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Respiratory System > Exercise physiology in healthy individuals > Flashcards

Exercise physiology in healthy individuals Flashcards

1
Q

Describe the RQ values for the metabolism of different substrates

A

Fats- 0.70
Carbohydrates- 1.0
Protein- 0.82

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2
Q

How do we calculate RQ

A

CO2 production/oxygen consumption - usually = 1

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3
Q

What is most of our energy at rest produced by

A

Aerobic metabolism

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4
Q

How many molecules of ATP are produced per molecule of glucose

A

37

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5
Q

What is a consequence of respiring more fat

A

less CO2 produced

lungs don’t have to work as hard to get rid of CO2

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6
Q

Summarise the RQ

A

§ The ratio of CO2: O2
§ 1 is the theoretical maximum.
§ Lowest for fat, intermediate for protein and highest for glucose.
§ O2 requirement at rest = 3.5mlmin-1kg-1.

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7
Q

Compare oxygen requirements for different activities

A

Oxygen requirements: sat at rest - O2 consumption roughly 3.5ml/min/kg - equal to 1 metabolic equivalent
Metabolic equivalents: standing = 1.5, walking = 2, running > 7

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8
Q

Describe the ventilation response to exercise

A

At the onset of exercise, there is a O2 deficit and post-exercise, there is an O2 debt (to refill the myoglobin stores).
O2 increases linearly with workload

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9
Q

What does the plateau of O2 consumption define

A

Max O2 consumption (VO2 max) and therefore max workload

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10
Q

Describe the muscular response to exercise

A

stored energy (ATP, PCr) used to generate muscular contraction; inorganic phosphates, ADP and creatine drive oxidative phosphorylation while Krebs/glycolysis increases; oxygen consumption at muscle increases, and initially CO2 production rises slowly (as buffered), but then rises to match O2

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11
Q

Describe how SV, Q and HR respond to exercise

A

Stroke volume initially increases but then decreases past a peak of 160mls while the CO and HR continue to rise.

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12
Q

Why does SV decrease

A

Q increases linearly with intensity until plateaus as maximum reached, alongside HR and oxygen consumption - exercise limited by cardiac output; when HR too fast, filling time in diastole reduced, which reduces SV after a peak

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13
Q

Describe the response of the lungs to exercise

A

TV increases with ventilation up to a peak where plateaus, and breathing frequency increases - will breathe at half vital capacity in exercise (increase further not as efficient); VQ matching at rest not ideal, but in exercise increases

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14
Q

How does the human body perform exercise

A

Gas exchange, O2, CO2

The muscle
The circulatory system
The lungs

Anaerobic metabolism/Acidosis

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15
Q

What is the purpose of gas exchange

A

Transport of oxygen to tissues

Removal of waste products (namely CO2)

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16
Q

Summarise the flow of oxygen and carbon dioxide

A

Negative pressure is generated within the chest cavity
Air travels from the mouth down the airways and into the alveoli of the lungs.
Assuming normal atmospheric concentrations of O2 (21%) it will diffuse down a concentration gradient across the alveolar surface to the pulmonary capillaries (venous O2 content 16%)
Binds to haemoglobin, raising blood oxygen levels
Blood travels through the heart, to target organs
Here capillaries, get smaller and densely infiltrate the tissue to allow easy diffusion of oxygen, again down a concentration gradient, into metabolising cells
Carbon dioxide diffuses in the opposite direction (largely dissolves into plasma) and returns to the lungs via the venous system
Carbon dioxide diffuses from the high concentration venous blood (approx 4%) to the low concentration alveolar air (0.04%)
Positive intrathoracic pressures cause expiration

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17
Q

What do we breathe out

A

FEO2 ~16%

FECO2 ~4%

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18
Q

What do we breathe in

A

FIO2 21%

FICO2 0.0%

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19
Q

Summarise the response of the muscle to exercise

A

Onset of exercise
Stored energy muscular contraction

Inorganic phosphates, ADP and creatine drive oxidative phosphorylation
Kreb’s cycle and glycolysis increase
Oxygen consumption at the muscle (QO2) increases
Initially CO2 production only slightly increases (buffered as HCO3-) but then rises, matching O2

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20
Q

How does oxygen consumption change during exercise

A

Cardiac Output rises 4-7 fold
Oxygen consumption rises 10-15 fold
Mixed venous sats typically ~75-80% at rest dropping to 15-20% at peak exercise
Up to 85% of oxygen can be extracted during exercise

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21
Q

Recall Fick’s equations

A

Cardiac Output = Oxygen Consumption/
(a-v) O2 Content

VO2= Cardiac Output x (a-v) O2 Content

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22
Q

What is the response of the lungs to exercise

A

TV increases with ventilation up to a peak where plateaus, and breathing frequency increases - will breathe at half vital capacity in exercise (increase further not as efficient); VQ matching at rest not ideal, but in exercise increase

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23
Q

Compare VQ at rest and during exercise

A

At rest VQ matching not ideal
PAO2 = 102mmHg
PaO2 = 92mmHg
P(A-a)O2 = 10mmHg

Early exercise
VQ matching improves
PaO2

Close coupling of VE to VCO2 
Decreasing P(A-a)
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24
Q

Describe incremental aerobic metabolism in exercise

A

Aerobic metabolism - oxygen flow matches demand

Total body RQ rises towards 1 as glucose becomes the predominant fuel source

Ventilation increases to match CO2 production and attempts to maintain steady-state

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25
Q

Describe anaerobic metabolism

A

Central to human exercise physiology is the anaerobic production of energy
Probable evolutionary role in flight or fight
Highly inefficient but short-term solution when greater energy is required

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26
Q

Describe the bohr effect

A

as pH increases, Bohr shift of ODC to right so at given PO2 Hb has less affinity to oxygen so offload more to acidotic muscles
why oxygen consumption quadruples as o2 delivery doubles

27
Q

How does the body deal with acidosis

A

lactate converted to protons, and is buffered by bicarbonate to increase CO2, increased ventilation allows pH to remain relatively stable; when [H+] exceeds HCO3- cannot buffer and begin hyperventilation
lactic acid is handled by increased ventilation- we see an increase in ventilation above the aerobic threshold

28
Q

Describe the phases of exercise

A

VE increases until anaerobic threshold and in isocapnic buffering
Increases further in respiratory compensation (H+ exceeds buffering)
PCO2 increases until anaerobic threshold, same in isocapnic buffering, increases in respiratory compensation
VO2 increases throughout- not as much as the other two

29
Q

How does ventilation change through the anaerobic threshold and ventilation compensation point

A

Exponentially- see graph

30
Q

How does PaCO2 change through the anaerobic threshold and ventilation compensation point

A

Decreases after ventilation compensation point- constant before

31
Q

How does VO2 change through the anaerobic threshold and ventilation compensation point

A

DELAY THEN INCREASES LINEARLY THROUGH BOTH

32
Q

Summarise exercise terminology

A 
QO2/CO2 	- At muscle
VO2/CO2  	- At mouth
VE			- Minute ventilation
PAO2/CO2 	- Alveolar partial pressure
PaO2/CO2 	- Arterial partial pressure
PETO2/CO2	- End-tidal partial pressures
33
Q

What is seen in fit people

A

max heart rate and FEV at the same time

Peak Q limits you

34
Q

How do we calibrate

A

volume - blow fix amount of volume
bike- apply known force
calibrate with biological control- who repeats the test in the same conditions each time

35
Q

Describe a cardiopulmonary exercise test

A

patient on a bike has continuous ECG and gas exchange monitoring and the power is slowly increased to put cardiopulmonary strain on the patient - can be used to detect heart/lung conditions/restrictions on exercise etc.

36
Q

Describe the Nurse’s health study

A

Nurses health study – followed up for 18 years (ages 30-55 yrs)

Starts to rise from a BMI 21
Risk of type 2 DM rises by 8 fold at BMI 25
CHD rises 2 fold at BMI 25 and 4 fold at BMI 30

37
Q

Describe the Forsyth report

A

Mapped which factors affected one’s intake
societal changes
jigsaw of factors- just one bit doesn’t do anything- but public health focusses on one change

38
Q

Does BMI on its own determine risk

A

Subject A: BMI 26.5 kg/m2, 1.3 litres visceral adipose tissue
Subject B: BMI 26.8 kg/m2, 5.5 litres visceral adipose tissue

visceral fat dictates metabolism- as it has a blood supply from G.I tract- increased risk of CHD and T2DM-
blood has to go through adipose tissue and the inflammatory cells- inflammatory mediators reduce liver function

39
Q

Describe the consequences of increased visceral adiposity

A 
Deteriorated lipid profile
Impaired insulin sensitivity
Increased susceptibility to thrombosis
Increased inflammation markers
Impaired endothelial function
40
Q

How do we measure waist circumference

A

Mid point between the lowest rib and ileac crest.

~1 cm above navel

Accuracy difficult if BMI>35

41
Q

Describe action level 1 in waist circumference

A

Action level 1
Women ≥80cm / 31.5 in Health risk increasing
Men ≥ 94cm / 37 in Take personal action to
avoid weight gain

42
Q

Describe action level 2

A

Action level 2
Women ≥ 88 cm /34.5 in Multiple health problems
Men ≥ 102 cm / 40 in Professional help needed

Lower for south asians

43
Q

Describe the impact of a 10% decrease in weight loss

A 
Improves all aspects of the metabolic syndrome, including:
50% fall in FBS
10% decrease in total cholesterol
15% reduction in LDL
30% fall in triglycerides
8% rise in HDL
Ave improvement of BP by 10/20mmHg

Overall relates to:
20-25% reduction in all mortality
30-40% reduction in diabetes related mortality
40-50% reduction in certain cancers

44
Q

What are NICE recommendations for obese patients

A 
Recommends:
Diet
Exercise
Behavioural therapy
Drug treatment
Surgery (if BMI >40)
45
Q

Essentially, what leads to T2DM

A

Genetic defect in pancreas + obesity (adipotoxicity)- insulin resistance

46
Q

Do we have targets for waist circumference

A

No- only weight

diet or liposuction- no reduction in risk- only weight provides benefit

47
Q

Describe the issue with perception

A

Patients want to be thin

But health professionals want reductions in complications

48
Q

Describe the issue with lifestyle advice

A

Short half-life

loses a lot of weight initially- but will put it back on

49
Q

Compare weight loss outcomes with different managements

A

§ With lifestyle changes, there was a 58% improvement (in the study on the left) in diabetic patients.
§ With lifestyle changes, it’s much harder to keep the weight off in this environment (without constant monitoring).
§ Using Orlistat (vs. placebo) and lifestyle changes, the same pattern is observed but Orlistat provides a much greater loss of weight.
o There is a GREAT reduction in weight over the first year which is gradually put back on and then plateaus.

50
Q

Describe the different types of bariatric surgery

A

There are 3 main procedures:
o Adjustable band.
§ A fluid can be injected into the sub-cutaneous bag to increase or decrease to food into the stomach.
o Sleeve gastrectomy.
o Gastric bypass (GBP) – Gold-standard.
§ The duodenum and part of the ileum only see bile and no food – may play a role in success of procedure.

51
Q

How can we make lifestyle advice more effective

A

Messages are simple
They are individualised
There is frequent follow-up

52
Q

What are the criteria for bariatric surgery

A

o BMI > 40, no co-morbidities.
o BMI > 35, co-morbidities.
o BMI 30-35, short duration of T2DM.

53
Q

Describe the benefits of bariatric surgery

A

§ GBP surgery was also found to be the most effective in patients with diabetes at glycaemic control.
o This could be due to a number of hypothesised reasons – as the effect occurs immediately after GBP:
§ Change in insulin resistance.
§ Change in insulin secretion.
§ Changes in the gut microbiota.
§ Changes in bile salt secretion.
o GBP also found to reduce mortality and to reduce occurrence of long-term CVD events.
§ Health benefits of bariatric surgery include; resolution/improvement of T2DM and hypertension, reduced cardiac risk, resolution of obstructive sleep apnoea, resolution of PCOS (improved fertility), reduction in cancer-related deaths, regression of non-alcoholic fatty liver disease, reduced MORTALITY.

54
Q

Describe the duodenal-jejunal sleeve

A

Duodenal-Jejunal Sleeve – Metabolic/Endocrinological control for diabetes and obesity.
o This results in less food digested and thus can improve glycaemic control.

55
Q

Describe the pharmacological control

A

§ Victoza – Liraglutide injection, patients with diabetes AND obesity.
o Oral GLP-1 – Oral version of liraglutide.
§ Saxenda – Liraglutide injection at a higher dose for obese patients.
§ Belviq – Lorcaserin pills, serotonin agonist that supresses appetite, results in a ~5% weight loss.
§ Qsymia – Phenteremine to supress appetite and topiramate (unknown method of action, acts as a pain killer), results in ~7-8% weight loss.
§ Contrave – Naltrexone to supress appetite, results in a ~5% weight loss, side effects on the heart and depression.

56
Q

Describe the use of sibutarmine

A

serotonin appetite system- effects on depression and hypertension

57
Q

Describe ghrelin

A

makes you hungry as you lose weight
losing weight is not easy
sees it as a state of starvation
tries to drive you back to your previous state

58
Q

Describe peptide gamma

A

Produced by colon
makes you hungry
physiologically works against you

59
Q

Describe energy intake as a cause of obesity

A

Energy Intake:

a. The energy per person of food sold has been fairly constant BUT there has been a shift in the content of the foods from carbohydrates to fats – i.e. percentage of CHO has dropped while fats has risen.
i. Autoregulation of fats in the body is bad – the body preferentially stores fat instead (unlike CHO and protein which the body has little ability to store).
ii. When we ingest fat we don’t feel as full as when we ingest CHO and protein (endocrine).
b. There has been an increase in fast food outlets.

60
Q

Describe energy usage as a cause of obesity

A

a. Reduction in energy expenditure – we now use cars, trains, laptops etc.
i. Quantified using Amish community studies

61
Q

Describe genes as a cause of obesity

A

a. While most obesity is NOT monogenic, the amount a person gains and WHERE they gain it is genetic.
i. One example of a variant gene contributing to obesity = FTO gene.
ii. Encode for hormones – e.g. Ghrelin, PYY, Leptin, Insulin.

62
Q

Which factors can lead to obesity

A 
Societal influence
Food production
Biology
Food consumption
Individual physiology 
Individual activity
Activity environment
63
Q

Describe the issue with obesity in the UK

A

At the present time obesity is fuelling much of the ill health in the UK

On a primary prevention level we have no answer to this

There is urgent need for be better treatment algorithms

Respiratory System (23 decks)

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