breathing during exercise We breathe oxygen into the body from the atmosphere. While this oxygen does not itself contain useable energy, it is the key that unlocks the energy stored in previously-ingested food. As the energy demands of the contracting muscles change during exercise, so must their energy and oxygen provision. But oxygen comprises only 21% of the atmospheric air; one therefore needs to inhale a volume of air each minute which is at least five times the volume of oxygen which is being absorbed out of the lungs by the body.

Lung ventilation — the volume breathed in and out per minute — however, is not five times that of the rate of oxygen utilization for metabolism, rather, it is twenty-five times. This is because most of the oxygen is breathed back into the atmosphere during expiration: only 20% or so of the inspired oxygen is actually taken up by the blood coursing through the lungs en route to the cells.

The air taken into the lungs does not all reach the gas-exchange regions (the alveoli). Airways that conduct air to the alveoli do not themselves take part in this exchange: only the volume of air that gets beyond this dead space into the alveoli contributes to the gas exchange. Consequently the alveolar ventilation is less than the total ventilation — and this is the volume which provides the oxygen to be taken up into the body.

The alveolar oxygen concentration, and its equivalent oxygen pressure, is determined by the balance between the supply of oxygen to the alveoli and the demand for its uptake into the blood: the alveolar ventilation per minute and the oxygen consumption per minute. The alveolar oxygen pressure in turn establishes the oxygen pressure in the arterial blood, which is normally maintained at, or close to, a constant level during exercise, the same level as when at rest, despite the body's oxygen consumption increasing more than 10-fold. This can only be achieved if the alveolar ventilation increases proportionally. Normally it does so, increasing so that it maintains a ratio of about twenty times the oxygen uptake rate, for moderate exercise, with the ratio for total ventilation being about twenty five.

While this characterizes the ventilation needed to maintain the level of oxygen in the arterial oxygen, it may or may not be appropriate for the other vital breathing requirement during exercise — the defence of blood and tissue acidity.

The exercise-induced challenge to the body's acidity levels has two different origins. Firstly, foodstuffs that serve as energy sources for exercise (carbohydrates and fats) are composed entirely of hydrogen, carbon, and oxygen atoms. During the progressive metabolic fragmentation of food molecules, hydrogen atoms are stripped away, to link with oxygen, yielding energy.

For example, for glucose:C₆H ₁₂O₆ + 6O₂ → 6H₂O + 6CO₂This leaves the carbon and oxygen to be vented into the atmosphere as carbon dioxide. As the body's carbon dioxide production from this source is normally approximately equal to its oxygen consumption during exercise, the same level of ventilation can serve both purposes: intake and exhaust. However, if ventilation does not increase sufficiently during exercise, the oxygen level will fall in the blood and tissues, and the carbon dioxide level will rise. Such an increase in carbon dioxide would increase blood and tissue acidity.

The body's acidity is determined by the concentration of hydrogen ions [H⁺] — the positively-charged protons which form the nuclei of the smallest of all atoms. An increase in carbon dioxide in body fluids increases the concentration of [H⁺]. For [H⁺] to be stabilized in the arterial blood leaving the lungs, the carbon dioxide level needs to be regulated by exhaling the carbon dioxide at a rate equivalent to its production rate.

Normally, for moderate exercise, ventilation does indeed increase in proportion to the increased metabolic rate, thereby maintaining arterial blood levels of both oxygen and carbon dioxide (and hence [H⁺]) at, or close to, resting levels. This control is mediated through an interaction of neural and blood-borne mechanisms. The neural mechanisms which lead to muscle contraction also simultaneously signal the breathing control centres of the brain; these receive neural information from the contracting muscles as well. If the resulting drive to breathe is not appropriate, then an ‘error’ in the arterial oxygen, carbon dioxide, and [H⁺] levels is sensed by chemoreceptors which ‘sample’ the blood in the carotid arteries perfusing the brain. This provides the ‘fine tuning’ of the control system.

The second challenge to arterial [H⁺] stability occurs only at higher work rates, where the energy demands cannot be met entirely through aerobic (i.e. oxygen-linked) metabolism. At these work rates the aerobic transfer of energy is supplemented by degradation of carbohydrates to lactic acid — present in the form of a lactate ion [L^-] and [H⁺]. This component is anaerobic metabolism (it utilizes no oxygen). The fitter the subject, the higher the work rate at which it begins to contribute (see figure). The resulting increase in [H⁺] has a number of deleterious effects on exercise tolerance: impaired muscle contraction; perception of limb fatigue; and ‘shortness of breath’.

As exercise continues at this high intensity, the body's acidity level can only be maintained (or its increase constrained) if the carbon dioxide-related component of the acidity is reduced. The body therefore ‘compensates’ by increasing ventilation proportionally more relative to carbon dioxide production. This reduces alveolar and arterial carbon dioxide levels (see figure) as a result of the increased carbon dioxide ‘washout’. Clearly, the greater the amount of carbon dioxide ‘washed out’ under these conditions, the less will be the increase in acidity for any given level of lactic acid production.

The additional drive to breathe which is linked to the increased lactic acid levels is thought to result predominantly from the effects of the [H⁺] (and other mediators such as potassium ions released from the active muscles) stimulating the carotid chemoreceptors. Neither hydrogen ions nor potassium ions readily cross the blood–brain barrier, so they do not stimulate the other chemoreceptors on the surface of the brain stem (which in other circumstances also influence ventilation).

The increase in ventilation during exercise could, theoretically, be accomplished by an infinite variety of depths (tidal volumes) and number (breathing frequency) of breaths per minute. Very deep and slow breathing requires extra effort because the thorax, and the lungs in particular, become very stiff at high volumes. Rapid shallow breathing, on the other hand, mostly ventilates the dead space. The spontaneously-chosen pattern is typically the one which most effectively combines low breathing effort with a high fraction of the breaths reaching the alveoli. Consequently, most people initially increase ventilation predominantly by increasing tidal volume up to a certain optimal maximum; higher ventilatory demands are then achieved predominantly by increasing breathing frequency. In many sporting events, however (e.g. swimming, rowing, and even running), athletes must, or choose to, link the duration of each breath to the cadence of their limb motions.

Physical training or increased fitness does little to improve the lung as a mechanical pump or gas exchanger, unlike the beneficial effects of exercise on skeletal muscles and the heart. Luckily, however, the limits of operation of the lungs normally far exceed the demands placed upon them. For example, at maximum levels of exercise, not only is full blood oxygenation maintained in normal subjects, but also ventilation has not reached a maximum: it can be increased further by volitional effort (see figure). Elite athletes may be different in this regard. The unusually high metabolic rates they can achieve require unusually high levels of ventilation and of blood flow through the lungs. Those athletes who have not been graced by their genetic make-up to have large lungs with large airways (allowing high levels of airflow), and large capillary volumes (allowing the high cardiac output of rapidly-flowing blood to be exposed to the gas-exchange surface at the alveoli long enough for oxygenation to be completed), can show a component of ‘pulmonary limitation’ to exercise. This is manifest, only at a very high work rates, by airflow rate reaching a limiting maximum, and by a reduction in arterial oxygenation — but only in those without the appropriate genetically-superior lung structure.

Normal individuals also experience ‘shortness of breath’ (dyspnoea) during exercise. This is quite modest at low work rates — except when the carotid chemoreceptors are sensitized, such as during sojourns at high altitude. At high work rates the dyspnoea is usually more marked and sustained. There is a narrow range of work rates — high but usually sustainable for long periods — for which dyspnoea develops but which then subsides as the exercise continues. This relief of dyspnoea has been termed second wind. This proves difficult to reproduce in the laboratory; consequently its mechanisms are poorly understood. Reduction in the lactic acid-related drive to breathe, as aerobic mechanisms catch up with the high-energy demands, is likely to be contributory.

Brian J. Whipp

See also acid–base homeostasis; breathing; exercise; lungs; metabolism; respiration.