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respiratory muscles are the effectors of ventilation. It is important to remember that respiratory muscles are skeletal striated.
voluntary muscle controlled by alpha motorneurons.
Inspiration is initiated by a burst of action potentials in the spinal motor nerves.
The control of ventilation affects:
• The frequency of respiration
• The volume of each breath (depth of breath)
1) Voluntary control: This type of control is mediated by our will and arises from the cortex. The cortex sends fibers along the corticospinal tract.
2) Emotional control: This type of control is mediated by the limbic lobe.
3) Autonomic control: arises from pacemaker cells located in the medulla oblongata.
Pacemaker cells then synapse on lower motorneurons:
◦ Cervical spinal cord levels affecting the diaphragm via phrenic nerves
◦ Thoracic spinal cord levels affecting the diaphragm via intercostal nerves.
4) metabolic control : mediated by a complex reflex; to maintain homeostasis.
- receptors, afferent pathways, integrative centers, efferent pathways and finally the effectors, the muscle of respiration. The integrative centers of this complex reflex arc are the respiratory centers located in the medulla oblongata and in the pons.
- peripheral chemo receptors; carotid body, aortic body, located outside of wall, thorugh small arteries, control respiration
!!!! baroreceptors - in the wall, mechanoreceptor, control cardiovascular
The peripheral chemoreceptors, located high in the
neck at the bifurcation of the common carotid arteries and in the thorax on the arch of the aorta.
There they provide excitatory synaptic input to the medullary inspiratory neurons. The carotid body input is the predominant peripheral chemoreceptor involved in the control of respiration.
- central chemoreceptor
neurons sensitive to H+ in CSF (depends on CO2 in blood). The central chemoreceptors are located in the medulla and, like the peripheral chemoreceptors, provide excitatory synaptic input to the medullary inspiratory neurons. They are stimulated by an increase in the H+ concentration of the brain's extracellular fluid. As we will see later, such changes result mainly from changes in blood PCO2.
Inputs from both the peripheral and central chemoreceptors stimulate the medullary inspiratory neurons to increase ventilation. The end result is a return of arterial and brain extracellular fluid PCO2 and H+ concentration toward normal. Of the two sets of receptors involved in this reflex response to elevated PCO2 , the central chemoreceptors are the more important, accounting for about 70% of the increased ventilation.
5) Drug control : that can act on medullary inspiratory neurons. these centers are very sensitive to drugs effects
6) Pulmonary stretch receptors(mechanoreceptors) control
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When the pulmonary stretch receptors are activated by an increase in respiratory volumes, inspiratory centers in the medulla are inhibited; this phenomenon is known as Herin-Breuer reflex It would seem logical that, as the exercising muscles produce more carbon dioxide, blood PCO2 would increase. This is true,however, only for systemic venous blood but not for systemic arterial blood. Why is it that arterial PCO2 does not increase
during exercise? Recall two facts from the section on alveolar gas pressures: (1) Arterial PCO2 is determined by alveolar PCO2 , and (2) alveolar PCO2 is determined by the ratio of carbon dioxide production to alveolar ventilation. <<During moderate exercise, the alveolar ventilation increases in exact proportion to the increased carbon dioxide production>>, so alveolar and therefore arterial PCO2 do not change. In fact, in very strenuous
exercise, the alveolar ventilation increases relatively more than carbon dioxide production. In other words, during strenuous exercise, a person may hyperventilate; thus, alveolar and systemic arterial PCO2 may actually decrease. 1.work load up - O2 consumption up - ventilation up
*Over the maximal work load, the work load
can increase with no increase in oxygen
consumption, because of lactate.
Lactate is comes from anaerobic metabolism and
is responsible for the oxygen debt.
2. ventilation and moderate exercise [6.3 note 10p graph]
at start of exercise, a sudden increase of ventilation by proprioceptor and phychological factors -> and then ventilation gradually increases (this mechanism is unclear, cannot explain because there is no changes of pCO2, pO2 and pH2 during moderate exercise. During moderate exercise, the alveolar ventilation increases in exact proportion to the increased carbon dioxide production, so alveolar and therefore arterial PCO2 do not change)
Several hypothesis could explain this increase in ventilation such as:
• Proprioceptors and stretch receptors in muscles of respiration and lungs
• Increase in body temperature
• Inputs from motor pathways to
respiratory neurons or reflexes
• Increase in plasma potassium coming
from muscles
• Increase in plasma epinephrine.
• Reflexes conditioned
3.After strenuous exercise, there is an increased rate of oxygen intake(excess post-exercise oxygen consumption) to repay oxygen debt.
- increased H+ keeps ventilation higher till all the
oxygen debt is repaid
Some factors that contribute to EPOC include the replenishment of Phosphocreatine and ATP, the conversion of lactate to pyruvate, and the re-synthesis of glycogen.
4. The maximum rate at which O2 is transported to the mitochondria(O2 uptake limit in exercising muscle) is not depends on saturation of Hb(it's always 100%) or O2 uptake in lungs; it depends on
1) 3 fold increase in O2 extraction from a unit of blood
◦ Muscles use more O2 and consume more CO2, causing a change in partial pressure
◦ More gases diffuse from and to the blood.
◦ more O2 is removed from Hb
◦ Dilation of capillaries and vasodilation.
2) 30 fold increase in blood flow
3) 100 fold increase in metabolic rate in muscle
during strenuous exercise