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O2 Requirement Of Breathing
small at rest and during light-to-moderate exercise
up to 100 L/min
O2 Cost
1.5 mL/L of air breathed each minute
O2 Represents A
small portion of VO2 at rest and low-to-moderate exercise intensities
O2 Can Increase
substantially at max exercise
During Exercise an Increased VO2 Means
more oxygen travels from your lungs to your muscles
During Exercise an Increased VCO2 Means
more CO2 travels from your muscles to lungs to be breathed out
Ventilations Increase Mainly Through
increase in tidal volume
Pulmonary Ventilation is Precisely Regulated At
both rest and during exercise
Clusters of Neurons in the Medulla Oblongota Act As
a “pacemaker”
Change in Ventilation is Determined By
exercise intensity
Control of Ventialtion at Rest
inspiration is active process (expiration is passive)
respiratory muscles controlled by somatic MNs and SC
Activity of MNs Is Controlled By
respiratory control centers (in medulla oblongata)
Respiratory Control Center is Located in
brain stem within 2 distinct areas
medulla oblongota and pons
RCC Controls The
rhythm and rate of beathing
3 Distinct Rhythm Centres
PreBotZ - inspiration
RTN/pFRG - expiration
Pontine respiratory center - rate and pattern
Normal Rhythm is Due to
interaction between clusters of the MNs
both +ve and -ve feedback to tightly regulate breathing
At Rest preBotzinger Interacts With
other centres to regulate
RCC Receives Input From
higher brain centers and periphery
Neural Input - Higher Brain Centres and Afferent Pathways
motor cortex can alter breathing in proportion to the amount of exercise
afferent input from muscle spindles, GTOs, joint pressure receptors
Neural Input is Important to Regulating Breathing During
submaximal, steady-state exercise
Humoral Input
chemoreceptors detecting blood
Chemoreceptors
specialized neurons detecting changes in internal environment
Humoral Input - Central
loacted in the medulla
PCO2 and H+ concentrations in CSF
Humoral Input - Peripheral
located in aortic arch and carotid artery
PO2, PCO2, H+ and K+ in blood
At Rest Greatest Respiratory Stimulus Is
PCO2 in arterial pressure
small ↑ in PCO2 in inspired air trigger large ↑ in VE
1 mmHg ↑ in PCO2 ↑ VE in 2 L/min
Blood pH Affects VE
acidosis reflects CO2 retention
breathing must ↑ to remove CO2
At Sea Level, Changes in PO2 Have
a small affect on ventilation
Environmental Changes Can
decrease PO2 and stimulate peripheral chemoreceptors
Carotid Bodies Monitor
arterial blood as it perfuses the brain
protection agaisnt decrease PO2 in inspired air
Plasma PO2 and VE Stimulate Ventilation During Exercise Due to
increase temperature
increase acidity
CO2 and K+
Central Chemoreceptors
stimulus: PCO2 ↑
↑ VE
Peripheral Chemoreceptors - Carotid Body
stimulus: PCO2 ↑, pH and PO2 ↓
↑ VE
Peripheral Chemoreceptors - Aortic Body
stimulus: PCO2 ↑, pH ↓
↑ VE
Muscle Mechanoreceptors
stimulus: muscle activity
↑ VE
Muscle Chemoreceptors
stimulus: pH ↓, K+ ↑
↑ VE
Regulation of VE During Exercise: Cortical Influence
anticipation of exercise stimulate respiratory neurons in the medulla to initiate the abrupt increase in exercise VE
Regulation of VE During Exercise: Peripheral Influence
sensory input from joints, tendons, and muscles influence bentilatory adjustments during exericse
Ventilatory Control During Submaximal Exercise
primary drive: higher brain denters
fine tuned by: humoral chemoreceptors and neural feedback
Ventilatory Control During Heavy Exercise
a linear rise in VE
increase blood H+ stimulates carotid bodies
K+, body temp, and catecolamines play a role
Control of Ventilation - How it Works Together
you start exercising
higher brain centers signal increased breathing, while receptors and chemoreceptors provide feedback
respiratory control center (medulla oblongata) receives these signals
respiratory muscles increase breathing rate and depth
ventilation increase to bring in more O2 and remove more CO2
Phase I of VE in Exercise and Recovery
neurogenic stimuli from the cerebral cortex and feedback from the active limbs stimulate the medulla to increase VE abruptly
neural control
Phase II of VE in exercise and recovery
after a short plateau minute ventilation rises expontentially to achieve a steady level related to metabolic gas exchange demands
humoral control
Phase III of VE in exercise and recovery
fine-tuning of the steady-state ventilation through peripheral sensory feedback mechanisms
sensory control
Effect of Training on Ventilation
no effect on lung structure and function at rest
normal lung exceeds demand for gas exchange - adaption no required
Effect of Training on VE - Elite Endurance Athletes
failure of lung to adapt to TR results in hypoxemia
Does the Pulmonary System Limit Exercise Performance - Low-to-Moderate Intensity
pulmonary system not seen as a limitation
Does the Pulmonary System Limit Exercise Performance - Maximal Exercise
respiratory muscle fatigue does occur during high intensity exercise
may be limiting in elite endurance athletes (40-50% experience hypoxemia)
Maximum Voluntary Ventilation
evaluates ventilatory capacity
rapid and deep breathing for 15 seconds
extrapolated to volume if subject continued for 1 min
25% > VE in Maximal Exercise
exercise does not maximally stress healthy person
140 to 180 L/min in college aged men
80 to 120 L/min healthy, college-aged women
Training Ventilatory Muscles Increases
ST
endurance
inspiratory muscle function
MVV