The activity and movement of the human diaphragm muscle is coordinated for both ventilatory and postural tasks. Thus, dynamic exercise-induced hyperpnoea might elicit larger pressure and kinetic responses than static CO2-induced hyperpnoea. Subcostal ultrasonography offers a direct measure of diaphragm kinetics in the form of craniocaudal displacement and displacement velocity. Our primary aim was to investigate the feasibility of diaphragm ultrasonography for the quantification of diaphragm kinetics during CO2-induced hyperpnoea and ramp cycle exercise. Methods: Ten healthy participants (5 women; mean ± SD age 22 ± 2 years) underwent modified Read CO2 rebreathing method (3.1 ± 1.0 min) and maximal ramp exercise on a recumbent cycle ergometer (8.0 ± 2.1 min). Initially, the closed-circuit rebreathing bag contained 5% CO2 and 95% O2, and the test was terminated at PETCO2 of 55 mmHg. A low-frequency (2.4 – 5.0 MHz), curve-linear ultrasound probe (Vivid 7, GE Health), positioned subcostally on the right mid-clavicular line, provided 15 s cine-loops twice each minute. These cine-loops were time-matched offline with breath-by-breath pressure and ventilatory responses. Diaphragm displacement was measured with anatomic M-mode, and displacement velocity was calculated by dividing inspiratory diaphragm displacement by inspiratory displacement time. Results: Diaphragm displacement and displacement velocity were quantifiable in 94% (range 72-100%) and 97% (84-100%) of the ultrasound-derived cine-loops during exercise and CO2 rebreathing, respectively. Feasibility was independent of test mode, minute ventilation (VE) and tidal volume. VE increased similarly between the two tests (p = 0.920). When matched for similar VE, Pdi was significantly higher during exercise than CO2 rebreathing (p = 0.023); increasing from 12.0 ± 1.5 to 18.9 ± 3.0 cmH2O (exercise) and from 10.0 ± 2.6 cmH2O to 15.8 ± 2.6 cmH2O (CO2 rebreathing). Although diaphragm displacement was similar for the two tests at rest (18.6 ± 7.6 mm; p = 0.327), the diaphragm showed significantly larger (p = 0.015) displacement during CO2 rebreathing (34.10 ± 1.07 mm) than during exercise (27.87 ± 2.90 mm). During both tests, displacement velocity increased as a function of inspiratory flow (CO2 rebreathing: r = 0.959; exercise: r = 0.982), and the displacement velocity did not differ significantly between the test modes (p = 0.371). Conclusion: Kinetic responses of the human diaphragm can be quantified during reflexively driven hyperpnoea. When matched for similar VE, the diaphragm muscle generates higher pressures during exercise, but moves significantly less. Diaphragm displacement may be constrained during exercise due to the quasi-isometric contraction required for simultaneous postural support and meeting ventilatory demands.