Ventilatory response to exercise

Beyond this point, during more severe exercise associated with anaerobic metabolism, minute ventilation increases faster than the rate of oxygen consumption, but proportionally to the increase in carbon dioxide production. The mechanism of the ventilatory response to severe exercise involves metabolic acidosis caused by anaerobic metabolism. The lactic acid produced under these conditions liberates an H+ ion that effectively stimulates the peripheral chemoreceptors to increase ventilation. 

During exercise, the increase in minute ventilation results from increases in tidal volume and breathing frequency. Initially, the increase in tidal volume is greater than the increase in breathing frequency. As discussed earlier in this chapter, increases in tidal volume increase alveolar ventilation more effectively. Subsequently, however, as metabolic acidosis develops, the increase in breathing frequency predominates. 

The mechanisms involved with the ventilatory response to exercise remain quite unclear. No single factor, or combination of factors, can fully account for the increase in ventilation during exercise. Therefore, much of this response remains unexplained. Factors that appear to play a role include  

Proprioceptors originating in muscles and joints of the exercising limbs provide substantial input to the medullary respiratory center. In fact, even passive movement of the limbs causes an increase in ventilation. Therefore, the mechanical aspects of exercise also contribute to the ventilatory response. The increased metabolism associated with exercise increases body temperature, which further contributes to the increase in ventilation during exercise. (Not surprisingly, ventilation is also enhanced in response to a fever.) Exercise is associated with a mass sympathetic discharge. As a result, epinephrine release from the adrenal medulla is markedly increased. Epinephrine is believed to stimulate ventilation. 

Levitsky, M.G., Pulmonary Physiology, 5th ed., McGraw-Hill, New York, 1999. 

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In a series of studies of ACE inhibitor-induced improvement in pulmonary function, treatment with aspirin 325 mg/day for 8 weeks in patients with mild to moderate heart failure due to primitive dilated cardiomyopathy did not affect ventilation and peak oxygen consumption during exercise when the patients were not taking an ACE inhibitor but worsened pulmonary diffusion capacity and made the ventilatory response to exercise (tidal volume, ventilation to carbon dioxide production) less effective in those who were, regardless of the duration of ACE inhibition (108). 

Witte KK, Thackray S, Nikitin NP, Cleland JG, Clark AL. The effects of long-term beta-blockade on the ventilatory responses to exercise in chronic heart failure. Eur J Heart Fail 2005 7 612-7. 

Schoene RB, Lahiri S, Hackett PH, Peters RM, Jr., Milledge JS, Pizzo CJ, Samquist FH, Boyer SJ, Graber DJ, Maret KH, West JB. Relationship of hypoxic ventilatory response to exercise performance on Moimt Everest. J Appl Physiol 1984 56 1478-1483. 

In contrast, hypnotic doses of benzodiazepines may worsen sleep-related breathing disorders by adversely affecting control of the upper airway muscles or by decreasing the ventilatory response to CO2. The latter effect may cause hypoventilation and hypoxemia in some patients with severe COPD, although benzodiazepines may improve sleep and sleep structure in some instances. In patients with obstructive sleep apnea (OSA), hypnotic doses of benzodiazepines may exaggerate the impact of apneic episodes on alveolar hypoxia, pulmonary hypertension, and cardiac ventricular load. Caution should be exercised with patients who snore regularly partial airway obstruction may be converted to OSA under the influence of these drugs. 

In earlier researches [8], it was suggested that normal ventilatory responses to CO2, exercise inputs, and mechanical loading could be predicted by the minimization of a controller objective function consisting of total chemical and mechanical cost of breathing. The optimal respiratory control model was later proposed and verified by optimizing a quadratic inspiratory neural drive [9]. The optimal instantaneous airflow and lung volume were derived based on a lumped-parameter RC model [10] for the relation between respiratory neural and mechanical outputs. 

Vallebona A, Gigli G, Orlandi S, Reggiardo G. Heart rate response to graded exercise correlates with aerobic and ventilatory capacity in patients with heart failure. Clin. Cardiol. 2005 28 25-9. 

Modeling of gas transport is also useful for correlating dose-response data obtained under different conditions. Brain suggested that the total dose of an inhaled gas is relate to ventilation rate, duration of exposure, and gas concentration before inhalation. Folinsbee et al. exposed human subjects to ozone at 0.37, 0.5, or 0.75 ppm for 2 h while they were at rest or exerdsing intermittently. The primary response of the subjects was an alteration in the exercise ventilatory pattern. They... 

A potential drawback of such a hierarchical system is that it is nonrobust to perturbations. Changes in ventilatory load, for example, would disrupt the ventilatory command from the feedforward signal. This is at variance with the experimental observation of a load compensation response of the controller which protects ventilation against perturbations of the mechanical plant at rest and during exercise [Poon et al, 1987a, b Poon, 1989a, b]. Furthermore, if the prime objective of the controller were indeed to meet the metabolic demand (i.e., to maintain chemical homeostasis), then the hierarchical control system seems to perform quite poorly it is well known that arterial chemical homeostasis is readily disrupted environmental changes. 

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