D3 is converted to 1,25(OH)2-D3 which is the active form. The transformation is limited by 1α(OH)-ase which in turn is regulated by levels of calcium and PTH and degraded by renal 24-OH-ase, which previous work has shown is upregulated by high 1,25(OH)2-D3, and 25(OH)D (formed in the liver from the oral cholecalciferol), thereby providing a brake on the system. It has also been shown that the upregulation of 24(OH)ase can be enough to actually decrease 1,25(OH)2-D3 levels, thereby resulting in osteoclastic activity. PTH is also suppressed by high 1.25(OH)2-D3.

tl;dr there are homeostatic mechanisms in place in calcium metabolism that result in a "counterintuitive" reduction in the active metabolite with supraphysiologic supplementation. Also, this is actually in line with prior work, though the authors don't mention any of it until the discussion at the end, and then only two papers. In about 5 minutes of searching, I found papers going back to 1995 suggesting the same thing.