Newborns: 44 breaths per minute
Infants: 20-40 breaths per minute
Preschool children: 20-30 breaths per minute
Older children: 16-25 breaths per minute
Adults: 12-20 breaths per minute
Adults during strenuous exercise: 35-45 breaths per minute
Athletes peak: 60-70 breaths per minute
Dyspnea: Low breathing rate
Driven by contraction and relaxation of the diaphragm.
Located in the brain stem (pons and medulla oblongata).
Comprised of neurons that depolarize and send efferent impulses to the diaphragm—functions as a "pacemaker" for breathing.
Intrinsic rate and depth of breathing can be modified based on various factors.
Breathing is precisely controlled by a combination of brain activity and sensory feedback from peripheral and central sources.
Primary Goal: Ensure that tissues receive adequate oxygen to satisfy metabolic needs.
Respiratory control center located in brain stem (medulla oblongata and pons) controls the rate and depth of breathing.
Located in the medulla oblongata, respond to changes in:
PCO2
pH (H+ concentration)
Located in aortic and carotid bodies, respond to changes in blood:
PCO2
pH (H+ concentration)
[K+] (exercise only in carotid bodies)
PO2 (extreme changes only in carotid bodies)
Located in aortic arch and carotid artery, detect:
Decreases in arterial PO2 (Pao2)
Increases in arterial PCO2 (Paco2)
Decreases in blood pH (increased H+ concentration)
Send signals to the respiratory control center in the brain to increase ventilation, initiating impulses to contract the diaphragm.
Found in the brain (medulla); respond to:
Increases in CO2
Increases in H+
Important to understand effects of hyperventilation and breath-holding on these receptors.
As exercise begins, the limbic system and cerebral cortex stimulate the respiratory center.
As exercise continues, muscles produce more CO2 and H+, sensed by chemoreceptors and leading to increased ventilation.
Oxygen binding to hemoglobin (Hb) is a reversible process influenced by:
PO2 in the blood: High in arteries travelling to tissues.
Affinity between Hb and O2: Resting state involves unloading 1 molecule of O2 from 4.
Steep increase in unloading during exercise as PO2 decreases.
Rightward shift indicates increased unloading under low pH conditions.
A decreased pH lowers Hb-O2 affinity; results in a rightward shift favoring unloading of O2 to tissues.
Increased blood temperature decreases Hb-O2 affinity; contributes to rightward shift of the curve.
Acid: A molecule that releases H+ ions.
Base: A molecule that combines with H+ ions.
Blood pH decreases during heavy exercise, mainly due to lactic acid (H+) binding to Hb.
This results in a rightward shift, facilitating O2 offloading (known as the "Bohr effect").
Opposite occurs for high pH conditions, leading to a leftward shift (higher affinity).
Maintaining acid-base balance is crucial for exercise performance:
H+ can inhibit ATP production by interfering with Krebs cycle enzymes.
H+ affects muscle contraction by binding to troponin, inhibiting calcium interaction.
Acid-Base Buffer Systems:
Resist changes in pH by releasing H+ when pH is high or accepting H+ when pH is low.
Intracellular Buffers: 60% from proteins (PCr), 20-30% from bicarbonate, 10% from phosphate groups.
Extracellular Buffers: Limited blood proteins, Hemoglobin binds H+ when deoxygenated.
Ventilation removes H+ from blood via the HCO3 reaction, contributing to acid-base balance.
Use bicarbonate to buffer acid load, critical during high-intensity exercise due to limited intracellular buffering capacity.
Extracellular buffers become important when exercise exceeds 50% VO2 max.
Increased blood temperature results in a weaker bond between Hb and O2, leading to a rightward shift in the curve, facilitating O2 unloading at tissues.
Demonstrates the relationship between hemoglobin saturation (y-axis) and the partial pressure of oxygen (x-axis).
The curve levels off as hemoglobin fills its maximum capacity of four oxygen molecules.
High intensity increases CO2 and lactic acid (producing H+) and causes pH drop.
During incremental exercise, expire ventilation (VE) increases linearly up to ~50-75% VO2max.
The ventilatory threshold is where VE increases exponentially due to H+ accumulation from lactate.
Respiratory centers located in the medulla and pons involuntarily control respiration by generating a rhythmic pattern of inspiration and expiration.
Input from higher brain centers and peripheral signals modifies this pattern.
Central chemoreceptors in the medulla (especially sensitive to acidity) and peripheral chemoreceptors in aortic and carotid bodies (sensitive to pH and PCO2, with carotid also sensitive to PO2).
Training does not change lung structure, but increases aerobic capacity, reducing lactic acid (H+) production and leading to lower ventilation during exercise.
Exercise ventilation is 20–30% lower at the same submaximal work rate post-training.
Graphical representation shows reduced ventilation (liters/min) at the same absolute work rate following training, highlighting the efficiency gained through training.