838
UNIT 4
Maintenance of the Body
22
Pulmonary Irritant Reflexes
Te lungs contain receptors that respond to an enormous variety
of irritants. When activated, these receptors communicate with
the respiratory centers via vagal nerve afferents. Accumulated
mucus, inhaled debris such as dust, or noxious fumes stimulate
receptors in the bronchioles that promote reflex constriction of
those air passages. Te same irritants stimulate a cough in the
trachea or bronchi, and stimulate a sneeze in the nasal cavity.
The Inflation Reflex
Te visceral pleurae and conducting passages in the lungs con-
tain numerous stretch receptors that are vigorously stimulated
when the lungs are inflated. Tese receptors signal the medul-
lary respiratory centers via afferent fibers of the vagus nerves,
sending inhibitory impulses that end inspiration and allow ex-
piration to occur.
As the lungs recoil, the stretch receptors become quiet,
and inspiration is initiated once again. Tis reflex, called the
inflation reflex
, or
Hering-Breuer reflex
(her
9
ing broy
9
er), is
thought to be more a protective response (to prevent the lungs
from being stretched excessively) than a normal regulatory
mechanism.
Check Your Understanding
19.
Which brain stem respiratory area is thought to generate the
respiratory rhythm?
20.
Which chemical factor in blood normally provides the most
powerful stimulus to breathe? Which chemoreceptors are
most important for this response?
For answers, see Appendix H.
Respiratory Adjustments
Compare and contrast the hyperpnea of exercise with
hyperventilation.
Describe the process and effects of acclimatization to high
altitude.
Exercise
Respiratory adjustments during exercise are geared both to in-
tensity and duration of the exercise. Working muscles consume
tremendous amounts of O
2
and produce large amounts of CO
2
,
so ventilation can increase 10- to 20-fold during vigorous ex-
ercise. Increased ventilation in response to metabolic needs is
called
hyperpnea
(hi
0
perp-ne
9
ah).
How does hyperpnea differ from hyperventilation? Te res-
piratory changes in hyperpnea do not alter blood O
2
and CO
2
levels significantly. By contrast, hyperventilation is excessive
ventilation, and is characterized by low P
CO
2
and alkalosis.
Exercise-enhanced ventilation does
not
appear to be
prompted by rising P
CO
2
and declining P
O
2
and pH in the blood
for two reasons. First, ventilation increases abruptly as exercise
begins, followed by a gradual increase, and then a steady state
of ventilation. When exercise stops, there is an initial small but
abrupt decline in ventilation rate, followed by a gradual decrease
to the pre-exercise value. Second, although venous levels change,
arterial P
CO
2
and P
O
2
levels remain surprisingly constant during
exercise. In fact, P
CO
2
may fall below normal and P
O
2
may rise
slightly because the respiratory adjustments are so efficient.
Our present understanding of the mechanisms that produce
these observations is sketchy, but the most accepted explanation
is as follows.
Te abrupt increase in ventilation that occurs as exercise be-
gins reflects interaction of three neural factors:
1.
Psychological stimuli (our conscious anticipation of
exercise)
2.
Simultaneous cortical motor activation of skeletal muscles
and respiratory centers
3.
Excitatory impulses reaching respiratory centers from
proprioceptors in moving muscles, tendons, and joints
Te subsequent gradual increase and then plateauing of res-
piration probably reflect the rate of CO
2
delivery to the lungs
(the “CO
2
flow”). Te small but abrupt decrease in ventilation
that occurs as exercise ends reflects the three neural factors
listed above being shut off. Te subsequent gradual decline to
baseline ventilation likely reflects a gradual decline in CO
2
flow
a±er exercise ends.
Te rise in lactic acid levels during exercise results from
anaerobic respiration. However, it is
not
a result of inadequate
respiratory function, because alveolar ventilation and pulmo-
nary perfusion are as well matched during exercise as during
rest (hemoglobin remains fully saturated). Rather, it reflects
cardiac output limitations or inability of the skeletal muscles to
further increase their oxygen consumption.
In light of this fact, the practice of inhaling pure O
2
by
mask, used by some football players to replenish their “oxygen-
starved” bodies as quickly as possible, is useless. Te panting
athlete
does
need more oxygen, but inspiring extra oxygen will
not help, because the shortage is in the muscles—not the lungs.
High Altitude
Most people live between sea level and an altitude of approxi-
mately 2400 m (8000 feet). In this range, differences in atmo-
spheric pressure are not great enough to cause healthy people
any problems when they spend brief periods in the higher-
altitude areas.
However, if you travel quickly from sea level to elevations
above 8000 ±, where atmospheric pressure and P
O
2
are lower,
your body responds with symptoms of
acute mountain sick-
ness
(
AMS
)—headaches, shortness of breath, nausea, and diz-
ziness. AMS is common in travelers to ski resorts such as Vail,
Colorado (8120 ±), and Brian Head, Utah (a heart-pounding
9600 ±). In severe cases of AMS, lethal pulmonary and cerebral
edema may occur.
When you move on a
long-term
basis from sea level to the
mountains, your body makes respiratory and hematopoietic
adjustments via an adaptive response called
acclimatization
.
As we have already explained, decreases in arterial P
O
2
cause
the peripheral chemoreceptors to become more responsive
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