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Exercise Physiology > Midterm 1 Content > Flashcards

Midterm 1 Content Flashcards

1
Q

Lecture 1:

What are 3 types of Muscle Tissue?

A

1.) Skeletal Muscle
2.) Cardiac Muscle
3.) Smooth Muscle

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2
Q

Lecture 1:

What is Skeletal Muscle?

A

Generates force production to move limbs & is under voluntary control & has striated muscle fibres

main focus of the course

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3
Q

Lecture 1:

What is Cardiac Muscle?

A

Striated muscle proteins but not under voluntary control as muscle generates own rhythm

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4
Q

Lecture 1:

What is Smooth Muscle?

A

Muscle fibres contract involuntarily
- vessels constrict/dilate to regulate blood flow

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5
Q

Lecture 1:

What are Myofibrils?

A

Muscle proteins that are the smallest unit of the muscle (muscle —> fasciculi—>muscle fibre —> myofibril)
Hundreds of thousands of them per muscle fibre

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6
Q

Lecture 1:

What are Sarcomeres?

A

The basic contractile element of skeletal muscle & go end to end for full myofibril length

The individual functional units of a muscle fibre with the power stroke cross bridge cycling that shortens the muscle

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7
Q

Lecture 1:

When discussing Sarcomeres, what are the different bands/zones that cause the striations (striped appearance)?

A

A-bands - dark stripes (contain both actin & myosin)
I-bands - light stripes (only actin here when relaxed)
H-zone - middle of A-band
M-line - middle of H-zone (where myosin group together)

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8
Q

Lecture 1:

What are the 2 types of Protein Filaments in Sarcomeres?
- describe each & what zone/band they are

A

1.) Actin (thin filaments)
- lighter under microscope & form the I-band
- composed of globular proteins joined together to make a chain
2.) Myosin (thick filaments)
- darker under microscope & forms the H-zone
*A-band contains both actin & myosin filaments

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9
Q

Lecture 1:

What does Myosin look like?

A

2 intertwined filaments with globular heads 360degs out of the thick filament axis & interact with actin for contraction

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10
Q

Lecture 1:

What are the 3 proteins that actin is composed of?

A

1.) Actin - contains myosin-binding site
2.) Tropomyosin - covers active site (for myosin head) at rest
3.) Troponin (anchored to actin) - moves tropomyosin when muscle is ready for muscle contraction

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11
Q

Lecture 1:

What is Titan & a few points on it

A

Third myofilament that acts like a spring (tension increases with muscle activation & force)
- attaches myosin to the Z-disk of actin
- Calcium binds to titan to increase muscle force when stretched
- stabilizes sarcomeres, centers myosin, & prevents overstretching

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12
Q

Lecture 1:

What is a Motor Unit?

A

Consists of a single motor neuron & all fibres it innervates (the nerve & the muscle fibres)
- more operating motor units = more contractile force

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13
Q

Lecture 1:

What is the Neuromuscular Junction?

A

Consists of the synapse between a motor neuron & muscle fibre (between nerve & motor unit connection)
- site of communication between a neuron & muscle

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14
Q

Lecture 1:

When discussing Muscle fibre contraction, What is Excitation-Contraction Coupling?

A

The combined process of turning a nerve on (exciting it) to the contraction of proteins in a muscle fibre

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15
Q

Lecture 1:

What are the 6 main steps of Excitation-Contraction Coupling?

A

1.) Action Potential (AP) develops in the brain
2.) AP arrives at the axon terminal & releases Acetylcholine (ACh)
3.) ACh crosses the synapse & binds to ACh receptors on plasmalemma
4.) AP travels down Plasmalemma & T-tubules
5.) triggers release of Ca2+ from sarcoplasmic reticulum (SR)
6.) Ca2+ enables actin-myosin contraction & muscle movement occurs

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16
Q

Lecture 1:

What is the role of Calcium in Muscle Fibres?

A

Calcium is an ion that causes muscle contraction as it signals muscle proteins to contract
- Calcium is released into SR & bind to troponin on thin filament to move tropomyosin and reveal the sites on actin for myosin heads to binds to

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17
Q

Lecture 1:

In the sliding filament theory, What happens in relaxed vs contracted states?

A

1.) Relaxed State - no actin-myosin interaction occurs at binding sites & myofilaments only overlap a little
- no calcium as binding sites covered by troponin
2.)Contracted State - myosin head pulls actin towards sarcomere center (power stroke) & filaments slide past eachother
- sarcomeres, myofibrils, & muscle fiber all shorten

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18
Q

Lecture 1:

In the sliding filament theory, what happens after the power stroke ends?

A

After power stroke ends, myosin detaches from active sites & myosin head rotates back to original position
- myosin attaches to another active site farther down

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19
Q

Lecture 1:

What causes the sliding filament theory to end?

A

Either the Z-disk reaches myosin filaments or AP stops & Calcium is pumped back into sarcoplasmic reticulum

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20
Q

Lecture 1:

What is the energy source for muscle contractions?

A

Adenosine Triphosphate (ATP) is necessary for muscle contraction
- it binds to the myosin head & ATP becomes ADP + Pi + energy

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21
Q

Lecture 1:

What are the 3 main types of muscle fibres?

A

1.) Type I
2.) Type IIa
3.) Type IIx

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22
Q

Lecture 1:

What percentage of muscle fibres does type I make & what is its peak tension?
- type of twitch?

A

Approx 50% of fibres in an average muscle & peak tension is 110ms
- slow twitch fibres as take a long time to reach peak force production (slow oxidative fibres)

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23
Q

Lecture 1:

What percentage of muscle fibres does type II make & what is its peak tension?
- type of twitch?

A

Type IIa & IIx both make up approx 25% of fibres in average muscle & peak muscle tension is 50ms
- fast twitch muscle fibres as they are fast to contract but quicker to fatigue
- IIa = fast oxidative fibre & IIx = fast glycolytic fibre

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24
Q

Lecture 1:

When comparing Type I & Type II muscle fibres, what is the difference in speed of myosin ATPase?

A

Fast myosin ATPase = fast contraction cycling (type I?)

Slower myosin ATPase = slower contraction cycling (type 2?)

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25
Q

Lecture 1:

What are Gel Electrophoresis?

A

Type I & II fibres have different types of myosin so this process separates types of myosin by size

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26
Q

Lecture 1:

What is the difference in the Sarcoplasm Reticulum’s of Type I vs Type II fibres?

A

Type II fibres have a more highly developed SR & the calcium release is faster & Vo is 3-5times faster

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27
Q

Lecture 1:

What is the difference in motor units in Type I vs Type II muscle fibres?

A

Type I motor units have smaller neurons with <300 fibres & type II motor units have larger neurons with >300 fibres
- more units in type II, meaning more connections to the brain

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28
Q

Lecture 1:

How are fibre types distributed?

A

Each person has a unique ratio that is mostly based on genetics
- arm & leg ratios are similar in one person
- typically more type I in endurance athletes & more type II in power athletes

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29
Q

Lecture 1:

What is the only muscle in the body that is 100% type I fibres in everyone?

A

The Soleus is type I in everyone

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30
Q

Lecture 1:

What happens to Type I muscle fibres during exercise?

A

The possess high aerobic endurance & maintain prolonged exercise
- require oxygen for ATP production
- recruited for low-intensity aerobic exercise & DPA
- ATP efficiently produced from fat & carbs

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31
Q

Lecture 1:

What happens to Type II muscle fibres during exercise?
- in general, Type IIa, & type IIx

A

In general, they fatigue quickly as poor aerobic endurance & produce ATP anaerobically
- Type IIa: produce more force & fatigue slower than I
- Type IIx: seldom used for everyday activities

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32
Q

Lecture 1:

When are Type IIa vs Type IIx muscle fibres used?

A

IIa - used for short, intense endurance (1,600m run)

IIx - used for short, explosive sprints (100m)

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33
Q

Lecture 1:

What are 2 main determinants of fibre type?
- explain each

A

1.) Genetics - determine which motor neurons innervate fibres & differentiate based on neuron
2.) Training - differentiate endurance, strength, & detraining. Training can induce small fibre type changes (10%)

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34
Q

Lecture 1:

What effect does aging have on muscle fibre type?

A

Aging causes a loss of type II motor units as they begin behaving like type I fibres

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35
Q

Lecture 1:

What is Motor Unit Recruitment?
- what order are units recruited in?

A

A method used for altering force production
- recruitment order = Type I, Type IIa, Type IIx

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36
Q

Lecture 1:

When discussing motor unit recruitment, how is force production altered?

A
  • less force production = fewer/smaller motor units
  • more force production = more/larger motor units
  • type I units are smaller than type II
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37
Q

Lecture 1:

What are the 2 main types of Muscle Contraction?

A

1.) Static (isometric)
2.) Dynamic

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38
Q

Lecture 1:

What is Static Muscle Contraction?

A

Isometric contraction where muscle produces force but doesn’t change length
- joint angle doesn’t change & myosin cross-bridges form & recycle with no sliding

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39
Q

Lecture 1:

What is Dynamic Muscle Contraction?

A

Muscle produces force & changes length
- joint movement is produced. Muscle lengthens/shortens

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40
Q

Lecture 1:

What are the 2 types of Dynamic Muscle Contractions?

A

1.) Concentric (most common) - muscle shortens as sarcomere shortens & filaments slide towards eachother

2.) Eccentric - muscle lengthens as cross-bridges form but sarcomere lengthens (eg; lowering heavy weight)

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41
Q

Lecture 2:

What are Substrates?

A

Fuel sources we make energy from (eg; adenosine triphosphate ATP)

Macronutrients absorbed from the diet - carbs, proteins, & fat (lipids)

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42
Q

Lecture 2:

What is Bioenergetics?

A

The process that converts substrates into energy
- a cellular-level process

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43
Q

Lecture 2:

What is Metabolism?

A

Chemical reactions that occur in the body

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44
Q

Lecture 2:

How is energy release measured?

A

Calculated from heat production
- calculated in calories — 1cal = heat energy req’d to raise 1g of water from 14.5 degrees to 15.5

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45
Q

Lecture 2:

what is 1,000 calories equal to?

A

1,000 cal = 1 kcal = 1 Calorie (dietary)

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46
Q

Lecture 2:

What are the 3 main substrates used as fuel for exercise?
- what are the key organic molecules they have?

A

1.) Carbohydrates
2.) Fat
3.) Protein
- all contain carbon, hydrogen, oxygen, &/or nitrogen

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47
Q

Lecture 2:

What type of substrate is used for short exercise? Which for long exercise?

A

Short = more carbohydrate

Long = carbohydrate & fat

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48
Q

Lecture 2:

What are Carbs converted into to be used as energy?

A

All carbs are converted to glucose & yield about 4.1kcal/g

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49
Q

Lecture 2:

Approximately how many kcals of glucose are stored in the body?

A

~2,500kcal

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50
Q

Lecture 2:

Where is extra glucose stored in the body & what is it stored as?

A

Extra glucose is stored as glycogen in the liver & muscles
- glycogen converted back to glucose when needed to make more ATP

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51
Q

Lecture 2:

How much energy does fat yield?

A

Fat yields almost double the amount of energy as carbs as it makes 9.4kcal/g
- yields high net ATP but slow ATP production

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52
Q

Lecture 2:

How much fat substrate can be stored in the body?

A

70,000+ kcal of fat stored in the body

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53
Q

Lecture 2:

What does fat get broken down into when used for energy?

A

Broken down into free fatty acids (FFAs) & glycerol
**only FFAs are used to make ATP

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54
Q

Lecture 2:

When is protein used for energy?
- how much energy does it yield?

A

Used for energy during starvation & yields 4.1kcal/g

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55
Q

Lecture 2:

How are proteins broken down & what are they broken down into?

A

Need to be broken down into individual amino acids & then into glucose in order to be used.
- convert into FFAs through lipogenesis for energy storage and cellular energy substrate

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56
Q

Lecture 2:

How is energy rate production controlled?

A

Energy is released at a controlled rate based on availability of primary substrate

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57
Q

Lecture 2:

What is the Mass Action Effect when discussing rate of energy production?

A

Explain how substrate availability affects metabolic rate
- more substrate available = higher pathway activity
- excess of given substrate = cells rely on that substrate more than others

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58
Q

Lecture 2:

How do enzymes control rate of energy production?

A

Energy release rate is controlled by enzyme activity in the metabolic pathway
- more enzymes = more ATP produced

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59
Q

Lecture 2:

What are Enzymes?

A

They facilitate breakdown (catabolism) of substrates & catalyze individual reactions to produce more ATP
- they can speed up or slow down reactions based on ATP requirements
- they lower the activation energy for a chemical reaction
- end with suffix “-ase”

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60
Q

Lecture 2:

What is PFK Enzyme?

A

Facilitates production of glucose when turned on or reduces rate of production when turned off
- used in glycolysis

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61
Q

Lecture 2:

What is Rate-Limiting Enzyme?

A

Can create a bottleneck effect at an early step
- activity is influenced by negative feedback & slows overall reaction to prevent runaway reaction

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62
Q

Lecture 2:

How is ATP stored?
- where & how much

A

ATP is stored in small amounts until needed & stored in phosphate bonds in muscle

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63
Q

Lecture 2:

When ATP is used for energy, how is it broken down to release energy?

A

ATP is broken down to release energy by using ATPase enzymes

ATP + Water + ATPase —> ADP + Pi + energy

*ADP is a lower-energy compound that is less useful

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64
Q

Lecture 2:

How is ATP formed from by-products?

A

ATP is synthesized through phosphorylation & can occur in either absence or presence of Oxygen

ADP + Pi + energy —> ATP

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65
Q

Lecture 2:

What are the three ATP synthesis Pathways?

A

1.) ATP-PCr System ~ anaerobic metabolism
2.) Glycolytic System ~ anaerobic metabolism
3.) Oxidative System ~ aerobic metabolism

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66
Q

Lecture 2:

What is the ATP-PCr System?
- oxygen required?
- ATP yield?
- duration?

A

Anaerobic system (no oxygen) with substrate-level metabolism and also called the Phosphate Creatine system
- ATP Yield = 1 ATP/1 PCr
- Duration = 3-15s
- Pathway is used to reassemble ATP because ATP stores are very limited

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67
Q

Lecture 2:

What is PCr?
- how is it broken down in the ATP-PCr System?

A

PCr = phosphocreatine & used for ATP recycling
- PCr + creatine kinase —> Cr + Pi + energy
- PCr energy cannot be used for cellular work but can be used to reassemble ATP
- it replenishes ATP stores @ rest & recycles ATP during exercise until used up

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68
Q

Lecture 2:

What is the main enzyme used in the ATP-PCr System?

A

PCr breakdown is cataloged by the CK enzyme (creatine kinase)
- CK controls rate of ATP production based on negative feedback
*low ATP & high ADP causes CK activity to increase
* high ATP levels cause CK activity to decrease

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69
Q

Lecture 2:

What is the Glycolytic System?
- oxygen required?
- ATP yield?
- Duration?

A

An anaerobic system for ATP synthesis that does not require oxygen
- ATP yield = 2-3 mol ATP/ 1 mol substrate
- Duration = 15s - 2min
- breaks down glucose via glycolysis

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70
Q

Lecture 2:

What substrate is used in the Glycolytic System?

A

Uses glucose or glycogen as its substrate
- costs 1 ATP for glucose & 0 ATP for glycogen
- must convert to glucose-6-phosphate

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71
Q

Lecture 2:

What is the Pathway for the Glycolytic System?
- where does it occur?
- ATP yield?

A

Pathway starts with glucose-6-phosphate & ends with pyruvic acid
- 10-12 enzymatic reactions total
- all steps occur int eh cytoplasm
- ATP Yield: 2 ATP for glucose & 3 for glycogen

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72
Q

Lecture 2:

What are 3 Cons of the Glycolytic System?

A

1.) low ATP yield & inefficient use of substrate
2.) lack of O2 converts pyruvic acid to lactic acid
3.) lactic acid impairs glycolysis & muscle contraction as it impairs ability to produce ATP

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73
Q

Lecture 2:

What are 2 Pro’s of the Glycolytic System?

A

1.) Allows muscles to contract when O2 is limited
2.) Permits shorter-term, high-intensity exercise than oxidative metabolism can sustain

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74
Q

Lecture 2:

In the Glycolytic System, What enzyme is used & how?

A

Phosphofructokinase (PFK) is a rate-limiting enzyme that regulates ATP production.
- lower ATP = higher PFK activity… higher ATP = lower PFK activity **PFK levels also regulated by products of Krebs cycle
- Glycolysis = ~2mins max exercise… need another pathway for longer durations

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75
Q

Lecture 2:

What is the Oxidative System?
- Oxygen required?
- ATP yield?
- Duration?
- location?

A

Aerobic system that yields way more ATP than other systems & is less intense as ATP is produced slowly
- ATP Yield is dependent on substrate… 32-33ATP/1g glucose & 100+ ATP/1 FFA
- Duration = steady supply for hours
- Location = mitochondria (not cytoplasm)
- most complex system of the 3 bioenergetic systems

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76
Q

Lecture 2:

What are the 3 stages of the Oxidation System when Oxidizing a Carbohydrate?

A

1.) Glycolysis
2.) Krebs Cycle
3.) Electron Transport Chain (ETC)

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77
Q

Lecture 2:

Explain the Electron Transport Chain

A

H+ & electrons are carried to the ETC via NADH & FADH2 molecules
- H+ & electrons travel down the chain….
1.) H+ combines with O2 & forms H2O
2.) Electrons & O2 help form ATP
3.) 2.5 ATP per NADH & 1.5 ATP per FADH2

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78
Q

Lecture 2:

How is Fat Oxidized in the Oxidative System?
- rate of entry into muscle?
- ATP yield compared to glucose?
- slower or faster than glucose oxidation?

A

Triglycerides (major fat energy source) are broken down into 1 glycerol & 3 FFAs through lipolysis (carried out by lipases)
- Rate of FFAs entry into muscle is dependent on concentration gradient
- Yields 3-4 times more ATP than glucose
- slower than glucose oxidation

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79
Q

Lecture 2:

What is the b-Oxidation (beta-oxidation) of fat?
- how much ATP used?

A

The process converting FFAs (fatty acids) to acetylene-CoA before entering Krebs Cycle
- uses 2 ATP right away

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80
Q

Lecture 2:

How many steps in the beta-Oxidation of fat?

A

of steps depends on # of carbons on FFA (fatty acids)

  • 16-carbon FFA yields 8 acetyl-CoA compared to 1 glucose yielding 2 acetyl-CoA
  • fat oxidation required more O2 at beginning & yields far more ATP later
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81
Q

Lecture 2:

When discussing fat oxidation… how does the Krebs cycle & ETC work?

A

Acetyl-CoA enters Krebs cycle & follows same path as glucose oxidation
- different fatty acids have different #’s of carbons meaning they… yield different #’s of acetyl-CoA molecules, & Yield different ATP

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82
Q

Lecture 2:

What is the Oxidation process of a protein?
- how is energy yield determined?

A

Protein rarely used as a substrate but can be converted to glucose & Acetyl-CoA
- energy yield not easy to determine as nitrogen presence is unique & excretion requires ATP

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83
Q

Lecture 2:

What are the 3 key ways that muscle can use lactate?

A

Lactate is an important fuel during exercise & can be used by muscles in 3 ways…
1.) lactate produced in cytoplasm is taken up by mitochondria (of same muscle fibre) & oxidized
2.) lactate transported via MCP transporters to another cell & oxidized there (lactate shuttle)
3.) lactate recirculates back to liver & reconverted to pyruvate & then glucose through gluconeogenesis

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84
Q

Lecture 2:

How do the 3 energy systems interact with eachother?

A

All 3 systems interact for all activities as no single system contributes 100% but one system will often dominate
- cooperation between systems increases during transition periods

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85
Q

Lecture 2:

What is the Crossover Concept?
- at rest vs at intensity & their intersection

A

**Cross-over point is the intersection of these 2, which is affected by exercise intensity & endurance training

  • at rest & exercise below 60% VO2max lipids are the primary substrate
  • at high intensity & above 75% VO2max carbohydrates are the primary substrate
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86
Q

Lecture 2:

What are the 3 main factors that determine Oxidative Capacity of a Muscle?

A

Not all muscles have maximal oxidative capability’s but can be determined by…
1.) Enzyme activity
2.) Fibre type composition & endurance training
3.) O2 availability versus need

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87
Q

Lecture 2:

Enzyme activity & Oxidative Capacity…. What are some representative enzymes?

A

Not all muscles exhibit optimal activity of oxidative enzymes
- representative enzymes include; succinate dehydrogenase & citrate synthase
- levels differ in endurance-trained vs untrained individuals

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88
Q

Lecture 3:

What is a Neuron?

A

The basic structural unit of nervous system also called a nerve & is an excitable tissue that sends nerve impulses down cellular membranes

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89
Q

Lecture 3:

What are the 3 major regions of the Neuron?

A

1.) Cell body (soma)
2.) Dendrites
3.) Axon

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90
Q

Lecture 3:

What 2 things speed up the propagation of action potentials?

A

Myelin speeds up propagation & axons with a larger diameter speed propagation as well

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91
Q

Lecture 3:

What is myelin & How does myelin speed up action potentials?

A

Myelin can be a fatty sheath around the axon & called Schwann cells or not continuous layers that are called nodes of Ranvier
- saltitory conduction

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92
Q

Lecture 3:

Schwann Cells vs Nodes of Ranvier

A

Schwann cells = continuous fatty myelin sheath around the axon made of glial cells

Nodes of Ranvier = non continuous myelination

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93
Q

Lecture 3:

What is the Synapse & its purpose?

A

The junction/gap between neuron’s that serves as a site of neuron-to-neuron communication
*AP must jump across the synapse

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94
Q

Lecture 3:

What is the pathway of Action Potential to the synapse?

A

Axon —> synapse —> dendrites
Presynaptic cell —> synaptic cleft —> postsynaptic cell
**signal changes form across synapse
Electrical —> Chemical —> Electrical

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95
Q

Lecture 3:

How do AP’s transmit across the Synapse?

A

AP can only move in one direction & axon terminals contain neurotransmitters that serve as chemical messengers
- they carry electrical AP across synaptic cleft
- bind to receptor on postsynaptic surface
- stimulate GP’s in postsynaptic neuron

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96
Q

Lecture 3:

What are Neurotransmitters?

A

50+ are known
- ACh & Noepinephrine (NE) govern exercise which increases acetylcholine (ACh)

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97
Q

Lecture 3:

What is the role of ACh neurotransmitter?

A

Governs exercise & stimulates skeletal muscle contraction, & mediates parasympathetic nervous system effects

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98
Q

Lecture 3:

What is the role of Noepinephrine (NE) neurotransmitter?

A

NE mediates sympathetic nervous system effects

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99
Q

Lecture 3:

What is the real name of the PGC-1a neurotransmitter?

A

Peroxisome Profilferator-activated receptor-y coactivator 1a

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100
Q

Lecture 3:

What are the 4 key points of the PGC-1a neurotransmitter?

A

A molecule that is more available during exercise
1.) increases branching of the presynaptic terminal motor neuron
2.) increases the # of presynaptic vesicles containing acetylcholine
3.) increase the # of acetylcholine receptors on the cell membrane
4.) decreases the size of the motor end plate

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101
Q

Lecture 3:

What are the 2 types of Postsynaptic responses?

A

1.) Excitatory Postsynaptic Potential (EPSP)
2.) Inhibitory Postsynaptic Potential (IPSP)

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102
Q

Lecture 3:

What is the Excitatory Postsynaptic Potential (EPSP) response?

A

This is a depolarization, excitatory response that promotes Action Potentials
- More EPSPs = more depolarization
- if you reach threshold depolarization that AP occurs

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103
Q

Lecture 3:

What is the Inhibitory Postsynaptic Potential (IPSP) response?

A

This is a hyperpolarization, inhibitory response that prevents Action Potentials
- multiple IPSPs = more hyperpolarizing

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104
Q

Lecture 3:

What sections of the brain form the Cerebrum?

A
  • Frontal lobe
  • Parietal lobe
  • Occipital lobe
  • Temporal lobe
    *basal ganglia
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105
Q

Lecture 3:

What is the primary motor cortex of the cerebrum?

A

Frontal lobe = primary motor cortex
- responsible for conscious control of muscle movement
- pathway = pyramidal cells > Corticospinal tract > spinal cord

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106
Q

Lecture 3:

What is the primary sensory cortex of the cerebrum?

A

Parietal lobe

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107
Q

Lecture 3:

What is the Basal ganglia in the cerebrum?

A

The cerebral white matter that include clusters of cell bodies deep in the cerebral cortex & initiate sustained or repetitive movements
Eg; walking, running, posture, muscle tone, etc

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108
Q

Lecture 3:

What are the 2 portions that form the Diencephalon?

A

1.) Thalamus
2.) Hypothalamus

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109
Q

Lecture 3:

What is the role of the Thalamus in the Diencephalon?

A

Serves as a major sensory relay center that determines what we are consciously aware of

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110
Q

Lecture 3:

What is the role of the Hypothalamus in the Diencephalon?

A

Maintains homeostasis & regulates internal environment using neuroendocrine control
- eg; appetite, thirst, fluid balance, sleep, blood pressure, heart rate, breathing, temperature, etc.
- controls systems typically under involuntary control

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111
Q

Lecture 3:

What is the role of the Cerebellum?

A

Controls rapid/complex movements & coordinates timing/sequence of the movements
- compares movements with intentions & initiated corrections
- accounts for body position & muscle status
- receives input from primary motor cortex (frontal lobe) to help execute/refine movements

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112
Q

Lecture 3:

What are the 3 sections that form the Brain Stem?

A

1.) Midbrain
2.) Pons
3.) Medulla Oblongata

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113
Q

Lecture 3:

What is the key role of the Brainstem?

A

To relay information between the brain & spinal cord

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114
Q

Lecture 3:

What is the purpose of Reticular Formation in the Brainstem?

A

To coordinate skeletal muscle formation/tone & control cardiovascular/respirator functions

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115
Q

Lecture 3:

What is the purpose of Analgesia System in the Brainstem?

A

Where pain is modulated by opioid substances as b-endorphins are released here with exercise

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116
Q

Lecture 3:

What is the Spinal Cord?
- location

A

Tract of nerve fibres that permit 2-way conduction of nerve impulses that is continuous with the medulla oblongata

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117
Q

Lecture 3:

What are the 2 tracts in the spinal cord?

A

1.) Ascending Afferent (sensory) fibres
2.) Descending Efferent (motor) fibres

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118
Q

Lecture 3:

What is the Peripheral Nervous System?
- how many cranial nerves?
- how many spinal nerves?

A

PNS is connected to brain & spinal cord
- 12 pairs of cranial nerves (connected to brain)
- 31 pairs of spinal nerves (connected to spinal cord)
*both types directly supply skeletal muscles

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119
Q

Lecture 3:

What are the 2 major divisions of the PNS?

A

1.) Sensory (Afferent) division
2.) Motor (efferent) division

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120
Q

Lecture 3:

What is the role of the Sensory Division of the PNS?

A

Transmits information from periphery to the brain & includes major families of sensory receptors

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121
Q

Lecture 3:

What are the 5 major families of sensory receptors in the PNS?

A

1.) Mechanoreceptors - physical forces
2.) Thermoreceptors - temperature
3.) Nociceptors - pain
4.) Photoreceptors - light
5.) Chemoreceptors - chemical stimuli (changes in o2 levels etc)

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122
Q

Lecture 3:

In the sensory division of the PNS, what are Joint Kinesthetics Receptors?

A

Receptors sensitive to joint angles & rate of angle change (degrees of flexion or extension)
- they sense joint position & movement

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123
Q

Lecture 3:

In the sensory division of the PNS, what are Muscle Spindle Receptors?

A
  • specialized intramural muscle fibres innervated by g-motor neurons
    Sensory fibres/nerve clusters sensitive to muscle length & rate of change
  • they sense muscle stretch and rate/amount of stretch
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124
Q

Lecture 3:

In the sensory division of the PNS, what are Golgi Tendon Organ Receptors?

A

They are sensitive to tension in the tendons & sense strength of contractions

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125
Q

Lecture 3:

What is the role of the Motor Division of the PNS?
- 2 subdivisions

A

Transmit information from the brain to periphery & has 2 subdivisions:
1.) Autonomic - regulates visceral activity
2.) Somatic - stimulates skeletal muscle activity

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126
Q

Lecture 3:

In the Motor Division of the PNS, what is the Autonomic Nervous System?

A

Regulates visceral activity & controls involuntary internal functions
- helps with exercise-related autonomic regulation such as heart rate, blood pressure, & lung functions

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127
Q

Lecture 3:

What are the 2 complimentary divisions of the Autonomic Nervous system?
- one key point on each

A

1.) Sympathetic Nervous System - fight or flight (prepares body for exercise)
2.) Parasympathetic Nervous System - rest & digest (state of conserving energy)

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128
Q

Lecture 3:

What is the Sympathetic Nervous System of the ANS?
- what happens when stimulation increases?

A

The fight or flight response in preparation for exercise… when stimulation increases…
- heart rate & blood pressure increase
- blood flow to muscles increase
- airway diameter increases (bronchodilation)
- metabolic rate, glucose levels, and FFA levels increase

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129
Q

Lecture 3:

What is the Parasympathetic Nervous System of the ANS?
- what happens when stimulation increases?

A

The rest & digest activity that opposes sympathetic effects as trying to conserve energy for next sympathetic event
- digestion & urination increases
- heart rate decreases
- diameter of vessels & airways decreases

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130
Q

Lecture 3:

What is Sensory-Motor Integration?

A

The communication & interaction between sensory & motor systems

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131
Q

Lecture 3:

What are the 5 Sequential Steps of Sensory-Motor Integration?

A

1.) Stimulus sensed by sensory receptor
2.) Sensory AP sent to sensory neurons in CNS
3.) CNS interprets sensory info & sends out response
4.) Motor AP sent out on alpha-motor neurons
5.) arrives at skeletal muscle & response occurs

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132
Q

Lecture 3:

What happens when level of control moves from spinal cord to cerebral cortex?

A

As level of control moves from spinal cord to cerebral cortex, movement complexity increases

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133
Q

Lecture 3:

What is the motor reflex activity like during sensory-motor integration?

A

Motor reflex is an instant, preprogrammed response to stimulus & is identical each time
- occurs before conscious awareness
- impulse is integrated at lower, simple levels

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134
Q

Lecture 4:

What is the role of the Endocrine System?

A

It’s a chemical communication system that maintains homeostasis via hormones

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135
Q

Lecture 4:

What is the speed of the endocrine system compared to the nervous system?

A

endocrine system is slower to respond than the nervous system but is longer lasting

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136
Q

Lecture 4:

What are the 2 key ways the endocrine system maintains homeostasis?

A

1.) controls substrate metabolism
2.) regulates fluid & electrolyte balance

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137
Q

Lecture 4:

What are the 4 key organs of the endocrine system we are going to look at?

A

Thyroid gland, adrenal glands, pancreas, & kidneys

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138
Q

Lecture 4:

What are steroid hormones?
- derived from what & soluble or not?

A

Derived from cholesterol & are lipid soluble as they can diffuse through membranes
- aldosterone is an important for fluid balance

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139
Q

Lecture 4:

What are the 4 major glands that secrete Steroid Hormones?
- & what hormone is secreted?

A

1.) Adrenal Cortex - cortisol & aldosterone
2.) Ovaries - estrogen & progesterone
3.) Testes - testosterone
4.) Placenta - estrogen & progesterone

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140
Q

Lecture 4:

What are Non-steroidal Hormones & their 2 types?

A

Non lipid-soluble hormones that are unable to cross membranes & include 2 types; Protein/Peptides & Amino-Acid Derived

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141
Q

Lecture 4:

What are the Protein/Peptide Non-Steroidal hormones?

A

The most common type of non-steroidal hormones that are secreted from the pancreas, hypothalamus, & pituitary glands

142
Q

Lecture 4:

What are the Amino-Acid Derived Non-Steroidal hormones?

A

Includes the thyroidal hormones (T3 & T4) and the Adrenal Medulla Hormones including epinephrine & noepinephrine

143
Q

Lecture 4:

How are Hormones secreted?

A

Secreted in bursts (pulsatile) as plasma concentrations fluctuate over minutes/hours & days/weeks

144
Q

Lecture 4:

How is Hormone Secretion Regulated?

A

Regulated by negative feedback as hormone release causes a change in the body
- large downstream change reduces secretion
- small downstream change increases secretion
- eg; home thermostat

145
Q

Lecture 4:

What is downregulation (when discussing hormone actions)?

A

The decrease in # of receptors during high plasma concentration & causes desensitization for receiving hormones

146
Q

Lecture 4:

What is upregulation (when discussing hormone actions)?

A

The increase in # of receptors during high plasma concentration & causes sensitization for hormones

147
Q

Lecture 4:

How do hormone receptors work?

A

Use hormone-specific receptors to limit the scope of their effects & bind to correct receptors
*if no receptors than there is no hormone effect

148
Q

Lecture 4:

Why is there no hormone effect if there is no receptor on the cell surface?

A

1.) hormone affects only tissues with specific receptors
2.) hormone exerts effects after binding with receptors
- typical cells have 2,000-10,000 receptors

149
Q

Lecture 4:

Where are steroid hormone receptors found & their actions?

A

Inside the cell in the cytoplasm or nucleus
-hormone-receptor complex enters nucleus & binds DNA to direct gene activation & regulate the synthesis of mRNA & proteins

150
Q

Lecture 4:

Where are non-steroid hormone receptors found & their actions?

A

Receptors on cell membranes go to second membrane systems to carry out hormone effects

151
Q

Lecture 4:

What are the 3 common second messengers of non-steroidal hormones & their roles

A

Second messengers carry out & intensify the effects of hormones
1.) Cyclic Adenosine Monophosphate (cAMP)
2.) Cyclic Guanine Monophosphate (cGMP)
3.) Inositol Triphosphate (IP3) & Diacylglycerol (DAG)

152
Q

Lecture 4:

Where is the Pituitary Gland located?

A

Attached to the inferior hypothalamus of the brain

153
Q

Lecture 4:

What are the 3 lobes of the Pituitary gland?

A

1.) Anterior (most important)
2.) Intermediate
3.) Posterior

154
Q

Lecture 4:

What is the role of the Pituitary Gland?

A

Secretes hormones in response to hypothalamic hormone factors:
- releasing & inhibiting factors
- exercise increases secretion of all anterior pituitary hormones

155
Q

Lecture 4:

What is the most common hormone released from the Anterior Pituitary Gland?
- what is it’s role

A

Growth Hormone (GH) is a potent anabolic hormone that’s release is proportional to exercise intensity (increased GH release when increase in intensity)
- helps build tissue & organs, promotes muscle growth (hypertrophy), & stimulates fat metabolism

156
Q

Lecture 4:

What are the 2 key hormones released from the Thyroid Gland?

A

Triiodothyronin (T3) & Thyroxine (T4)

157
Q

Lecture 4:

In the Thyroid Gland, T3 & T4 led to increases in what?

A

T3 & T4 increase…
- metabolic rates of all tissues
- protein synthesis
# & size of mitochondria
- glucose uptake by cells
- rate of glycolysis & gluconeogenesis
- FFA mobilization

158
Q

Lecture 4:

How is the release of T3 & T4 stimulated?

A

1.) The Anterior Pituitary releases thyrotropin (Thyroid-stimulating hormone/TSH) that travels to the thyroid gland and stimulates release of T3 & T4
2.) Exercise speeds up release of TSH
- short exercise = T4 increases & long exercise = T4 constant & T3 decreases

159
Q

Lecture 4:

What is the role of the Adrenal Medulla?

A

Releases catecholamines (80% Epinephrine & 20% NE) that help with the fight or flight response
- exercise increases which increases SNS & increases release of E & NE

160
Q

Lecture 4:

When Catecholamines are released from the Adrenal Medulla, what 3 things are increased?

A

1.) heart rate, contractile force, & blood pressure increase in the heart
2.) Glycolysis & FFAs increase
3.) Blood flow to skeletal muscle increases

161
Q

Lecture 4:

What hormones are released from the Adrenal Cortex?

A

Releases corticosteroids which include:
- glucocorticoids
- mineralocoticoids
- gonadocorticoids

162
Q

Lecture 4:

What is the most common glucocorticoid released from the Adrenal Cortex?
- function?

A

Cortisol is the major glucocorticoid & stimulates glucogenesis while increasing FFA mobilization & protein catabolism
- acts as an anti-inflammatory & depresses anti-immune reactions

163
Q

Lecture 4:

What are the 2 key hormones in the Pancreas & their main function?

A

1.) Insulin - used to lower blood glucose levels
2.) Glucagon - used to raise blood glucose levels

164
Q

Lecture 4:

How does insulin work when released from Pancreas?

A

Lowers blood glucose by countering hyperglycaemia and opposing glucagon
- facilitates glucose transport into cells
- enhances synthesis of glycogen, protein, & fat
- inhibits (stops) gluconeogenesis

165
Q

Lecture 4:

How does Glucagon work when released from the Pancreas?

A

Glucagon raises blood glucose levels by countering hypoglycemia & opposes insulin
- promotes glycogenolysis & gluconeogenesis

166
Q

Lecture 4:

3 key ways of regulating carbohydrate metabolism during exercise?

A

1.) Glucose must be available to tissues
2.) Adequate glucose during exercise requires glucose re;ease from liver & glucose uptake by muscles
3.) some hormones help increase circulating glucose such as; glucagon, epinephrine, noepinephrine, & cortisol

167
Q

Lecture 4:

What is Glycogenolysis?

A

The process of turning glycogen into glucose

168
Q

Lecture 4:

What is Gluconeogenesis?

A

The process of turning FFAs & proteins into glucose

169
Q

Lecture 4:

How does Growth Hormone affect glucose circulating during exercise?

A

GH causes an increase in FFA mobilization which causes a decrease in cellular glucose uptake

170
Q

Lecture 4:

How do T3 & T4 hormones affect glucose circulating during exercise?

A

T3 & T4 hormones cause an increase in glucose catabolism & fat metabolism

171
Q

Lecture 4:

What does the amount of glucose released from the liver depend on?

A

Exercise intensity & duration

172
Q

Lecture 4:

When discussing the regulation of Carbohydrate Metabolism during exercise, what happens when exercise intensity increases?

A
  • catecholamine release increases
  • glycogenolysis rate increases in liver & muscles
  • muscle glycogen is used before the liver glycogen
173
Q

Lecture 4:

When discussing the regulation of Carbohydrate Metabolism during exercise, what happens when exercise duration increases?

A
  • more liver glycogen is sued
  • increase in muscle glucose uptake causes increase in liver glucose release
  • glycogen stores decrease causes glucagon ;evils to increase
174
Q

Lecture 4:

During Exercise, what happens to insulin levels?

A

Insulin concentrations decrease & cellular insulin sensitivity increases causing more glucose to be taken up into the cells & less insulin is used

175
Q

Lecture 4:

How does the CNS interact with the Endocrine SYstem?

A

CNS regulates carbohydrate metabolism through hormones (insulin) & nutrients (glucose, FFAs, & amino acids)
- brain sensitive to glucose & helps control insulin release
- Leptin & GLP-1 hormones are released by adipose tissue & act through the CNS to decrease glucose production
*glucose is the only substrate for brain metabolism

176
Q

Lecture 4:

How is Fat Metabolism regulated during exercise?

A

FFA mobilization & fat metabolism is critical to endurance exercise as glycogen is depleted & fat energy is required, causing lipolysis acceleration
- Triglycerides broken down into FFAs & glycerol

177
Q

Lecture 4:

During exercise, how are triglycerides broken down to maintain metabolism using the fat substrate?

A

Tryglycerides broken down into FFAs & Glycerol
- fat is stored as tryglycerides in adipose tissue
- broken into FFAs & transported to muscles
- rate of this breakdown is a possible determinant of the rate of cellular fat metabolism

178
Q

Lecture 4:

What is Lipolysis & how is it stimulated?

A

Lipolysis is the breakdown of fat & is stimulated by:
- decreased insulin levels
- epinephrine & norepinephrine
- cortisol
- Growth Hormone
*they stimulate lipolysis via lipase enzyme

179
Q

Lecture 4:

During exercise, plasma volume decreases in the blood. What does this cause?

A

1.) increases hydrostatic pressing & tissue osmotic pressure
2.) decreases plasma water content through sweating
3.) increases heart strain, which decreases blood pressure

180
Q

Lecture 4:

During exercise, hormones work to correct fluid imbalances, where are these secreted from?
- name 3 organs/glands

A

1.) Posterior Pituitary Gland
2.) Adrenal Cortex
3.) Kidneys

181
Q

Lecture 4:

How does the Posterior Pituitary gland help regulate fluid & electrolytes during exercise?
- what is the main hormone?

A

Posterior pituitary secretes Antidiuretic hormone (ADH) & oxytocin which are produced in the hypothalamus & travel to posterior pituitary & secreted when brain signals from hypothalamus
- Only ADH is involved with exercise to increase water reabsorption in kidneys & less water in urine (antidiuresis)

182
Q

Lecture 4:

How is the ADH hormone from the Posterior Pituitary stimulated to regulate fluid & electrolytes?

A

1.) decrease in plasma volume (hemoconcentration) causes increase in osmolality
2.) increases osmolality & stimulates osmoreceptors in hypothalamus
*ADH is released & increases water retention by kidneys (minimizes water loss & severe dehydration)

183
Q

Lecture 4:

What hormones do the Adrenal Cortex release to maintain fluid & electrolyte regulation?

A

They secrete mineralocorticoids, the main one is aldosterone which acts on kidneys & causes sodium retention from urine into the blood so water is reabsorbed to maintain osmolaty

184
Q

Lecture 4:

What effects does Aldosterone have on Fluid & electrolyte retention?

A

Aldosterone released from the Adrenal Cortex causes…
1.) increases Na+ retention by kidneys
2.) increases Na+ retention to increase water retention via osmosis
3.) increases Na+ retention to increase K+ excretion

185
Q

Lecture 4:

What is the stimuli for Aldosterone release?

A

Decrease in plasma Na+

Decrease in blood volume & blood pressure

Increase in Plasma K+

186
Q

Lecture 4:

How do the kidneys help regulate fluid & electrolytes?

A

Kidneys are target tissues for ADH & they secret erythropoietin (EPO) & renin

187
Q

Lecture 4:

How does EPO (erythropoietin) released from the kidneys work to maintain fluid & electrolyte balance?

A

EPO released in response to low blood O2 in the kidneys
- simulates red blood cell production which is critical for adapting to training & altitude

188
Q

Lecture 4:

What is the stimulus for renin (enzyme) release from the kidneys?

A

Decreased blood volume & decreased blood pressure
- sympathetic nervous system impulses

189
Q

Lecture 4:

What is the Renin-Angiotensin-Aldosterone Mechanism?

A

Process where renin converts angiotensinogen into angiotensin I & then ACE converts Angiotensin I into Angiotensin II which stimulates the release of Aldosterone

190
Q

Lecture 4:

What does Angiotensin II hormone do?

A

Constricts blood vessels to increase pressure causes kidneys to release aldosterone & brainstem to increase thirst to increase water intake

191
Q

Lecture 4:

What is Osmolality?

A

The measure of concentration of dissolved particles (proteins, ions, etc) in the body’s fluid compartments
- normal value + ~300mOsm/kg

192
Q

Lecture 4:

How does Osmolality & Osmosis help with fluid & electrolyte regulation?

A

If compartments osmolality increases than water is drawn in but is compartment osmolality decreases than water is drawn out (osmosis)

193
Q

Lecture 4:

Relationship between Aldosterone & Osmosis & what does osmotic water movement minimize?

A

Na+ retention causes increased osmolality which leads to increased water retention because where Na+ moves, water follows
- Osmotic water movement minimizes loss of plasma volume & maintains blood pressure

194
Q

Lecture 5:

What is Direct Calorimetry?

A

The measurement of temperature change from heat produced during energy production/expenditure

195
Q

Lecture 5:

When turning substrates into energy, what is metabolism efficiency of it?

A

40% of substrate energy turns into ATP
60% of substrate energy turns into heat

196
Q

Lecture 5:

What are the 2 laws of Thermodynamics?

A

1.) Energy can be created or destroyed
2.) any chemical reaction in the body will release heat

197
Q

Lecture 5:

What happens to heat as energy is produced?

A

Heat production increases with energy production
- can be measured with calorimeter
- water flows through walls & body temp increases the water temp

198
Q

Lecture 5:

What are 2 Pros of Direct Calorimetry?

A

1.) Accurate over time & more precise
2.) Good for resting metabolic measurements

199
Q

Lecture 5:

What are the 4 Cons of Direct Calorimetry?

A

1.) expensive & slow (box is very pricey)
2.) heat added by exercise equipment (eg; treadmill creates friction heat)
3.) Measurement errors created by sweat
4.) Neither practical nor accurate for exercise

200
Q

Lecture 5:

What is Indirect Calorimetry?
- what does it measure?

A

Way of measuring expiratory gases under certain conditions & estimates total body energy expenditure based on O2 used & CO2 produced
- measures respiratory gas concentration

201
Q

Lecture 5:

When is Indirect Calorimetry accurate?

A

Is accurate for steady-state oxidative metabolism

**older methods are accurate but slow & newer methods are faster but expensive

202
Q

Lecture 5:

What is VO2 & how is it calculated?

A

VO2 = volume of O2 consumed per minute (rate of O2 consumption) & units = L/min
*volume of inspired O2 minus volume of expired O2
Formula = (Vi x FiO2) - (Ve x FeO2)

203
Q

Lecture 5:

What is VCO2 & how is it calculated?
- formula & units?

A

The volume of CO2 produced per minute (rate of CO2 produced) & units = L/min
*VCO2 = volume expired CO2 minus Volume inspired CO2
*Formula = (Ve x FeCO2) - (Vi x FiCO2)

204
Q

Lecture 5:

When Calculating VCO2 & VO2, what does FiO2 & FeO2 represent? FeO2 & FeCO2?

A

FiO2 = fraction of O2 in the air we inhale

FiCO2 = fraction of CO2 in the air we inhale

FeO2 = fraction of O2 expired into the air

FeCO2 = fraction of CO2 expired into the air

205
Q

Lecture 5:

What is the % of FiO2 always?

A

Always 20.93% or 21%

206
Q

Lecture 5:

What is the % of FiCO2 always?

A

Always 0.03%

207
Q

Lecture 5:

What is the Respiratory Exchange Ratio (RER)?
- formula?
- units?

A

The ratio between rates of CO2 production & O2 usage
- RER = VCO2/VO2
- no units as it is a ratio

208
Q

Lecture 5:

What does O2 usage during metabolism depend on?

A

Depends on type of fuel being oxidized
- more carbon atoms = more O2 needed

209
Q

Lecture 5:

What does RER predict?

A

Predicts substrate usage & how much energy is required which is measured in Kcal/O2 efficiency

RER = efficiency of energy substrate

210
Q

Lecture 5:

What is the typical range for RER?

A

Between 1.0 & 0.7
*use chart to see these ratios

211
Q

Lecture 5:

What are the limitations of Indirect Calorimetry?

A

1.) CO2 production may not = CO2 exhalation
2.) RER is inaccurate for protein oxidation
3.) RER near 1.0 may be inaccurate when lactate buildup increases CO2 exhalation
4.) Glucogenesis produces RER <0.70
5.) doesn’t work on someone malnourished

212
Q

Lecture 5:

What are the 5 steps to solving indirect Calorimetry questions?

A

1.) Calculate VO2
2.) Calculate VCO2
3.) Calculate RER
4.) use RER to obtain kcal/LO2 (on chart)
5.) Use kcal/LO2 & VO2 to calculate EE

213
Q

Lecture 5:

What is Metabolic Rate & what is it based on?

A

The rate of energy use by the body based on whole body O2 consumption & corresponding caloric equivalent
*@ rest RER = 0.80 & O2 = 0.3L/min
* @ rest metabolic rate = 2,000 kcal/day

214
Q

Lecture 5:

What is Basal Metabolic Rate?

A

BMR = rate of energy expendature @ rest
- found when in supine position, thermoneutral environment, & after 8hrs of sleep & 12hrs fasting

215
Q

Lecture 5:

What are a few things that affect BMR?

A

BMR find the minimum energy required for living & can be affected by body surface area, age, stress, hormones, body temp, etc

216
Q

Lecture 5:

What is Resting Metabolic Rate (RMR)?

A

Typically what we measure as rules are not as strict & is like BMR but easier (within 5-10% range)
- stringent standardized conditions not required
- 1,200 - 2,400 kcal/day
- looks @ total daily metabolic activity

217
Q

Lecture 5:

What occurs to energy expenditure during submaximal aerobic exercise?

A
  • metabolic rate increases with exercise intensity
  • slow component of O2 uptake kinetics (at higher outputs, VO2 increases as more Type II fibre recruitment occurs)
  • VO2 drift = upward drift at low power outputs possibly due to ventilators hormone changes (occurs when recruiting Type II fibres)
218
Q

Lecture 5:

What occurs to energy expenditure during submaximal aerobic exercise?

A
  • metabolic rate increases with exercise intensity
  • slow component of O2 uptake kinetics (at higher outputs, VO2 increases as more Type II fibre recruitment occurs)
  • VO2 drift = upward drift at low power outputs possibly due to ventilators hormone changes (occurs when recruiting Type II fibres)
219
Q

Lecture 6:

What are the 2 Definitions of Fatigue?

A

1.) decrements in muscular performance with continued effort, accompanied by sensations of tiredness
2.) inability of muscle(s) to maintain required power output to continue muscular work at given intensity

220
Q

Lecture 6:

Is fatigue reversible?

A

Fatigue is reversible by rest & isn’t necessarily catastrophic but is a continuum @ reduced rate

221
Q

Lecture 6:

What are the 4 major causes of fatigue?

A

1.) inadequate energy delivery/metabolism
2.) accumulation of metabolic by-products
3.) failure of muscle contractile mechanism
4.) altered neural control of muscle contraction

222
Q

Lecture 6:

How does PCr depletion coincide with fatigue?

A

PCr (phospho-creatine) is used for short-term, high-intensity effort & gets depleted more quickly than total ATP (Pacing helps defer depletion)
*Pi accumulation may be potential cause

223
Q

Lecture 6:

How is Glycogen Depletion associated with Fatigue?

A

Glycogen depletion is correlated with fatigue as reserves are limited & get depleted quickly
- fatigue related to total glycogen depletion but unrelated to rate of glycogen depletion

224
Q

Lecture 6:

Does glycogen depletion increase or decrease with intensity?

A

Glycogen is depleted more quickly with high intensity & depleted more quickly during first few minutes of exercise

225
Q

Lecture 6:

How is glycogen depleted in fibres recruited first?

A

Fibres recruited first/most often get depleted fastest
- type I fibres depleted after moderate endurance exercise

226
Q

Lecture 6:

How are Muscle fibre types recruited (what order)?

A
  • Type I fibres recruited first (for light/moderate intensity)
  • Type IIa fibres recruited next (for moderate/high intensity)
  • Type IIx fibres recruited last (for maximal intensity)
227
Q

Lecture 6:

What is glycogen depletion like in different muscle groups?

A

Activity-specific muscles are depleted faster as they’re recruited the earliest & for he longest time

228
Q

Lecture 6:

How is glycogen depletion & blood glucose levels related?
- role of liver?

A

When muscle glycogen isn’t enough for prolonged exercise, liver glycogen turns to glucose & enters blood stream
- when muscle glycogen decreases, liver glycogenolysis increases

229
Q

Lecture 6:

What are the 3 Metabolic By-Products that cause fatigue?

A

1.) Pi - from rapid breakdown of PCr to form ATP
2.) Heat - retained by body & core temp increases
3.) Lactic Acid - product of anaerobic glycolysis

230
Q

Lecture 6:

How does Heat alter metabolic rate?
- how does heat impact muscle function?

A

Heat increases rate of carbohydrate utilization
& speeds up glycogen depletion
- high muscle temperature may impair muscle function

231
Q

Lecture 6:

How does time to fatigue change with surrounding temperatures?
- what degree is longest to fatigue? Which is shortest?

A
  • longest time to exhaustion = 11degC
  • shortest time to exhaustion = 31degC
  • *muscle precooking prolongs exercise
232
Q

Lecture 6:

If lactic acid isn’t cleared immediately from the muscles, what does it convert to?

A

Lactic acid converts to Lactate & H+ which causes decrease in muscle pH (causing acidosis)

233
Q

Lecture 6:

What happens when muscle pH levels drop below 6.9? PH = 6.4?

A

pH <6.9 inhibits the glycolytic enzymes used for ATP synthesis

pH = 6.4 prevents further glycogen breakdown

234
Q

Lecture 6:

How does fibre recruitment contribute to fatigue?

A

Fibre recruitment may be reduced due to…
- stress of exhaustive exercise may be too much
- someone may be unwilling to endure more pain
- discomfort of fatigue is a warning sign to stop
- elite athletes learn proper pacing to tolerate fatigue

235
Q

Lecture 6:

What is Muscle Soreness & what does it result from?

A

Muscle soreness = accuse soreness during & immediately after exercise & felt anytime (delayed-onset 1-2 days later)
- Results from exhaustive/high-intensity exercise (especially when performed for the first time)

236
Q

Lecture 6:

What is Acute Muscle Soreness?
- duration?

A

Felt during or immediately after strenuous/novel exercise caused by accumulation of metabolic by-products (H+) & disappears in minutes-hours

237
Q

Lecture 6:

What is tissue Edema?

A

Tissue edema occurs due to plasma fluid in the interstitial place & causes acute muscle swelling

238
Q

Lecture 6:

What does DOMS stand for?

A

Delayed-onset muscle soreness

239
Q

Lecture 6:

What are DOMS?
- major cause of them?

A

Delayed-onset muscle soreness that appears 1-2 days after exercise causes predominantly by eccentric contractions
- stiffness to restrictive pain
-eg; level-run pain < downhill-run pain (not caused by increase in blood lactate oncentrations)

240
Q

Lecture 6:

How is structural damage of muscle indicated in DOMS?

A

Structural damage caused by DOMS is indicated by muscle enzymes in blood
- enzyme concentrations in blood increase 2-10 times after heavy training
- onset of DOMS parallels the onset of increased muscle enzymes in blood

241
Q

Lecture 6:

Hoe are DOMS and inflammation connected?

A

Inflammation & DOMS are connected as white blood cells count increases with soreness and neutrophils are released due to damaged muscle cells

242
Q

Lecture 6:

What are some sequence of events in DOMS?

A

Increase muscle tension leads to structural damage to muscle/cells
- membrane damage disturbs Ca2+ homeostasis & inhibits cellular respiration causing activation of enzymes that degrade Z-disks
- circulating neutrophils increase as products of macrophage activity accumulate & stimulate pain
- fluid & electrolytes shift to the area & create edema

243
Q

Lecture 6:

How do DOMS impact Performance?
- 3 factors causing loss of strength?

A

DOMS reduce muscle force generation as there is a loss of strength due to 3 factors…
1.) physical disruption of muscle
2.) failure in excitation-contraction coupling
3.) loss of contractile protein

244
Q

Lecture 6:

3 Strategies for reducing DOMS?

A

1.) minimize eccentric work early in training
2.) start with low intensity & increase slowly
3.) start with higher-intensity (exhaustive training) - soreness starts bad but much less later on

245
Q

Lecture 6:

What are EAMC Muscle Cramps?
- caused by…?
- reduced by…?

A

EAMC = exercise-associated muscle cramps that are localized to an overworked muscle
- due to lack of conditioning, improper training, & depletion of muscle energy stores
- treated with stretching & reduced by changing excitatory properties of neuron

246
Q

Lecture 6:

What are heat cramps?

A

Associated with large sweat & electrolyte losses (sodium & chloride)
*coupled with dehydration
- treated with high sodium solution, ice, & massage

247
Q

Lecture 7:

What are the 6 Major functions for the Cardiovascular System?

A

1.) Delivers O2 & nutrients
2.) removes CO2 & wastes
3.) transports hormones & other molecules
4.) Supports temperature balance & fluid regulation
5.) maintains acid-base balance
6.) regulates immune function

248
Q

Lecture 7:

What are the 3 major circulatory elements of the Cardiovascular system?

A

1.) Heart (pump)
2.) Blood Vessels (channels/tubes)
3.) Blood (fluid medium)

249
Q

Lecture 7:

What is the role of the right side of the heart?
- route of the blood flow?

A

Pulmonary circulation ( deoxygenated blood from body & pumped to lungs)
- superior & inferior vena cava to RA to tricuspid valve to RV to pulmonary valve to pulmonary arteries to lungs

250
Q

Lecture 7:

What is the role of the left side of the heart?
- route of the blood flow?

A

Systemic Circulation (pumps oxygenated blood from the lungs to the body)
- lungs to pulmonary veins to LA to mitral valve to LV to aortic valve to aorta

251
Q

Lecture 7:

what is Myocardium?

A

Myocardium is heart muscle & left ventricular has most myocardium beacause it must pump blood to entire body so its largest & has thickest walls

252
Q

Lecture 7:

How are cardiac muscle fibres of the myocardium connected?

A

Connected by intercalated discs with desmosomes holding the cells together
- gap junctions rapidly conduct action potentials

253
Q

Lecture 7:

What is the difference between Myocardium & Skeletal Muscle?

A

Skeletal muscle: large, long, unbranded, multinucleated cells with intermittent, voluntary contractions & Ca2+ released from SR

Myocardial Cells: small, short, branched, single nucleus cells with continuous, involuntary rhythmic contractions & calcium-induced calcium release
- high capillary density & mitochondria count

254
Q

Lecture 7:
What is the route of electrical signal through the heart?

A

Sinoatrial (SA) Node —> Atrioventricular (AV) Node —> AV bundle (bundle of his) —> Purkinjee fibres

255
Q

Lecture 7:

How do electrical signals spread through the heart?

A

Electrical signals spread through gap junctions

256
Q

Lecture 7:

What is the role of the SA Node in the cardiac conduction system?

A

SA node initiates contraction signals
- made of pacemaker cells in the upper posterior RA wall
- signals spread from SA node via RA/LA to AV node
- stimulates

257
Q

Lecture 7:

What is the role of the AV Node in the cardiac conduction system?

A

The AV node, located in the RA (right atrial) wall, delays the signal & relays it to ventricles
- the delay lets R&L atrial to contract before R&L ventricles
- then relays signals to AV bundle

258
Q

Lecture 7:

What is the role of the AV Bundle in the cardiac conduction system?

A

AV bundle relays signal to R&L ventricles which travels along interventricular septum (which then splits into R&L bundle branches) & sends signal to the apex of the heart

259
Q

Lecture 7:

What is the role of the Purkinje Fibres in the cardiac conduction system?

A

Purkinje fibres forming the terminal branches of R&L bundle branches send a signal into the R&L ventricles & spread it through the entire ventricle wall
- contraction of R&L ventricles

260
Q

Lecture 7:

How does the Parasympathetic Nervous System help with Extrinsic control of the hearts activity?
- 3 key points

A

1.) PNS accesses heart through vagus nerve (cranial nerve X)
2.) PNS carries impulses to SA & AV nodes as it releases Acetylcholine to hyper-polarize cells (brings membrane potential down to decrease threshold & heart-rate)
3.) PNS decreases HR below intrinsic HR (100bpm)

261
Q

Lecture 7:

What is intrinsic heart rate normally? Normal resisting heart rate? Resting heart rate in endurance athletes?

A

1.) intrinsic = 100bpm
2.) resting = 60-100bpm
3.) elite endurance athletes = 35-45bpm

262
Q

Lecture 7:

What effect does the Sympathetic Nervous System have on heart activity?

A

Opposite effect of the PNS
- carries impulses to the SA & AV nodes which release NE for depolarization (increases HR & contractile force)
- increases HR above intrinsic HR (determines HR during physical & emotional stress)

263
Q

Lecture 7:

What is the max HR someone can have?

A

250bpm

264
Q

Lecture 7:

Define Cardiac Cycle
- 2 periods?

A

Tall mechanical & electrical events that occur during one heart beat
- 2 periods; diastole (relaxation phase, chambers fill with blood, & 2x length of systole) & systole (contraction phase to pump blood to body)

265
Q

Lecture 7:

In the Cardiac Cycle, what occurs during Ventricular Systole?
- how is it shown on an electrocardiogram?

A

1/3 of the cardiac cycle where contraction begins as a result of…
- increased ventricular pressure
- AV valses closing (heart sound 1 “lub”)
- semilunar valve opens & blood is ejected
*End-systolic volume (ESV) is the blood remaining in the ventricle
*QRS complex to T wave on electrocardiogram

266
Q

Lecture 7:

In the Cardiac Cycle, what occurs during Ventricular Diastole?
- how is it shown on an electrocardiogram?

A

2/3 of the cardiac cycle where relaxation begins due to the ventricular pressure dropping
- semilunar (SV) valves close (heart sound 2 “dub”)
- AV valves open & ventricle fills 70% passively & 30% by atrial contraction
*End-diastolic volume (EDV) = amount of blood in ventricles
* T wave to the next QRS complex

267
Q

Lecture 7:

What is Stroke Volume (SV)?
- calculation for SV?

A

The volume of blood pumped out of heart in one heartbeat
- occurs during systole where most, not all, blood is ejected
- EDV - ESV = SV
Eg; 100mL - 40mL = 60mL

268
Q

Lecture 7:

What is Ejection Fraction (EF)?
- formula for calculating

A

The % of EDV pumped
- SV / EDV = EF
Eg; 60mL/100mL = 0.6 =60%
- clinical index of heart contractile function

269
Q

Lecture 7:

What is Cardiac Output (Q)?
- units & formula?

A

The total volume of blood that is pumped per minute measured in L/min (Q= HR x SV)
- Resting cardiac output = ~4.2 - 5.6 L/min
(Average total blood volume is ~5 L & total blood volume circulates once every minute)

270
Q

Lecture 7:

What is Functional Syncytium?

A

The pumping of the heart as one unit

271
Q

Lecture 7:

What is Torsional Contraction?
- explain how it works in systole & diastole

A

The increased contractility during intense exercise to enhance left ventricle filling
*Increases hearts efficiency
- Systole: heart twists gradually, storing energy like a spring
- Diastole: abrupt untwisting that allows atrial filling (dynamic relation)

272
Q

Lecture 7:

What are the 5 things that form the vascular system?

A

1.) Arteries - carry blood away from heart
2.) Arterioles - control blood flow & feed capillaries
3.) Capillaries -site for nutrient & waste connection
4.) Venules - collect blood from capillaries
5.) Veins - carry blood from venules back to heart

273
Q

Lecture 7:

What is Systolic Blood Pressure (SBP)?

A

Highest pressure in the artery that occurs during systole (contraction)
- top number of blood pressure (~110 to 120 mmHg)

274
Q

Lecture 7:

What is Diastolic Blood Pressure (DBP)?

A

The lowest pressure in the artery that occurs during diastole (relaxation)
- bottom number of blood pressure (~ 70-80 mmHg)

275
Q

Lecture 7:

What is Mean Arterial Pressure (MAP)?

A

The average pressure over entire cardiac cycle & is important for pressure differential
- MAP = 2/3 DPB + 1/3 SBP

276
Q

Lecture 7:

Define General Hemodynamics

A

The way your blood flows through your arteries and veins and the forces that affect your blood flow

277
Q

Lecture 7:

What is Pressure & why is it important to blood flow?

A

The force that drives blood flow & provided by heart contraction
- blood flows from area of high pressure (LV, & arteries) to are of low pressure (veins, & RA)
*pressure gradient = 100mgHg

278
Q

Lecture 7:

What is Resistance & how does it impact blood flow?

A

The force that opposes blood flow & is provided by physical properties of vessels
- radius of vessels is most important
- controls pressure differences through the body

279
Q

Lecture 7:

What is the easiest way to change blood flow in the body?

A

1.) Change the radius of vessels through; vasoconstriction (smaller diameter) & Vasodilation (larger diameter)
2.) Arterioles (resistance vessels) - site for most VC & VD & responsible for 70-80% of pressure drop from LV to RA

280
Q

Lecture 7:

How is blood distributed throughout the body?
- distribution @ rest vs @ heavy exercise

A

1.) blood flow (BF)s to sites where there is most need
- regions of high metabolism have increased BF
2.) @ rest cardiac output (Q) = 5L/min
- liver & kidneys receive 50% of Q
- skeletal muscle receives ~20% of Q
3.) Heavy exercise (Q = 25 L/min)
- exercising muscles receive 80% of Q via VD
- flow to liver & kidneys decreases via VC

281
Q

Lecture 7:

What are the 3 types of Intrinsic Control of Blood Flow?

A

1.) Metabolic
2.) Endothelial
3.) Myogenic

282
Q

Lecture 7:

When discussing Intrinsic Control of Blood Flow, How do Metabolic Mechanisms help?

A

Metabolic mechanisms (VD) form a buildup of local metabolic by-products such as a decrease in oxygen levels and increase carbon dioxide, K+, H+, & lactic acid

283
Q

Lecture 7:

When discussing Intrinsic Control of Blood Flow, How do Endothelial Mechanisms help?

A

Endothelial mechanisms (mostly VD) include substances secreted by vascular endothelium & includes nitric oxide (NO), prostaglandins (relax smooth muscle), & EDHF (hyperpolarizing)

284
Q

Lecture 7:

When discussing Intrinsic Control of Blood Flow, How do Myogenic Mechanisms help?

A

Local pressure changes that causes VC & VD
- increase in pressure causes increased vasoconstriction whereas decreased pressure causes increased vasodilation

285
Q

Lecture 7:

What are a few things that help with the extrinsic control of blood flow?

A

Autonomic process where blood flow may be redistributed to a different organ at same level

SNS (@autonomic branch) innervates smooth muscle in arteries & Arterioles and increase in sympathetic activity increases VC but decrease in activity leads to decrease in VC

286
Q

Lecture 7:

How does the Local Control of muscle Blood Flow work?

A

Blood flow to exercising muscle increases to match its metabolic demand

This is seen through local alteration of blood flow & improved extraction at tissue level)

287
Q

Lecture 7:

How does Functional Sympatholysis help with local control of muscle blood flow?

A

Functional Sympatholysis is the inhibition of sympathetic vasoconstriction by reducing vascular responsiveness to adrenergic receptor activation
*sympathetic nerve cannot do job bc we’ve inhibited neurotransmitters by EDHF + ND inhibitors
*review slide 38

288
Q

Lecture 7:

What are Baroreceptors and how do they control blood pressure?

A

Assist with integrative control of blood pressure
- sensitive to changes in arterial pressure
- Afferent signals sent from baroreceptors to brain
- Efferent signals from brain sent to heart & vessels
- Adjustments of arterial pressure are back to normal

289
Q

Lecture 7:

What three mechanisms assist with blood return to the heart?

A

1.) One-way venous valves
2.) muscle pump
3.) respiratory pump
*upright posture makes venous return to heart more difficult (eg; compared to laying down)

290
Q

Lecture 7:

How does the Muscle Pump work to assist with blood return to heart?

A

Skeletal muscles contract and increases pressure in vein causing the superior valve to open so the blood can rush through
Eg; walking helps activate muscle pump so blood doesn’t pool in legs & decreases risk for deep vein thrombosis

291
Q

Lecture 7:

What are the 3 major functions of blood?

A

1.) transportation (O2, Nutrients, & waste)
2.) temperature regulation
3.) acid-base (pH) balance

292
Q

Lecture 7:

How much blood volume typically in a male? In a female?

A

Male = 5-6L Female = 4-5L

293
Q

Lecture 7:

What is the composition of blood?

A

1.) Plasma - 55-60% of blood volume
2.) Formed Elements - 40-45% of blood volume
- includes… red blood cells, white blood cells, & platelets

294
Q

Lecture 7:

How can blood plasma levels increase & decrease?
- composition of plasma?

A
  • can decrease by 10% with dehydration in heat
  • can increase by 10% with training & heat acclimation
  • 90% water, 7% protein, 3% nutrients & ions
295
Q

Lecture 7:

What are the 3 things that make the formed elements of blood?
- their percentages

A
  • red blood cells (erythrocytes) - 99%
  • white blood cells (leukocytes) - <1%
  • platelets - <1%
296
Q

Lecture 7:

Define “Hematocrit”

A

The total percent of blood volume composed of formed elements

297
Q

Lecture 7:

What are Red Blood Cells?
- Composition?
- lifespan?

A

Red blood cells have no nucleus & cannot reproduce
- replaced by hematopoiesis
- lifespan of 4months
- produced & destroyed @ equal rates

298
Q

Lecture 7:

What is Hemoglobin & its role in red blood cells?

A

An oxygen-transporting protein found in red blood cells
- 250million hemoglobin per red blood cell
- carries 20mL O2 per 100mL of blood

299
Q

Lecture 8:

What is the Purpose of the respiratory system?

A

To carry Oxygen to & remove CO2 from all body tissues

300
Q

Lecture 8:

What are the 4 Processes of the Respiratory System?

A

1.) Pulmonary Ventilation
2.) Pulmonary Diffusion
3.) Transport of Gases via Blood
4.) Capillary Diffusion

301
Q

Lecture 8:

What is Pulmonary Ventilation?
- 2 zones?

A

Process of moving air into & out of the lungs
- transport zone & exchange zone
- Pathway = nose/mouth > Nasal conchae > pharynx > larynx > trachea > bronchial tree > alveoli

302
Q

Lecture 8:

What occurs during Inspiration of Pulmonary Ventilation

A

An active process where the diaphragm flattens, ribcage/sternum move up & out, and the thoracic cavity expands thus increasing the volume of thoracic cavity & lungs

303
Q

Lecture 8:

What happens to lung volume & intrapulmonary pressure during inspiration?

A

Lung volume increases & intrapulmonary pressure decreases
- boyles law helps explain this movement
- due to pressure difference, air passively rushes in due to pressure difference

304
Q

Lecture 8:

What additional muscles are used for forced breathing?

A

Scalenes, sternocleidomastoid, & pectoralis
- ribs raise even further

305
Q

Lecture 8:

What occurs during Expiration of pulmonary ventilation?

A

A passive process where inspiratory muscles relax, decreasing lung volume & increasing intrapulmonary pressure
- air is forced out of the lungs

306
Q

Lecture 8:

What occurs during forced breathing when exhaling?
- what muscles are used?

A

Forced breathing, is an active process where internal intercostals pull ribs down
- uses latissimus dorsi, Quadratus lumborum, and abdominal muscles to force diaphragm back up

307
Q

Lecture 8:

What is Pulmonary Diffusion?

A

The gas exchange between alveoli and capillaries (alveoli are surrounded by capillaries)
- air path = bronchiole tree to alveoli
- blood path = right ventricle > pulmonary trunk > arteries > capillaries

308
Q

Lecture 8:

what are the 2 major functions of Pulmonary Diffusion?

A

1.) Replenishes blood oxygen supply
2.) Removes Carbon dioxide from blood

309
Q

Lecture 8:

During Pulmonary Diffusion, How does the blood flow to the lungs?
- how much? How fast? Where from?

A

At rest, lungs receive about 4-6 L of blood/min
- RV cardiac output to lungs = LV cardiac output
*lung blood flow = systemic blood flow
- Blood moves to lungs via Low Pressure Circulation
- Lung MAP = 15mmHg vs aortic MAP = 95mmHg
- small pressure gradient (15 to 5 mmHg)
* resistance much lower as vessel walls thinner

310
Q

Lecture 8:

What is Oxygen’s diffusion capacity?
- normally? at rest? At exercise?

A

O2 diffusion capacity is the O2 volume that is diffused /min/mmHg of gradient
*gradient calculated from capillary mean PO2 (11mmHg)
- @ rest = 21mLO2/min/mmHg of gradient OR 231mLO2/min for 11mmHg gradient
- @ max exercise = venous O2 levels decrease & PO2 has a bigger gradient (diffusion capacity increases by 3 times)

311
Q

Lecture 8:

Why is Oxygen diffusion capacity limited at rest?

A

Limited due to incomplete lung perfusion
- only bottom 1/3 of lung perfused with blood & top 2/3 lung surface area has poor gas exchange

312
Q

Lecture 8:

Why does Oxygen diffusion capacity increase with exercise?

A

Increases with exercise as there is more even lung perfusion as systemic blood pressure rises to open the top 2/3 of lungs for perfusion
- gas exchange now occurs over entire lung surface area

313
Q

Lecture 8:

What is the carrying capacity of blood for oxygen transport?

A

Carrying capacity is 20mL O2/100mL blood

Approx 1L O2/ 5 L blood

314
Q

Lecture 8:

How is oxygen transported in blood?

A
  • greater than 98% of O2 is bound to hemoglobin (Hb) in red blood cells (oxyhemoglobin if carrying o2 & deoxyhemoglobin if not carrying)
  • less than 2% of O2 dissolved in plasma
315
Q

Lecture 8:

Review Oxyhemoglobin Dissociation Curve

A

Slide 25

316
Q

Lecture 8:

What are 2 factors that affect Hemoglobin Saturation?

A

1.) Blood pH - more acidic = more O2 unloaded @ acidic exercising muscles (Bohr effect as O2Hb curve shifted to right)

2.) Blood Temp - warmer blood causes more tissue O2 unloading during exercise (causes O2Hb curve to shift right)

317
Q

Lecture 8:

What happens to hemoglobin oxygen-saturation during rest? During exercise?

A

@ rest, Hb is 98-99% saturated with 0.75 seconds of transit time

During exercise, Hb saturation levels lower ( transit time is shorter than at rest)

318
Q

Lecture 8:

What are the 3 ways Carbon Dioxide is transported in the blood?

A

1.) as bicarbonate ions
2.) dissolved in plasma
3.) bound to Hb (carbaminohemoglobin)

319
Q

Lecture 8:

What is the role of Bicarbonate Ions for Carbon dioxide Transport?

A

Bicarbonate ions transport 60-70% of CO2 in blood to lungs
1.) CO2 & water forms carbonic acid (H2CO3) - in red blood cells & catalyzed by carbonic anhydrase
2.) Carbonic acid dissociates into bicarbonate - H+ binds to Hb & triggers Bohr Effect
- bicarbonate ion diffuses from red blood cells into plasma

320
Q

lecture 8:

What is a Carbaminohemoglobin?

A

A hemoglobin molecule in the blood with CO2 bound to it for transport

321
Q

Lecture 8:

How is Carbon Dioxide Transported with Carbaminohemoglobin?

A

20-33% of CO2 transported is bound to Hb
- CO2 binds to protein (-globin) part of Hb
- deoxyhemoglobin binds CO2 more easily as PCO2 levels affect CO2 binding
*higher PCO2 = easier to bind CO2
* lower PCO2 = easier CO2 dissociation

322
Q

Lecture 8:

What is the difference between Arterial and venous Oxygen?

A

The difference reflects the tissue O2 extraction (higher exteraction = venous O2 lower& difference increases)
- Atrial O2 content = 20mL O2/100mL blood
- Mixed Venous O2 = 15-16mLO2/100mL blood (rest) or 4-5mLO2/100mL blood (exercise)

323
Q

Lecture 8:

How is Oxygen Transported in muscle?

A

Myoglobin
- similar structure to hemoglobin but higher affinity for O2

324
Q

Lecture 8:

3 key factors influencing Oxygen delivery & uptake

A

1.) O2 content of blood - represented by PO2 & Hb % saturation
2.) Blood flow - decreased blood flow = decreased opportunity to deliver O2 to tissue… increase exercise = increase blood flow to muscle
3.) Local conditions (pH/Temp) - shift in O2Hb dissociation curve & decreased pH causes increased temp to promote O2 unloading in tissue

325
Q

Lecture 8:

3 ways to regulate pulmonary ventilation

A

1.) maintain bodies homeostatic balance between blood PO2 & PCO2 & pH
2.) coordination between cardiovascular & respiratory systems
3.) coordination via involuntary regulationn

326
Q

Lecture 9:

During acute exercise, what are some cardiovascular responses?

A
  • heart rate
  • stroke volume
  • cardiac output
  • blood pressure
  • blood flow
  • blood
327
Q

Lecture 9:

What are the normal Resting Heart Rate (RHR) levels?
- untrained vs trained
- how is RHR affected?

A

Normal ranges of untrained RHR = 60 to 80 bpm
Trained Ranges of trained RHR = 30 to 40 bpm
* RHR affected by neutral tone, temperature, & altitude
* anticipatory response increases heart rate above RHR before exercise starts

328
Q

Lecture 9:

What is heart rate during exercise directly proportional to?

A

Heart rate when exercising is directly proportional to exercise intensity

329
Q

Lecture 9:

What is Maximum Heart rate?
- how is it calculated?

A

HR max is the highest HR achieved in all-out effort to volitional fatigue
- it’s highly reproducible & see slight decline with age
- Estimated HRmax = 220 - age
- Better Estimated HRmax = 280 - (0.7 x age)

330
Q

Lecture 9:

What is Steady-State HR?

A

The point of plateau & the optimal HR for meeting circulatory demands at a given submaximal intensity
- increase intensity = increased steady-state HR (2-3mins to adjust)
-It is a basis for simple exercise tests estimating aerobic fitness & HRmax

331
Q

Lecture 9:

Why does heart rate fluctuate during exercise?
- causes & influencing factors?

A

Measure of HR rhythm fluctuates due to continuous changes in sympathetic & parasympathetic balance
- influenced by; body core temp, sympathetic nerve activity, respiratory rate, etc
- analyzed in respect to frequency (not time)

332
Q

Lecture 9:

How does Stroke Volume respond during acute exercise?
- does it increase or decrease?

A

SV increases with intensity to 40-60% of VO2max (past this is plateau leading to exhaustion)
- max exercise SV is approx. double standing SV but only slightly higher than supine SV
* supine SV Musca higher than Standing SV due to supine EDV being way larger

333
Q

Lecture 9:

What are 3 factors that increase Stroke Volume (during exercise)?

A

1.) increased preload (end-diastolic ventricular stretch) = frank-starling mechanism
- increase stretch = increase contraction strength
2.) increased contractility (inherent ventricle property)
- increase in epinephrine or NE which increases contractility
3.) decreased after load: aortic resistance

334
Q

Lecture 9:

How is blood pressure altered during exercise?
- systolic BP up or down? Diastolic?

A

During endurance exercise, there is an increase in mean arterial pressure (MAP)
- systolic BP increases in proportion to intensity
- diastolic BP has a slight increase or decrease

335
Q

L:ecture 9:

How is MAP calculated during exercise?

A

MAP = Q (cardiac output) x total peripheral resistance (TPR)
* Q increases & TPR slightly decreases

336
Q

Lecture 9:

How is blood distribution altered in acute exercise?

A

cardiac output increases causing an increase in available blood flow
- increase in blood flow redirected to areas with greatest metabolic need (working muscle)
- blood is shunted away from less active regions by sympathetic vasoconstriction
- local vasodilation allows additional blood flow to exercising muscle (triggered by metabolic products)

337
Q

Lecture 9:

How does cardiovascular drift assist in cardiovascular response during exercise?

A

Cardiovascular drift is associated with increased core temp & dehydration
- Stroke Volume decreases as skin blood flow increases & plasma volume/venous return & prelod decrease
- Heart Rate drift increases to compensate

338
Q

Lecture 9:

How is plasma volume altered during exercise?

A

Upright exercise causes a decrease in plasma volume to compromise with exercise performance
- decreased plasma volume causes increased MAP & capillary hydrostatic pressure
- sweating further decreases plasma volume

339
Q

Lecture 9:’

What does the decrease in blood plasma lead to?

A

Hemoconcentration of blood due to decrease in fluid % in blood & increase in cell %
(Hematocrit increases up to 50%)

340
Q

Lecture 9:

What are the net effects of Hemoconcentration during exercise?

A

Red blood cell concentration increases as plasma levels decrease
- hemoglobin concentration increases, thus increasing O2 carrying capacity

341
Q

Lecture 9:

What stimulates rapid changes in HR, Q, & BP during exercise?

A

1.) precede metabolic buildup in muscle
2.) HR increases within 1s of onset of exercise
3.) Central Command - higher brain centers & coactivation of motor & cardiovascular centers

342
Q

Lecture 9:

When exercising what is the first priority of cardiovascular response?

A

First priority is to maintain blood pressure
- blood flow is maintained as long as BP is stable
- BP prioritized before other needs

343
Q

Lecture 9:

How is Ventilation changed during exercise?

A

There is an immediate increase in ventilation that occurs before muscles contract due to anticipatory responses from central command
- second phase of ventilation increase is driven by chemical changes in arterial blood (increase in CO2 & H+ triggers chemoreceptors)

344
Q

Lecture 9:

What is ventilation increase proportional to?
- what changes from low intensity to high intensity activities?

A

Ventilation increase is proportional to metabolic needs of the muscle
- at low intensity, only tidal volume increases but at high exercise ventilation rate increases also

345
Q

Lecture 9:

How long is ventilation recovery & what is it regulated by?

A

Ventilation recovery occurs several minutes after delay of exercise
- regulated by blood pH, PCo2 & temperature

346
Q

Lecture 9:

When discussing breathing irregularities, what is Exercise-Induced Asthma?

A

Occurs due to lower airway obstruction & more water being evaporated from airway surface
- related to disruption of airway epithelium & injury to microvasculature
- results in coughing, wheezing, or dyspnea

347
Q

Lecture 9:

When discussing breathing irregularities, what is Dyspnea?

A

Dyspnea is shortness of breathe that is common with poor aerobic fitness & caused by the inability ro adjust to high blood PCO2 & H+
- fatigue in respiratory muscles

348
Q

Lecture 9:

When discussing breathing irregularities, what is Hyperventilation?

A

Excess ventilation/breatjing that may be anticipatory or anxiety driven
- caused by increase in PCO2 gradient between blood & alveoli
- must decrease blood PCO2 to decreased drive to breathe (slow breathing)

349
Q

Lecture 9:

When discussing breathing irregularities, what is Valsalva Maneuver?

A

A potentially dangerous irregularity accompanied with certain exercises that causes the glottis to stay closed (increased intra-abdominal Pressure & intrathoracic Pressure)
- the great veins collapse from high pressures causing decrease in venous return, decreased cardiac output, & decreased arterial BP

350
Q

Lecture 9:

What is Ventilatory Threshold?

A

The point where Litres of air breathed is greater than Litres of O2 consumed
- associated with lactate threshold and increased PCO2

351
Q

Lecture 9:

Is Ventilation normally a limiting factor on exercise performance?

A

Ventilation normally not a limiting factor as respiratory muscles are very fatigue resistant (account for 10% of VO2 & 15% of cardiac output [Q] during exercise)

Exercise Physiology (11 decks)

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