The response of bacteria to sub-lethal injury is an important aspect of food microbiology as many inimical processes to which bacteria are subjected during processing are non-lethal. For pathogens like Salmonella and Escherichia coli, the difference in injury levels of exponential phase cells compared to their stationary phase counterparts in this regard is well recognised and evident for a variety of inimical processes. The expression of a range of stress resistance genes under the control of the sigma factor RpoS provides some explanation for the greater resistance of stationary phase cells. However in 1997 the suicide response hypothesis was put forward as an explanation for the observed response of Salmonella and E. coli to sub-lethal stresses. This hypothesis arose as an explanation for the observed protection of Salmonella and E. coli strains to heat and freeze-thaw injury by the presence of a high level of competitor organisms, a protection that had been shown to be RpoS independent. The central tenet of this theory was that under sub-lethal stress bacteria produce a burst of intracellular free radicals and it is these that lead to sub-lethal injury and/or death. Exponential phase cells because of their more active metabolism are more susceptible to this effect and suffer greater damage. This paper reviews the origins of this theory, the evidence for a free radical response and explores the potential mechanisms by which competitor cells produce a protective effect.