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Anttila, K.

Publications and source records attributed to Anttila, K..

4 recordsLinked to original sources

Can exercise training improve mitochondrial thermal responses in rainbow trout cardiomyocytes?

1.Climate-driven warming is challenging the physiological limits of aquatic ectotherms, with cardiac performance emerging as one of the key determinants of thermal tolerance. Cardiac function relies on mitochondrial ATP production, and mitochondrial dysfunction has been linked to cardiac failure at critical temperatures. However, mitochondria are plastic and may represent a target for interventions aimed at improving thermal tolerance in fish. Exercise training improves whole-animal performance in fish, including cardiac thermal performance, and improves mitochondrial function in other taxa. However, its effects on the thermal sensitivity of cardiac mitochondria remain unknown. This study investigated whether exercise-training alters cardiac mitochondrial performance at optimal and critical temperatures in rainbow trout Oncorhynchus mykiss. Farmed rainbow trout were subjected to a four-week exercise training regime, while control fish remained under standard rearing conditions. Cardiac mitochondrial respiration was assessed in permeabilised heart fibres at 16{degrees}C (optimal growth temperature) and 26{degrees}C (temperature associated with cardiac arrhythmia) and several biochemical and nuclear indicators were measured. No significant differences were detected between treatments for any measured variable. However, trained fish generally exhibited higher maximal respiratory capacities and respiratory control ratios, particularly at the elevated temperature, suggesting subtle improvements in mitochondrial function despite considerable inter-individual variation. Temperature influenced mitochondrial performance, increasing proton leak and reducing coupling efficiency. These findings demonstrate that cardiac mitochondrial function is thermally sensitive and represents a potential targeted for improving thermal resilience in aquaculture species. 2. Summary StatementExercise training did not significantly alter cardiac mitochondrial function in rainbow trout but small improvements were observed under heat stress, suggesting modest improvements in mitochondrial function despite considerable inter-individual variation.

physiology↗

Early-life adversity modulates growth trajectories and red blood cell mitochondrial metabolism in king penguin chicks

In many avian species, variation in breeding phenology is known to affect reproductive success. In king penguins, the breeding cycle lasts more than a year, and the start of egg-laying extends over 3 months, with early-breeders laying eggs around December and late-breeders around February. Consequently, late-born chicks have less time to grow and build up their energy reserves before the Austral winter. It is however not known whether late-born chicks display alternative physiological strategies to catch up before winter. Variation in metabolic rate is one important pathway driving differences in growth patterns, as it is directly involved both in energy allocation processes and fitness. The conversion of resources into energy occurs in mitochondria, and the efficiency of this conversion is likely to play a fundamental role in explaining individual heterogeneity in growth and survival. The purposes of this study were to investigate the differences in red blood cell mitochondrial metabolism between early- and late-born king penguin chicks and to assess whether morphometric phenotypes could be explained by differences in mitochondrial metabolism. Late-chicks expressed higher mitochondrial metabolism compared to early-chicks at 100 days post-hatching, probably linked to the stress related to winter environmental conditions and a decrease in parental feeding rates. We did not find a clear association between chick mitochondrial metabolism and growth patterns, suggesting that mostly environmental conditions contributed in explaining different metabolic phenotypes. As king penguin populations in Crozet may face changing breeding conditions (changes in feeding area and foraging trips duration) in relation to global changes, studying the physiological traits and adaptations underlying the chick growth and survival may help understanding the response of king penguins facing challenging conditions.

physiology↗

Early-life environmental effects on mitochondrial aerobic metabolism: an experimental brood size manipulation in wild great tits

Parental care (including postnatal provisioning) is a major component of the offsprings early-life environment. In avian species, the number of chicks in the nest and subsequent sibling competition for food are known to affect chicks growth, leading in some cases to long-lasting effects for the offspring. Because of its central role in converting energy, variation in the offsprings mitochondrial metabolism could be an important pathway underlying variation in growth patterns. Here, we performed a brood size manipulation in great tits (Parus major) to unravel its impact on offsprings mitochondrial metabolism and reactive oxygen species (ROS) production in red blood cells. We investigated the effects of brood size on chicks growth and survival, and tested for long-lasting effects on juvenile mitochondrial metabolism and phenotype. As expected, chicks raised in reduced broods had a higher body mass compared to enlarged and control groups. However, mitochondrial metabolism and ROS production were not significantly affected by the treatment either at chick or juvenile stages. Chicks in very small broods were smaller in size and had higher mitochondrial metabolic rates. The nest of rearing has a significant effect on nestling mitochondrial metabolism, yet variation in mitochondrial metabolism at the early-life stages are not associated with survival chances. The contribution of the rearing environment in determining offspring mitochondrial metabolism emphasizes the plasticity of mitochondrial metabolism in changing environments. Further studies would be needed to closely investigate what are the major environmental cues affecting the offspring mitochondrial metabolism during the growth period.

physiology↗

Transgenerational endocrine disruption? Experimental copper exposure, but not heat stress, leads to elevated egg thyroid hormone levels

Climate change and pollution are some of the greatest anthropogenic threats to wild animals. Transgenerational plasticity - when parental exposure to environmental stress leads to changes in offspring phenotype - has been recently highlighted as a potential mechanism to respond to various environmental and anthropogenic changes across taxa. Transgenerational effects may be mediated via multiple mechanisms, such as transfer of maternal hormones to eggs/fetus. However, sources of variation in hormone transfer are poorly understood in fish, and thus the first step is to characterize whether environmental challenges alter transfer of maternal hormones to eggs. To this end, we explored the genetic and environmental variation (in response to temperature and endocrine disrupting copper) in maternal thyroid hormone (TH), transfer to offspring in a common fish model species, the three-spined stickleback (Gasterosteus aculeatus) using multiple approaches: (i) We compared ovarian TH levels among six populations across a wide geographical range in the Baltic Sea, including two populations at high water temperature areas (discharge water areas of nuclear power plants) and we experimentally exposed fish to (ii) environmentally relevant heat stress and (iii) copper for 7 days. We found that populations did not differ in intraovarian TH levels, and short-term heat stress did not influence intraovarian TH levels. However, copper exposure increased both T4 and T3 levels in ovaries. The next step would be to evaluate if such alterations would lead to changes in offspring phenotype. Capsule: We show that experimental copper exposure, but not heat stress (experimental or among-population variation), leads to elevated ovarian thyroid hormone levels in sticklebacks.

physiology↗