The coordination of respiratory muscle activity is essential to move air in and out of the lungs. At rest, inspiration is an active process with contractions of diaphragmatic (DIA) and external intercostal muscles (eIC), while the expiratory airflow is generated by elastic recoil forces of the thorax and lungs. Exposure to reduced oxygen (hypoxia) or elevated carbon dioxide levels (hypercapnia) transforms expiration into an active process, with the recruitment of abdominal (ABD) and internal intercostal muscles (iIC) that increase the expiratory flow. It remains unclear how the ABD and iIC muscles are coordinated during active expiration and how their entrainment modifies the expiratory flow to improve pulmonary ventilation. In the present study, we examined the ABD and iIC muscle activity patterns and the corresponding alterations in the expiratory flow during conditions of hypoxia and hypercapnia. Electrodes were implanted in the DIA, eIC, iIC, and ABD muscles of anesthetized (urethane, 1.2 mg/kg, i.v.) adult male Holtzman rats (n=8, 250-300 g). These animals also received a snout mask that allowed exposure to gas mixtures while monitoring nasal airflow. Experiments were performed under anesthesia. Physiological parameters were recorded under resting conditions and during 10-min exposure to hypoxia (7% O₂) and hypercapnia (7% CO₂). All procedures were approved by the institutional Ethics Committee (#17/2020). Values are expressed as mean±SD and compared using one-way ANOVA followed by Bonferroni or Friedman post-tests. Under resting conditions, DIA and eIC showed synchronized bursts during the inspiratory phase, ABD and iIC were silent, and the expiratory flow peaked during the first expiration stage. Hypoxia caused an initial increase in the respiratory frequency (fR) (resting: 88±11 vs 2^nd-min: 113± 19 bpm, P<0.01), elicited a sustained increase in DIA (∆: 25-41%) and eIC (∆: 37-58%) burst amplitudes (P<0.05), and brought about phase-locked ABD (∆: 60-120%) and iIC (∆: 116-325%) expiratory bursts (P<0.05) during the initial six minutes of exposure. These hypoxia-induced respiratory motor changes were accompanied by increased airflow during the second stage of expiration. Under hypercapnic conditions, fR increased during the last 2 min of exposure (resting: 85±12 vs 10^th-min: 97±14 bpm, P=0.0299), DIA (∆: 45-56%) and eIC (∆: 111-128%) burst amplitudes were higher throughout the exposure time (P<0.05), and ABD (∆: 105-144%) and iIC (∆: 219-255%) expiratory activities were higher during the last four minutes of exposure (P<0.02). The respiratory motor responses to hypercapnia did not change the airflow pattern, peaking during the first stage of expiration as noted during resting conditions. Our data indicate that hypoxia and hypercapnia exposures evoke entrained ABD and iIC bursts during the expiratory phase. However, their recruitment timing differs between gas conditions, occurring earlier under hypoxia than in hypercapnia. Moreover, their impact on the expiratory airflow is different, indicating that the adjustments of active expiration on the pulmonary mechanics involve stimulus-dependent recruitment of additional respiratory muscles.