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Cardiorespiratory CC > Exercise Physiology > Flashcards

Exercise Physiology Flashcards

1
Q

Dynamic Exercise

A

Rhythmical movement of joint and contraction and relaxation of muscles
Swimming, running + cycling

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2
Q

Static Exercise

A

Maintained contraction for a length of time

Weight-lifting

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3
Q

Immediate Energy system

A

Fastest supply of ATP (creatine phosphate/phosphocreatine)
Rapid mobilisation of high energy phosphates
No oxygen

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4
Q

Anaerobic glycolysis

A

Can supply ATP when requirements high
Less efficient at ATP generation
No oxygen

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5
Q

Aerobic (oxidative metabolism)

A

Sustained supply of ATP

Uses O2

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6
Q

Immediate Energy MOA

A

Phosphocreatine in muscles at high conc.
Creatine phosphate provides store of high-potential phosphate to maintain contraction
Catalysed by creatine kinase

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7
Q

Non-oxidative Energy MOA

A 
ATP generated from glucose via glycolytic pathway
Less efficient
Excess pyruvate --> lactate
Lactic acid build up
Drop in pH --> muscle fatigue
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8
Q

Oxidative Energy MOA

A

Require molecular O2 (oxidative phosphorylation)

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9
Q

VO2

A

Vol of oxygen consumed

Determined by Fick equation

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10
Q

Fick equation

A 
VO2= Q x (CaO2-CvO2)
Q= CO
CaO2= arterial oxygen content
CvO2= venous oxygen content
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11
Q

CaO2-CvO2

A

Arteriovenous oxygen difference

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12
Q

Vol of O2 consumed at ret

A

VO2= 250ml/min (70kg person)

3.6ml O2 consumed/min for each kg of body mass

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13
Q

VO2 max

A

Highest peak O2 uptake that an individual can obtain during dynamic exercise using large muscle groups during a few minutes performed under normal conditions at sea level

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14
Q

When is VO2 max reached

A

When O2 consumption remains at steady state despite an increase in workload

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15
Q

COPD/advanced heart disease VO2 max

A

10-20 ml O2/(min x kg)

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16
Q

Mildly active middle aged adults VO2 max

A

30-40ml O2/(min x kg)

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17
Q

Elite endurance athletes VO2 max

A

80-90ml O2/(min x kg)

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18
Q

Anaerobic threshold

A

Point where lactate begins to accumulate in bloodstream

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19
Q

Lactic acid metabolism

A

Produced faster than it can be metabolised –> metabolic acidosis –> exercise endurance reduced

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20
Q

2 Major consequences of increased exercise

A

Rise in CO

Redistribution of CO to active muscles

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21
Q

Exercise Begins…

A

Reduced parasympathetic activity
Increased sympathetic nerve activity
Increased HR + mobilisation of blood from great veins (vasoconstriction)

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22
Q

Exercise change in parameters

A

Increased venous return
Increased End-Diastolic Volume
Increased SV according to Starling’s Law
Positive inotropic response on heart

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23
Q

Change in end-diastolic vol. in exercise

A

Increase

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24
Q

Change in venous return during exercise

A

Increase

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25
Q

Positive inotropic response

A

Increase in rate + force of contraction

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26
Q

SV + HR changes with Increased O2 uptake

A

SV increases –> reaches maximum levels + plateaus at moderate exercise intensity
Heavy exercise- CO sustained by increasing HR

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27
Q

Heart remodelling

A

Heart adapts to sustained increases in BP by increasing muscle mass mostly by hypertrophy

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28
Q

Heart remodelling MOA

A

Physiologically (pregnancy/athletes)

Pathologically (hypertension)

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29
Q

Athlete’s heart

A

Increase muscle mass
Thickening LV wall + LV dilation
Normal cardiac function
Reversible

30
Q

Failing heart

A

Increased muscle mass
Reduced cardiac function
Irreversible
Cell death + fibrosis

31
Q

Endurance athlete

A

Runner, swimmer
Thickening LV wall
LV dilation

32
Q

Strength athlete

A

Weightlifter
Thickening LV wall
Mild LV dilation

33
Q

Combination athlete

A

Gross thickening LV wall

LV dilation

34
Q

Hypertension on heart

A

LV wall thickening

No dilation early stages of disease

35
Q

Dilated cardiomyopathy, HF

A

Thinning LV walls

Significant LV dilation

36
Q

Hypertrophic cardiomyopathy

A

Gross thickening LV wall

No dilation/decrease in LV chamber size

37
Q

Bradycardia in Athletes

A

Vol-induced cardiac hypertrophy increases resting end diastolic vol. and SC
Slower resting HR than untrained individuals

38
Q

Distribution of CO at rest

A

20-25% resting CO to muscles (1L/min)

39
Q

Distribution CO at max exercise

A

80-90% increased CO goes to muscle (22L/min)

40
Q

Systemic regulation redistribution blood flow

A

Adrenergic receptors

Alpha, beta 1 and beta 2

41
Q

Alpha adrenoreceptors

A

Constrict vessels in gut + cause vasoconstriction of veins

42
Q

Beta 1 adrenoreceptors

A

Found in heart

Increase rate and force of myocardial contraction

43
Q

Beta 2 adrenoreceptors

A

Relax smooth muscle (i.e. in bronchi) and increase ventilation and O2 uptake
Cause vasodilation of blood vessels (specifically ones supplying skeletal muscle)

44
Q

Blood vessels themselves response to exercise

A

Endothelial factors + myogenic mechanisms

NO acts to relax smooth muscle cells –> dilation of blood vessels

45
Q

Surrounding tissues (tissue factors)

A 
Tissue factors
Adenosine + inorganic phosphates
CO2
H+ 
K+
Released from contracting muscles
46
Q

Total Peripheral Resistance during exercise

A

Drops dramatically

Approx. 1/3rd of resting resistance

47
Q

Decrease in TPR

A

Offset by increases in CO

Can lead to decrease in diastolic pressure

48
Q

Systolic BP change in exercise

A

Increased force of ventricular contraction causes increase in systolic BP

49
Q

Diastolic BP change in exercise

A

Diastolic BP remains relatively stable or even decreases

50
Q

Resp system in exercise

A

Increased pulmonary minute ventilation + oxygen extraction in tissues

51
Q

Pulmonary ventilation at rest

A

8l/min

52
Q

Pulmonary ventilation heavy exercise

A

100l/min

53
Q

Increased ventilation

A

Rise in resp. rate and tidal volume

54
Q

Moderate work rates

A

Steady state ventilation is directly proportional to the work done as measured by O2 consumption

55
Q

Severe exercise

A

Increase in ventilation is disproportionately large in relation to O2 uptake (limiting factor)

56
Q

Uptake of O2 in lungs

A

pulmonary ventilation

57
Q

Delivery of O2 to muscle

A

blood flow and O2 content

58
Q

Extraction of O2 from vlood

A

delivery + PO2 gradient between blood/cell/mitochondria

59
Q

O2 blood gases high exercise

A

Partial pressure O2 in arterial blood declines slightly

As O2 consumption rises, partial pressure of O2 in mixed venou blood also declines

60
Q

CO2 blood gases high exercise

A

Partial pressure CO2 rises

61
Q

Arteriovenous difference in oxygen content in exercise

A

Rises
As exercise increases, arteriovenous difference also increases
Increase gradient –> drives O2 uptake into cells

62
Q

O2 delivery to tissues in exercise

A

Facilitated by decrease in Hb-O2 binding affinity
During exercise, Increased CO2, H+ and temp
Cause right shift in Hb binding curve
Reduced affinity of Hb for O2–> increases delivery in tissues

63
Q

Post-exercise O2 consumption

A

Measurable increase in rate of O2 intake/uptake following strenuous activity

64
Q

Oxygen debt

A

At beginning of exercise body builds up O2 debt

Measurable increase in rate of O2 intake following strenuous activity to eliminate O2 debt

65
Q

Oxygen decline initial phases

A

ATP + creatine phosphate are resynthesized (via oxidative pathways)
Excess lactate is resynthesized into glucose + glycogen

66
Q

Central command

A

Modulate baroreceptor reflex sensitivity

Receives feedback from increased activity in afferent nerves from exercising limbs

67
Q

Metaboreceptors

A

Respond to changes in metabolite concentrations (mainly pH and K+)

68
Q

Factors involved in Resp. response to exercise

A

Neural mechanisms activate resp. muscles

Initiation of motor activity from premotor area of cerebra cortex –> increase ventilation

69
Q

Chemoreception

A

Contributes to Resp Response to exercise

CO2 Major driver for ventilation

70
Q

Denervated carotid bodies

A

Slower ventilatory response compared to normal subjects

71
Q

Plasma K+ concentrations

A

Elevated during exercise

Extra stimulus to peripheral chemoreceptors

Cardiorespiratory CC (34 decks)

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