The lack of structural adaptability to exercise is a major weakness in the pulmonary system. 2 For example, when pulmonary blood flow and VO2 increases with aerobic training, lung diffusion capacity and pulmonary capillary blood volume remain unchanged in highly trained individuals. 2 Furthermore, when the rate of ventilation increases with duration or intensity of an aerobic training session, there is no change in the capability of the airways or lungs to produce higher flow rates to facilitate the increase in ventilation that is needed. 2 (more…)
Ventilatory threshold is the point at which pulmonary ventilation (minute ventilation) increases in a non-linear fashion in relation to oxygen consumption (Fig. 1). This occurs when exercise intensity increases and becomes more anaerobic, closely coinciding with the shift towards blood and muscle acidosis caused by onset of lactate accumulation. The underlying cause of this involves sodium bicarbonate buffers acting to counteract the acidosis resulting from dissociation of the accumulated lactic acid. (more…)
Pulmonary ventilation is controlled via neural (afferent) feedback receptors located in the brain, lungs, and other parts of the body. These control mechanisms act to regulate alveolar and arterial gas pressures during exercise of varying intensities. Neurons within the medulla are responsible for controlling the physical mechanisms involved with normal respiration by causing the diaphragm and intercostal muscles to contract, in turn causing the lungs to fill with air. (more…)
Pulmonary ventilation is one of the three naturally occurring buffer mechanisms that regulate the body’s pH during exercise. As exercise intensity increases, more CO2 is produced, which reacts with H2O to form H+ protons. This process results in acidosis, or lowering of pH, which continues to drop as exercise intensity increases. (more…)
