The ion damage produced in alloys of AlxGa1−xAs (x = 0.6, 0.7, 0.8, and 0.85) by implantation at 77 K with Kr ions (500, 700, and 1500 keV) was studied by using Rutherford backscattering channeling and transmission electron microscopy. In addition, the accumulation of ion damage at 50 K was studied by performing the ion implantations in situ in the transmission electron microscope. In Al0.8Ga0.2As, damage accumulation at 77 K was independent of dose rate, indicating that dynamic annealing is not occurring at 77 K. The in situ studies demonstrated that planar defects are produced on warm-up from 50 K to room temperature, indicating that they are not the nucleation site for amorphization. The lower energy implantations revealed that amorphization initiated within the AlxGa1−xAs layer, showing that heterointerfaces are not required for amorphization. These results, along with the similarity of the room-temperature microstructures in the different alloys, imply that the amorphization mechanism is independent of Al content. It is proposed that the observed dependence of the amorphization dose on Al content is related to an increase in the number of cascade overlaps needed to initiate and to produce a continuous amorphous layer. A mechanism explaining the microstructural changes with composition, based on the thermal and physical properties of the alloy and on the distribution of energetic cascade events, is presented.