Abstract
Elasmobranchs (i.e., sharks, skates, and rays) are considered highly vulnerable to population declines, largely due to their life history strategy and their global exploitation in directed and non-directed fisheries. Despite recent attempts to preserve shark populations through mandatory release of certain species upon capture, the outcomes of catch-and-release fishing are poorly understood. Moreover, the large degree of capture-induced physiological stress experienced by sharks may result in mortality in the minutes to days following release (i.e., post-release mortality). Work on sharks suggests that elevated levels of plasma potassium (i.e., hyperkalemia) may be correlated with higher rates of post-release mortality, and work on bony fish suggests that other physiological disruptions associated with capture-stress (e.g., low oxygen and pH of the blood), or unfavorable environmental conditions (e.g., elevated ambient temperature) may also impact survival following release. In bony fishes, physiological disruptions arising from capture may alter the contraction-relaxation cycling of the heart by shifting intracellular ion gradients within the muscle cells and reducing heart contractility. While these physiological disruptions of the blood are also well documented in the blood of elasmobranchs, their influence on cardiac function is unknown. Cardiac recovery from capture may be possible through an increased adrenaline response (e.g., restoring contractile force), including enhanced release of calcium from the sarcoplasmic reticulum (SR). My research focuses on how changes in blood biochemistry arising from capture may impact myocardial function in elasmobranchs, and the potential role of adrenaline and SR calcium in counteracting these effects. Findings from this work show that hyperkalemia, low oxygen, low pH, and temperature change (i.e., "stressors") had negative, species-specific effects on cardiac function, however, these effects were unexpectedly lessened when stressors were applied concurrently. Adrenaline improved cardiac function in some situations and for some species, and SR calcium did not enhance myocardial function under stressful conditions, indicating it does not appear to aid in recovery following capture stress in the study species. Given the global decline in shark populations, identifying physiological causes that may correspond with elevated levels of post-release mortality and exploring the extent to which the heart may recover from capture is the first step in identifying interspecific sensitivities to capture and considering mitigation plans for reduced post-release mortality.