Linking extrinsic with intrinsic factors: the effects of stress on reproduction may be adaptive

In small mammal population cycles, after explosive reproduction during the phase of increasing population density the animals slow their reproductive rate during the high-mortality decline phase. Existing theory about reproductive restraint involves delayed compensating benefits, but those are of little value during the decline phase when survival is very unlikely. Changing prevalence of differing genotypes has been ruled out for small mammal populations, so now the reproductive slowdown is attributed to stress, which is known to suppress reproduction and have trans-generation effects. But why are there no stress-immune animals that keep reproducing at a high rate regardless of circumstances? This analysis shows why there is an immediate benefit of reproductive restraint: it both slows the rate of decline and diminishes the probability of local extinction. With a simple model I calculate how reproduction should vary to maximize the probability of persistence under differing mortality rates, and then simulate the evolution of a reaction norm of reproductive effort under cycling mortality rates. I find that animals should restrain reproduction when mortality rates are high or very low. These results link the death rates produced by extrinsic factors with the intrinsic change in reproductive output and show why the effects of stress on reproductive output seem appropriate.