KELLEY, KM; GALIMA, MM; REYES, JA; SAK, K; SMOLKO, S; BAKER, ME; LOWE, CG; CA State Univ. Long Beach; CA State Univ. Long Beach; CA State Univ. Long Beach; CA State Univ. Long Beach; CA State Univ. Long Beach; Univ. CA San Diego; CA Sate Univ. Long Beach; : Temporal Relationships in the Stress- and Growth-Endocrine Axes in Marine Fishes. Are the Growth Impacts of Stress Prolonged?

Cortisol mediates physiological adaptations to stressors, including fuel mobilization to support increased energy demands and reduction of energy-expensive processes such as growth or immune function. Long-term stress, however, can be maladaptive since inhibition of important physiological processes cannot be prolonged without serious consequences. Upon encountering a stressor such as catching-&-releasing, fish exhibit rapid (in minutes) and profound (>50-fold) surges in plasma cortisol that are sustained so long as the stressor remains. Cortisol returns toward baseline at a rate that differs among species, regulated in part by metabolizing enzymes that inactivate cortisol, e.g., 11beta-hydroxysteroid dehydrogenase-type-2 (11-beta-HSD-2). The cortisol surge affects endocrine regulators of tissue growth & repair. An insulin-like growth factor-binding protein (IGFBP) is increased by cortisol and in several physiological conditions in which cortisol is elevated and growth is inhibited. The consistent presence of the IGFBP in growth-inhibited fish suggests its utility as a biomarker of the growth impacts of stress. Importantly, the IGFBP may remain elevated even after the cortisol surge has subsided, suggesting that the physiological impacts of cortisol outlast its initial stress-induced surge. Thus, the nature of the stress response itself (e.g., role of 11β-HSD-2) and its secondary effects (e.g., on growth) are significant considerations when assessing the biological impacts of catch-&-release or other stressors. [Funded by CA Sea Grant College Prog. NOAA NA06RG042 2002-03, proj. # R/F-192, & NSF grant IBN0115975.]