Exercise Physiology Flashcards

1
Q

what are the two types of exercise

A

dynamic

static

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2
Q

what is dynamic exercise

A
  • This is the rhythmical movement of joints and contraction and relaxation of muscles – such as swimming, running and cycling
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3
Q

what is static exercise

A
  • Static – maintained contraction for a length of time – weight lifting
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4
Q

what is the energy requirements of the exercising muscle

A
  • At rest skeletal muscle has relatively low metabolic needs but during exercise as the muscles perform work their metabolic requirements increase
  • Energy comes in the form of ATP
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5
Q

name the energy sources

A
  • immediate energy system
  • anaerobic glycolysis
  • aerobic
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6
Q

describe energy sources

A

Immediate energy system

  • fastest supply of ATP (creatine phosphate/phosphocreatine)
  • rapid mobilisation of high energy phosphate
  • uses no oxygen

anaerobic glycolysis

  • can supply ATP when requirements are high
  • less efficient at generating ATP
  • uses no oxygen

aerobic

  • sustained supply of ATP
  • uses oxygen
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7
Q

what is creatine phosphate catalysed by in order to release ATP

A

creatine kinase

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8
Q

how is ATP generated from anaerobic glycolysis

A

• ATP is generated from glucose via the glycolytic pathway.

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9
Q

describe lactic acid synthesis

A
  • made when excess pyruvate is converted to lactate
  • happens by lactate dehydrogenase
  • lactic acid build up can cause a drop in the pH and the muscle can begin to fatigue
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10
Q

what is the VO2

A

the rate of oxygen uptake by skeletal muscle

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11
Q

how can VO2 be determined

A
- by the Fick equation 
VO2 = Q x (CaO2-CvO2)
–	Q is the cardiac output of the heart (blood flow to muscle)
–	CaO2 is the arterial oxygen content
–	CvO2 is the venous oxygen content
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12
Q

what is CaO2-CvO2

A

CaO2 – CvO2) is also known as the arteriovenous oxygen difference.
– Difference between what is going into the capillary bed versus (in terms of arterial oxygen) what is being removed (in terms of venous)

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13
Q

what should the VO2 be at rest

A
  • VO2: 250ml/min (70kg person) (oxygen consumption)

- 3.6 ml O2 consumed/min for each kg of body mass (ml O2/(min x kg).

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14
Q

define the maximal oxygen uptake

A

VO2 max is the highest peak oxygen uptake that an individual can obtain during dynamic exercise using large muscle groups during a few minutes performed under normal conditions at sea level. – this is when you are performing maximally at a constant rate

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15
Q

what is VO2 max reached

A

• VO2 max is reached when oxygen consumption remains at steady state despite an increase in workload.

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16
Q

what does the VO2 max reflect

A
  • it reflects the aerobic physical fitness of the individual
  • important in determinant of their endurance capacity during prolonged, sub-maximal exercise
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17
Q

what is the VO2 max in

  • COPD/advanced heart disease
  • mildy active middle aged adults
  • elite endurance athletes
A
  • 10-20 ml o2/(minxkg)
  • 30-40 ml O2/(min x kg)
  • 80-90 ml O2/(min x kg)
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18
Q

what is the anaerobic threshold

A

• The anaerobic threshold (also known as the lactate threshold) is the point where lactate (lactic acid) begins to accumulate in the bloodstream.

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19
Q

what happens in the anaerobic threshold

A

• Lactic acid is produced faster than it can be metabolized, the development of metabolic acidosis occurs and exercise endurance is reduced.

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20
Q

how does the anaerobic threshold vary

A
  • The AT measurements vary from person to person, and, within a given individual, sport to sport.
  • Untrained individuals have a low AT whilst elite endurance athletes have a high AT.
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21
Q

what are the aims of adjustments of the cardiovascular system that accompany exercise

A
  • Aim of the adjustments during exercise the muscles are actively working and you need to increase oxygen delivery to these muscles
  • As well as remove carbon dioxide
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22
Q

what are the two major changes in the cardiovascular system as a result of increased exercise

A
  1. Rise in cardiac output – through increases in SV and HR

2. Redistribution of larger proportion of cardiac output to the active muscles

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23
Q

how does a rise in cardiac output happen when you start exercise

A
  • Heart rate is kept low by the action of the parasympathetic nervous system (vagus nerve)
  • Partial vasoconstriction of blood vessels by activity of sympathetic nerves.
  • As exercise begins there is reduced activity of parasympathetic and increased activity of sympathetic nerves.
  • Increased HR and mobilisation of blood from great veins (vasoconstriction)
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24
Q

what are the cardiovascular changes in exercise due to an increase in sympathetic activity

A
  • Increased venous return
  • Increased end diastolic volume (EDV) (increased preload)
  • According to Starlings law, increased SV
  • Sympathetic activity has a positive inotropic response on the heart.
  • The increase in HR and SV act to increase cardiac output during exercise.
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25
Q

what increases CO the most in exercise

A
  • In mild exercise small changes in CO are achieved largely by changes in heart rate and stroke volume
  • Stroke volume reaches maximum levels at fairly moderate exercise intestate
  • Further increases in CO during heavy exercise are achieved via heart rate changes
  • During heavy maximal exercise the increase is achieved by heart rate as stroke volume can be limiting
26
Q

what are the long term changes of exercise

A
  • heart remodelling
27
Q

what are the ways in which hypertrophy can happen

A

hypertrophy can either happen via physiologically such as pregnancy or exercise, or pathologically in diseases such as hypertension

28
Q

what happens to the heart during exercise

A
  • The heart can adapt to sustained increases in blood pressure by increasing muscle mass largely via an increase in cardiac myocytes size (hypertrophy)
29
Q

describe the difference between the athletes heart and the failing heart

A

THE ATHLETE’S HEART
• Increased muscle mass
• Normal cardiac function
• Reversible

THE FAILING HEART
•	Increased muscle mass
•	Reduced cardiac function
•	Irreversible
•	Cell death and fibrosis
30
Q

describe why athletes have bradycardia

A
  • Volume induced cardiac hypetrophy in atheletes increases resting end diastolic volume (EDV) and SV
  • therefore Athletes typically have a slower resting HR (bradycardia) when compared to untrained individuals
31
Q

Why are cardiac overloading stimuli (e.g. those experienced during exercise) beneficial whilst others are harmful

A
  • could it be because of different signaling pathways
32
Q

describe the redistribution of CO to active muscles

A
  • At rest 20-25% of the resting cardiac output is distributed to the skeletal muscles at about 1 l/min.
  • During maximal exercise about 80-90% of the increased cardiac output goes to the skeletal muscle with a blood flow of about 22 l/min.
33
Q

what are the two main mechanisms that control redistribution of blood flow

A
  • Systemic regulation

- Local control

34
Q

how does systemic regulation control the redistribution of blood flow

A
  • At the start of exercise there is an increase in the sympathetic outflow to the heart and systemic resistance vessels.
  • Adrenergic receptors (adrenoceptors) play an important role directing blood flow from non-essential organs to skeletal muscle.
  • via alpha adrenorecepotrs, beta 1 and 2 adrenoreceptors
35
Q

what do alpha adrenoreceptors do

A

• Alpha adrenoreceptors constrict the vessels in the gut and cause vasoconstriction of veins.

36
Q

what do beta 1 adrenoreceptors do

A

• Beta 1 adrenoreceptors (found in the heart) act to increase the rate and force of myocardial contraction

37
Q

what do beta 2 adrenoreceptors do

A

• Beta 2 adrenoreceptors act to relax smooth muscle and increase ventilation and oxygen uptake and cause vasodilation of blood vessels, especially those supplying skeletal muscle

38
Q

how is blood flow locally regulated

A
  • Blood flow is strongly determined by local regulatory factors either from the blood vessels themselves (endothelial factors and myogenic mechanisms) or from the surrounding tissues (tissue factors).
39
Q

name the endothelial/myogenic mechanisms that help control blood flow locally

A
  • Endothelial/myogenic mechanisms: Nitric oxide acts to relax smooth muscle cells and this causes dilation of blood vessels
40
Q

name the tissue factors mechanism that help control blood flow locally

A
  • Tissue factors: include adenosine and inorganic phosphates, carbon dioxide, hydrogen ions (H+) and potassium ions (K+) released from contracting muscles.
41
Q

describe how blood flow to the skin changes

A

– vasodilation at the skin initially during exercise so it increases initially during light exercises and strenuous exercises but decreases during maximal exercise,
- blood flow to the skin is diverted to skeletal muscles in expense to blood flow to the skin, this means you have not got good thermoregulation

42
Q

how does total peripheral resistance TPR change during exercise

A

• Total peripheral resistance (TPR) during maximal dynamic exercise drops dramatically – it is approximately one-third of the resting resistance.

43
Q

how do you work out MAP

A

• MAP = (CO x TPR) + CVP

44
Q

if the TPR decreases why is MABP only slightly increased or normal

A
  • Decreases in TPR are offset by increases in CO

* MABP only rises slightly

45
Q

describe how systolic and diastolic pressure changes

A
  • Increased force of ventricular contraction (increased SV) causes an increase in systolic pressure.
  • In dynamic exercise the diastolic pressure remains relatively stable or even decreases.
  • Decrease in the TPR can lead to a decrease diastolic pressure.
46
Q

how does the respiratory system adjust for exercise

A
  • increased pulmonary minute ventilation

- increased oxygen extraction in tissues

47
Q

how does ventilation change in exercise

A
  • At rest pulmonary ventilation is about 8l/min but in heavy exercise can increase to 100 l/min or more
  • Increased in ventilation is achieved via a rise in respiratory rate and tidal volume (increase in minute ventilation)
  • At moderate work rates the steady state ventilation is directly proportional to the work done as measured by the oxygen consumption
  • However during severe exercise the increase in ventilation is disproportionately large in relation to oxygen uptake (limiting factor
48
Q

how is ventilation increased in exercise

A
  • achieved by a rise in respiratory rate and tidal volume( due to increase in minute ventilation)
49
Q

what is the pathway of oxygen uptake from the atmosphere to the mitochondria during exercise

A
  • Uptake of O2 in lungs - pulmonary ventilation
  • Delivery of O2 to muscle - blood flow and O2 content
  • Extraction of O2 from blood - delivery and PO2 gradient between blood/cell/mitochondria
50
Q

how does the blood gases change in oxygen

A
  • At high levels of exercise the partial pressure of oxygen in the arterial blood declines slightly
  • As the oxygen consumption rises the partial pressure of oxygen in the mixed venous blood also declines
  • The partial pressure of carbon dioxide rises
  • Overall the arteriovenous difference in oxygen content rises markedly
  • The increase in gradient drives oxygen diffusion into the cells
51
Q

define the term post exercise oxygen consumption

A
  • There is a measurable increase in the rate of oxygen intake/uptake following strenuous activity (excess post-exercise oxygen consumption (EPOC).
52
Q

describe oxygen consumption during exercise

A
  • Oxygen consumption does not rise immediately to match the energy requirements, it rises progressively over several minutes until it matches a stead state of the needs of the exercising muscles
  • As the work continues the oxygen uptake remains at a level that is appropriate to the degree of exercise
  • Thus at the beginning of exercise the body builds up on an oxygen deficit
53
Q

what happens at the end of exercise to oxygen consumption

A
  • At the end of the exercise period the oxygen consumption declines rapidly but may not reach resting levels for up to 60 minutes
  • There is a measurable increase in the rate of oxygen intake following strenuous activity (excess post-exercise oxygen consumption (EPOC)) proposed to be necessary to eliminate the “oxygen debt.”
  • During the initial phase of oxygen decline ATP and creatine phosphate are resynthesised (via oxidative pathways). Excess lactate is resynthesised into glucose and glycogen.
54
Q

what is the challenge of matching cardiac output and ventilation to the metabolic demands of exercise

A
  • The primary site for coordination/integration is the brain central controller/command with input from sensors
55
Q

what are the factors that regulate the cardiovascular response to exercise

A
  • As exercise begins HR increases and force of contraction increases
  • Initially changes due to autonomic factors (inhibitor of parasympathetic and increase in sympathetic)
  • Changes are through to be due to signals from higher brain levels (central command)
56
Q

what does central command receive feedback from

A
  • Central command acts to modulate baroreceptor reflex sensitivity. – the set point changes slightly
  • Central command also receives feedback from increased activity in afferent nerves from exercising limbs.
57
Q

what do metabaroreceptors respond to

A

• Metaboreceptors respond to changes in metabolite concentrations (mainly pH and K+) – these are stimulated by metabolites in the skeletal muscle, these feedback information about what is going on during exercise

58
Q

what is the major drive fro ventilation

A

• Chemoreception also contributes. CO2 major driver for ventilation

59
Q

what do patients with denervated carotid bodies have

A

• Patients with denervated carotid bodies have slower ventilatory responses compared to normal subjects. Therefore the response of the peripheral chemoreceptors also involved.

60
Q

what provides extra stimulus to the peripheral chemoreceptors

A

• Plasma potassium concentrations are elevated during exercise and are thorugh to provide an extra stimulus to the peripheral chemoreceptors

61
Q

during exercise there is increased neural input from..

A

• Increased neural input from afferent activity in the joints