Module 3 focuses on the respiratory system's adaptation to exercise and stressors.
Exercise training and athlete studies are used to understand respiratory function improvements.
A large study compared 493 elite athletes to 16 sedentary individuals.
The athletes were from 15 different sports.
Athletes showed higher vital capacities, forced vital capacities, and forced expiratory volume in one second (FEV1).
Improvements were observed in basketball, water polo, and rowing athletes.
Cross-sectional data highlights that stature influences lung function.
Lung volumes correlate with body size.
Lung volumes and capacities are generally not significantly affected by exercise training.
Genetics primarily determine lung volumes.
No relationship exists between fitness and lung capacity (FVC) in healthy, untrained individuals.
Maximal voluntary ventilation (MVV) tends to be larger in athletes with exercise training, irrespective of exercise type.
Continued exercise into older age blunts the natural decrement of increased residual lung volumes.
Residual lung volume temporarily increases after acute exercise due to peripheral airway closure and increased thoracic blood volumes.
Hormesis: "What doesn't kill you makes you stronger."
Temporary increases in residual lung volume with exercise, but overall beneficial with age.
No significant relationship between aerobic fitness and lung function if values are within a normal range.
Groups should be matched for body size in studies.
Athletes come in diverse body types.
Boyle's Law: Inverse relationship between volume and pressure.
As volume increases, pressure decreases, and vice versa.
P1V1 = P2V2
Air moves in and out of the lungs due to pressure differentials induced by volume changes.
Ventilation is influenced by lung properties: compliance, elasticity, and surface tension.
Pulmonary ventilation is driven passively by changes in volume.
Inhalation: Alveolar pressure is lower than atmospheric pressure.
Exhalation: Alveolar pressure is higher than atmospheric pressure.
Lung compliance: The ease at which a lung can expand under pressure.
Lung compliance = change in lung volume / change in transpulmonary pressure.
Reduced by resistance to distension (stretch).
Pulmonary Fibrosis: Lung tissues infiltrated with connective tissue proteins causing scarring and stiffness, reducing lung compliance.
Increased mechanical work required to breathe.
Caused by autoimmune diseases, infections, toxins, radiation, or chemotherapy.
Managed with medication and exercise rehabilitation; scarring is irreversible.
Lungs have high elastin concentration for elasticity.
Lungs are always in a state of elastic tension, increasing with inspiration.
Elastic Recoil: Lungs springing back during expiration.
Pneumothorax: Air enters the interpleural space, equalizing pressure, causing lung collapse.
Air enters into in interpleural space, due to open chest wound. Lungs can no longer expand and start collapsing from chest wall because of elastic recoil. Can be a life threatening situation.
Fluid inside alveoli creates surface tension.
Forces resist distension, including surface tension exerted by fluid in alveoli.
Lungs secrete and absorb fluid to maintain a minimal layer on the alveolar surface, driven by osmosis and transport of sodium and chloride.
Water molecules stick together, increasing surface tension.
Water molecules pull together, creating an inward force and increasing alveolar pressures.
Law of Laplace
P = arc{2T}{r}
Pressure is directly proportional to the radius.
Surfactant reduces surface tension, preventing alveolar collapse.
Impact of surfactant molecules is higher as alveoli get smaller.
Cystic Fibrosis: Genetic disorder where malfunctioning chloride carriers result in imbalance and fluid absorption/secretion.
Airways fill with viscous mucus, difficult to clear.
Alveolar surfactant composition changes with exercise, related to cardiorespiratory fitness.
Higher fitness leads to higher changes.
May benefit individuals with cystic fibrosis.
May counteract increased susceptibility to lung diseases associated with aging.
Exercise training per se doesn't significantly increase lung function or size.
Athletes don't generally have larger or better functioning lungs than non-athletes.
Ventilation generally does not limit maximal human performance; exception is swimmers.
Swimmers generally have slightly better lung function.
Respiratory muscles can improve with exercise training, but requires high intensity and long durations.
The diaphragm is the main muscle of inspiration, moving about 10 cm per breath.
Diaphragm flattens and moves down, increases volume and changes pressure.
Scalene and external intercostal muscles also contract, expanding volume and rotating/lifting ribs.
Accessory muscles of inspiration: PEC minor, serratus anterior, scaleni, and sternocleidomastoid.
Give extra lift to the thorax to increase dimension and ensure more oxygenated air intake.
Diaphragm spasms (stitch) may occur with overexertion.
Increasing diaphragm resilience allows longer durations of exercise.
Expiration is passive recoil of the diaphragm and lung tissue.
During strenuous exercise, abdominal muscles contract to aid expiration by increasing abdominal pressure and forcing diaphragm up.
Internal intercostal muscles lower and move ribs closer together to shrink thoracic dimensions.
Training increases strength and endurance capacity of respiratory muscles.
Muscles become more efficient at utilizing oxygen.
Can be used in rehabilitation clinics for individuals with chronic airway disease.
Central and peripheral chemoreceptors monitor the body and signal the brain to adjust pulmonary ventilation.
Exercise stimulates peripheral chemoreceptors (reduced blood lactate, potassium, sodium; increased core temperature).
Exercise may increase chemoreceptor sensitivity centrally.
Lungs can regenerate (pneumonectomy).
Lung structures are sensitive to caloric intake.
Increased caloric intake in mice increased cell division, alveolar size/number, and elastic recoil pressures (reversible).
Individuals at high altitudes have increased pulmonary diffusion pressures.
Accessory muscles of respiration adapt to high loads.
Chronic lung overloading (COPD) shifts towards a more oxidative phenotype of diaphragm and accessory muscles.
Emphysema reduces elastic recoil, causes airway closure and increased volumes.
Diaphragm operates at a shorter, flatter length with fewer sarcomeres.
Slumping forwards during exhaustive exercise is to stabilise these muscles.
Bending forward and bracing on knees helps stabilize upper body, supporting accessory muscles and decreasing effects of gravity.
Increases thoracic volume and aids in use of core muscles for expiration.
Dyspnea (shortness of breath) during exercise is common.
Athletes may be misdiagnosed with asthma.
Common causes include asthma or airway hyper-responsiveness (AHR).
The most common medical condition in Olympians.
High minute ventilation and environmental conditions (cold, dry air, pollution, chlorinated pools) cause micro-injuries to airway epithelium.
Repeated injury and repair cycles lead to structural changes and AHR.
Swimming-induced subclinical pulmonary edema.
Exercise-induced arterial hypoxemia is common in highly trained endurance athletes.
Inadequate oxygen supply to working muscles limits performance.
High pulmonary pressures may injure alveolar capillary membranes, causing interstitial edema.
Reports of coughing up blood and lung hemorrhaging after intense exercise at sea level.
High altitudes exacerbate risk due to non-uniform hypoxic pulmonary vasoconstriction.
Upper airway dysfunction (laryngeal dysfunction, vocal cord dysfunction) often seen.
Sudden narrowing of the glottis leads to the immediate onset of shortness of breath and a stridor on inspiration.
May be associated with GERD (gastroesophageal reflux disease).
Cough is common in athletes, especially in winter sports, and may not always be related to asthma but can be associated with different things or symptoms such as; sinusitis or rhinitis and laryngitis.
Upper respiratory tract infections are common, with overtraining/overreaching impairing immune function.
Prevention: Avoid dehydration and exercising in cold/polluted environments.
Heat and moisture exchange devices warm up inspired air.
Limit the number of competitions and exposure to extreme environments.
Warm up reduces severity of symptoms by increasing blood flow to bronchi.
Pharmacological interventions: Inhaled corticosteroids, L-arginine, antioxidants, leukotriene receptor antagonists.
Expiratory muscles are used when we cough or when we sneeze. That is why can get such stomach pain and sore stomach muscles.
Are used to stabilise the abdominal and chest cavities during strenuous activity.
Valsalva maneuver: Closing off the glottis to increase pressure during heavy lifting.
Full inspiration, closing off throat, maximally activating inspiratory muscles.
Increases intrathoracic pressure from 3 mm Hg at rest to 150 mm Hg.
Prolonged Valsalva can collapse veins, reducing venous return, stroke volume, and blood pressure, potentially causing fainting.
High pressure nitrogen in seawater is generally safe and physiologically inert.
Nitrogen narcosis: Nitrogen becomes harmful under high pressure (hyperbaric) conditions.
Similar to alcohol intoxication (dizziness, drowsiness).
Decompression sickness: Nitrogen bubbles form in tissue fluids and blood if ascending too quickly.
Causes muscle and joint pain (the bends).
Treated with hyperbaric oxygen.