ig 10.20
m During prolonged
submaximal
exercise:
entilation tends
to drift upward
Little change in
PCO2
Higher ventilation
not due to
increased PCO2
ig 10.21
m Linear increase in ventilation
0p to ~50-75% O2max
m Exponential increase beyond this point
m entilatory threshold (·vent)
3nflection point where E increases
exponentially
m 3n the trained runner
Decrease in arterial PO2 near exhaustion
pH maintained at a higher work rate
·vent occurs at a higher work rate
ig 10.22
ig 10.22
m 1980·s: 40-50% of elite male endurance
athletes were capable of developing
m 1990·s: 25-51% of elite female endurance
athletes were also capable of
developing
m Causes:
entilation-perfusion mismatch
Diffusion limitations due to reduce time of
R½C in pulmonary capillaries due to high
cardiac outputs
m Respiratory
control center
Receives neural
and humoral input
M eedback from
muscles
M CO2 level in the
blood
Regulates
respiratory rate
ig 10.23
m Humoral chemoreceptors
Central chemoreceptors
M Located in the medulla
M PCO2 and H+ concentration in cerebrospinal
fluid
Peripheral chemoreceptors
M ortic and carotid bodies
M PO2, PCO2, H+, and K+ in blood
m Neural input
rom motor cortex or skeletal muscle
ig 10.24
ig 10.25
m rubmaximal exercise
Linear increase due to:
M Central command
M Humoral chemoreceptors
M Neural feedback
m Heavy exercise
Exponential rise above ·vent
M 3ncreasing blood H+
ig 10.26
m entilation is lower at same work rate
following training
Day be due to lower blood lactic acid levels
Results in less feedback to stimulate
breathing
ig 10.27
m Low-to-moderate intensity exercise
Pulmonary system not seen as a limitation
m Daximal exercise
Not thought to be a limitation in healthy
individuals at sea level
Day be limiting in elite endurance athletes
New evidence that respiratory muscle
fatigue does occur during high intensity
exercise