Respiratory acidosis and O2 supply capacity do not affect the acute temperature tolerance of rainbow trout (Oncorhynchus mykiss).

The mechanisms that determine the temperature tolerances of fish are poorly understood, creating barriers to disentangle how additional environmental challenges-such as CO2-induced aquatic acidification and fluctuating oxygen availability-may exacerbate vulnerability to a warming climate and extreme heat events. Here, we explored whether two acute exposures (~0.5 hours or ~72 hours) to increased CO2 impact acute temperature tolerance limits in a freshwater fish, rainbow trout (Oncorhynchus mykiss). We separated the potential effects of acute high CO2 exposure on critical thermal maximum (CTmax), caused via either respiratory acidosis (reduced internal pH) or O2 supply capacity (aerobic scope), by exposing rainbow trout to ~1 kPa CO2 (~1% or 10 000 µatm) in combination with normoxia or hyperoxia (~21 or 42 kPa O2, respectively). In normoxia, acute exposure to high CO2 caused a large acidosis in trout (blood pH decreased by 0.43 units), while a combination of hyperoxia and ~1 kPa CO2 increased the aerobic scope of trout by 28%. Despite large changes in blood pH and aerobic scope between treatments, we observed no impacts on the CTmax of trout. Our results suggest that the mechanisms that determine the maximum temperature tolerance of trout are independent of blood acid-base balance or the capacity to deliver O2 to tissues.

Rapid blood acid-base regulation by European sea bass (Dicentrarchus labrax) in response to sudden exposure to high environmental CO2.

Fish in coastal ecosystems can be exposed to acute variations in CO2 of between 0.2 and 1 kPa CO2 (2000-10,000 µatm). Coping with this environmental challenge will depend on the ability to rapidly compensate for the internal acid-base disturbance caused by sudden exposure to high environmental CO2 (blood and tissue acidosis); however, studies about the speed of acid-base regulatory responses in marine fish are scarce. We observed that upon sudden exposure to ∼1 kPa CO2, European sea bass (Dicentrarchus labrax) completely regulate erythrocyte intracellular pH within ∼40 min, thus restoring haemoglobin-O2 affinity to pre-exposure levels. Moreover, blood pH returned to normal levels within ∼2 h, which is one of the fastest acid-base recoveries documented in any fish. This was achieved via a large upregulation of net acid excretion and accumulation of HCO3- in blood, which increased from ∼4 to ∼22 mmol l-1. While the abundance and intracellular localisation of gill Na+/K+-ATPase (NKA) and Na+/H+ exchanger 3 (NHE3) remained unchanged, the apical surface area of acid-excreting gill ionocytes doubled. This constitutes a novel mechanism for rapidly increasing acid excretion during sudden blood acidosis. Rapid acid-base regulation was completely prevented when the same high CO2 exposure occurred in seawater with experimentally reduced HCO3- and pH, probably because reduced environmental pH inhibited gill H+ excretion via NHE3. The rapid and robust acid-base regulatory responses identified will enable European sea bass to maintain physiological performance during large and sudden CO2 fluctuations that naturally occur in coastal environments.

Motor deficits in children with autism spectrum disorder: a cross-syndrome study.

Recent research suggests that children with autism spectrum disorder (ASD) experience some level of motor difficulty, and that this may be associated with social communication skills. However, other studies show that children with language impairments, but without the social communication problems, are at risk of motor difficulties as well. The aim of the present study was to determine if children with ASD have syndrome-specific motor deficits in comparison to children with specific language impairment (SLI). We used an independent groups design with three groups of children (8-10 years old) matched on age and nonverbal IQ: an ASD group, an SLI group, and a typically developing (TD) group. All of the children completed an individually administered, standardized motor assessment battery. We found that the TD group demonstrated significantly better motor skills than either the ASD or SLI groups. Detailed analyses of the motor subtests revealed that the ASD and SLI groups had very similar motor profiles across a range of fine and gross motor skills, with one exception. We conclude that children with ASD, and SLI, are at risk of clinically significant motor deficits. However, future behavioral and neurological studies of motor skills in children with ASD should include an SLI comparison group in order to identify possible autism-specific deficits.

Comorbid motor deficits in a clinical sample of children with specific language impairment.

The aim of the present study was to compare the motor function of a clinical sample of children with specific language impairment (SLI) to a language-matched comparison group that had not been referred for SLI assessment. A typical language comparison group with similar nonverbal IQ was also included. There were approximately 35 children in each group, aged 9- to 10-years-old, and the children completed a range of standardised language, motor and literacy measures. The results showed that the SLI group scored significantly lower than the language-matched and typical language comparison groups on all of the motor and literacy measures. We conclude that language factors alone are insufficient to explain the extensive comorbid motor and literacy deficits shown by the children with SLI in this study. We suggest that the clinical diagnosis of SLI may be influenced by the presence of additional developmental difficulties, which should be made explicit in assessment procedures, and that intervention strategies, which address the broad range of difficulties experienced by children with a clinical diagnosis of SLI, should be prioritised.