Exercise And Illness Flashcards
(43 cards)
what is the effect of illness on exercise capacity (generally)
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.
what is the advice about exercise whilst unwell?
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.
What is the effect if beta blockers on exercise response ?
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
What is the definition of pulmonary hypertension?
Increased pressures across the pulmonary vasculature, resting mean PAP>25mmhg.
How is pulmonary hypertension classified?
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
How do patients with group 1 PAH present?
Progressive increase in exertional dyspnoea, loss of exercise tolerance, generalised fatigue, chest pain,exertional light headedness
What cardiovascular changes will be present for a patient with PAH on the CPET?
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
What Ventilatory changes might be shown on the CPET in a patient with PAH?
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
What effect does COPD have on maximal expiratory flow or FEV1?
It reduces, this is because as the patient breathes out the diseased Airways narrow rapidly as the pleural pressure becomes positive.
What limits maximal exercise in patients with severe COPD?
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.
What happens to tidal volume in exercising COPd patients ?
It is smaller relative to their FVC, if also may actually decrease at their highest tolerated level of exercise
What is exercise associated air trapping in COPD?
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.
How does ventilation perfusion mismatch affect patients with COPD?
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
What happens to physiological dead space in COPd?
It increases because of the disproportionate contribution of high VA/VQ units to total ventilation.
How is physiological dead space represented on CPET?
VE/VCO2
How is peripheral muscle function affected in COPD?
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.
How does COPD cause cardiovascular issues during exercise?
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
What is the earliest and most characteristic exercise abnormality in a patient with ILD? What other findings suggest this?
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.
Why do ILD patients show an elevated VE/VCO2?
- They develop a compensated Respiratory alkalosis but also due to scarring they have a v/Q mismatch and elevated dead space
What effect will iron deficiency have on exercise ?
Relatively early Ventilatory threshold and modest loss in maximal oxygen consumption
What effect does anaemia have on exercise?
Loss of maximal oxygen uptake but it is not strictly proportional to severity of anaemia because stroke volume and circulating plasma volume increase
What effect does subclinical hypothyroidism have on exercise ?
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.
What effect will POTS have on the CPET?
Failure to raise systolic blood pressure despite a maximal exercise effort. Can be confirmed with tilt table testing ,
What happens to muscle fibres as we age ? How does this affect exercise
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.
