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28. 6. 2012.

Respiratory responses to acute exercise

Pulmonary ventilation during dynamic exercise

The onset of exercise is accompanied by an immediate increase in ventilation. In fact, like the HR response, the marked increase in breathing may occur even before the onset of muscular contractions. This is shown in the picture below for light, moderate and heavy exercise. Because of its rapid onset, this initial respiratory adjustment to the demands of exercise is undoubtedly neural in nature, mediated by respiratory control centers in the brain(central command), although neural input can also come from receptors in the exercising muscle.

The more gradual second phase of the respiratory increase shown in the picture is controlled primarily by changes in the chemical status of the arterial blood. As exercise progresses, increased metabolism in the muscles generates more carbon dioxide and H+. Recall that these changes enhance oxygen unloading in the muscles, which increases the (a-ṽ)O2 difference.  Increased CO2 and H+ are sensed by chemoreceptors primarily located in the brain, carotid bodies, and lungs, which in turn stimulate the inspiratory center, increasing rate and depth of respiration. Some researchers have suggested that chemoreceptors in the muscles might also be involved. In addition, data suggest that receptors in the right ventricle of the heart send information to the inspiratory center so that increases in cardiac output can stimulate breathing during the early minutes of exercise. These humoral influences on breathing rate and pattern serve to fine-tune the respiratory response to exercise so as to match oxygen delivery with aerobic demands without overtaxing respiratory muscles.
At the end of exercise, the muscles’ energy demands decrease almost immediately to resting levels. But pulmonary ventilation returns to normal at a slower rate. If the rate of breathing perfectly matched the metabolic demands of the tissues, respiration would decrease to the resting level within seconds after exercise. But respiratory recovery takes several minutes, which suggests that postexercise breathing is regulated primarily by acid-base balance, the partial pressure of dissolved carbon dioxide(PCO2), and blood temperature.

Breathing irregularities during exercise

Ideally, breathing during exercise is regulated in a way that maximizes aerobic performance. However, respiratory dysfunction during exercise can hinder performance.


The sensation of dyspnea(shortness of breath) during exercise is common among individuals in poor physical condition who attempt to exercise at levels that significantly elevate arterial carbon dioxide and H+ concentrations. Both stimuli send strong signals to the inspiratory center to increase the rate and depth of ventilation. Although exercise – induced dyspnea is sensed as an inability to breathe, the underlying cause is an inability to adjust breathing to blood PCO2 and H+.
Failure to reduce these stimuli during exercise appears to be related to poor conditioning of respiratory muscles. Despite a strong neural drive to ventilate the lungs, the respiratory muscles fatique easily and are unable to reestablish normal homeostasis.


The anticipation of or anxiety about exercise, as well as some respiratory disorders, can cause an increase in ventilation in excess of that needed for exercise metabolism. Such overbreathing is termed hyperventilation. At rest, hyperventilation can decrease the normal PCO2 of 40mmHg in the alveoli and arterial blood to about 15mmHg. As arterial carbon dioxide concentrations decrease, blood pH increases. These effects combine to reduce the ventilatory drive. Because the blood leaving the lungs is nearly always about 98% saturated with oxygen, an increase in the alveolar PO2 does not increase the oxygen content of the blood. Consequently, the reduced drive to breathe – along with the improved ability to hold one’s breath after hyperventilating – results from carbon dioxide unloading rather than increased blood oxygen. Even when performed for only a few seconds, such deep, rapid breathing can lead to light-headedness and even loss of consciousness. This phenomenon reveals the sensitivity of the respiratory system’s regulation of carbon dioxide and pH.

Valsalva maneuver

The Valsalva maneuver is a potentially dangerous respiratory procedure that frequently accompanies certain types of exercise, in particular the lifting of heavy objects. This occurs when the individual:
  • Closes the glottis(the opening between the vocal cords);
  • Increases the intra-abdominal pressure by forcibly contracting the diaphragm and the abdominal muscles,
  • Increases the intrathoracic pressure by forcibly contracting the respiratory muscles.

As a result of these actions, air is trapped and pressurized in the lungs. The high intra-abdominal and intra-thoracic pressures restrict venous return by collapsing the great veins. This maneuver, if held for an extended period of time, can greatly reduce the volume of blood returning to the heart, decreasing cardiac output and altering arterial blood pressure.  Although the Valsalva maneuver can be helpful in certain circumstances, this maneuver can be dangerous and should be avoided.

Ventilation and energy metabolism

During long periods of mild steady-state activity, ventilation matches the rate of energy metabolism, varying in proportion to the volume of oxygen consumed and the volume of carbon dioxide produced(VO2 and VCO2 respectively) by the body.

Ventilatory equivalent for oxygen

The ratio between the volume of air expired or ventilated(Ve) and the amount of oxygen consumed by the tissues(VO2) in a given amount of time is referred to as the ventilatory equivalent for oxygen, or Ve/VO2. It is typically measured in liters of air breathed per liter of oxygen consumed per minute.
At rest, the Ve/VO2 can range from 23 to 28L of air per liter of oxygen. This value changes very little during mild exercise, such as walking. But when exercise intensity increases to near-maximal levels, the Ve/VO2 can be greater than 30L of air per liter of oxygen consumed. In general, however, the Ve/VO2 remains relatively constant over a wide range of exercise intensities, indicating that the control of breathing is properly matched to the body’s demand of oxygen.

Ventilatory threshold

As exercise intensity increases, at some point ventilation increases disproportionately to oxygen consumption. The point at which this occurs is called the ventilatory threshold, illustrated in the figure below. When work rate exceeds ~55% to 70% of VO2max, at approximately the same point as the ventilatory threshold, more lactate starts to appear in the blood. This may result from greater production of lactate or less clearance of lactate. This lactic acid combines with sodium bicarbonate(which buffers acid) and forms sodium lactate, water, and carbon dioxide. As it is known, the increase in carbon dioxide stimulates chemoreceptors that signal the inspiratory center to increase ventilation. Thus, the ventilatory threshold reflects the respiratory response to increased carbon dioxide levels. Ventilation increases dramatically beyond the ventilatory threshold.

Respiratory limitations to performance

Like all tissue activity, respiration requires energy. Most of this energy is used by the respiratory muscles during pulmonary ventilation. At rest, the respiratory muscles account for only about 2% of the total oxygen uptake. As the rate and depth of ventilation increase, so does the energy cost of respiration. The diaphragm, the intercostal muscles, and the abdominal muscles can account for up 11% of the total oxygen consumed during heavy exercise and can receive up to 15% of the cardiac output. During recovery from dynamic exercise, sustained elevations in ventilation continue to demand increased energy, accounting for 9% to 12% of the total oxygen consumed postexercise.
Although the muscles of respiration are heavily taxed during exercise, ventilation is sufficient to prevent an increase in alveolar PCO2 or a decline in alveolar PO2 during activities lasting only a few minutes. Even during maximal effort, ventilation usually is not pushed to its maximal capacity to voluntarily move air in and out of the lungs. This capacity is called the maximal voluntary ventilation and is significantly greater than ventilation at maximal exercise. However, considerable evidence suggests that pulmonary ventilation might be a limiting factor during very high intensity(95~100% VO2max) exercise in highly trained subjects.
Can heavy breathing for several hours(such as during marathon running) cause glycogen depletion and fatique of the respiratory muscles? Animal studies have shown a substantial sparing of their respiratory muscle glycogen compared with muscle glycogen in exercising muscles. Although similar data are not available for humans, our respiratory muscles are better designed for long-term activity than are the muscles in our extremities. The diaphragm, for example, has two to three times more oxidative capacity(oxidative enzymes and mitochondria) and capillary density than other skeletal muscle. Consequently, the diaphragm can obtain more energy from oxidative sources than can skeletal muscles.
Similarly, airway resistance and gas diffusion in the lungs do not limit exercise in a normal, healthy individual. The volume of air inspired can increase 20- to 40-fold with exercise – from ~5L/min at rest up to 100 to 200 L/min with maximal exertion. Airway resistance, however, is maintained at near-resting levels by airway dilation(through an increase in the laryngeal aperture and bronchodilation). During submaximal and maximal efforts in untrained and moderately trained individuals, blood leaving the lungs remains nearly saturated with oxygen(~98%). However, with maximal exercise in some highly trained elite endurance athletes, there is too large a demand on lung gas exchange, resulting in a decline in arterial PO2 and arterial oxygen saturation(i.e. exercise-induced arterial hypoxemia, EIAH). Approximately 40% to 50% of elite endurance athletes experience a significant reduction in arterial oxygenation during exercise approaching exhaustion. Arterial hypoxemia at maximal exercise is likely the result of a mismatch between ventilation and perfusion of the lung. Since cardiac output is extremely high in elite athletes, blood is flowing through the lungs at a high rate and thus there may not be sufficient time for that blood to become saturated with oxygen. Thus, in healthy individuals, the respiratory system is well designed to accommodate the demands of heavy breathing during short- and long-term physical effort. However, some highly trained individuals who consume unusually large amounts of oxygen during exhaustive exercise can face respiratory limitations.
The respiratory system also can limit performance in patient populations with restricted or obstructed airways. For example, asthma causes constrtiction of the bronchial tubes and swelling of the mucous membranes. These effects cause considerable resistance to ventilation, resulting in a shortness of breath. Exercise is known to bring about symptoms of asthma, or to worsen those symptoms in select individuals. The mechanism or mechanisms through which exercise induces airway obstruction in individuals with so-called exercise-induced asthma remain unknown, despite extensive study.

Respiratory regulation of acid-base balance

As already noted, high-intensity exercise results in the production and accumulation of lactate and H+. Although regulation of acid-base balance involves more than control or respiration, it is discussed here because the respiratory system plays such a crucial role in rapid adjustment of the body’s acid-base status during and immediately after exercise.
Acids, such as lactic acid and carbonic acid, release H+. The metabolism of carbohydrate, fat, or protein produces inorganic acids that dissociate, increasing the H+ concentration in body fluids, thus lowering the pH. To minimize the effects of free H+, the blood and muscles contain base substances that combine with, and thus buffer or neutralize, the H+:

H+ + buffer ---> H-buffer

Under resting conditions, body fluids have more bases(such as bicarbonate, phosphate, and proteins) than acids, resulting in a slightly alkaline tissue pH that ranges from 7.1 in muscle to 7.4 in arterial blood. The tolerable limits for arterial blood pH extend from 6.9 to 7.5, although the extremes of this range can be tolerated only for a few minutes(see figure below). An H+ concentration above normal(low pH) is referred to as acidosis, whereas a decrease in H+ below the normal concentration(high pH) is termed alkalosis.
The pH of intra- and extracellular body fluids is kept within a relatively narrow range by:
  • Chemical buffers in the blood,
  • Pulmonary ventilation,
  • Kidney function.

The three major chemical buffers in the body are bicarbonate(HCO3-), inorganic phosphates(P), and proteins. In addition to these, hemoglobin in the red blood cells is also a major buffer. Table below illustrates the relative contributions of these buffers in handling acids in the blood. Recall that bicarbonate combines with H+ to form carbonic acid, thereby eliminating the acidifying influence of free H+. The carbonic acid in turn forms carbon dioxide and water in the lungs. The CO2 is then exhaled and only water remains.

Buffering capacity of blood components

The amount of bicarbonate that combines with H+ equals the amount of acid buffered. When lactic acid decreases the pH from 7.4 to 7.0, more than 60% of the bicarbonate initially present in the blood has been used. Even under resting conditions, the acid produced by the end products of metabolism would use up a major portion of the bicarbonate from the blood if there were no other way of removing H+ from the body. Blood and chemical buffers are required only to transport metabolic acids from their sites of production(the muscles) to the lungs or kidneys, where they can be removed. Once H+ is transported and removed, the buffer molecules can be reused.
In the muscle fibers and the kidney tubules. H+ is primarily buffered by phosphates, such as phosphoric acid and sodium phosphate. Less is known about the capacity of the buffers intracellularly, although cells contain more protein and phosphates and less bicarbonate than do the extracellular fluids.
As noted earlier, any increase in free H+ in the blood stimulates the respiratory center to increase ventilation. This facilitates the binding of H+ to bicarbonate and removal of carbon dioxide. The end result is a decrease in free H+ and in increase in blood pH. Thus, both the chemical buffers and the respiratory system provide short-term means of neutralizing the acute effects of exercise acidosis. To maintain a constant buffer reserve, the accumulated H+ is removed from the body via excretion by the kidneys and eliminated in urine. The kidneys filter H+ from the blood along with other waste products. This provides a way to eliminate H+ from the body while maintaining the concentration of extracellular bicarbonate.
During sprint exercise, muscle glycolysis generates a large amount of lactate and H+, which lowers the muscle pH from a resting level of 7.1 to less than 6.7. As shown in the table below, an all-out 400m sprint decreases leg muscle pH to 6.63 and increases muscle lactate from a resting value of 1.2 mmol/kg to almost 20 mmol/kg of muscle. Such disturbances in acid-base balance can impair muscle contractility and its capacity to generate adenosine triphosphate(ATP). Lactate and H+ accumulate in the muscle, in part because they do not freely diffuse across the skeletal muscle fiber membranes. Despite the great production of lactate and H+ during  the nearly 60s required to run 400m, these by-products diffuse throughout the body fluids and reach equilibrium after only about 5 to 10 min of recovery. Five minutes after the exercise, the runners described in the table below had blood pH values of 7.10 and blood lactate concentrations of 12.3 mmol/L, compared with a resting pH of 7.40 and a resting lactate level of 1.5 mmol/L.

Blood and muscle pH and lactate concentration 5 minutes after a 400m run


Reestablishing normal resting concentrations of blood and muscle lactate after such an exhaustive exercise bout is a relatively slow process, often requiring 1 to 2h. As shown in the figure below, recovery of blood lactate to the resting level is facilitated by continued lower-intensity exercise, called active recovery. After a series of exhaustive sprint bouts, the participants in this study either sat quietly(passive recovery) or exercised at an intensity of 50% of VO2max. Blood lactate is removed more quickly during active recovery because the activity maintains elevated blood flow through the active muscles, which in turn enhances both lactate diffusion out of the muscles and lactate oxidation.
Although blood lactate remains elevated for 1 to 2h after highly anaerobic exercise, blood and muscle H+ concentrations return to normal within 30 to 40 min of recovery. Chemical buffering, principally by bicarbonate, and respiratory removal of excess carbon dioxide are responsible for this relatively rapid return to normal acid-base balance.

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