Many of the profound changes in metabolism that are caused by O 2 deficiency also occur in well-aerated tissues when oxidative phosphorylation is partially or wholly inhibited. For these well-aerated tissues, reduction in energy formation occurs during exposure to inhibitors of oxidative phosphorylation, cold/chilling and wounding, so we prefer the term 'energy crisis' metabolism over 'anaerobic' metabolism. In this review, we note that the overwhelming body of data on energy crises has been obtained by exposure to hypoxia-anoxia, which we will indicate when discussing the particular experiments. We suggest that even transient survival of an energy crisis requires a network of changes common to a large number of conditions, ranging from changes in development to various adverse conditions such as high salinity, drought and nutrient deficiency, all of which reduce growth. During an energy crisis this general network needs to be complemented by energy specific proteins, including the so called 'anaerobic proteins' and the group of ERFVII transcription factors, which induces the synthesis of these proteins. Crucially, the difference between anoxia-intolerant and -tolerant tissues in the event of a severe energy crisis would mainly depend on changes in some 'key' energy crisis proteins: we suggest these proteins would include phytoglobin, the V-H+ PP i ase and pyruvate decarboxylase. A second characteristic of a high tolerance to an energy crisis is engagement of energy efficient transport. This feature includes a sharp reduction in rates of solute transport and use of energy-efficient modifications of transport systems by primary H+ transport and secondary H+-solute transport systems. Here we also discuss the best choice of species to study an energy crisis. Further, we consider confounding of the acclimative response by responses to injury, be it due to the use of tissues intolerant to an energy crisis, or to faulty techniques.