Cellular calcium homeostasis is disturbed during brief periods of ischemia, with free cytosolic Ca ([Ca2+]i) rising severalfold within 10-15 minutes (or even sooner). Nevertheless, the myocardial cells' ability to regulate Ca recovers quickly after reperfusion, unlike the lingering depression of contractile function known as stunning. This brief commentary considers the hypothesis that the rise in cell calcium during ischemia and during early reperfusion leaves behind stunning as an unwelcome legacy. This idea by no means excludes the involvement of other factors, such as free radicals; instead, it suggests a possible common pathway for cell injury by a variety of specific agents. A provocative feature of the formulation is the idea that the crucial lesion in stunning occurs at the level of the contractile proteins, rather than more proximally.