Exercise, Altitude And Diving
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.
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 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.