Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

c2 > exercise physiology > Flashcards

exercise physiology Flashcards

1
Q

what are the types of exercise?

A

dynamic

static

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define dynamic exercise. give examples

A

rhythmical movement of joints and contraction and relaxation of muscles. Swimming, running & cycling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

define static exercise. give examples

A

maintained contraction for a length of time. Weight-lifting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what ATP supply is the immediate energy system? what is its function?

A 
fastest supply of ATP - creatine phosphate (phosphocreatine)
function - rapid mobilisation of high energy phosphates. uses no O2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what ATP supply does anaerobic glycolysis provide? what is its function?

A

can supply ATP when requirements are high

less efficient at making ATP. uses no O2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what ATP supply does oxidative metabolism provide? what is its function?

A
  • sustained supply of ATP

- function; uses O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the 3 sources of metabolism that support skeletal muscle function?

A
  1. Immediate
  2. Non-oxidative
  3. Oxidative (aerobic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where are high concentrations of creatine phosphate found?

A

in the muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the function of creatine phosphate?

A

• Provides a store of high potential phosphate to maintain contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is phosphocreatine broken down to and what catalyses this reaction?

A

• Phosphocreatine  creatine produces ATP

o Catalysed by creatine kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how is ATP generated in anaerobic glycolysis?

A

ATP generated from glucose via the glycolytic pathway – less efficient at making ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what causes muscles to fatigue?

A
  • Excess pyruvate  lactate
  • Lactic acid build-up
  • Drop in pH – muscle begins to fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where is energy derived from in sustainable exercise?

A

aerobic metabolism

need O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is VO2?

A

the rate of O2 uptake by skeletal muscle (amount of O2 consumed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what equation can determine VO2?

A

VO2 can be determined by the Fick equation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is Fick’s equation? define each term

A

VO2 = Q x (CaO2 – CvO2)

Q – cardiac output of the heart (blood flow to muscle)
CaO2 – arterial oxygen content
CvO2 – venous oxygen content
(CaO2 – CvO2) is also known as the arteriovenous oxygen difference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the VO2 in a 70kg person?

A

250ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how much O2 is consumed/min/kg body mass?

A

3.6ml/min/kg of body mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is VO2 max?

A

– highest peak O2 uptake obtained during dynamic exercise using large muscle groups during a few mins performed under normal conditions at sea level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

when is VO2 reached?

A

when O2 consumption remains at a steady state even in an increase in workload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does VO2 show?

A

Reflects aerobic physical fitness of the individual – important determinant of endurance capacity during prolonged, sub-maximal exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the anaerobic threshold?

A

point where lactate begins to accumulate in the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how does lactic acid reduce exercise endurance?

A

Lactic acid produced faster than it can be metabolised  metabolic acidosis  exercise endurance = reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

would elite athletes have a high or low anaerobic threshold?

A

high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the 2 major consequences of increased exercise?

A
  • Rise in cardiac output – through increases in SV and HR

* Redistribution of larger proportion of cardiac output to the active muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how is HR kept low?

A

action of the parasympathetic nervous system (vagus nerve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how are HR and SV increased at the start of exercise?

A
  • As exercise begins, there’s reduced activity of the parasympathetic nerves and increased activity of sympathetic nerves
  • Increased HR and mobilisation of blood from great veins (vasoconstriction)
  • Increased venous return  Increased EDV (increased preload)  increased SV
  • Sympathetic activity has a positive inotropic response to the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

define hypertrophy

A

increase in cardiac myocyte size to increase muscle mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how can hypertrophy of the heart muscle occur?

A

physiologically

pathologically

30
Q

how can physiological hypertrophy occur?

A

pregnancy or exercise

31
Q

how are the left ventricles affected for;

  • endurance athletes
  • strength athletes
  • combination athletes?
A

 Endurance athlete – thickening of LV walls  LV dilation
 Strength athlete  mild LV dilation
 Combination athlete  gross thickening of LV walls  LV dilation

32
Q

how can heart muscle hypertrophy occur pathologically?

A

 Hypertension – thickening of LV walls  no dilation in early stages of disease
 Dilated cardiomyopathy, heart failure  thinning of LV walls  significant LV dilation
 Hypertrophic cardiomyopathy  gross thickening of LV walls  no dilation/decrease in LV chamber size

33
Q

what physiological remodelling occurs in an athlete’s heart? is it reversible?

A

o Increased muscle mass
o Normal cardiac function
o Reversible

34
Q

what physiological remodelling occurs in a failing heart? is it reversible?

A

o Increased muscle mass
o Reduced cardiac function
o Irreversible
o Cell death and fibrosis

35
Q

how does volume-induced cardiac hypertrophy occur?

A

increases resting EDV and SV

36
Q

how does the HR of athletes compare to untrained individuals?

A

athletes have bradycardia

37
Q

at rest, what % of resting CO is distributed to the muscles?

A

20-25%

38
Q

during maximal exercise, how much of the increased CO goes to the muscle?

A

80-90%

39
Q

what mechanisms control redistribution of blood flow?

A

systemic regulation

local control

40
Q

how does systemic regulation control distribution of blood flow?

A
  • Start of exercise – increase in sympathetic outflow to the heart and systemic resistance vessels
  • Adrenergic receptors play an important role directing blood flow from non-essential organs to skeletal muscle
41
Q

what do alpha adrenoreceptors do?

A

constrict vessels in the gut - cause vasoconstriction of veins

42
Q

what do beta-1 adrenoreceptors in the heart do?

A

increase rate and force of myocardial contraction

43
Q

what do beta-2 adrenoreceptors do?

A

relax smooth muscle and increase ventilation + oxygen uptake and cause vasodilation of blood vessels, esp those supplying skeletal muscle

44
Q

where do local regulatory factors that control blood flow come from?

A

blood vessels themselves

surrounding tissue

45
Q

what local regulatory factors come from the blood vessels?

A

endothelial factors and myogenic mechanisms e.g. NO relaxes smooth muscle and causes dilation of blood vessels

46
Q

what local regulatory factors come from the surrounding tissue?

A

tissue factors. E.g. adenosine and inorganic phosphates, carbon dioxide, hydrogen ions (H+) and potassium ions (K+) released from contracting muscles

47
Q

how does increasing vasodilator metabolites increase muscle blood flow?

A

decreases TPR which increases skeletal and cardiac muscle blood flow

48
Q

how do you calculate MAP?

A

MAP = (CO x TPR) + CVP

49
Q

why does MABP rise only slightly in exercise?

A

decrease in TPR is counteracted by increases in CO

50
Q

how does systolic pressure change in exercise and why?

A

increases bc of increase in ventricular contraction force

51
Q

how does diastolic pressure change in dynamic exercise?

A

stable/decreass slightly

52
Q

how is the body’s increased need for O2 met?

A

met through increased pulmonary minute ventilation and oxygen extraction in tissues

53
Q

what is the pulmonary ventilation at rest?

A

8L/min

54
Q

what is the pulmonary ventilation during heavy exercise?

A

100L or more

55
Q

what causes the increase in minute ventilation in exercise?

A

increase in resp rate

increase in tidal volume

56
Q

how is O2 taken up into the lungs?

A

pulmonary ventilation

57
Q

how is O2 delivered to the muscle?

A

blood flow and O2 content

58
Q

how is O2 extracted from the blood?

A

delivery and Po2 gradient between blood/cell/mitochondria

59
Q

how do blood gases change during exercise?

A
  • High exercise levels – arterial PaO2 declines slightly
  • As O2 consumption rises, PaO2 in the mixed venous blood also declines
  • Partial pressure of CO2 rises
  • Arteriovenous difference in O2 content rises
  • Increase in gradient drives O2 diffusion into cells
60
Q

why is there reduced affinity of Hb for O2 during exercise?

A
  • Increased CO2
  • Increase H+
  • Increase in temperature
61
Q

what effect does reduced affinity of Hb for O2 have on O2 delivery to tissues?

A

increases O2 delivery to the tissues

62
Q

define excess post-exercise oxygen comsumption

A

measurable increase in the rate of oxygen intake/uptake following strenuous activity

63
Q

how does the body build up an oxygen deficit?

A
  • O2 consumption doesn’t rise immediately – rises over several mins until it matches the needs of the exercising muscles
  • As work continues, O2 uptake remains at a level that’s appopriate for exercise levels
64
Q

why is EPOC needed?

A

eliminates O2 debt

65
Q

what is made during the initial phase of O2 decline?

A

ATP and creatine phosphate are resynthesised via oxidative pathways
• Excess lactate is resynthesised into glucose and glycogen

66
Q

what causes changes to HR and contraction force occur after autonomic factors?

A
  • Changes bc of signals from central command of the brain
  • Central command acts to regulate baroreceptor reflex sensitivity
  • CC also gets feedback from increased activity in afferent nerves from exercising limbs
  • Metaboreceptors respond to changes in metabolite concentrations (mainly pH + K+)
67
Q

what mechanisms activate respiratory muscles?

A

neural mechanisms

68
Q

what part of the brain causes an increase n ventilation?

A

initiation of motor activity from premotor area of the cerebral cortex
chemoreceptors also contribute

69
Q

what is the major driver for ventilation?

A

CO2

70
Q

what effect does a denervated carotid body have on patients?

A

they have slower ventilatory responses

71
Q

what effect do elevated potassium concentrations have on the body during exercise?

A

thought to provide an extra stimulus to peripheral chemoreceptors.

c2 (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions