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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
Positive inotropic response
Increase in rate + force of contraction
26
SV + HR changes with Increased O2 uptake
SV increases --> reaches maximum levels + plateaus at moderate exercise intensity Heavy exercise- CO sustained by increasing HR
27
Heart remodelling
Heart adapts to sustained increases in BP by increasing muscle mass mostly by hypertrophy
28
Heart remodelling MOA
Physiologically (pregnancy/athletes) | Pathologically (hypertension)
29
Athlete's heart
Increase muscle mass Thickening LV wall + LV dilation Normal cardiac function Reversible
30
Failing heart
Increased muscle mass Reduced cardiac function Irreversible Cell death + fibrosis
31
Endurance athlete
Runner, swimmer Thickening LV wall LV dilation
32
Strength athlete
Weightlifter Thickening LV wall Mild LV dilation
33
Combination athlete
Gross thickening LV wall | LV dilation
34
Hypertension on heart
LV wall thickening | No dilation early stages of disease
35
Dilated cardiomyopathy, HF
Thinning LV walls | Significant LV dilation
36
Hypertrophic cardiomyopathy
Gross thickening LV wall | No dilation/decrease in LV chamber size
37
Bradycardia in Athletes
Vol-induced cardiac hypertrophy increases resting end diastolic vol. and SC Slower resting HR than untrained individuals
38
Distribution of CO at rest
20-25% resting CO to muscles (1L/min)
39
Distribution CO at max exercise
80-90% increased CO goes to muscle (22L/min)
40
Systemic regulation redistribution blood flow
Adrenergic receptors | Alpha, beta 1 and beta 2
41
Alpha adrenoreceptors
Constrict vessels in gut + cause vasoconstriction of veins
42
Beta 1 adrenoreceptors
Found in heart | Increase rate and force of myocardial contraction
43
Beta 2 adrenoreceptors
Relax smooth muscle (i.e. in bronchi) and increase ventilation and O2 uptake Cause vasodilation of blood vessels (specifically ones supplying skeletal muscle)
44
Blood vessels themselves response to exercise
Endothelial factors + myogenic mechanisms | NO acts to relax smooth muscle cells --> dilation of blood vessels
45
Surrounding tissues (tissue factors)
``` Tissue factors Adenosine + inorganic phosphates CO2 H+ K+ Released from contracting muscles ```
46
Total Peripheral Resistance during exercise
Drops dramatically | Approx. 1/3rd of resting resistance
47
Decrease in TPR
Offset by increases in CO | Can lead to decrease in diastolic pressure
48
Systolic BP change in exercise
Increased force of ventricular contraction causes increase in systolic BP
49
Diastolic BP change in exercise
Diastolic BP remains relatively stable or even decreases
50
Resp system in exercise
Increased pulmonary minute ventilation + oxygen extraction in tissues
51
Pulmonary ventilation at rest
8l/min
52
Pulmonary ventilation heavy exercise
100l/min
53
Increased ventilation
Rise in resp. rate and tidal volume
54
Moderate work rates
Steady state ventilation is directly proportional to the work done as measured by O2 consumption
55
Severe exercise
Increase in ventilation is disproportionately large in relation to O2 uptake (limiting factor)
56
Uptake of O2 in lungs
pulmonary ventilation
57
Delivery of O2 to muscle
blood flow and O2 content
58
Extraction of O2 from vlood
delivery + PO2 gradient between blood/cell/mitochondria
59
O2 blood gases high exercise
Partial pressure O2 in arterial blood declines slightly | As O2 consumption rises, partial pressure of O2 in mixed venou blood also declines
60
CO2 blood gases high exercise
Partial pressure CO2 rises
61
Arteriovenous difference in oxygen content in exercise
Rises As exercise increases, arteriovenous difference also increases Increase gradient --> drives O2 uptake into cells
62
O2 delivery to tissues in exercise
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
Post-exercise O2 consumption
Measurable increase in rate of O2 intake/uptake following strenuous activity
64
Oxygen debt
At beginning of exercise body builds up O2 debt | Measurable increase in rate of O2 intake following strenuous activity to eliminate O2 debt
65
Oxygen decline initial phases
ATP + creatine phosphate are resynthesized (via oxidative pathways) Excess lactate is resynthesized into glucose + glycogen
66
Central command
Modulate baroreceptor reflex sensitivity | Receives feedback from increased activity in afferent nerves from exercising limbs
67
Metaboreceptors
Respond to changes in metabolite concentrations (mainly pH and K+)
68
Factors involved in Resp. response to exercise
Neural mechanisms activate resp. muscles | Initiation of motor activity from premotor area of cerebra cortex --> increase ventilation
69
Chemoreception
Contributes to Resp Response to exercise | CO2 Major driver for ventilation
70
Denervated carotid bodies
Slower ventilatory response compared to normal subjects
71
Plasma K+ concentrations
Elevated during exercise | Extra stimulus to peripheral chemoreceptors

Cardiorespiratory CC (34 decks)

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