Figure 1.

Framework for understanding the effects of thermal stress on glucocorticoid physiology, life history, and fitness across generations. (A) Repeated acute or chronic exposure to heat stress is expected to result in elevated glucocorticoid levels because chronic thermal stressors increase baseline glucocorticoid levels (e.g., Jessop et al., 2016; Mentesana & Hau 2022; Narayan & Hero 2014). Such effects are predicted to increase energy demand, which will reduce body condition (assuming resources are limited), and compromise reproduction and survival probability over the long term; (B) focusing on offspring from F₀ adults exposed to thermal stress, as indicated by the dashed lines to F₁ box, intergenerational effects (e.g., maternal effects) are expected to result in either (i) sensitization of the HPA (i.e., Developmental Sensitization Hypothesis) or (ii) desensitization of HPA responses (i.e., Developmental Desensitization Hypothesis) in F₁ offspring. The yellow dot on the y-axis in each figure represents the hypothetical GC concentration of F₀ adults. Under the Developmental Sensitization Hypothesis, baseline glucocorticoid levels in the F₁ are expected to increase because the offspring HPA is more reactive to stressors (i.e., higher peak responses and slower return to baseline—denoted by differences in red response curve “R”). If offspring are exposed to repeated thermal stressors (i.e., an environment like their parents), repeated acute responses lead to elevated glucocorticoid levels (denoted by higher baseline “B” glucocorticoid levels) and we expect reduced growth, slower age at maturity, and decreased life span and reproduction in offspring. Under the Developmental Desensitization Hypothesis, maternal effects are expected to cause the HPA axis in offspring to become less responsive to stressors (i.e., reduced peak glucocorticoid levels and faster return to baseline). (C) Transgenerational effects of glucocorticoids can be long lasting (i.e., epigenetic, or behavioral perpetuation—across many generations) or transient (hormonal, resource driven—across one or a couple generations) with their effects on population persistence depending on environmental predictability (i.e., matched or unmatched environments). Under the Developmental Sensitization Hypothesis, positive feedback could occur, such that responses are compounded across generations under repeated environmental stress. The HPA axis (H = Hypothalamus; P = Pituitary gland; A = Adrenal glands) is expected to become more sensitive for a larger fraction of the population. In this scenario, reduced population growth is expected because of the negative effects of chronically elevated glucocorticoids on life-history traits, affecting survival and reproduction,increases the probability of population extinction. In contrast, developmental desensitization could reduce the sensitivity of the HPA axis in subsequent generations, reducing glucocorticoid levels and exerting a neutral or beneficial effect on organism fitness.