Isocitrate Dehydogenase
Alpha - ketogluterate dehydrogenase
Pyruvate Dehydrogenase

Front 70

Hydrolysis of Triglyceride

Back 70

Adipose triacylglyceride lipase
Hormone sensitive lipase
Monoacylglyceride lipase

Front 71

Protein Metabolism

Back 71

N cannot be used as an energy source. Must be removed.
Deamination - removal of nitrogen from protein (in liver)
Transamination - the nitrogen is passed to other compounds

Front 72

Deamination

Back 72

N gets removed fromt he body after being taken off, it is expelled in urine. Produces Urea

Front 73

Transamination

Back 73

N is passed to other molecules in skeletal muscle, alpha-ketogluterate. These molecules are shittled to the liver and are deaminated.

Front 74

Protein

Back 74

Recommended 0.84 - 1.7 g/kg/day