Environment, damage and senescence: modelling the life-history consequences of variable stress and caloric intake

1. Senescence is intimately connected with physiological state, which is affected by the environment. Two aspects of the environment - stress and caloric intake - are investigated in the context of senescence, particularly in the context of repair of damage caused by endogenous and exogenous stressors. 2. In a simple life-history model, the organism is characterized by size (affecting reproductive success) and accumulated damage (affecting survival) at age. The modelled organism experiences an imprinting period, at the end of which it estimates the level of food and damaging sources in the environment. From those, an optimal life history is determined, assuming that reproduction is an allometric function of size. 3. The optimal life history involves a behavioural trait (intensity of foraging) and an allocation process (amount of energy allocated to repair of damage). Subsequent to the imprinting period, the organism lives experiencing levels of stress or caloric intake that differ from those during the imprinting period. The mismatch is such that either the caloric intake is greater post-imprinting than during imprinting or environmental stress is smaller post-imprinting that during imprinting. 4. Since reproduction is given allometrically and the organism cannot shrink, there is no reproductive senescence. In all cases, mortality increases with age. Senescence is caused by accumulated damage and we focus on the allocation of potential growth to repair and environmental mismatch. 5. In the case of stress mismatch, the general qualitative result is that both the optimal level of activity and the allocation to repair are greater than their values in the case of no mismatch and they are positively correlated. For caloric mismatch, during the post-imprinting period the intensity of foraging is greater than that predicted if there were no mismatches. However, we predict either a negative correlation between genes characterizing activity and repair (for small mismatch), no correlation (for moderate mismatch) or positive correlation (for large mismatch). Furthermore, caloric mismatch is predicted to lead to a considerable reduction in lifetime reproduction, but stress mismatch is predicted to induce an increase in stress resistance throughout life with little cost to lifetime reproduction.