topic 8: pulmonary system - ex phys

diffusion of gases

gases diffuse and dissolve into a liquid (air to blood) down their concentration gradient

• high concentration of O2 in the atmosphere to low concentration of O2 in blood

• O2 from air → O2 inhaled in alveoli → high PO2 goes into capillaries (100 mmHg, 40 mmHg CO2) → pulm vein (red) → LA/LV → systemic arteries → O2 into exercising muscle → low PO2 passing muscles (40 mmHg)

• CO2 from exercising muscles → increases PCO2 into capillaries (46 mmHg, 40 mmHg O2) → systemic veins → RA/RV → pulm artery (blue) → alveoli → PCO2 into alveoli to be exhaled

O2 transport

oxyhemoglobin (98%)

plasma (2%)

CO2 transport

from exercising muscle to alveoli because we want to get rid of it by exhaling (drops pH and impedes performance)

bicarbonate (70-75%)

carbaminohemoglobin (20%)

plasma (5-10%)

oxyhemoglobiin

how 98% of oxygen is transported and has 4 binding sites for O2

• deoxyhemoglobin: Hb not bound to O2 (RBC in venous blood)

• oxyhemoglobin →← deoxyhemoglobin + o2 (in capillaries surrounding alveoli)

• Hb is saturated when all 4 binding sites are filled with O2 (highest in pulm vein PO2 = 100 mg to be delivered to muscles)

• loading: when O2 binds to Hb near alveoli

  • high affinity (tight bond) to be transported

  • promotes oxyhemoglobin and high PO2

• unloading: when O2 is released from Hb at the tissues

  • low affinity (weak bond) to be delivered (easier for O2 to be picked up by myoglobin protein)

  • promotes deoxyhemoglobin and low PO2

oxygen-hemoglobin dissociation curve (curve)

describes percent oxyhemoglobin saturation over different PO2 levels

• high PO2 as blood leaves from aorta, high affinity, oxyhemoglobin state (TOP of curve)

• blood travels through tissues so O2 is unloaded from Hb there, decreasing affinity as it reaches muscles/tissues— drops to 80% and 40 mmHg PO2 (veins at rest) (MID of curve)

• blood travels back to lungs with deoxyhemoglobin state and low mmHg PO2 (BOTTOM of curve)

bohr effect

rightward shift in increasing temp, drop in pH, and accumulation of RBC byproduct 2-3 DPG

• promotes unloading (decreasing affinity) from Hb in muscle tissue during exercise

• meaning even at the same PO2, Hb holds less O2 so more O2 is delivered to tissues mainly during exercise

• increasing temp: heat lowers affinity of oxyhemoglobin

• drop in pH: H+ binds to hb

• 2-3 DPG: binds to Hb and prevent tight binding

myoglobin

protein that shuttles O2 from the cell membrane to the mitochondria inside muscles

• has a higher affinity for O2 than Hb → leaves blood and moves from Hb to Mb

• needed for continuous O2 for mitochondria and aerobic metabolism during long-duration activities (slow twitch fibers)

• at a low PO2, Mb is fully saturated and can hold/deliver more O2 vs Hb not fully saturated

CO2 transport in blood

CO2 from exercising muscle to blood and plasma

• CO2 dissolved in plasma

• CO2 combines with Hb to form carbaminohemoglobin: high PCO2 into blood (gradient), further releases O2

• CO2 from exercising muscle — formation of bicarbonate in RBC: CO2 + H2O → H2CO3 → H+ + HCO3- → then into plasma

  • CO2 + water → carbonic acid → bicarbonate and hydrogen ion

  • H+ combines with Hb so it can release O2 and prevent acidity

• chloride shift: Cl- from plasma to RBC, HCO3- to plasma with its negative charge

  • Cl- is an anion that maintains the negative electrical charge of RBC

  • removing HCO3- from RBCs allow more CO2 to be carried and blood and exhaled

CO2 transport to alveoli

CO2 from RBC and plasma in blood to alveoli

• bicarbonate ion enters RBC: HCO3- + H+ → H2CO3 → CO2 + H2O and takes to alveoli

  • Cl- leaves RBC

• carbaminohemoglobin breaks down into Hb and CO2 and takes to alveoli

• CO2 dissolved in plasma goes into alveoli

rest to work

transition where ventilation increases at the onset of exercise, while arterial PO2 and PCO2 are unchanged

• anticipation before exercise sends neural signals (in central command) — immediate breathing changes (muscle mechanoreceptors)

  • happens before CO2 rises or O2 drops

• VE increases proportionally to match metabolic demand

  • as exercise starts, muscles used more O2 and produce more CO2

  • arterial PO2 = 100 mmHg taken in/used

  • arterial PCO2 = 40 mmHg produced/removed

hot prolonged exercise

type of exercise and environment where ventilation increases with blood temperature while arterial PCO2 remains constant

• rise in blood temp stimulates the brain → ventilation increases (ex: panting, regulate body temp)

• VE matches increased demand for CO2 removal

• muscles produce more CO2 and ventilation increases to remove it

  • if VE didn’t increase, CO2 would buildup and drop pH

  • O2 delivery increases but does not drive VE here

incremental exercise

exercise where as intensity increases, there is a linear increase in ventilation until 50-75% (mod intensity) where it exponentially increases

• aka ventilatory threshold

  • marker for programs: following workouts below VT (long duration) or above VT (shorter spurts)

  • HR continues to increase linearly (SNS and O2 demand), but VE after VT driven by lactate and H+

• linear: CO2 production matches O2 use and VE increases proportionally

• at VT: intensity is high where lactate accumulates

  • extra CO2 from using bicarbonate to buffer so you breathe harder

• 1st threshold: intensity where breathing increases and can conversate during exercise

  • more lactate, aerobic to mainly anaerobic

• 2nd threshold: point of unsustainable, high intensity where breathing is heavier and faster and cannot maintain convo

  • accumulation of lactate higher than the clearance of lactate

trained vs untrained (incremental exercise)

trained/elite: 40-50% see sudden drop in PO2 — exercise induced hypoxemia

• VQ mismatch: not enough O2 in alveoli but O2 can still be transferred to blood and vice versa

  • blood flowing fast bc of HR and cannot capture enough O2

  • PO2 drops and lungs couldn’t fully keep up with demand

• maintains higher PO2 until extreme exertion

• pH drops more at high work rate

• VE increases and can maintain higher work rate and reaches higher absolute workload (%VO2max) before exhaustion (140 L/min)

untrained:

• maintains higher PO2 levels but steadier/gradual decline

• pH decreases but drops faster

• VE increases but reaches lower max ventilation (110 L/min)

arterial PO2 and ventilation

normal PO2 in arterial blood has little effect on ventilation until PO2 is at low levels

• read graph right to left

• Hb already fully saturated — no need to breathe more

  • moderate drops (65 mmHg) — Hb still carries enough O2

• below hypoxic threshold: ventilation increases sharply because chemoreceptors (carotid and aortic bodies) detect low O2 and signal to breathe more

  • bring in more O2 and protect tissues from hypoxia

arterial PCO2 and ventilation

as arterial PCO2 increases, ventilation increases linearly and sharply (primary control)

• CO2 is important bc it directly affects pH

• CO2 + H2O → H2CO3 → H+ + HCO3-

• increasing CO2 increases H+ and drops pH

• central chemoreceptors (brain) detect pH changes

• muscles produce more CO2, ventilation increases to remove CO2

breathing patterns

as exercise gets harder (increasing VO2max), your body increases minute ventilation

• factors that change to result in an increase in ventilation:

  • tidal volume: volume of air breathed in and out at rest (primary at low-mod exercise vs frequency levels off) — more work to fill the lungs

  • frequency: how many breaths taken (primary at heavy exercise vs tidal volume reaches max the lungs can inhale)

• IRV: additional vol of air inspired + tv

• ERV: additional vol of air expired + tv

stitch

exercise related abdominal pain caused by irritation of the parietal peritoneum

• common in running, swimming, jumping

• repetitive movements that cause it: torso movement, bouncing, twisting, diaphragm movement with breathing

• friction between abdominal organs and wall

• most susceptible: younger people who are more PA

• gain relief: rhythmic pattern to reduce diaphragm strain, firm pressure to stabilize wall

• prevent: avoid large meals (1-2 hours, full stomach increases friction), posture/core stability

respiratory control center

central command (cerebral cortex, higher brain)/humeral chemoreceptors/skeletal muscle receptors tells _____ _____ _____ in medulla oblongata to increase ventilation during exercise

• humeral chemoreceptors

  • peripheral

  • central

• skeletal muscle

  • chemoreceptors

  • mechanoreceptors

• deliver to: respiratory muscle

  • inspiration: increases ventilation — CC (PCO2 and pH) and PC (PO2, PCO2, pH) → center → ext intercostals up and out and diaphragm down → increase vol of thorax → draw air into lungs

  • expiration: decreases ventilation

humeral

chemoreceptors that measure chemical composition of arterial blood, sending info to RCC to increase ventilation

• peripheral: monitor changes in aortic and carotid bodies (in blood) — PO2, PCO2, H+, K

• central: in medulla oblongata and monitor changes in cerebrospinal fluid (NOT blood) — PCO2, H+

• both measure PCO2 and H+

• these and signals from active muscles stimulate RCC to increase ventilation

skeletal muscle

receptors detect chemical composition and stretch in/of skeletal muscle

• chemoreceptors: located in skeletal muscle — info on pH, temp, H+, PO2, PCO2

• mechanoreceptors: located in bronchioles — info on stretch, smooth muscle surrounding either expand or contract

  • dont want lungs to overinflate

  • also in skeletal muscle that control muscle movement (length/stretch/tension/force)

acid base balance and ventilation

during exercise, CO2 levels in blood rises and lower blood pH

• CO2 + water → carbonic acid → ph blood drops

• central chemoreceptor in medulla oblongata detect CO2 increase, pH drop, and receive nerve signal that O2 is low → RCC → impulse to respiratory muscles

• result in increased ventilation

mod intensity and ventilation

start of exercise: see immediate increase in ventilation bc of central command preparing respiratory muscles

• no change in PO2 or PCO2 yet

• neural input, chemoreceptor input, and afferent signals sent from exercising muscles to RC throughout exercise

  • afferent signals of movement/stretch/metabolites

• increases body temp

• increases epinephrine due to SNS activation→ to carotid arteries → stim carotid bodies of peripheral chemoreceptors

  • respond to PO2, PCO2, H+

heavy intensity and ventilation

as intensity increases, there is a linear rise in ventilation throughout heavy exercise

• very heavy: near/after lactate threshold (ventilatory threshold) — starts to rise steeply

  • increased H+ from VT bc anaerobic glycolysis increases, and pH drops

• H+ stim peripheral chemoreceptors → RCC → increases breathing

  • bicarbonate buffers H+ and makes more CO2 to further stim breathing

• increases K: muscles depolarize more from APs, K+ leaves muscles to blood

• increases body temp: blood temp rises

• increases epinephrine: stronger SNS activation and stim carotid bodies

• increases neural input to RCC: more muscles are active

• increases motor unit recruitment and afferent signaling: more muscle fibers and larger fast twitch → stronger afferent signals from receptors

lung adaptation

VE is higher before training than after training as intensity increases, but lungs do not structurally adapt as much

• at the same work rate (time), trained individuals breathe less after endurance training

• trained: muscles more aerobically efficient — more mitochondria, capillaries, o2 extraction, less reliant on anaerobic → less lactate and H+ → less VE

• exercise can cause respiratory muscle fatigue bc they are working continuously

  • endurance training increases respiratory muscle endurance capacity — build fatigue resistance

  • accessory muscles gain more mitochondria → better ATP production

• lung size is mostly fixed since thoracic cavity limits expansion

  • most adaptations happen in the heart (higher CO), blood, skeletal muscle, and respiratory muscles