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Cardiorespiratory physiological phenotypic plasticity in developing air‐breathing anabantid fishes (Betta splendens and Trichopodus trichopterus)
Developmental plasticity of cardiorespiratory physiology in response to chronic hypoxia is poorly understood in larval fishes, especially larval air‐breathing fishes, which eventually in their development can at least partially “escape” hypoxia through air breathing. Whether the development air brea...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5555888/ https://www.ncbi.nlm.nih.gov/pubmed/28778991 http://dx.doi.org/10.14814/phy2.13359 |
Sumario: | Developmental plasticity of cardiorespiratory physiology in response to chronic hypoxia is poorly understood in larval fishes, especially larval air‐breathing fishes, which eventually in their development can at least partially “escape” hypoxia through air breathing. Whether the development air breathing makes these larval fishes less or more developmentally plastic than strictly water breathing larval fishes remains unknown. Consequently, developmental plasticity of cardiorespiratory physiology was determined in two air‐breathing anabantid fishes (Betta splendens and Trichopodus trichopterus). Larvae of both species experienced an hypoxic exposure that mimicked their natural environmental conditions, namely chronic nocturnal hypoxia (12 h at 17 kPa or 14 kPa), with a daily return to diurnal normoxia. Chronic hypoxic exposures were made from hatching through 35 days postfertilization, and opercular and heart rates measured as development progressed. Opercular and heart rates in normoxia were not affected by chronic nocturnal hypoxic. However, routine oxygen consumption [Formula: see text] (~4 μmol·O(2)/g per hour in normoxia in larval Betta) was significantly elevated by chronic nocturnal hypoxia at 17 kPa but not by more severe (14 kPa) nocturnal hypoxia. Routine [Formula: see text] in Trichopodus (6–7 μmol·O(2)/g per hour), significantly higher than in Betta, was unaffected by either level of chronic hypoxia. P (Crit), the PO(2) at which [Formula: see text] decreases as ambient PO(2) falls, was measured at 35 dpf, and decreased with increasing chronic hypoxia in Betta, indicating a large, relatively plastic hypoxic tolerance. However, in contrast, P (Crit) in Trichopodus increased as rearing conditions grew more hypoxic, suggesting that hypoxic acclimation led to lowered hypoxic resistance. Species‐specific differences in larval physiological developmental plasticity thus emerge between the relatively closely related Betta and Trichopodus. Hypoxic rearing increased hypoxic tolerance in Betta, which inhabits temporary ponds with nocturnal hypoxia. Trichopodus, inhabiting more permanent oxygenated bodies of water, showed few responses to hypoxia, reflecting a lower degree of developmental phenotypic plasticity. |
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