Activity Exercise High Altitude Diving

Physiological Stresses - Body needs a greater amount of oxygen to meet the - At higher altitudes, atmospheric pressure is lower due to - Increased partial pressure of gases (as you dive deeper
increased metabolic demands of the muscle tissues less dense air because of the effects of gravity every 33 ft/10 m, atmospheric pressure will increase by 1
- Great amount of carbon dioxide produced by exercising - Therefore, at high altitudes pO2 in the alveoli decreases as atm and volume of gases will be reduced by 50%
tissues also have to be removed percentage availability of O2 in the air decreases - The increased partial pressure will force the gases from the
- Decrease in pO2 causing acute hypoxia alveoli into the bloodstream and dissolve
- Other physiological stresses include ambient pressure,
decreased effects of gravity, altered respiration,
hypothermia and sensory impairment
Control of Breathing - CNS (Primarily) - Peripheral Chemoreceptors - Central and Peripheral Chemoreceptors

Monitors changes in parameters such as paO2, paCO2, pH,
Primary Motor Cortex Decreased paO2 (Hypoxemia)
etc.
via collateral branches 
(+)
from the descending
detected by Frequent divers will have desensitized Hypoxic and
corticospinal tract Peripheral Chemoreceptors (in carotid and Hypercapnic respiratory drives due to prolonged use of
aortic bodies) hyperbaric oxygen supply
Medullary Respiratory Centres (DRG & VRG)
via cranial nerves IX &X
(+)
(+) via intercostal nerve (glossopharyngeal
and phrenic nerve nerve
and vagus nerve)

Intercostal muscles and Diaphragm

Medullary Respiratory Centres (DRG & VRG)
Increased contraction of the
respiratory muscles (+)
via intercostal nerve
and phrenic nerve

Increased RR and respiratory depth (Hyperpnea)

but no change in blood chemistry Intercostal muscles and Diaphragm

- Proprioception Increased contraction of the

respiratory muscles
Increased muscle contraction
detected by Increased RR and respiratory depth
(Hyperventilation)
(in muscle spindles, Golgi tendon
Proprioceptors and Joint Kinaesthetic Receptors)

via sensory afferent neurones

(+)
(which bundles into the dorsal
spinothalamic tract) Initial increase in pO2 Decrease in pCO2 (Hypocapnia)
via collateral
fibres
Decrease in CSF H+ (↑ pH)
Primary Somatosensory Cortex
[Respiratory Alkalosis]

detected by
At the same time, the DST will Process signals
Central Chemoreceptors
branch into the DRG while and relays to
ascending to the PSC Primary Motor
(-)
(+) Cortex
Medullary Respiratory Centres (DRG & VRG)
DRG and then VRG (-)

(+)
Alveolar Ventilation
Phrenic nerves and intercostal
nerves

Hyperpnea

- Chemoreceptors do not involve here due to the negligible

change in arterial pO2 and pCO2, only provides “final
adjustments” for respiration
Work of Breathing - Increases - Increases - Increases
 ↑ TV causing more work to overcome resistive recoil  ↑ TV to generate greater transpulmonary pressure  To expand the chest against a less negative intrapleural
forces of the lungs  ↑ Airflow causing more turbulence / airway resistance pressure due to exertion of pressure by water outside of
 ↑ Airflow causing more turbulence / airway resistance the chest
* One of the reasons of mouth breathing during hyperventilation
Alveolar Ventilation (Change in Lung Volumes) - Increases - Increases - Increases (as seen in partial immersion up to the neck)
Due to ↑ TV & ↑ RR  Due to ↑ TV & ↑ RR  Pressure outside the thorax increases
↓ IRV  Causing reduce in outward elastic recoil of the chest wall
- ↓ TLC  Thus, ↓ FRC as the ERV ↓
 Due to ↑ venous return & ↑ pulmonary blood volume  ↑ IRV
- RV & FRC unchanged  TLC and VC remain the same
Oxygen consumption - Increases - Increases - Increases
Arterial pO2 - No change - Increases due to hyperventilation, but will eventually - Increases
decrease [Refer to Respiratory Alkalosis]
Arterial pCO2 - No change - Decreases due to hyperventilation - Slight to no increase
Additional Arterial pH - No change (small decrease in intense exercises) - Increases in Respiratory Alkalosis - Decreases during Hypoxia
Parameters Venous pCO2 - Increased - Decreased - Increased
Pulmonary BF and CO - Increased due to - Increased due to - Increased due to
 ↑ venous return (skeletal muscle pump, respiratory  Hypoxic pulmonary vasoconstriction and sympathetic  ↑ venous return
pump, mild fall in venous capacitance) activity  This causes ↑ mean pulmonary artery pressure → ↑
 ↑ HR & SV  This causes ↑ mean pulmonary artery pressure → ↑ capillary hydrostatic pressure
capillary hydrostatic pressure  More capillaries will be recruited for better pulmonary
 More capillaries will be recruited for better pulmonary perfusion
perfusion
 However, at the same time can cause HAPE
V/Q ratio Better distribution towards all zones, less regional differences Increased due to increase in both pulmonary blood flow and Under-ventilated but over-perfused alveoli due to capillary
pulmonary ventilation engorgement
Physiologic Dead Space - Decreases - Not stated - Not Stated
 Due to better ventilation → perfusion match
 But anatomic dead space increases due to slight
distension of large airways
Hb Oxygen Dissociation Curve Shifts to right, P50 ↑, affinity ↓ - Shifts to right, P50 ↑, affinity ↓ - Shifts to right, P50 ↑, affinity ↓
Pulmonary Diffusion Capacity - Increases - Decreases - Increases
 Due to ↑ pulmonary blood flow and velocity of blood 
Due to low pO2 causing partial pressure for oxygen  Due to vascular engorgement and central pooling of blood
* depends on the partial pressure difference of the gas, diffusion flow (↑ HR & CO) diffusion to decrease during diving, especially during cold water immersion
coefficient of the gas and thickness of the membrane  Also, lungs are expanded due to increased ventilation 
Causes ↑ CO to ↑ pulmonary artery O2 content
* Decreases in Emphysema, Pulmonary Fibrosis, Pulmonary  Pulmonary capillaries will be more recruited at the upper
Edema, Anemia, etc. zones of the lungs
 Thus, there will be an ↑ perfusion across all zones of the
lungs (↑ ventilation amongst all lung surfaces)
 Efficient gaseous exchange is achieved
- Note that at rest, usually the upper zones of the lungs are
least perfused due to gravity
Loading of O2 and unloading of CO2 - Both increased (right shifting of O2 dissociation curve) due - Decreased pO2 loading (before acclimatization) - Loading of O2 shows little increase as pO2 increases with
to ↑ temperature, ↑ pCO2, ↑ 2,3-DPG and ↓ pH 
Hypocapnia and Alkalosis may help increase O2 loading in depth
- Hemoglobin has less affinity to O2 lungs - However, increase in pO2 increases dissolved oxygen in
-
[Refer to Bohr Effect] 
↑ CO help increases tissue perfusion plasma [Refer to Henry’s Law] when supplied with 100%

Tissue metabolic acidosis (↑ temperature, ↑ pCO2, ↑ hyperbaric oxygen
-
2,3-DPG and ↓ pH) causes right shifting of O2 dissociation Oxygen will be forced to dissolve in plasma while also
curve binding to Hb
-
This helps perfuse divers in higher ambient pressure
- Increased pO2 loading (after acclimatization) conditions

Erythropoiesis increases RBC O2 carrying capacity - Unloading of CO2 remains constant, depending on the
workload of the diver
Acid-base balance
Related Mechanisms / Pathologies
Changes in exercise summary
- In hypoxic conditions, muscle tissues will switch to - Respiratory Alkalosis - Depending on activity
anaerobic respiration causing the production of lactic acid 
Increased ventilation reduces pCO2
- Results in metabolic acidosis which will be detected by 
pH of blood and CSF drops
peripheral chemoreceptors 
This inhibits respiratory centers and decreases ventilation
- Causing Chemoreceptor Reflex to pay the oxygen debt 
Further worsening tissue hypoxia
(break down lactic acids) in order to switch back to aerobic
respiration
- Increased respiratory drive
- Training effect in athletes - Acclimatization - Immersion Diuresis

↑ maximal O2 uptake  Renal compensation for Respiratory Alkalosis
 Immersion of body in water
↑ maximal CO  Intercalated B-cells reduces blood pH by pumping H+

↓ resting HR actively into the bloodstream while excreting more HCO3-

↑ resting SV via the collecting duct Decrease in body Hydrostatic

↑ arteriovenous O2 difference (Improved tissue oxygen  Increase in H+ will be cause acidosis which will be temperature pressure of water
extraction) detected by Central Chemoreceptors, thus stimulating (Hypothermia) increases blood

Muscle adaptions for ↑ efficiency (↑ capillaries & ↑ the respiratory centers and then increasing alveolar
enzymatic activity ventilation pressure

↑ blood volume  Hypoxia (↓ O2) will cause the release of Hypoxia Peripheral
Increase in BP & VR

↑ exercise loads with ↓ minute ventilation Inducible Factors (HIF) which will mediate hypoxia- vasoconstriction to

↑ respiratory muscle endurance induced genes conserve heat detected by, via

↑ pulmonary diffusing capacity  These genes will synthesize Erythropoietin (EPO) vagal afferent
nerves
 EPO stimulates the bone marrow to produce more RBC
(Erythropoiesis) Low Pressure Volume
How stress is our gas exchange  Increased RBC mass (Polycythemia) causes ↑ blood Receptors (stretch
• Oxygen diffusing capacity viscosity and ↑ O2 carrying capacity (pO2 does not receptors in LA)
• partial pressure difference of the gas (ΔP) change)
• diffusion coefficient of a gas (D) (effect of  Increased V/Q ratio (perfusion match) for efficient gas
molecular weight and solubility exchange Aldosterone Decreased Increased
• thickness of the membrane (ΔX)  Angiogenesis to increase the number of blood capillaries suppression secretion of ADH secretion of ANP
• Decreases in emphyses, fibrosis, pulmonary in the tissues for better tissue perfusion via ↓ RAA
oedema, anaemia  Due to no change in pO2, hypoxic stimulation of arterial activity
• Increases in exercise (effects may be acute and chemoreceptors persists, but after a few days CSF pH will
due to training) increase back to normal
• At rest (non-athlete) 23ml/min VS Maximal exercise  Due to persistent pulmonary hypertension, hypoxic
48ml/min pulmonary vasoconstriction and increased blood viscosity,
• Athlete-skater pulmonary vessel smooth muscles remodeling and RV ↑ Diuresis
64ml/min hypertrophy will occur - Diving Reflex
• Athlete-swimmer  Activated via unknown sensors located in the face or nose
70ml/min - Acute Mountain Sickness when the face is immersed in cold water
 Occurs when an unacclimatized person ascends to high  Impulses are then sent to the heart via afferent vagal
altitudes nerves
 Respiratory Alkalosis persists and causes prolonged  Causes bradycardia to lower cardiac workload
• Diffusing capacity increases in exercise mainly due to hypoxemia  Increases TPR (except for heart and brain due to their
increase pulmonary blood flow  Hypocapnia in the brain can also cause cerebral powerful autoregulation properties)
• Increased speed of blood flow vasoconstriction thus resulting in brain hypoperfusion  This reflex can be used as a measure to treat tachycardias
• Recruit of capillaries increases the surface areas for  Risk factors: Prior episodes of AMS, can develop easily at such as PSVT
diffusion night when RR drops during sleeping  Reflex also can be seen in voluntary apnea (breath hold)
• Mixed venous PO2 may be lower than normal, and venous  Symptoms are Neurologic (sleepiness, laziness, false when cold water/press/ice is in contact with the face
PCO2 may be higher than normal due to the effect of the sense of well-being, impaired judgment, blunted pain
exercise perception, increasing errors of simple tasks, decreased - Note that a normal person would not be able to dive more
Oxygen unloading at tissues is increased (righ shift of the visual activity, clumsiness, tremors) than 3 feet (1 meter) with a snorkel
disspciation curve)  This is because the maximum intrapleural pressure
Increased temperature, lower pH, Increased CO2 , possibly - High Altitude Cerebral Edema (HACE) generated by our lungs are not enough to inflate the lungs
increased 2,3 DPG  End of stage of Acute Mountain Sickness beyond the 3 feet limit as the water pressure is very high
• metabolic acidosis secondary to the increased lactic acid  Hypoxemia (↓ paO2) will cause systemic vasodilation of when descending
production the blood vessels [Refer to CVS Regulation of Blood Flow]
• Arterial chemoreceptors may play a role in supporting  This will increase cerebral blood flow and the
increased respiratory drive to increase in alveolar leakiness/permeability of the vessels
ventilation
How stressed is our pulmonary ventilation in exercise?
• Maximum Breathing capacity= 150 to 170 L/min
• Pulmonary ventilation at rest= TV X RR= 6l/min
• Pulmonary ventilation at maximal exercise rates=
100-120l/min
• Conclusion our breathing capacity is in excess of
pulmonary ventilation requirements at maximal exercise rate
• ie  some reserve for conditions like high altitude, extreme
hot weather, to certain extent in respiratory disease
Stimulus driving this increase in ventilation
• Could it be chemoreceptors? PO2 and PCO2 show
negligible change in exercise
• Most of the response Neurogenic
• Proprioceptors
• Central at level of respiratory centres: collateral
from motor cortex
• Chemoreceptors provide “final adjustment”
Blood Gas concentration and alvelor ventilation during exercise
• Alveolar ventilation increases without any increase in PCO 2
• PCO2 remains within normal limits during exercise
- High Altitude Pulmonary Edema (HAPE)
- Treatment for AMS and associated symptoms
 At the same time, disrupted ionic balance causes
Astrocyte swelling, resulting in cytotoxic edema
 Fluid will accumulate in the interstitial spaces causing
cerebral edema
 The ↑ in ICP will result in brain herniation. This
compresses the respiratory centers in the brainstem,
thus decreasing pulmonary ventilation
 Symptoms: ataxia, fatigue
  This will cause “shallow water blackout” due to the

↓ pO2 at the alveoli will cause vasoconstriction of
pulmonary blood vessels

Blood flow will be redirected to vessels that are not
constricted

Blood flow through these vessels will then significantly
increase

The increase in hydrostatic pressure/permeability of the
pulmonary vessels will cause fluid accumulation in the
interstitial spaces (pulmonary edema)
Barotrauma


Supplemental oxygen (portable hyperbaric O2) –
prevent/treat cerebral edema and reduces tissue hypoxia

Descend to lower altitudes ASAP/ Ascend to higher
altitudes slowly

Acetazolamide – inhibits carbonic anhydrase thus
preventing respiratory alkalosis to be detected by the
central chemoreceptors. This enables the body to mimic
Hypercapnic conditions which help drive respiration and
increase ventilation

Memitol & Dexamethasone (corticosteroid) – Removes
cerebral edema
a)
 Breath-hold Diving
 One would hyperventilate before breath-
holding and then dive
 Once reaching the Breakpoint, voluntary
apnea is stopped and overridden by
involuntary control (pO2, pCO2, lung volume
mediated)
 As the person further descends the increasing
gas pressure (and decrease in gas volume) will
cause an increase in pO2
 This causes more oxygen to diffuse into the blood
stream and tissues
 At the same time pCO2 does not increase much due
to CO2 being actively produced via metabolism and
removed from tissues rather than taken in
 However, during ascent, air expands instead of
being compressed
rapid
decrease in pO2 leading to hypoxia
 Self-Contained Underwater Breathing Apparatus
(SCUBA) Diving
 One would dive with a tank filled with compressed
(high pressure) gas which is slightly less than the
ambient pressure
 A regulator will detect and open the valve of the
tank whenever the user wants to breath
 Expired gas will be released into the water as gas
bubbles
 At any depth, the pressure of the lungs will remain
close to the ambient pressure
 Work of breathing will increase due to
increased gas densities supplied by the tank
 High pO2 flow will desensitize the hypoxic drive
 ambient pressure increases or decreases but the
body cannot equilibrate with ambient pressure
 barotrauma of descent is called “squeeze.”
 middle ear, if the eustachian tube is clogged or
oedematous, air pressure cannot equilibrate
pressure in the middle ear;
 the sinuses; the lungs, resulting in pulmonary
congestion, oedema, or haemorrhage; and even
cavities in the teeth
 expanding pulmonary gas “burst lung”,
hemorrhage, pneumothorax, or air embolism.
 In the gastrointestinal tract abdominal discomfort
and eructation or flatus
 In the ears, sinuses, and teeth may also occur on
rapid ascent from great depths.
 If upper respiratory tract infection is present, the
eustachian tube membranes swell and produce
mucus which may plug the air passage
 During descent, the diver can suffer severe pain as
the ear drum becomes stretched and moves inward
Aerotitis
 In URTIs, Eustachian tube membranes will swell and
produce mucus/edema/inflammation which will block
the tube
 This causes the diver’s middle ear to fail to equilibrate
 with the ambient pressure
 Thus, during descending the increase in ambient
pressure will stretch the eardrum inwards as the
pressure inside the body is lower
 The diver will experience pain

b) Pulmonary congestion/edema/hemorrhage
 Lungs and sinuses are subjected to the high ambient
pressure while descending

c) Decompression Sickness
 When descending, ambient pressure will increase the
patrial pressure of gases in the body thus forcing them
to diffuse into the body tissues [Henry’s Law]
 When ascending, trapped gases in the alveoli and
tissues (esp. fat tissues) will expand rapidly due to
decrease in ambient pressure

- Erythropoietin
 Increased PVC
 Increased oxygen caring capacity
 Help to reduce hypoxemia
 Increase viscosity
 Increased vascular resistance

- Hypoxia Pulmonary Vasoconstriction

 Increases pulmonary resistance
Compared to systemic vessels which dilate During ascent: ambient pressure falls gases bubble
Increases afterload on RV out esp nitrogen in body tissues and fluids.
Cor pulmonale may enter the venous blood trapped in the
pulmonary circulation and rarely cause symptoms
If they do “the chokes” by divers, include substernal
- Muscular Adaptation chest pain, dyspnoea, and cough and may be
• Cellular metabolism responds by accompanied by pulmonary hypertension, pulmonary
• increasing capacity of oxidative enzymes, oedema, and hypoxemia
• increased mitochondrial number, bubbles in the circulation of the central nervous
• increased capillary density system, which may result in brain damage and
paralysis.
- Respiratory Adaptation Bubbles that form in the joints of the limbs cause pain
 (“the bends”).
Hypoxic drive persists
 Osteonecrosis of joints may also be caused by
Response tends to decrease slightly inadequate decompression

Due to compensatory renal mechanisms to respiratory
alkalosis (reduction in HCO3)

The body tolerates more hypoxia and so saves energy by The Pulmonary Blood Flow
reducing the energy spent on breathing • Venous return increases

Increased diffusing capacity and TLC (seen as large chest • Increased capillary hydrostatic pressure recruitment
increased diffusing capacity
of high altitude dwellers)
 • somewhat improved matching of ventilation and
perfusion
 
Gas bubbles (esp. N2) will form in the blood and
tissues

Arterial Gas Embolism occurs when the gas bubbles
escape into the blood vessels due to airway
obstruction causing alveoli rupture.

They will occlude the arterial vasculature causing
ischemia, infarction and stroke.

This normally happens when a diver forgets to exhale
the trapped air from the body

Rapid decompression can also rupture the
lungs/alveoli causing pneumothorax, hemorrhage or
air embolisms

GI discomfort such as eructation (burping) or flatus
(stomach gases) can be seen

Air Embolism in the CNS can result in brain damage
and paralysis

Air Embolism in the joints can cause pain and
osteonecrosis

d) Nitrogen Narcosis
 Increased solubility of Nitrogen during descent as
partial pressure of N2 increases
 Directly affects the CNS, causing euphoria, memory
loss, clumsiness, irrational behavior, limb numbness,
motor impairment, disorientation and unconsciousness

e) Oxygen Toxicity
 Inhalation of 100% at atmospheric or high ambient
pressures
 Causes visual impairment and alveolar damage,
convulsions & death

f) High-Pressure Nervous Syndrome

 Occurs at depths >250 feet while using a breathing gas
containing helium
 Helium is used to prevent nitrogen narcosis and help
avoid decompression sickness
 However, when helium replaces nitrogen in the tissues
it will cause its own set of adverse effects
 Causes tremors, decreased mental ability, nausea,
vomiting, dizziness, decreased manual dexterity
Challenges Ventilation Prefusion ration in Exercise A high altitude Diving Challenges
- In general V/Q ratios improve in all alveolar unit 1. Air pressure decreases as we ascend to higher altitude. ambient pressure
-
- At rest they may vary but during exercise the average increases to 2. This is due to the effect of gravity.
3. This makes the air less dense as we ascend. - decreased effects of gravity
2.5, less scatter indicating areas receiving more blood are also
receiving more ventilation 4. The air particles remain further apart from each other the - altered repiration
less the air pressure - hypothermia
Factor affecting ventilation 5. This is expressed as a reduced partial pressure of each of - sensory impairment
• Voluntary control the component gases in the atmosphere.
• Irritant receptors in the airways involved in coughing and 6. All the while the composition (% of each component gas in
sneezing the air mixture) remains constant
• J receptors: located juxtaposed to capillaries, detect increased 7. As per the table, PO2 at 8000 m is less than arterial PO2 at
blood volume and congestion, cause tachypnoea sea level!
• Cerebral oedema: acute oedema and compress cerebral blood 8. Can diffusion of oxygen into the lungs occur?
vessels respiratory depression As the ambient pressure reduce , partial pressure of oxygen reduce
Parameter that changes
 Barometer pressure
 External ambient

High altitude affect PO2 Immersion up to the neck

 Alveolar PO2 depends to a large extend on the atmospheric • Pressure outside thorax increases
Po2 • outward elastic recoil of the chest wall
• ↓functional residual capacity
•  ↓ expiratory reserve volume
• ↑inspiratory reserve volume
• TLC and VC normal
• Work of breathing increases as intraplueral
 pressure is less negative and respiratory muscles
 This cause low diffusion gradient for oxygen must work harder to expand chest
 This drop in the partial pressure of oxygen is a major
challenge
 It means the gradient for diffusion of oxygen is now less,
compared to at sea level
Consequences / Effect Consequences of Low ambient PO2
• If exposed to extremely low arterial PO2 (< 20 mmHg)
• Unconsciousness in a few seconds
• Brain death
• If exposed to arterial PO2 between 25-40 mmHg
• Lack of coordination, slowed reflexes, slurred
speech, overconfidence, unconsciousness, coma and
death id prolonged
• If Chronic (between 40 -60 mmHg)
• Bedridden, with limited capacity for motor activity
• Fatigue, dyspnoes, SOB,
• Periodic breathing especially during sleep
Compensatory response
1. Hyperventilation: Due to activation of peripheral
chemoreceptors
• Increase in tidal volume, better distribution of
ventilation
• Leads to reduced PCO2; allows alveolar PO2 to
increase
2. Respiratory alkalosis can lead to a lowered respiratory
drive
3. Tachycardia due to increased sympathetic stimulation as a
result of the peripheral chemoreceptors
4. This increases CO and helps supply more blood to tissues
5. DPG concentration increases: helps shift curve to right and
deliver more O2
Effect of High Pressure
Breathing air under high pressure for a long time
•
• Amount of nitrogen dissolved in the body fluids
increases
• More gases dissolve in pulmonary capillaries
due to high pressure
• Gradually these gases also saturate the tissue
• Since most of this gas is nitrogen which is not
metabolised it remains dissolved in body tissues
• The pressure is reduced during ascent
• Nitrogen pressure in the lungs is decreased to
some lower level
• The large amount of nitrogen dissolved needs to
come out of solution to equalise the new low
pressure.
• Nitrogen bubbles form in tissues bad cause
decompression sickness.
