Exercise, Altitude And Diving
Exercise
Resting arterial oxygen saturation is close to 100% and
oxygen content cannot be raised significantly during exercise. Oxygen delivery (arterial
oxygen content blood flow) to exercising muscle is increased by increasing
muscle blood flow, made possible by metabolic vasodilatation. Oxygen
extraction from the delivered blood is also increased.
For the whole body, oxygen consumption (mL/min)
cardiac output (mL/min) (arterial-mixed venous oxygen content) (mL/mL). In
active muscle, oxygen unloading from haemoglobin is aided by the reduced tissue
Po2 and the rightward shift of the oxyhaemoglobin dissociation
curve caused by local increases in Pco2, [H+] and
temperature. Maximum oxygen extraction does not vary greatly with fitness and
the main factor determining maximum oxygen consumption (V" O2
max) is the maximum cardiac output. V" 02 max is an index of fitness and in a young man
this might be 12 times resting oxygen consumption (Table 1) and more in an
athlete.
In exercise, mixed venous blood has a reduced Po2
and increased Pco2. As blood passes through the pulmonary
capillaries, the increased alveolar to blood partial pressure gradients
increase 02 uptake and C02 output. In mild to moderate
exercise, alveolar ventilation is accurately matched to metabolism and Pao2,
Paco2 and arterial pH (pHa) are maintained at
resting values (Fig. 15a). The mechanisms initiating and controlling the
ventilatory response remain uncertain. In heavy exercise, increased anaerobic
metabolism increases lactic acid production and reduces arterial pH. This gives
an extra stimulus to breathing via the peripheral chemoreceptors, and at this anaerobic
threshold the relationship between ventilation and oxygen consumption
becomes steeper and Paco2 falls (Fig. 15a).
Exercise intolerance is a common symptom of many
diseases, and the inability to raise the cardiac output adequately is the main
underlying mechanism in many diseases. In anaemia oxygen delivery to the muscles
is reduced because of reduce arterial oxygen content. In some respiratory
diseases, limited ability to increase ventilation or incomplete equilibrium in
the pulmonary capillary may limit exercise.
Altitude
Barometric pressure falls progressively with increasing
altitude from about 101 kPa (760 mmHg) at sea level to 33.6 kPa (252 mmHg) on
the summit of Everest (see Chapter 4), but oxygen fraction remains constant at
0.209. Moist inspired Po2 (0.209 (PB PH20))
is about 19.9 kPa (149 mmHg) at sea level and about 5.7 kPa (43 mmHg) on the
summit of Everest. If ventilation remains unchanged, reduced inspired Po2
inevitably leads to reduced Pao2 but Paco2
( C02 production/alveolar ventilation) will be unaltered. This is
the situation initially when a person ascends to altitudes up to about 3000 m
(9840 fit)
(Fig. 15b). Hypoxic carotid body chemoreceptor stimulation occurs, but any
ventilatory increase lowers Paco2, which depresses
ventilation. Above 3000 m the more severe hypoxia does increase ventilation and
Paco2 falls (Fig. 15b). Acute mountain sickness
commonly develops some hours after rapid ascent to altitudes above 3600 m
(12 000 fit)
with symptoms such as fatigue, nausea, anorexia, dizziness, headaches and sleep
disturbance. It can progress to life-threatening high-altitude pulmonary
oedema and/or high-altitude cerebral oedema, which usually require
immediate descent. The more benign symptoms improve with time, a process known
as acclimatization. 0ver the next few days, ventilation increases,
raising Pao2 and lowering Paco2
(A to B, Fig. 15b). During this period the initial alkalosis of arterial blood
and cerebrospinal fluid (CSF) is corrected by bicarbonate transport out of the CSF and
renal bicarbonate excretion. A gradual normalization of arterial and CSF
pH was originally thought to explain the gradual increase of ventilation, but
other mechanisms, such as increased sensitivity of the peripheral
chemoreceptors to hypoxia and changes in the central nervous system reflex
pathways, are also important. Erythropoietin production by the kidney is
stimulated by hypoxia, and haemoglobin concentration rises from 150 g/L to
around 200 g/L after a few weeks at high altitude, aiding acclimatization by increasing
arterial oxygen content.
At altitude the concentration of 2,3-diphosphoglycerate
in red blood cells increases and Paco2 falls,
and they cause opposite shifts (right and left respectively) of the
oxyhaemoglobin dissociation curve, which at many altitudes results in little
net change in oxygen aff nity. At very high altitude the very low Paco2
shifts the curve to the left and the beneficia effect of increased oxygen
binding in the lungs outweighs the impaired oxygen release in the tissues.
With acclimatization humans can live at much higher
altitudes than it is possible to tolerate acutely. The highest long-term human
settlement was Quilcha, Chilie (5334 m, 17 500 fit), from where miners walked to work at the
Aucanquilcha mine 610 m (2000 fit) higher. Sudden exposure to the summit of Everest would cause a
healthy sea level dweller to lose consciousness in less than 2 minutes but a
few very f t and fully acclimatized people have climbed it without
supplementary oxygen.
The hypoxic pulmonary vasoconstriction that aids
ventilation- perfusion matching at sea level causes an unhelpful global vasocon
striction at high altitude. In some people living above 2500 m (8200 fit) this becomes
excessive, leading to pulmonary hypertension and right ventricular failure.
Excessive polycythaemia also often occurs in these patients, contributing to
this chronic mountain sickness (Monge’s disease).
Diving
Diving into water affects the respiratory system in many
ways. Breath-hold diving initiates several reflexes, leading to the
cardiovascular and respiratory effects of the diving response. Immersion
of the face in water stimulates receptors around the eyes and nose supplied by
the trigeminal nerves, leading to reflex apnoea, bradycardia and widespread
vasoconstriction. The apnoea helps prevent water in- halation. The
oxygen-conserving bradycardia and vasoconstriction are enhanced by reflexes
from the carotid body chemoreceptors but antagonized by reflexes from lung
stretch receptors. The cardiovascular responses are usually modest in humans,
but excessive bradycardia sometimes occurs, especially following unexpected
immersion during expiration, and this may explain some accidental deaths in
water.
The weight of the water increases the pressure on the
body by 1 atmosphere (101 kPa, 760 mmHg) for every 10 m (33 fit) below the surface.
Even 1 m below the surface breathing through a snorkel becomes difficult
because the pressure on the chest opposes inspiration. In SCUBA diving greater
depths are made possible by pressurizing the inspired, and hence alveolar gas,
to ambient pressure, but this brings other problems. Using compressed air, the
increased alveolar Pn2 raises arterial Pn2,
which has effects on the brain similar to alcohol intoxication and eventually
leads to nitrogen narcosis. Dissolved nitrogen may also cause problems
if the diver surfaces too rapidly. Decompression sick-ness or the
bends occurs when the rapidly decreased pressure causes nitrogen to comes
out of solution, forming bubbles in the blood and tissues, leading to
musculoskeletal pains and neurological symptoms. The high pressure compresses
the gas in the lungs and this expands during ascent. If the diver fails to
exhale while ascending, this can rupture the lungs.
