We examined the separate effects of acute hypercapnia and acute hypoxia on the electromyographic activity (EMG) of the costal and crural diaphragm in 6 anesthetized spontaneously breathing piglets (age 12–23 days, weight 3.00–4.37 kg). Bipolar wire electrodes were inserted into the anterior paratendinous costal diaphragm and the midportion of the crural diaphragm. EMG activity was quantified in arbitrary units (au) of peak moving time average while the animals breathed 50% O2/50% N2(baseline) and after 30 min of either hypercapnia (12% CO2) or hypoxia (12% O2) exposure. After 30 min of hypercapnia, the peak moving time average EMG increased in both parts of the diaphragm with the increase in crural diaphragm EMG activity (from baseline: 20 ± 2 au to 30 min 12% CO2: 83 ± 20 au) not being significantly different from that observed in the costal diaphragm (from baseline: 21 ± 2 au to 30 min 12% CO2: 72 ± 20 au,p= 0.17). Similarly, the peak moving time average EMG increased in both parts of the diaphragm after 30 min of hypoxia with the increase in the crural diaphragm EMG activity (from baseline: 21 ± 2 au to 30 min 12% O2: 28 ± 6 au) not being significantly different from that observed in the costal diaphragm (from baseline: 21 ± 1 au to 30 min 12% O2: 26 ± 7 au,p= 0.51). These data indicate that the inspiratory EMG activity of the diaphragm is not differentially distributed between its costal and crural components during chemically stimulated breathing in piglets.