The Commentary by Pörtner, Bock and Mark ([Pörtner et al., 2017][1]) elaborates on the oxygen- and capacity-limited thermal tolerance (OCLTT) hypothesis. Journal of Experimental Biology Commentaries allow for personal and controversial views, yet the journal also mandates that ‘opinion and fact

As a consequence of increasing atmospheric CO2, the world's oceans are becoming warmer and more acidic. Whilst the ecological effects of these changes are poorly understood, it has been suggested that fish performance including growth will be reduced mainly as a result of limitations in oxygen transport capacity. Contrary to the predictions given by the oxygen- and capacity-limited thermal tolerance hypothesis, we show that aerobic scope and cardiac performance of Atlantic halibut (Hippoglossus hippoglossus) increase following 14–16 weeks exposure to elevated temperatures and even more so in combination with CO2-acidified seawater. However, the increase does not translate into improved growth, demonstrating that oxygen uptake is not the limiting factor for growth performance at high temperatures. Instead, long-term exposure to CO2-acidified seawater reduces growth at temperatures that are frequently encountered by this species in nature, indicating that elevated atmospheric CO2 levels may have serious implications on fish populations in the future.

Temperature acclimation may offset the increased energy expenditure (standard metabolic rate, SMR) and reduced scope for activity (aerobic scope, AS) predicted to occur with local and global warming in fishes and other ectotherms. Yet, the time course and mechanisms of this process is little understood. Acclimation dynamics of SMR, maximum metabolic rate, AS and the specific dynamic action of feeding (SDA) were determined in shorthorn sculpin (Myoxocephalus scorpius) after transfer from 10°C to 16°C. SMR increased in the first week by 82% reducing AS to 55% of initial values, while peak postprandial metabolism was initially greater. This meant that the estimated AS during peak SDA approached zero, constraining digestion and leaving little room for additional aerobic processes. After eight weeks at 16°C, SMR was restored, while AS and the estimated AS during peak SDA recovered partly. Collectively, this demonstrated a considerable capacity for metabolic thermal compensation, which should be better incorporated into future models on organismal responses to climate change. A mathematical model based on the empirical data suggested that phenotypes with fast acclimation rates may be favoured by natural selection as the accumulated energetic cost of a slow acclimation rate increases in a warmer future with exacerbated thermal variations.

Marine ecosystems provide essential resources and services, with fishes being of prime socio-economic importance. There are alarming global trends of excessive exploitation and habitat degradation of marine fishes, with most commercial stocks either overfished or nearing capacity ( Pauly et al., 2002; FAO, 2014; Pauly and Zeller, 2016). Global climate change is also altering patterns of marine biodiversity, with more pronounced effects expected in the future ( Perry et al., 2005; IPCC, 2014; McNeil and Sasse, 2016). The consequences of over-exploitation, habitat degradation and global climate change are unknown, but there is legitimate concern about irreversible loss of fisheries resources and biodiversity, leading to reduced food security and even direct threats to ecosystem integrity ( Perry et al., 2005; Cheung et al., 2009; Sumaila et al., 2011; Duarte, 2014; Elliott et al., 2015; Pauly and Zeller, 2016). There is a need, therefore, to improve the scientific knowledge base underpinning advice on the sustainable management of marine fish biodiversity and fisheries resources.

SUMMARY: The hypothesis that the increase in post-prandial splanchnic blood flow will be reduced during hypoxia to prioritise blood flow to other organs was tested by measuring cardiac output and gut blood flow during a stepwise hypoxic challenge (five steps, from 20.6 to 3.9 kPa, 5 min of exposure to each level) before and after feeding (equivalent to 2.9% of body mass). Splanchnic blood flow, both absolute and relative to cardiac output, increased after feeding. Mean post-prandial gut blood flow increased by 71% (from 9.6±1.6 to 14.9±1.6 ml min-1 kg-1, means± S.E.M.). Before feeding, gut blood flow was 24.0% of cardiac output,and this increased significantly 24 h after feeding to 34.0%. The absolute post-prandial increase in gut blood flow (5.3±0.9 ml min-1kg-1) was paralleled by an increase in cardiac output(5.4±2.1 ml min-1 kg-1). Hypoxia decreased gut blood flow significantly from 9.6±1.6 to 3.7±1.1 ml min-1 kg-1, corresponding to a decrease in relative gut blood flow from 24 % to 13%. Contrary to our initial hypothesis, and although post-prandial absolute blood flow decreases during hypoxia, the relative proportion of cardiac output reaching the gut did not decrease (34.6%pre-hypoxia versus 26.7% during hypoxia), unlike the situation in non-feeding fish. We propose that, following feeding, relative gut blood flow is maintained because splanchnic hyperaemia occurs as a result of the release of local factors; consequently the reflex vasoconstriction of the gastrointestinal vasculature during hypoxia is not as effective in decreasing gut blood flow as it was before feeding because local hyperaemia out-competes the reflex regulation.