SUMMARY This study is an attempt to gain an integrated understanding of the interactions between temperature, locomotion activity and metabolism in the European sea bass (Dicentrarchus labrax). To our knowledge this study is among the few that have investigated the influence of the seasonal changes in water temperature on swimming performance in fish. Using a Brett-type swim-tunnel respirometer the relationship between oxygen consumption and swimming speed was determined in fish acclimatised to 7, 11, 14, 18, 22, 26 and 30°C. The corresponding maximum swimming speed(Umax), optimal swimming speed (Uopt),active (AMR) and standard (SMR) metabolic rates as well as aerobic metabolic scope (MS) were calculated. Using simple mathematical functions, these parameters were modelled as a function of water temperature and swimming speed. Both SMR and AMR were positively related to water temperature up to 24°C. Above 24°C SMR and AMR levelled off and MS tended to decrease. We found a tight relationship between AMR and Umax and observed that raising the temperature increased AMR and increased swimming ability. However, although fish swam faster at high temperature, the net cost of transport (COTnet) at a given speed was not influence by the elevation of the water temperature. Although Uopt doubled between 7°C and 30°C (from 0.3 to 0.6 m s-1), metabolic rate at Uopt represented a relatively constant fraction of the animal active metabolic rate (40-45%). A proposed model integrates the effects of water temperature on the interaction between metabolism and swimming performance. In particular the controlling effect of temperature on AMR is shown to be the key factor limiting maximal swimming speed of sea bass.

Equatorial populations of marine species are predicted to be most impacted by global warming because they could be adapted to a narrow range of temperatures in their local environment. We investigated the thermal range at which aerobic metabolic performance is optimum in equatorial populations of coral reef fish in northern Papua New Guinea. Four species of damsel fishes and two species of cardinal fishes were held for 14d at 29, 31, 33, and 34°C, which incorporated their existing thermal range (29–31°C) as well as projected increases in ocean surface temperatures of up to 3°C by the end of this century. Resting and maximum oxygen consumption rates were measured for each species at each temperature and used to calculate the thermal reaction norm of aerobic scope. Our results indicate that one of the six species, Chromisatripectoralis, is already living above its thermal optimum of 29°C. The other five species appeared to be living close to their thermal optima (approximately 31°C). Aerobic scope was significantly reduced in all species, and approached zero for two species at 3°C above current-day temperatures. One species was unable to survive even short-term exposure to 34°C. Our results indicate that low-latitude reef fish populations are living close to their thermal optima and may be more sensitive to ocean warming than higher-latitude populations. Even relatively small temperature increases (2–3°C) could result in population declines and potentially redistribution of equatorial species to higher latitudes if adaptation cannot keep pace.

Increases in environmental temperature predicted to result from global warming have direct effects on performance of ectotherms. Moreover, cardiac function has been observed to limit the tolerance to high temperatures. Here we show that two wild populations of Atlantic salmon originating from northern and southern extremes of its European distribution have strikingly similar cardiac responses to acute warming when acclimated to common temperatures, despite different local environments. Although cardiac collapse starts at 21-23°C with a maximum heart rate of B150 beats per min (bpm) for 12°C-acclimated fish, acclimation to 20°C considerably raises this temperature (27.5°C) and maximum heart rate (B200 bpm). Only minor population differences exist and these are consistent with the warmer habitat of the southern population. We demonstrate that the considerable cardiac plasticity discovered for Atlantic salmon is largely independent of natural habitat, and we propose that observed cardiac plasticity may aid salmon to cope with global warming.

The oceans are absorbing excess atmospheric CO2, and this is causing ocean acidification. Surprisingly, one coral reef damselfish exhibits enhanced aerobic performance after living at projected future ocean CO2 levels for 17 days. Identifying both the winners and losers under climate change scenarios is vital to conserving marine biodiversity.

Ocean surface CO2 levels are increasing in line with rising atmospheric CO2 and could exceed 900 μatm by year 2100, with extremes above 2000 μatm in some coastal habitats. The imminent increase in ocean pCO2 is predicted to have negative consequences for marine fishes, including reduced aerobic performance, but variability among species could be expected. Understanding interspecific responses to ocean acidification is important for predicting the consequences of ocean acidification on communities and ecosystems. In the present study, the effects of exposure to near-future seawater CO2 (860 μatm) on resting (Ṁ O2rest) and maximum (Ṁ O2max) oxygen consumption rates were determined for three tropical coral reef fish species interlinked through predator-prey relationships: juvenile Pomacentrus moluccensis and P. amboinensis, and one of their predators: adult Pseudochromis fuscus. Contrary to predictions, one of the prey species, P. amboinensis, displayed a 28 – 39 % increase in Ṁ O2max after both an acute and four-day exposure to near-future CO2 seawater, while maintaining Ṁ O2rest. By contrast, the same treatment had no significant effects on Ṁ O2rest or Ṁ O2max of the other two species. However, acute exposure of P. amboinensis to 1400 and 2400 μatm CO2 resulted in Ṁ O2max returning to control values. Overall, the findings suggest that: (1) the metabolic costs of living in a near-future CO2 seawater environment were insignificant for the species examined at rest; (2) the ṀO2max response of tropical reef species to near-future CO2 seawater can be dependent on the severity of external hypercapnia; and (3) near-future ocean pCO2 may not be detrimental to aerobic scope of all fish species and it may even augment aerobic scope of some species. The present results also highlight that close phylogenetic relatedness and living in the same environment, does not necessarily imply similar physiological responses to near-future CO2.

We have investigated the role of the membrane molecules CD11/CD18 and CD14 which may mediate the binding of lipopolysaccharide (LPS) to human monocytes, in the induction of the production and release of interleukin (IL)-1 and tumor necrosis factor-alpha (TNF-alpha) by LPS-stimulated cells. Blockade of CD11a, CD11b and CD18 with saturating concentrations of specific mAb did not inhibit the release of cytokines from LPS-stimulated monocytes. In contrast, inhibition of the release of IL-1 beta and TNF-alpha occurred in monocytes cultures that had been pretreated with either of two monoclonal antibodies (mAb) recognizing different epitopes on the CD14 molecule. The binding of LPS to CD14 has been previously shown to require serum factors. In the present study, we found that serum had an enhancing effect on the release of IL-1 and TNF-alpha from LPS-stimulated cultures of normal human monocytes. The inhibitory effect of anti-CD14 mAb was, however, observed in cultures performed in the presence or in the absence of serum, suggesting that triggering of IL-1/TNF-alpha release by CD14 is independent of LPS-binding proteins or other serum proteins. IL-1 beta and TNF-alpha were also released from LPS-stimulated cultures of monocytes from patients with paroxysmal nocturnal hemoglobinuria lacking expression of CD14. Thus, CD14 but not CD11/CD18 can trigger serum-dependent and independent cytokine release from endotoxin-stimulated normal human monocytes; CD14 is not, however, the only LPS receptor that is involved in the secretory response of endotoxin-stimulated cells.

Serum-free culture of human monocytes in the presence of monoclonal antibodies to the LFA-1 alpha chain (CD11a), CR3 alpha chain (CD11b) or beta chain (CD18) bound to Sepharose induced the dose-dependent production of cell-associated interleukin (IL) 1 activity and of IL 1 alpha and IL 1 beta antigens, but no release of extracellular IL 1 activity or antigen in the culture medium. Triggering of IL 1 production was also observed with insolubilized anti-CD11/CD18 F(ab')2 antibodies. Two cross-linked antibodies recognizing distinct epitopes on the CD11b molecule induced cell-associated IL 1. Soluble antibodies did not induce IL 1 production. The kinetics of induction of IL 1 by stimulation of adhesion-promoting proteins differed from those of IL 1 induction by adhesion to plastic. The lack of induction of IL 1 release by stimulation of the CD11/CD18 molecules resembled the intracellular accumulation of IL 1 induced by lipid A. Induction of IL 1 by adhesive processes may be a mechanism by which T cells trigger IL 1 production by monocytes during antigen presentation.

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