Respiratory Physiology
475
arterial H
+
concentration (see Figure 13–41), due to the gen-
eration and release of lactic acid into the blood. This change
in H
+
concentration is responsible, in part, for stimulating the
hyperventilation accompanying strenuous exercise.
Other Factors
A variety of other factors play some role in stimulating ven-
tilation during exercise. These include (1) refl ex input from
mechanoreceptors in joints and muscles; (2) an increase in body
temperature; (3) inputs to the respiratory neurons via branches
from axons descending from the brain to motor neurons sup-
plying the exercising muscles; (4) an increase in the plasma epi-
nephrine concentration; (5) an increase in the plasma potassium
concentration due to movement of potassium out of the exercis-
ing muscles; and (6) a conditioned (learned) response mediated
by neural input to the respiratory centers. The operation of this
last factor can be seen in
Figure 13–42
. There is an abrupt
increase—within seconds—in ventilation at the onset of exer-
cise and an equally abrupt decrease at the end; these changes
occur too rapidly to be explained by alteration of chemical con-
stituents of the blood or by altered body temperature.
Figure 13–43
summarizes various factors that infl u-
ence ventilation during exercise. The possibility that oscilla-
tory changes in arterial
P
O
2
,
P
CO
2
, or H
+
concentration occur,
despite unchanged average levels of these variables, and play
some role has been proposed, but this remains unproven.
Other Ventilatory Responses
Protective Refl
exes
A group of responses protect the respiratory system from irri-
tant materials. Most familiar are the cough and the sneeze
refl exes, which originate in receptors located between airway
epithelial cells. The receptors for the sneeze refl ex are in the
nose or pharynx, and those for cough are in the larynx, tra-
chea, and bronchi. When the receptors initiating a cough are
stimulated, the medullary respiratory neurons refl exly cause a
deep inspiration and a violent expiration. In this manner, par-
ticles and secretions are moved from smaller to larger airways,
and aspiration of materials into the lungs is also prevented.
100
80
60
40
20
0
110
100
90
40
30
60
36
48
Minute
ventilation
(L/min)
Arterial
P
O
2
(mmHg)
Arterial
P
CO
2
(mmHg)
Rest
Maximal
exercise
O
2
consumption (ml/min)
Arterial [H
+
]
(nmol/L)
Figure 13–41
The effect of exercise on ventilation, arterial gas pressures, and
hydrogen ion concentration. All these variables remain constant during
moderate exercise; any change occurs only during strenuous exercise,
when the person is actually hyperventilating (decrease in
P
CO
2
).
Adapted from Comroe.
Minute ventilation (L/min)
Rest
Exercise
Recovery
(1)
(2)
Time
Figure 13–42
Ventilation changes during exercise. Note (1) the abrupt increase at
the onset of exercise and (2) the equally abrupt but larger decrease
at the end of exercise.
Figure 13–43
Summary of factors that stimulate ventilation during exercise.
Note: ? indicates a theoretical input.
Figure 13–43
physiological
inquiry
The existence of chemoreceptors in the pulmonary artery has been
suggested. Hypothesize a function for peripheral chemoreceptors
located on and sensing the
P
O
2
and
P
CO
2
of the blood in the
pulmonary artery.
Answer can be found at end of chapter.
Respiratory center
? Oscillatory changes
in arterial
P
O
2
,
P
CO
2
, [H
+
]
Via chemoreceptors
Conditioned response
Temperature
Joints
Skeletal
muscle
Plasma epinephrine
and
potassium concentrations
Motor cortex
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