Exercise And Illness Flashcards

1
Q

what is the effect of illness on exercise capacity (generally)

A

illness can cause lack of sleep, cough, congestion all of which can hamper training
fever can impair body temperature regulation and increased fluid losses may occur.
inadequate nutrition whilst unwell can lead to an energy deficit.

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2
Q

what is the advice about exercise whilst unwell?

A

if a simple URTI ie cough/ common cold generally can continue
however intense training during an infectious illness can increase risk of myocarditis and heat exertional illness.

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3
Q

What is the effect if beta blockers on exercise response ?

A

They depress exercise heart rate, blood pressure and cardiac output. At submaximal exercise they impede lipolysis in adipose tissue. Non selective beta blockers decrease lipolysis in skeletal muscle, leading to less fatty acids to use as fuel. Glycogenolysis Decreases at maximal output. Plasma levels of K+ increase as reuptake into skeletal muscle is blocked. This increases fatigue.
General people taking beta blockers on a long term basis see a slower improvement in their VO2 max.
They also cause bronchoconstriction- Decreased expiratory flow rate and smaller tidal volume

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4
Q

What is the definition of pulmonary hypertension?

A

Increased pressures across the pulmonary vasculature, resting mean PAP>25mmhg.

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5
Q

How is pulmonary hypertension classified?

A

1- idiopathic, heritable, scleroderma, drug associated
2- due to any cause of elevated L atrial pressure
3- due to underlying lung disease eg COPD
4- secondary to thromboembolic disease
5- miscellaneous hematologic causes

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6
Q

How do patients with group 1 PAH present?

A

Progressive increase in exertional dyspnoea, loss of exercise tolerance, generalised fatigue, chest pain,exertional light headedness

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7
Q

What cardiovascular changes will be present for a patient with PAH on the CPET?

A

Reduction in maximal oxygen uptake proportional to disease severity
High resting heart rate and low O2 pulse
O2 pulse may fail to increase despite increasing oxygen consumption, this suggests progressive loss of right ventricular stroke volume with exercise effort

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8
Q

What Ventilatory changes might be shown on the CPET in a patient with PAH?

A

Have a Ventilatory threshold between 60% and 80%, high resting ventilation, exceptionally brisk ventilation response to exercise. This is because the diffuse pulmonary vascular damage produces small regions in the lung that are poorly perfused but well ventilated, increasing physiological dead space. Also increased pulmonary artery pressures and RV failure increases Respiratory drive
End tidal CO2 and arterial CO2 are consistently low throughout
Also exercise hypoxaemia

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9
Q

What effect does COPD have on maximal expiratory flow or FEV1?

A

It reduces, this is because as the patient breathes out the diseased Airways narrow rapidly as the pleural pressure becomes positive.

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10
Q

What limits maximal exercise in patients with severe COPD?

A

It is impaired by the ability of ventilation to keep pace with increasing CO2 production. Essentially they experience acute Respiratory failure with acidosis during any sustained maximal exercise effort.

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11
Q

What happens to tidal volume in exercising COPd patients ?

A

It is smaller relative to their FVC, if also may actually decrease at their highest tolerated level of exercise

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12
Q

What is exercise associated air trapping in COPD?

A

With exercise increase in Respiratory rate the available time for exhalation Decreases therefore the only way a copd patient can increase expiratory flow rates is to inspire to a higher volume which increases work of breathing. Essentially they cannot exhale completely back to FRC.

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13
Q

How does ventilation perfusion mismatch affect patients with COPD?

A

Parts of the lung will have saturation in the 70-75% range which brings down the overall arterial saturation to 85-90% with exercise this worsens

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14
Q

What happens to physiological dead space in COPd?

A

It increases because of the disproportionate contribution of high VA/VQ units to total ventilation.

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15
Q

How is physiological dead space represented on CPET?

A

VE/VCO2

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16
Q

How is peripheral muscle function affected in COPD?

A

They show signs of deconditioning and disuse atrophy, diminished muscle mass, reduced aerobic oxidative capacity and Decreased mitochondrial and capillary density. This can still be improved with training even in severe COPD.

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17
Q

How does COPD cause cardiovascular issues during exercise?

A

Untreated chronic hypoxia leads to pulmonary hypertension and right heart failure. With significant pulmonary hypertension, exercise causes increased RV volume which impinges on the interventricular septum which impairs LV stroke volume.
Also the development of dynamic hyperinflation during exercise will produce positive intrathoracic pressure which impairs venous return

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18
Q

What is the earliest and most characteristic exercise abnormality in a patient with ILD? What other findings suggest this?

A

Increased Ventilatory demand, demonstrated by increased VE/VCO2, however it can be highly variable so it not necessarily useful unless you have a previous value to compare it to.
Other findings include a consistently reduced ETCO2 and maximal exercise tidal volume that does not reach 60% of resting vital capacity.

19
Q

Why do ILD patients show an elevated VE/VCO2?

A
  1. They develop a compensated Respiratory alkalosis but also due to scarring they have a v/Q mismatch and elevated dead space
20
Q

What effect will iron deficiency have on exercise ?

A

Relatively early Ventilatory threshold and modest loss in maximal oxygen consumption

21
Q

What effect does anaemia have on exercise?

A

Loss of maximal oxygen uptake but it is not strictly proportional to severity of anaemia because stroke volume and circulating plasma volume increase

22
Q

What effect does subclinical hypothyroidism have on exercise ?

A

Loss of exercise tolerance
It produces a reduction in stroke volume, this can be corrected by thyroid supplementation to drop TSH levels back to normal range.

23
Q

What effect will POTS have on the CPET?

A

Failure to raise systolic blood pressure despite a maximal exercise effort. Can be confirmed with tilt table testing ,

24
Q

What happens to muscle fibres as we age ? How does this affect exercise

A

The proportion of fast twitch fibres begins to progressively decline after age 30. Therefore lactate levels and metabolic acidosis are less and type 1 fibres become the primary source of power for elderly subjects. This causes the Ventilatory threshold to come much later than in young subjects.

25
Q

How does muscle mitochondrial efficiency change with ageing ? How does this affect exercise?

A

By 60s or 70s all normal subjects will demonstrate some loss of mitochondrial efficiency. This is because hydrogen ions leak back across the mitochondrial membrane , bypassing ATP synthetase ans thereby reducing ATP production. This means that the amount of oxygen required for a given power output will be higher.
Interestingly the effect is smaller in chronically fit elderly and can be reduced in sedentary elderly if they undergo aerobic training over several months.

26
Q

How does diastolic function change as we age and how does this affect exercise ?

A

As we age we may develop impaired diastolic filling and this reduces stroke volume during exercise. This can mean that the O2 pulse will fail to increase in the latter portion of the exercise effort.
Therefore at higher exercise heart rates they will have a lower cardiac output and lower oxygen consunption

27
Q

How does vascular recruitment change as we age , how does this affect exercise ?

A

Blood flow to exercising muscles Is delayed. This is because normal vasodilation is nitric oxide dependent and this is especially reduced in sedentary elderly subjects. This causes even moderate levels of sustained exertion to be more difficult in the first few minutes. The effect of this can be reduced with training.

28
Q

How does our Respiratory system change with ageing?

A

Vital capacity and FEV1 slowly decline, with a more rapid decrease in FEV1, so FEV1/ FVC ratio will decrease. However the effect of these changes in elderly patients without lung disease does not seem to influence maximal exercise capacity because their minute ventilation is well below their MVV, also there are no age related changes in pulmonary gas exchange with ageing with those with normal lungs

29
Q

Why are beta blockers not recommended for diabetics ?

A

They block signs of hypoglycaemia

30
Q

What effect do ACE inhibitors and ARBs have on exercise ?

A

Not much at all- no reduction in VO2 max or metabolic affects

31
Q

Why do calcium channel blockers not affect skeletal muscle?

A

Skeletal muscle uses intracellular calcium stored in the sarcoplasmic reticulum whereas calcium channel blockers affect uptake of extracellular calcium.

32
Q

What effect does amlodipine have on exercise ?

A

It has little or no negative chonotropic, inotropic or dromotropic effects. There is no change in resting heart rate, blood pressure or catecholamines response during exercise, nor any change in VO2 max

33
Q

What effect do ACE inhibitors have on muscle ?

A

They may have a use in treating sarcopenia

34
Q

What effect do alpha blockers have on exercise ?

A

They decrease exercise blood pressure, they have little effect on cardiac output. There is little or no effect on VO2, lactate, duration or performance in moderate exercise

35
Q

What effect do diuretics have on exercise?

A

They decrease VO2 max, cause dehydration, potassium loss contributes to muscle fatigue and they also interfere with exercise induced hypervolaemia, which improves cardiovascular performance and thermoregulation

36
Q

How does asthma affect exercise?

A

A lower FEV1 correlates with a lower VO2 max

37
Q

How can exercise improve asthma control?

A

It increases the number or sensitivity of beta receptors in the Airways. This may improve bronchodilation but this will not significantly affect performance as exercise is not limited by ventilation in healthy individuals

38
Q

What effect do beta 2 agonists have in muscle cells?

A

They cause hypertrophy and increased responsiveness of fast twitch muscle cells.

39
Q

What effect do beta 2 agonists have in muscle cells?

A

They cause hypertrophy and increased responsiveness of fast twitch muscle cells.

40
Q

How do benzodiazepines affect exercise ?

A

They reduce peak power and blood levels of epinephrine and lactate during maximal exercise.

41
Q

What type of exercise produces the best decrease in anxiety ?

A

Low to moderate intensity resistance training.

42
Q

What effect does exercise have on the brain?

A

Increases plasma norepinephrine, elevated central serotonin, increased dopamine synthesis, increased plasma endogenous cannabinoid, acute inflammatory response leads to chronic anti inflammatory response, enhanced hippocampal neurogenesis, growth of new blood vessels in the hippocampus, cortex and cerebellum. Increased BDNF in multiple brain regions

43
Q

How does exercise improve parkinsonism, multiple sclerosis, mood disorders, PTSD, schizophrenia?

A

Physical activity enhances BDNF release and this contributed to neuroplasticity and neurogenesis. Regular exercise improves the ability to maintain, repair and reorganise circuits damaged during ageing. Other mechanisms involve reduced inflammation, reduced stress response , improved gut biome activity, improved sleep and improved antioxidant defense.