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                <term xml:lang="en">O2</term>
                <term xml:lang="en">CO2</term>
                <term xml:lang="en">chemoreflex</term>
                <term xml:lang="en">modeling</term>
                <term xml:lang="en">delays</term>
                <term xml:lang="en">gain</term>
                <term xml:lang="en">exercise</term>
                <term xml:lang="en">hypoxia</term>
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                <term xml:lang="en">ventilatory oscillations</term>
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              <p>We evaluated the mechanisms responsible for the instability of ventilation control system under simultaneous metabolic (exercise) and environmental (hypoxia) stresses, promoting the genesis of periodic breathing. A model following the main concepts of ventilatory control has been tested, including cardiovascular and respiratory parameters, characteristics of peripheral and central chemoreceptors, at mild exercise in hypoxia (FIO 2 =0.145). Interaction between O 2 and CO 2 sensing was introduced following three different modalities. A sensitivity and multivariate regression analyses closely matched with physiological data for magnitude and period of oscillations. Low FIO 2 and long circulatory delay from lungs to peripheral chemoreceptors (DeltaTp) lengthen the period of oscillations, while high peripheral and central chemoresponses to O 2 and CO 2 , low FIO 2 and high DeltaTp increased their magnitude. Peripheral and central O 2 / CO 2 interactions highlight the role of CO 2 on peripheral gain to O 2 and the contribution of peripheral afferences on central gain to CO 2. Our model supports the key role of peripheral chemoreceptors in the genesis of ventilatory oscillations. Differences in the dynamics of central and peripheral components might be determinant for the system stability.</p>
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