Respiratory #10- Flashcards
What defines the capacity of performance of an individual?
It max O2 consumption (VO2 max in ml/kg/min)
- Higher in male than female
- Peaks ~ 20
How does PCO2, pH, minute ventilation change with ramping exercise?
- Decline in pH and in bicarbonate (production of lactic acid by anaerobic metabolism → consumes bicarbonate → reduction of bicarbonate)
- Increase in minute ventilation
- Increase in VCO2 (metabolic production of CO2) follow closely increase in ventilation → expiratory CO2 stays stable
*Both increase exponentially after flexion point - Expired CO2 goes down at peak intensity
- VO2 increases linearly → at peak exercise, starts to plateau off
*Chemoreceptors don’t really explain the matching of ventilation to exercise (because no increase in CO2)
What are the relationships between HR and VO2 and between Minute ventilation and VO2?
(VO2 = oxygen consumption)
HR and VO2 → linearly relationship
VE and VO2 → curvilinear relationship
What systems mostly limit trained vs untrained individuals?
Trained → Respiratory system (Cardio system it trained/pushed)
Untrained → Cardiovascular system
*A lot of increase in CO is from HR, more than SV
How is oxygen carrying capacity increased during exercise?
- Increasing cardiac output:
- Large increase in HR
- Tiny increase SV at the start of exercise
- Decrease in vascular resistance → increase blood flow
- Decrease in vascular compliance
*Recruitement of vessels + distention to accomodate larger volumes - More extraction of oxygen from the blood:
- Bigger difference between arterial and venous PO2 → gradient increases linearly
How does the respiratory system increase tidal volume during exercise?
Why does it do so?
Inspire more + Expire below FRC
*If kept same FRC and just inspired more → would require more muscle recruitement → more work to breathe (optimization)
What determines the anaerobic threshold?
Point where ventilation increases exp (not linearly anymore)
Anaerobic system is already working before that threshold, but point at which is produces lactate and reduces bicarbonate faster than can get rid of it
How does relative dead space change with increasing exercise?
Deadspace : tidal volume ration decreases as tidal volume increases
*Decreases very fast at first and then plateaus
VCO2 produced increases, but expired CO2 in each expiration does the increase because of the increase in minute ventilation
During exercise, how does the affinity of Hb for oxygen change?
Bohr → decrease in pH
Haldane → Decrease in arterial PCO2
Change in temperature → decrease in affinity for O2 with increased temperature (~40˚C) right shift
How does the increase in VCO2 affect the frequency of breathing and tidal volume?
With increase in VCO2, 1st increase in Tidal volume, when VT plateaus → bigger increase in frequency of breathing
*Not always, but in majority of subjects
*For flow-volume curve, at high exerices → approach max flow-volume curve on expiration
Even if try harder, can’t expire faster
How is the V/Q ration affected by increasing exercise?
What does it explain?
Ventilation increase much more than flow
A bit of increase V/Q ratio → reduction in PCO2 at peak exercise
Why do some athletes have mild arterial hypoxemia?
Female athletes are more likely
Corresponds to major dip in PaO2 → SaO2 (when get past the flat part of Hb saturation)
Alvealor → arterial oxygen gradient: increases a lot more in hypoxemic athletes = inefficiency of ventilation
Factors that can lead to that → decrease in pH, increase in body temperature → reduction affinity of Hb going through peripheral circulation will bring down oxygenation + shunts → bigger A → a oxygen gradient
*Supplemental Oxygen → better performance pretty systematically →respiratory system IS contributing to exercise limitation
What are some adverse respiratory consequences of high intensity exercise?
- Slight widening of the Alveolar → arterial O2 gradient (A-a Do2)
- Reduced oxygen saturation caused by fall in pH and increase in core temperature (also somtimes increase inlung water)
- Increased work of breathing and blood flow to the respiratory muscles
What is the difference in O2 uptake for sendentary vs highly trained athletes?
Highly trained athlete = more efficient taking up O2 for same
Need to ventilate less for the same O2 uptake, at the cost of having a higher PaCO2
Ve matched to CO2 production → if permit arterial CO2 to be higher, can have lower ventilation
How important is the oxygen cost of breathing during exercise vs at rest?
What changes for people with emphysema?
Increase because more respiratory muscles are recruited:
At rest → 2ml/min
During exercise → 100ml/min → 8-10% of the maximal O2 consumption (larger mass of muscle recruited)
*Exponential increase → Could be a limiting factor?
With emphysema (obstructive lung disease) → O2 consumption by the respiratory muscles increases much more with smaller increase in ventilation
How can inspiratory muscle Oxygen cost be assessed experimentally?
What was observed?
By reducing the inspiratory muscle work at > 85% VO2 max:
Individuals put on mechanical ventilator → proportional assist of ventilation → Pleural pressure (esophageal) becomes much less negative when insp. muscles are unloaded + Transdiaphragmatic pressure becomes much less positive
- Prevents exercise-induced diaphragm fatigue (loss of capacity of diaphragm to generate force after hard exercise is improved)
- Decrease sympathetic tone, increase vascular conductance, increase blood flow to locomotor muscles
- Decrease in locomotor muscle fatigue
- Less short of breathe, less limb discomfort
- Can las longer at peak exercise
- Less blood flow to accessory respiratory muscles
What characteristics of the diaphragm favour increase performance?
- Doesn’t show evidence of diaphragm fatigue generally (very resistant to fatigue)
- Diaphragm has greater mitochondrial volume, capillary density, aerobic capacity than locomotor muscles
- Vasculatur is protected agains vasoconstriction during exercise
- Extensive recruitement of “accessory” muscles distributes work of breathing
What is the respiratory muscle metaboreflex
Metabolites that accumulate in respiratory muscles → afferent signal to CNS → reduce blood flow in active blood flow → limits exercise performance
*Feedback that prevents exercise from excessive fatigue/dammage
