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Exercise + Health Physiology Flashcards

1
Q

Define fitness

A

Ability to perform physical tasks and the state of being physically healthy

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2
Q

How many deaths can be attributed to physical inactivity

A

Estimated 9.4% worldwide
(Kamada eg al 2017)

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3
Q

What did Taylor et al 1962, focusing on occupational activity + longevity find

A

Clerks (less active occupation) (11.83 per 1000) are more likely to die than railway workers (7.62 per 1000)

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4
Q

Limitations of Taylor et al 1962

A

May be a self-selection bias - people may become clerks because they have an illness that prevents them from doing physical jobs
Doesn’t account for confounders- smoking, alcohol, leisure activities

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5
Q

What did the Harvard alumni health study (paffenbarger et al 1986) do

A

Questionnaire about lifestyle with an estimated calorie expenditure for each activity

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6
Q

Harvard alumni health study key findings

A

There is a large decrease in mortality in those doing a bit of activity compared to extremely low activity.

Remained significant even after adjusting for various factors eg BP + Smoking

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7
Q

How does intensity of exercise impact mortality

A

Vigorous activity is associated with a greater mortality risk reduction, minute by minute, than moderate intensity (Samitz et al)

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8
Q

What is the problem with subjective studies about activity

A

Participants are likely to overestimate the amount of activity they do, therefore results may underestimate true benefits

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9
Q

What was the healthy ABC study?

A

Objective study following high functioning older adults for 6.5years, using doubly labelled water to quantify daily energy expenditure

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10
Q

Findings + limitations of healthy ABC study

A

55% decrease in mortality risk between the least active and moderately active

But v expensive and gives no info on intensity of activity

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11
Q

Ekelund et al 2019 metanalysis findings

A

Largest benefits are seen going from the 1st quartile to the second quartile
5-6mins of moderate activity per day is associated with 30% lower mortality

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12
Q

Impact of strength training on mortality

A

Decreases risk of all cause mortality
Benefits seen are additive to aerobic exercise
Benefits peaked at 82mins per week

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13
Q

Describe the relationship between sedentary behaviour and mortality

A

Non linear relationship
The risk of sedentary behaviour is only substantial at >8hrs per day (4% Inc in mortality)
Each additional hour after 8 increases the risk

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14
Q

TV viewing vs General sedentary behaviour

A

Inc risk of all cause mortality is sharper in TV viewing than general sedentary behaviour because it tends to be associated with other unhealthy behaviours- snacking, alcohol (Patterson et al 2018)

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15
Q

Can you outrun sedentary behaviour?

A

High physical activity seems to offset negative effects of sedentary time (Ekelund et al 2016)

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16
Q

Does timing of physical activity matter in relation to mortality?

A

No both ‘weekend warriors’ and those regularly active over 5 days have a similar reduction in mortality. (O’Donovan et al 2017)

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17
Q

How does fitness impact mortality

A

Higher fitness is associated with lower mortality in patients with and without CVD at baseline, even after accounting for confounders

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18
Q

How does fitness age 18 impact mortality

A

High fitness aged 18 is associated with decreased risk all cause mortality
(Hogstrom et al 2016)
Limitation - don’t know what the participants did in the 30 years in between

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19
Q

Impact of physical activity on obese populations (mortality)

A

The risk of mortality is ameliorated but not eliminated

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20
Q

Impact of cardio respiratory fitness in obese individuals

A

Obese pts with high levels cardio respiratory fitness have similar mortality risk as a fit normal weight adult

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21
Q

Define obesity

A

Abnormal or excessive fat accumulation that poses a risk to health
BMI >=30 (>=35 very obese)

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22
Q

Why use waist circumference alongside BMI

A

To get an idea of central obesity + fat distribution as this can have major impact on health

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23
Q

Problem with visceral adipose tissue

A

Inc risk of health conditions
Adipose tissue compresses organs + can lead to chronic inflammatory state + dyslipideamia which may promote insulin resistance

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24
Q

List some conditions associated with obesity

A

Osteoarthritis- Inc load on joints
Obstructive sleep apnoea - Inc pharyngeal soft tissue
T2DM - insulin resistance due to inc pro inflammatory cytokines
Heart failure + stroke - atherosclerosis due to dyslipidemia and inc lipid production

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25
Q

Implication of having NO subcutaneous fat

A

Same metabolic processes that happen in obesity may occur

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26
Q

How do genetics impact obesity

A

Genetic influence has been confirmed by twin and adoption studies
Monogenic- potent influence by single gene
Polygenic - combination of multiple genes

FTO gene if carry both high risk alleles have Inc risk obesity

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27
Q

Environmental impact on obesity

A

21st century diet, leisure, transport and work habits have lead to inc obesity
70yrs ago people with high risk genes weren’t fat due to their environment, it is the environment changing that has lead to more obese people

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28
Q

Obesity Mx

A

Depends on BMI
Overweight may be able to use lifestyle changes alone
Obese - trial medication alongside diet + exercise
Last resort BMI>40 (or 35 with co-morbidities) - surgery - banding or gastric bypass (exercise post surgery for maintenance)

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29
Q

Problems with ozempic

A

Expensive
Limited availability
Side effects

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30
Q

Effect of physical activity on weight gain over time

A

Being active helps prevent weight game over time
But most evidence is observational studies - don’t look at diet or consider bidirectional impact

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31
Q

Does regular exercise lead to weightloss

A

Can induce significant weightloss in a strictly controlled + motivated environment
But very difficult to replicate this is real life so most people won’t see any benefit from exercise alone

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32
Q

Is exercise or diet control better?

A

Diet control as you can control 100% of your input but only 20% of energy expenditure
+ it takes longer to expend energy than to consume it
Therefore easier to induce negative energy balance through diet

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33
Q

Impact of aerobic training alongside weightloss diet

A

One study showed additional weightloss of =1.5kg

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34
Q

Best way to prevent regaining weight

A

Combination of exercise and Liraglutide facilitated weightloss maintenance better than either alone

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35
Q

Define T2DM

A

Disorder of carbohydrate metabolism caused by combination of hereditary and environmental factors. Characterised by inadequate secretion or utilisation of insulin leading to sustained hyperglycaemia

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36
Q

T2DM S+S

A

Fatigue
Weightloss
Thirst
Excessive urination
Hunger

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37
Q

T1DM v T2DM

A

T1 - autoimmune condition, can’t produce insulin, typically occurs younger
T2 - often due to obesity, resistant to insulin (may eventually stop producing it)

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38
Q

What is HbA1c

A

Glycated haemoglobin
Gives a measure of the amount of sugar in the blood over a 2-3 month period
>=6.5% (48mmol) = Diabetes (2 measures over 2 days)

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39
Q

Blood sugar pattern in T2DM

A

High fasting glucose
Postprandial hyperglycaemia

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40
Q

Describe the OGTT

A

Oral glucose tolerance test
Measure plasma glucose 120 mins after consuming 75g glucose
If >7.8 suggests impaired glucose tolerance
Often used in pregnancy to dx gestational diabetes

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41
Q

Impact of T2DM on mortality

A

Diabetics have a 15% higher risk of death than general population
Each 1% increase in HbA1c is as 12% increased risk of Mortality

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42
Q

Macro vascular complications T2DM

A

Stroke
CVD

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43
Q

Micro vascular complications T2DM

A

Diabetic retinopathy, nephropathy and neuropathy

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44
Q

Describe normal glucose metabolism in a fasted state

A

Want glucose to enter circulation
Liver increases glucose output through glycolysis and gluconeogenesis

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45
Q

Describe normal glucose metabolism in fed state

A

High levels of insulin, want to remove glucose from circulation
Increased glucose uptake and glycogen synthesis in skeletal muscle
Increased glucose uptake, Inc de novo lipogenesis and dec lipolysis in adipose tissue
Inc glycogen synthesis, Inc de novo lipogenesis and dec glucose output from liver

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46
Q

Metabolism of glucose in insulin resistance

A

Decrease glucose uptake into muscle - more glucose remains in circulation
Dec glucose uptake and inc lipolysis in adipose tissue
Inc glucose output and glycogen synthesis in liver

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47
Q

Define gluconeogenesis

A

New formation of glucose from non carb sources including glycerol

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48
Q

Goals of diabetes management

A

Glycemic control
Weight management
Cardiovascular and renal risk management

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49
Q

Lifestyle management for T2DM

A

Physical activity and diet can be very effective
26% reduction if meet weekly exercise guidelines

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50
Q

Best exercise for T2DM Mx

A

Combination of aerobic and resistance training is most effective
The more intense the exercise the greater the improvement in Hba1c

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51
Q

Why can you only put diabetes into remission in the first 6 year

A

Pancreatic beta cells have often died after 6 years of hyper secretion of insulin, therefore pt is dependent on insulin injections

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52
Q

DARE Study results

A

HbA1c decreased significantly over a 6 month Period with exercise session 3x weekly
Combination training had the biggest effect

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53
Q

How does exercise impact pancreas for T2DM

A

Increased beta cell mass
Increased insulin
Decreased glucagon

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54
Q

How does exercise impact adipose tissue (T2DM)

A

Decreased inflammation
Decreased fat mass
Increased insulin sensitivity

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55
Q

Impact of exercise on muscle tissue (T2DM)

A

Inc glucose uptake, Inc glucose and fatty acid oxidation, Inc insulin sensitivity

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56
Q

Impact of exercise on liver (T2DM)

A

Inc insulin sensitivity, dec hepatic glucose production, dec triglyceride accumulation

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57
Q

Impact of exercise on circulation (T2DM)

A

Dec blood glucose, Dec BP, dec serum triglycerides

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58
Q

What happens to glucose in acute exercise

A

Contractions cause increased glucose uptake independent of insulin
Muscles remain more sensitive to insulin for up to 2 days after

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59
Q

5S’s in T2DM

A

Sitting - break up long periods of sitting with short walks every 30 mins
Sweating - do at least 150 min moderate intensity activity weekly
Strengthening - 2-3 resistance training sessions a week improve insulin sensitivity
Sleep - aim for consistent uninterrupted sleep 6-8hrs per night
Stepping - increasing daily steps by 500 is associated with a 2-9% decreased risk of CVD

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60
Q

When does risk of sudden cardiac events increase

A

During and shortly after exercise

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61
Q

Describe relative and absolute risk of sudden cardiac event during exercise

A

Relative risk increases during exercise (you are more likely to have SCR/MI during exercise than at rest) but absolute risk remains very low

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62
Q

How to measure manual BP

A

Find brachial artery
Wrap BP cuff around bicep + put bell of stethoscope on brachial artery
Pump up cuff
Release cuff until you can hear pulse - systolic
Slowly release more until can no longer hear pulse - diastolic

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63
Q

Smoking + CVD

A

Smoking is a well know risk factor for CVD
Damages lining of arteries, increases BP, + thickens blood

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64
Q

Describe bland Altman plot

A

Compares 2 sets of measurements to identify any systematic bias or random error in date

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65
Q

Factors contributing to differences between venous sampling and finger prick

A

Air bubbles in sample
Sample contamination
Length of time taken to get sample
Blood volume

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66
Q

What is Q risk 3

A

Calculates persons risk of having MI or stroke in next 10 years

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67
Q

Benefits of Q Risk

A

Includes additional risk factors compared to Framingham CVD risk prevention, providing greater risk prediction accuracy

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68
Q

Additional risk factors in Q risk

A

Ethnicity
Townsend deprivation score
Migraine
CKD stage 3+
SLE
RA
A Fib
BP treatment
Angina/MI in 1st degree relative under 60
Erectile dysfunction
Antipsychotics/ steroids
Severe mental illness

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69
Q

Framington CVD risk predictor variables

A

Age
HDL
Total cholesterol
Untreated systolic BP
Treated systolic BP
smoker
Diabetes

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70
Q

What is the Townsend deprivation score

A

Measure of material deprivation in a population based on unemployment, non car ownership
Non home ownership, household overcrowding

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71
Q

What risk factors are there that you can’t change for MI/Stroke

A

Male
Asian ethnicity
Family history

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72
Q

Aims of ACSM pre-participation screening algorithm

A

Identify Individuals who require medical clearance before initiating an exercise programme
Identify individuals who may benefit from partaking in a medically supervised exercise programme
Identify individuals with medical conditions who should be excluded from exercise until medical condition improves

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73
Q

3 factors that the ACSM pre participation screening is based on

A

Current exercise participation
Desired exercise intensity
Hx + Sx of CV, Metabolic or renal disease

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74
Q

When is medical clearance recommended for exercise

A

No regular exercise + S+S of CV/Metabolic/Renal disease
No regular exercise + Known CV/Metabolic/Renal disease
Currently active, known disease + want to engage in vigorous activity
Currently active + new onset of S+S (discontinue exercise until medically cleared)

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75
Q

What does detailed evaluation for medical clearance include

A

Hx, examination, bloods, resting ECG, Exercise ECG

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76
Q

Define CVD

A

Collective term for diseases affecting heart and circulatory system

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77
Q

List 8 cardiovascular diseases

A

Stroke
Angina
MI
Heart failure
Peripheral arterial disease
Congenital heart defects
Arrythmias
CHD
DVT

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78
Q

Number of CVD Deaths

A

27% of UK deaths 2022

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79
Q

Active jobs v sedentary jobs CVD risk

A

Sedentary 2x more likely to have MI
But self selection bias

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80
Q

Impact of cardio respiratory fitness on CVD deaths

A

1 met increase in baseline cardio respiratory fitness was associated with 18% decrease in CVD deaths after adjustment for confounders

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81
Q

Cardio respiratory fitness vs genetic components CVD

A

Increased cardio respiratory fitness decreases risk of CVD even in people with high genetic risk for CVD

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82
Q

What increases risk of CVD mortality

A

Low physical activity
Poor cardio respiratory fitness

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83
Q

Define atherosclerosis

A

Thickening and hardening of artery caused by build up of plaque in the inner layer of the artery wall
Harder for blood to flow through so Inc risk of MI + Stroke

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84
Q

Describe development of atherosclerosis

A
  1. RFs cause endothelial damage increasing permeability of endothelial layer
  2. Initimal smooth muscle proliferation stimulated by various mechanisms
  3. Plasma LDL enters intima and is oxidised
  4. Oxidised LDL is taken up by scavenger receptors on monocyte transforming it into lipid laden foam cells
  5. Fatty streaks are formed from lipid filled foam cells
  6. Atherosclerotic plaque forms over many years
  7. Plaques are susceptible to rupture, haemorrhage, athero-embolism + anneurysm formation
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85
Q

Contents of atherosclerotic plaque

A

Cells - smooth muscle, macrophages, T cells
Extra cellular contents - collagen, elastic fibres
Intra+ extra cellular lipid

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86
Q

Role of hyperlipidemia in atherosclerosis

A

Can increase endothelial permeability
Inc serum conc of LDL + VLDL, can promote formation of foam cells

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87
Q

Modifiable atherosclerosis RF

A

Hyperlipidemia
Hypercholestroaemia
HTN
Smoking
Diabetes
Obesity
Low physical activity

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88
Q

Chylomicron function

A

Transport dietary fat from intestines to adipose tissue, muscle + liver

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89
Q

VLDL function

A

Made in liver, transports triglycerides to tissues
Contributes to build up of atherosclerotic plaque

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90
Q

LDL function

A

Predominate carrier of serum cholesterol to tissues
Contributes to build up of atherosclerotic plaque

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91
Q

HDL function

A

Transports excess cholesterol from blood + peripheral tissues to liver
Protective against CVD

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92
Q

Effect of exercise on lipoproteins

A

Regular exercise elevates HDL and lowers VLDL + triglycerides

The changes are more likely if exercise also causes weight loss
Findings for LDL less consistent

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93
Q

Effect of walking on BP

A

Both accumulated + continuous walking lead to post exercise hypotension, in healthy individuals and those at risk of CVD

Effects lasted = 24hrs

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94
Q

Impact of exercise alongside anti hypertensive meds in African Americans

A

Significant decrease in diastolic BP
Significant decrease in intraventricular septum thickness + left ventricular mass

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95
Q

Mean arterial pressure calculation

A

MAP = CO*Systemic vascular resistance

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96
Q

How does aerobic exercise decrease systemic vascular resistance

A

Vasodilation

Histamine released during vasodilation increases endothelial dependant vasodilation

Arterial baroreceptor reflex is reset - decreased noradrenaline - less vasoconstriction

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97
Q

Adaptations to training that decrease systemic vascular resistance

A

Vascular structural changes
Decreased inflammation
Decreased adiposisity
Increased insulin sensitivity

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98
Q

Describe endothelial dysfunction

A

Endothelium should be able to interact with vascular smooth muscle to influence blood flow
Atherosclerosis hardens and thickens blood vessels- harder for this to happen
Get turbulent flow and thrombus formation

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99
Q

Describe NO induced vasodilation

A

Exercise
Increased endothelial shear stress
Increased endothelial nitric oxide synthesis
Inc nitric oxide availability
Nitric oxide vasodilates blood vessels
Improved endothelial function

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100
Q

Impact of regular exercise on cardiovascular system

A

Enlarged coronary artery diameter, lower BP, Dec risk blood clots, improved endothelial function, dec chronic inflammation

Therefore potential for it to contribute to cardiovascular health

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101
Q

Define inflammation

A

Local immune response to physical injury/ damage or infection

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102
Q

Inflammation signs

A

Rubor, Dolor, calor, tumour, loss of function

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103
Q

Inflammation functions

A

Phagocytic cells engulf and destroy infected or damaged tissues
Stimulate tissue repair

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104
Q

How does inflammation stimulate tissue repair

A

Causes cytokine release from tissues which stimulates liver to release acute phase proteins eg CRP

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105
Q

Describe interleukins

A

Group of cytokines released by immune cells that play important role in regulating immune response including inflammation, proliferation, differentiation + activation

106
Q

What is bad inflammation

A

Chronic low grade inflammation
Dysfunction of immune response leading to LT release of inflammatory cytokines by immune cells

107
Q

Causes of chronic low grade inflammation

A

Obesity - FFA uptake by immune cells
Smoking - high levels of toxins in circulation
Unresolved infection
Autoimmune response
Local tissue hypoxia

108
Q

Describe how obesity/ high levels visceral fat cause chronic long term inflammation

A

Adipocyte hypertrophy
Blood supply therefore stretched over larger area
Hypoxic areas cause Inc metabolic stress
Cytokine release

Obesity can’t be beaten in 2-3 days so stimulus remains + cytokines constantly released

109
Q

List conditions associated with chronic inflammation

A

Diabetes
CKD
Heart disease
Inflammatory arthritis
Dementias
Stroke
IBD
Endometriosis

110
Q

Role of pro-inflammatory cytokines in chronic inflammation

A

Mediates inflammation
Eg IL6, TNF-alpha

111
Q

What are elevated pro inflammatory cytokines, fibrinogen + CRP associated with

A

Inc prevalence of multiple inflammation related diseases
Inc risk all cause mortality
Inc CVD RF

112
Q

Impact of inflammation on liver

A

Insulin resistance
Sustained acute phase protein release

113
Q

Impact of inflammation on adipose tissue

A

Adipokine production + immune cell infiltration

114
Q

Impact of inflammation on brain

A

Build up of amyloidogenic proteins (IL6 can cross BBB)

115
Q

Impact of inflammation on endothelial cells

A

Endothelial dysfunction + arteriosclerosis

116
Q

Impact of inflammation on skeletal muscle

A

Sarcopenia, insulin resistance

117
Q

Inflammation + CVD

A

Chronic inflammation is a RF for CVD
IL6 is increases as number of other CVD RFs increase in otherwise healthy women

118
Q

Impact of using monoclonal antibodies to target inflammatory pathways

A

Dec incidence of atherosclerotic pathogens
Lowered CRP, NOT lipids
Dec incidence of having another CVD event/death over 4years

119
Q

Can exercise be ani-inflammatory

A

Yes
Study showed more active people had lower inflammatory markers
But same trend seen - more active people had less adipose tissue

120
Q

Impact of sedentary time on inflammation

A

People with higher sedentary time had higher inflammation levels even if also physically active

121
Q

List 4 mechanisms why LT physical activity is anti inflammatory

A

1.Decreased adipose tissue - biggest source of circulating IL6
2. Decreased numbers of inflammatory immune cells entering adipose tissue
3. Altered cytokine production from inflammatory immune cells
4. High intensity exercise + counter action of anti-inflammatory response

122
Q

How is decreasing numbers of inflammatory immune cells entering adipose tissue anti-inflammatory

A

Migration of immune cells from circuit tissues is a key event in chronic inflammation
Studies show monocyte migration decreases in obese individuals who move more
Mice studies show decreased inflammatory macrophages per gram adipose tissue in obese mice that exercise compared to obese mice

123
Q

How does altered cytokine production from inflammatory cells make LT physical activity anti inflammatory

A

Regular brisk walking in pts with CKD decrease inflammatory immune cell activation and release of pro inflammatory proteins into blood

124
Q

How is higher intensity activity anti-inflammatory

A

Causes skeletal muscle to release large amounts of IL6 as an acute response.
Stimulus leads to release of counter active anti-inflammatory response - IL10

Regular performance of higher intensity/longer duration activity can lead to persistent elevation of IL10

125
Q

Anti-inflammatory effects of regular physical activity

A

Reduced circulating levels of anti-inflammatory markers at rest
Lower pro-inflammatory cytokine release from immune cells at rest

126
Q

What is the gold standard measure of cardio respiratory fitness

A

VO2 max (maximum oxygen uptake)

127
Q

What is a low VO2 max indicative of

A

Inc risk CVD + Premature mortality

128
Q

Why is direct determination of VO2 max not always possible?

A

Cost, lack of specialised equipment, lack of trained personnel
May be dangerous in some people

129
Q

List 4 methods to estimate VO2 max

A

Bruce treadmill protocol - maximal graded exercise test
Astrand-ryhming cycle ergo meter test - submaximal
Chester step test - submaximal
Questionnaire

130
Q

Guidelines for safe conduct of laboratory exercise test

A

Physical activity readiness questionnaire should be completed
Ensure treadmill/ ergometer is safe
Fully describe all procedures to pt and provide participant info sheet
Familiarise participants with all equipment
Give participants opportunity to ask Qs
Watch participants closely in test + for 10 mins after
Provide opportunity for warm up/cool down

131
Q

Describe Bruce treadmill protocol

A

Maximal graded exercise test performed until exhaustion or til termination is indicated by S+S
3 minute stages of increasing treadmill speed and gradient
Duration of test sustained can be used to estimate VO2 max

132
Q

What variables are measured in the Bruce treadmill protocol

A

HR, BP, Ratings of perceived exhaustion
ECG if done in clinical practice

133
Q

Describe Astrand-rhyming cycle ergometer test

A

Single stage test lasting 6 minutes
Individuals pick a work rate based on sex and fitness status
Pedal rate set at 50
HR measured min 5 + 6 and mean is used to estimate VO2 max from a nomogram
Must then adjust value for age

134
Q

What assumptions are made when estimating VO2 max using sub-maximal tests

A

Steady state HR is obtained for each exercise work rate
Linear relationship exists between HR + work rate
Difference between actual + predicted maximum HR is minimal
Mechanical efficacy is the same for everyone
The participant is not affected by other factors that may affect HR - Caffiene, stress, hot environment

135
Q

Benefits + limitations of the Chester step test

A

Cheap and easy

May be difficult for people with balance issues
Few points for plotting- line of best fit less accurate

136
Q

Describe Chester step test

A

Step up and down in time with metronome which increases in pace as test stages progress
Stop when HR reaches 80% of max or feel breathless, overtired or dizzy
Maximal O2 uptake estimated based off of HR response to submaximal exercise stages

137
Q

How to decide what size step participants should use in the Chester step test

A

30 cm = under 40, regularly active, used to moderate-vigorous exertion
25cm = over 40, regularly active, used to moderate-vigorous exertion
20cm under 40 little active/ moderately overweight
15cm over 40 little active

138
Q

How to calculate max HR

A

220-age

139
Q

Benefits and limitations for estimating VO2 max from questionnaires

A

Quick, simple + easy
Rely on prior knowledge
People unlikely to be totally accurate

140
Q

What questionnaires are used in estimating VO2 Max

A

Perceived functional ability (PFA)
Physical activity rating (PA-R)

141
Q

What is the difference between RMR and basal metabolic rate

A

RMR is slightly higher (measured at rest, 3-4hrs post light meal)
BMR - minimum level of energy required to sustain vital functions. Measured at rest in post-absorbative state 12 hours after food

142
Q

How is RMR Measured

A

Indirect calorimetry
Direct calorimetry
Predictive equations provide an estimate

143
Q

What Are the four most common equations used to predict RMR?

A

Harris-Benedict
Owen
Who/FAO/UNU
Miffed St Jeor

144
Q

How are predictive equations developed

A

Based Off off measurements of direct and indirect calorimetry

145
Q

How Are predictive equations, validated

A

Used On a diverse population with a variety of weights ages And ethnicities

146
Q

How Much variation exists between the different productive equations

A

A fair bit, but Owens tends to be roughly 200kcal lower than the other 3

147
Q

What are The key limitations when using predictive equations

A

They are based off of a generalised population, which might not be representative of the individual

Maybe Unreliable for certain ages and ethnicity , particularly older adults and non-white

Risk Of individual error in calculations and measurements
Individual Variation

148
Q

Energy expenditure calculation

A

Energy expenditure = RMR * physical activity level

149
Q

Physical activity level associated with sedentary existence during work and leisure

A

1.4

150
Q

Physical activity level associated with very high PA levels during work and pleasure

A

2.5

151
Q

Estimated Physical activity level that is the maximum level of sustainable in humans

A

5 (Before body weight is lost)

152
Q

Physical Activity level associated with moderate activity levels

A

1.6 women
1.7 men

153
Q

Physical activity level associated with high activity levels

A

1.8 women
1.9 men

154
Q

What Is a MET

A

A multiple of the resting metabolic rate

155
Q

What Is 1met equivalent to?

A

Energy Expenditure of the body, at rest quantified as one kcal, per kilogram, body mass per hour

156
Q

Oxygen Consumption equivalent to one met

A

3.5mL/kg/min

157
Q

How Does exercise, intensity, affect energy expenditure?

A

Higher intensity equals higher energy expenditure

158
Q

What is exercise, intensity, dependent on

A

Physical Fitness and individual needs a good level of cardiovascular fitness to work at high exercise intensity

159
Q

How Many calories are expended for each litre of oxygen consumed

A

5kcal (21kJ)

160
Q

Why Does low energy intake cause a decline in energy expenditure?

A

Lower Metabolic rate due to lower metabolically Active tissue mass
Adaptive Thermogenesis an involuntary compensatory mechanism to conserve energy

161
Q

Why Are patients given new energy intake targets for body weight maintenance once their goal weight is achieved

A

To ensure they are in energy balance
It Is lower than pre-weight-loss maintenance calories, because lean mass is increased compared to Fat mass

162
Q

Define ectopic fat

A

Fat stored in places not designed for mass storage eg intraorgan

163
Q

How does accumulation of ectopic fat occur

A

1.positive energy balance
2. Inc inflammation, hypoxia, pro inflammatory cytokines and insulin resistance
3. Fat spillover occurs leading to more free fatty acids in circulation
4.FFA deposit within organs

164
Q

Stages of non alcoholic fatty liver disease

A
  1. Healthy
  2. Fatty liver (32% population)
  3. Non alcoholic steatohepatitis (NASH)
  4. Cirrhosis (+ Inc risk HCC)
165
Q

MASLD diagnostic criteria

A

Metabolic dysfunction related steatotic liver disease
= steatotoic liver disease plus 1 of
BMI>25/waist circumference >94(M) or >80 (f)
Fasting serum glucose >5.6 or 2hr glucose >7.8 or T2DM
BP >130/85
Plasma triglycerides >1.7
HDL cholesterol <1(m) or <1.3 (f)

166
Q

Gold standard Ivx for MASLD

A

Liver biopsy
Visible liver droplets in >5% hepatocytes
Able to identify different stages of MASLD
But invasive + specialised

167
Q

Gold standard non invasive Ivx for MASLD

A

MR spectroscopy
Liver fat% >5.56
Allows repeat measures
But expensive + specialised

168
Q

MASLD prevalence

A

Affects 32% adults
Most common form of liver disease worldwide
Often co-exists with other diseases T2DM(60%),Obesity (70%)
Individuals with MASLD 2x more likely to develop T2DM

169
Q

Strongest predictor of insulin resistance

A

Intra-organ liver fat

170
Q

Lipid supply to liver mechanisms

A

Adipose tissue lipolysis
Dietary fat
De novo lipogenesis

171
Q

Lipid disposal from liver mechanisms

A

Fat oxidation
VLDL-TAG export

172
Q

Hepatic steatosis pathogenesis

A

Inc dietary fat - Inc lipolysis - Inc FFA - Inc TAG synthesis
Inc dietary fat - Inc TAG rich chylomicrons, chylomicron remnants left, Inc TAG synthesis

Inc dietary fructose + glucose - Inc de novo lipogenesis

173
Q

Why does hepatic steatosis occur

A

Lipid supply to liver exceeds disposal due to over nutrition and insulin resistance
Disposal routes may also increase but not enough to offset Inc supply

174
Q

MASLD Mx

A

Resmetrion - 1st drug approved this year, some anti obesity drugs also look promising
Lifestyle modifications - exercise + hypocalorific diet.
5% weightloss - dec hepatic steatosis, 7% weightloss NASH resolution, 10% weightloss fibrosis regression

175
Q

Impact of exercise alone on MASLD

A

No change body weight
Significant decrease in liver fat
Significant increase in peripheral insulin sensitivity

176
Q

Why does exercise improve MASLD - adipose tissue

A

Improved adipose tissue insulin sensitivity
Decreased adipose tissue lipolysis

177
Q

Why does exercise improve MASLD - Skeletal muscle

A

Inc glucose uptake as enhanced insulin sensitivity
Leading to less substrate for de novo lipogenesis

178
Q

Why does exercise improve MASLD - liver supply

A

Dec uptake of lipids from circulation, decreased hepatic lipase activity
Dec de novo lipogenesis

179
Q

Why does exercise improve MASLD - liver disposal

A

Inc lipid oxidation
(Rodent studies showed Inc markers of B-oxidation + mitochondrial biogenesis)

180
Q

Impact of resistance exercise on MASLD

A

Similar improvements in BMI and liver fat between aerobic + resistance exercise despite lower intensity and energy consumption with resistance training.

May complement aerobic training by modulating liver fat through different mechanisms

181
Q

Resistance exercise mechanisms to dec liver fat

A

Hypertrophy of Type 2 muscle fibres
Activation of GLUT 4 + AMPK
Alteration in myokines

182
Q

How does hypertrophy of type 2 muscle fibres improve MASLD

A

Hypertrophy of skeletal muscle = increased glycotic demand by muscle
Decreased circulating glucose = less substrate for de novo lipogenesis

183
Q

What is GLUT 4

A

Insulin regulated transporter protein, responsible for glucose uptake into muscle.

184
Q

What is AMPK

A

Energy sensing kinase that promotes insulin sensitivity

185
Q

How does activation of GLUT 4 + AMPK improve MASLD

A

Inc insulin sensitivity so Inc GLUT 4 mediated uptake into muscle
Decreased circulating glucose + insulin, less substrate for de novo lipogenesis

186
Q

What is a myosin’s

A

Cytokine produced and secreted by skeletal muscle

187
Q

How does alteration in myokine improve MASLD

A

Irisin = myokine increased in resistance exercise, believed to inhibit key regulators and enzymes in de novo lipogenesis

188
Q

What is the athletes paradox

A

Skeletal muscle lipids are elevated in endurance athletes and T2DM compared to lean sedentary counterparts
But athletes remain insulin sensitive so this may be beneficial for them due to high fuel demand

Therefore believed the form in which lipids are stored is important
PUFA better than SFA and intermediates

189
Q

Describe inspiration

A

Process of breathing in
Diaphragm moves down, external intercostals move up and out
Chest cavity is increased therefore pressure in lungs is lower than atmospheric pressure
Air pulled into lungs

190
Q

Describe expiration

A

Process of removing CO2 from body through the lungs
Diaphragm relaxes, moving up, external intercostals move down + in
Intra thoracic pressure increases above atmospheric pressure
Air passively flows out

191
Q

Define tidal volume

A

Amount of air that moves in and out of lungs with each respiratory cycle
Typically 500ml ish

192
Q

Define inspiratory reserve volume

A

Amount of air that can be taken into the lungs after tidal volume, upon forced inspiration

193
Q

Define expiratory reserve volume

A

Extra volume of air that can be expired with maximal effort, beyond the level reached at the end of normal quiet breathing

194
Q

Define residual volume

A

Vol of air remaining in lungs after maximal forceful expiration

195
Q

Define vital capacity

A

Total vol of air that can be displaced from lungs following maximal inspiration

196
Q

Define ventilation

A

Movement of air in and out of airways

197
Q

Define asthma

A

Chronic inflammatory disease of airways that causes reversible airway obstruction + hypereactivity

198
Q

Asthma Sx

A

Cough, wheeze, chest tightness, SoB
Sx typically worse at night
Multiple triggers - exercise, cold weather, allergies etc

199
Q

Asthma prevalence

A

> 300 million affected worldwide
10% 6+7yr olds - greater incidence in children
60,000 uk hospital admissions per year

200
Q

Asthma attack pathophysiology

A

Airway Smooth muscle tightens
Air becomes trapped in alveoli

201
Q

Define COPD

A

Umbrella term for chronic bronchitis + emphysema
Chronic progressive lung disease characterised by persistent respiratory symptoms + airflow obstruction that’s not fully reversible

202
Q

Define emphysema

A

Enlargement of air spaces and destruction of lung parenchyma

203
Q

Define chronic bronchitis

A

Increased sputum production, obstruction of major and minor airways, chronic productive cough

204
Q

COPD Sx

A

“Air hunger”, exertional dyspnoea, chronic cough, decreased exercise tolerance, sputum production, Inc respiratory effort

205
Q

COPD Mx

A

Smoking cessation
Vaccines
Meds - SABA/LABA/LAMA/ICS
Oxygen therapy
Pulmonary rehab

206
Q

Describe pulmonary rehab

A

6-12week programme with twice weekly sessions (both exercise + educational)
Aims to improve exercise tolerance and lung function

207
Q

Does pulmonary rehab work

A

Yes - overwhelming evidence
Improves mood, dyspnoea, mastery, emotional function, functional + maximal exercise capacity

208
Q

Pulmonary rehab outcome measures

A

Strength
Exercise capacity
Quality of life
Mood
Dyspnoea + fatigue

209
Q

Describe COPD cycle of inactivity

A

Dec activity
Muscles weaker
Weaker muscles have increased oxygen consumption as less efficient
Feel breathless
Become fearful of tasks making you breathless
Avoid activities making you breathless
Decreased activity

210
Q

Describe COPD positive cycle of activity

A

Inc activity
Muscles stronger
Use O2 more efficiently
Decreased breathlessness- tasks feel easier
Feel better
More motivated to continue activity
Increased activity

211
Q

What is GOLD score

A

Global initiative for chronic obstructive lung disease
GOLD IV is worst

212
Q

Effect of physical activity on COPD

A

Some level activity = decreased risk COPD admissions + mortality
2hrs walking/cycling per week = 30-40% decrease in admission/ mortality

213
Q

Asthma + physical activity

A

Mixed results
Most studies suggest physical activity improves lung function, quality of life + asthma control
3 studies showed no improvement. No studies showed worsening

214
Q

describe trabecular bone

A

inside
network of cross bridges filled with bone marrow
more rapid turn over

215
Q

describe cortical bone

A

on the outside (very outer layer = periosteum)
dense strong structure
longitudinal cylindrical osteons

216
Q

what is bone tissue composed of

A

2/3rd ground substance
1/3rd portions
2% bone cells

217
Q

describe ground substance

A

predominately hydroxyapatite crystals + other Ca salts and ions

allows storage and release of Ca

218
Q

describe the protein component of bone

A

most abundant is type 1 collagen fibres

219
Q

describe bone cells

A

osteoblasts - develop from messenchymal stem cells, build bone by recreating osteoid protein which matures to osteocytes

osteocytes = mature bone cells, role in signalling

osteoclasts - resorb bone using acids and enzymes

220
Q

How is bone mineral distribution measured

A

DEXA scan - 2D image
pQCT - 3D scan of peripheral bones eg shin + forearm
Clinical QCT - 3D image

221
Q

describe trends in Bone mineral density

A

higher in men throughout life
significant drop in post menopausal women - due to decreased oestrogen

both men and women decrease slowly with age

222
Q

define osteoporosis

A

systemic skeletal disease characterised by low bone mass + microarchitectural deterioration of bone tissue, with consequent increase in bone fragility and fracture risk

223
Q

lifetime fracture risk in over 50s

A

1 in 2 women
1 in 5 men

224
Q

common fragility fracture sites

A

NOF, vertebrae, forearm

225
Q

why does osteoporosis increase risk fragility fracture

A

thinning of cortical bone and loss of trabeculae

226
Q

osteoporosis RF

A

older age
female
smoker
low BMI
FH
decreased oestrogen
cancer Tx
glucocorticoid use
T2DM
high falls risk

227
Q

describe mechanostat theory

A

bone adapts to its level of loading
1. Habitual loading - stress causes strain within bone
2. Moderately increased loading - increased strain
3. osteocytes detect additional strain -bone adapts
4. inc loading on adapted bone - less strain

228
Q

why is it important to not extremely overload bone

A

causes micro damage and fractures

229
Q

describe targeted remodelling

A

old bone undergoes osteocyte apoptosis + is replaced by new bone
total bone mineral density unchanged

230
Q

describe disuse mediated remodelling

A

build less bone than resorbed - lose bone mineral density

231
Q

describe formation modelling

A

increased load
leads to new bone being build independent of resorption

232
Q

describe resorption modelling

A

osteocyte apoptosis and osteoclast resorption occur without osteoblasts building new bone

233
Q

effect of exercise on children’s bones

A

regular jumping(impact activity) increases bone mineral density

effects long lasting - seen up to 7 yrs later

234
Q

effect of exercise on adolescent bones

A

thickens cortical bone

type of exercise impacts what bone is thickened
eg hockey - multidirectional impact - all-round thickening
running thickened at front and back

235
Q

effect of exercise on pre-menopausal women

A

spine - high load resistance training increased BMD
hip - high impact exercise increased BMD

236
Q

effect of exercise on fracture risk

A

observational studies suggest decreased 38% women + 45% in men

237
Q

factors contributing to fracture risk

A

bone strength - Bone mineral density + bone structure

falls risk - neuromuscular function + environmental hazards

238
Q

fall prevention exercise

A

most effective = challenges balance, includes lower limb strength training. > 3 hrs per week tailored to individual

239
Q

UK recommendations for exercise for osteoporosis

A

progressive resistance exercise, loading the hip = spine 2-3 days per week
build to 3 sets of 8-12 rep max

include impact exercise - 50 moderate impacts per day with rest breaks

if falls risk prioritise strength and balance training 2-3 days per week

240
Q

What Is cancer

A

Uncontrolled mitosis cells can metastasise to another part of the body

241
Q

How Does the thymus impact cancer incidence?

A

Thymus Produces t cells
Thymus Shrinks as you get older, less t cells produced
Greater Incidence of cancer as you get older

242
Q

Describe Non-specific cancer immunity

A

Natural Killer cells kill abnormal cells - identified as they have lost MHC class 1 receptors
2 Methods
Cytolytic activity - secrete granzymes- enzymes enter through pore and cause cells to lyse
Cytokine release- indirect method through recruiting specific immune cells

243
Q

Describe Specific antitumour immunity

A

Dendritic Cells such as macrophages do phagocytosis
B Cells produce specific antibodies, causing a humeral immune response
T cells - work with CD8 to induce apoptosis via cytotoxic cells
T cells work with CD4 to prime B cells

244
Q

Describe the 3 Es of immunosurveillence

A

Eliminatation - immune System destroys, weakest cancer cells
Equilibrium, small sub population of cancer cells, survive and lie, dormant
Escape - Clonal outgrowth of surviving cancer cells

245
Q

Define clonal

A

Every cell in the population has original mutation

246
Q

Describe Metastasis

A

Cancer Cells spread to other parts of the body
2/3 of cancer related deaths are due to mets
Metastasis are made of different cell types, including stem cells which are harder to treat

247
Q

Cancer RF

A

Nearly 50% preventable
Pathogens - EBV infection - nasopharyngeal ca + Burkitt lymphoma
Obesity
UV damage
Toxin exposure - asbestos, smoking

248
Q

How to reduce cancer risk

A

Exercise
Eat well
Healthy body weight
Limit UV a exposure
Don’t smoke
Avoid infectious agents

249
Q

Effect of exercise on cancer overview

A

Dec primary cancer risk
Improves chemo response
Improved recovery
Dec secondary cancer risk (probably, hard to research)

250
Q

Effect of leisure time PA on Ca risk

A

Dec risk oesophageal Adenocarcinoma, liver, lung, kidney, myeloma,colon, H+N

But Inc risk malignant melanoma- Inc UV exposure (outside more)

251
Q

How to exercise help prevent cancer

A

Sex hormones - breast cancer often driven by oestrogen, oestrogen produced by adipose cells, exercise decreases adiposity.

Metabolic hormones - exercise improves insulin sensitivity, dec risk T2DM, associated with some cancers

Chronic inflammation promotes cancer - exercise dec chronic inflammation (4 mechanisms)

252
Q

How does exercise effect existing Ca

A

Can decrease cell growth - voluntary wheel running in mice decreased tumour growth 67%
Cancer cells incubated with exercised serum produced fewer tumours in mice
Exercise decreased breast cancer cell viability, proliferation + tumourogenic potential in vitro

BUT
Can’t shrink tumours

253
Q

Effect of exercise on tumour metabolism

A

Cancer cells more susceptible to exercise induced energy stress

Cancer cells use up lots of glucose - always metabolise through lactate producing pathway - therefore adapted to inc number of GLUT 1 transporters to counteract quick build up of lactate.

254
Q

Why shouldn’t you completely cut out sugar if have cancer

A

Cancer cells have more GLUT 1 transporters therefore can use any available sugar faster
Cutting out majority of sugar will starve healthy cells as cancer cells will monopolise any available

255
Q

Effect of exercise on chemo

A

Cancer cells cause angiogenesis (new blood vessels, these tend to be more leaky + tortuous)
Exercise promotes this and makes the new blood vessels stronger
Therefore chemo can be delivered deeper into the tumour - better effects

Increased drug tolerance - able to withstand higher dose - more like likely to kill tumour

256
Q

Effect of exercise on immune cell function (Cancer)

A

Exercise mobilises cells involved in immune response
Natural killer cells first to be mobilised by exercise- as express more B-adrenergic receptors

Patients with Inc NK + Cytotoxic T cells = better prognosis

257
Q

Effect of exercise on NK cells

A

Inc NK cell cytotoxic activity
Inc lymphocytic production
Inc number of granulocytes

258
Q

Which cancer patients is exercise most beneficial for

A

Compromised immune function

259
Q

What can effect ability to exercise in Ca pts

A

Type + stage Ca
Ca Tx
Stamina, strength + fitness level

260
Q

Exercise + metastasis

A

Cancer stem cells are more chemo resistant
Exercise may alter cancer stem cell phenotypes

Research ongoing

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