Jackson 4 Flashcards
Rhythmical breathing is controlled by
skeletal muscles
inspiration requires action potentials in
motor neurons
expiration due to cessation of
motor neuron activity and lung recoil
rhythmic contraction controlled by
pacemaker neurons
Role of medulla oblongata and pacemaker cells
Activity of pacemaker neurons can be modulated by…
activity of pulmonary stretch receptors
drugs, e.g. barbiturates and opiates/morphine
partial pressures of respiratory gases and [H+]
↓ PO2 —->
↑ ventilation rate
↑ PCO2 or [H+] –>
↑ ventilation rate
regulation of ventilation rate by respiratory gases and [H+] involves
chemoreceptors in two locations
peripheral chemoreceptors are stimulated by
↑ [H+] or ↓ PO2
central chemoreceptors are stimulated by
↑ [H+] in extracellular fluid in brain
Ventilation rate can be modulated by
peripheral chemoreceptors responding to a change in PO2
ventilation rate increases below PO2 of about
60 mm Hg
note that at PO2 = 60, Hb is ———-, so ventilation rate begins to increase before blood is depleted of O2
90% saturated
Ventilation also can be modulated by
peripheral & central chemoreceptors responding to a change in PCO2 and [H+]
ventilation rate is much more sensitive to
PCO2 than to PO2
rate increases above PCO2 of about
40 mm Hg
central chemoreceptor response to decrease in brain pH is
primary regulator
CO2 poisoning symptoms depend on ———- – can lead to death
level of toxicity
Ventilation rate can be modified by
non-respiratory sources of H+
metabolic acidosis, e.g.
excess lactic acid
metabolic alkalosis, e.g.
severe vomiting
Note that anemia does not
change ventilation
, carbon monoxide poisoning does not
change ventilation
During exercise, alveolar ventilation can increase
20 fold, but mechanism underlying the increase is not completely understood.
arterial PCO2 ————- until exercise becomes strenuous; venous PCO2 ———-
typically unchanged
increases but no change in arterial values
ventilation increases in exact proportion to
CO2 production and with severe exercise, arterial PCO2 actually decreases due to hyperventilation
decreased PO2?
as with CO2, venous O2 decreases, but not arterial
increase in ventilation is proportional to O2 use
increased H+?
requires
intense exercise for this to be a factor due to lactic acid accumulation
Conclusion: multiple factors provide input to the respiratory center and contribute to increasing ventilation during exercise
Hypoxia =
a deficiency of O2 at the level of the tissues
old school - RBC packing or use
recombinant human EPO
modern option – use gene therapy to increase
endogenous EPO
Can also train at high altitude to stimulate
EPO production in response to low arterial PO2.
high altitude training effect: can be accomplished at sea level by
sleeping in a hypobaric atmosphere
training at low / normal altitude conditions body to utilize
increased O2 availability
Physiological principles in sports
How can physiological principles be applied to increase the
O2 carrying capacity of the blood in order to enhance athletic performance?
hypoxic hypoxia or hypoxemia -
decreased arterial PO2
anemic hypoxia –
normal arterial PO2; decreased hemoglobin and O2 content of blood
ischemic hypoxia–
blood flow to tissues is too low
histotoxic hypoxia -
cells unable to utilize O2
Hypoxic hypoxia can be caused by a number of conditions
hypoventilation –
diffusion impairment –
vascular shunt
ventilation-perfusion inequality
hypoventilation
increases arterial PCO2
diffusion impairment – thickened alveoli-blood interface
vascular shunt – blood bypasses alveoli
ventilation-perfusion inequality – can occur as a consequence of COPD
diffusion impairment –
thickened alveoli-blood interface
vascular shunt –
blood bypasses alveoli
ventilation-perfusion inequality –
can occur as a consequence of COPD
Because Patm decreases as altitude increases, PO2
also decreases (even though O2 still 21%)
Immediate responses T
stimulate ventilation –
increased dependence on anaerobic glycolysis –
Acclimatization to high altitude depends on delayed responses that take days or weeks
increased erythropoiesis which results in polycytothemia; stimulated by erythropoietin (EPO), a hormone from the kidney
increased 2,3 DPG synthesis which will shift the Hb-O2 curve to the right
increased synthesis of other components of O2 delivery and consumption
also change:
capillary density –
mitochondria –
myoglobin -
