Immediate and delayed effects of gill-net capture on acid–base balance and intramuscular lactate concentration of gummy sharks, Mustelus antarcticus ☆ Lorenz H. Frick a, ⁎, Terence I. Walker b , Richard D. Reina a a School of Biological Sciences, Monash University, Wellington Road, Clayton, Victoria 3800, Australia b Marine and Freshwater Fisheries Research Institute, Department of Primary Industries Queenscliff Centre, Bellarine Highway 2a, Queenscliff, Victoria 3225, Australia abstract article info Article history: Received 19 September 2010 Received in revised form 20 February 2011 Accepted 22 February 2011 Available online 3 March 2011 Keywords: Acid–base balance Capture stress Delayed mortality Gill-net Gummy shark Intramuscular lactate Metabolic scope Many sharks are captured as untargeted by-catch during commercial fishing operations and are subsequently discarded. A reliable assessment of the proportion of discarded sharks that die post-release as a result of excessive physiological stress is important for fisheries management and conservation purposes, but a reliable physiological predictor of post-release mortality has not been identified. To investigate effects of gill-net capture on the acid–base balance of sharks, we exposed gummy sharks, Mustelus antarcticus, to 60 min of gill-net capture in a controlled setting, and obtained multiple blood and muscle tissue samples during a 72-h recovery period following the capture event. Overall mortality of gummy sharks was low (9%). Blood pH was significantly depressed immediately after the capture event due to a combination of respiratory and metabolic acidosis. Maximum concentrations of plasma lactate (9.9±1.5 mmol L -1 ) were measured 3 h after the capture event. Maximum intramuscular lactate concentrations (37.0±4.6 μmol g -1 ) were measured immediately after the capture event, and intramuscular lactate concentrations were substantially higher than plasma lactate concentrations at all times. Sharks in poor condition had low blood pH and high intramuscular lactate concentration, but blood pH does not appear to be a reliable predictor of survival. Suitability of intramuscular lactate concentration as predictor of delayed mortality deserves further investigation. © 2011 Elsevier Inc. All rights reserved. 1. Introduction Fishing capture has been shown to elicit profound physiological changes in elasmobranchs (e.g. Cliff and Thurman, 1984; Manire et al., 2001; Mandelman and Skomal, 2009; Frick et al., 2010a; Frick et al., 2010b), but information on the post-release fate of sharks that are incidentally captured during fishing operations and subsequently discarded alive is still scarce compared with the large amount of publications addressing delayed effects of capture stress in teleosts. Discard rates of sharks are high in global fisheries (see Stevens et al., 2000), and reliable estimates of discard mortality are essential to assess the overall impact of fishing pressure on shark populations. Identification of a suitable physiological predictor of delayed mortality could facilitate an accurate assessment of the proportion of sharks that are discarded alive, but die post-release as a direct consequence of physiological capture stress. The problem of discard mortality will ultimately have to be addressed with data collected under natural conditions, but circumstances in the wild allow only one opportunity for blood sampling — immediately after the capture event and prior to the shark's release. Our recent study on the post-capture condition of gummy sharks, Mustelus antarcticus, found that sharks which died post-release displayed significantly higher blood lactate and potassium concentrations than surviving sharks, but these differences did not become apparent until hours after the capture event (Frick et al., 2010a). Blood lactate and potassium concentrations measured immediately after the capture event did not allow a prediction of a shark's probability of survival. The physiological mechanisms underlying delayed mortality are still not fully understood. Sharks undergo metabolic and/or respiratory blood acidosis following capture, handling, and release (e.g. Cliff and Thurman, 1984; Mandelman and Farrington, 2007), and Mandelman and Skomal (2009) found a positive correlation between the degree of blood acid–base disturbance and at-vessel mortality of carcharhinid sharks. However, Wood et al. (1983) concluded that blood acidosis was unlikely to cause delayed mortality in fish, and suggested that the key toxic event leading to delayed mortality occurred in the intracellular compartment as a consequence of an intracellular build-up of metabolic protons. Richards et al. (2003) found that white muscle lactate production was correlated with metabolic acidosis in spiny dogfish, Squalus acanthias, following exhaustive exercise, but a possible connection between the extent of blood acid–base disturbance or intramuscular lactate concentration and post-capture condition of sharks has not been investigated. Comparative Biochemistry and Physiology, Part A 162 (2012) 88–93 ☆ This paper stems from a presentation in the Symposium "The Physiological Stress Response in Elasmobranch Fishes", at the 26th annual meeting of the American Elasmobranch Society, held on July 11, 2010, in Providence, Rhode Island (USA). ⁎ Corresponding author at: Dorfstr. 43, CH-8712 Staefa, Switzerland. Tel.: +41 76 329 4536. E-mail addresses: lofrick@gmx.net (L.H. Frick), terry.walker@dpi.vic.gov.au (T.I. Walker), richard.reina@monash.edu (R.D. Reina). 1095-6433/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.cbpa.2011.02.023 Contents lists available at ScienceDirect Comparative Biochemistry and Physiology, Part A journal homepage: www.elsevier.com/locate/cbpa