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Flat hydrodynamic shells likely represent an evolutionary trade-off between adaptation to an aquatic lifestyle and the instability of more rounded shells, thought beneficial for self-righting. Trade-offs often result in compromises, this is particularly true when freshwater turtles, with flatter shells, must self-right to avoid the negative effects of inverting. These turtles, theoretically, invest more biomechanical effort to achieve successful and timely self-righting when compared to turtles with rounded carapaces. This increase in effort places these hatchlings in a precarious position; prone to inversion and predation and with shells seemingly maladapted to the act of self-righting. Here, we examine hatchling self-righting performance in three morphologically distinct freshwater turtle species (Apalone spinifera,Chelydra serpentinaandTrachemys scripta scripta) that inhabit similar environmental niches. We demonstrate that these hatchlings were capable of rapid self-righting and used considerably less biomechanical effort relative to adult turtles. Despite differences in shell morphology the energetic efficiency of self-righting remained remarkably low and uniform between the three species. Our results confound theoretical predictions of self-righting ability based on shell shape metrics and indicate that other morphological characteristics like neck or tail morphology and shell material properties must be considered to better understand the biomechanical nuances of Testudine self-righting.

 

In hypoxia, air-breathing fish obtain O₂from the air but continue to excrete CO₂into the water. Consequently, it is believed that some O₂obtained by air-breathing is lost at the gills in hypoxic water.Pangasionodon hypophthalmusis an air-breathing catfish with very large gills from the Mekong River basin where it is cultured in hypoxic ponds. To understand howP. hypophthalmuscan maintain high growth in hypoxia with the presumed O₂loss, we quantified respiratory gas exchange in air and water. In severe hypoxia (PO₂: ≈ 1.5 mmHg), it lost a mere 4.9% of its aerial O₂uptake, while maintaining aquatic CO₂excretion at 91% of the total. Further, even small elevations in water PO₂rapidly reduced this minor loss. Charting the cardiovascular bauplan across the branchial basket showed four ventral aortas leaving the bulbus arteriosus, with the first and second gill arches draining into the dorsal aorta while the third and fourth gill arches drain into the coeliacomesenteric artery supplying the gut and the highly trabeculated respiratory swim-bladder. Substantial flow changes across these two arterial systems from normoxic to hypoxic water were not found. We conclude that the proposed branchial oxygen loss in air-breathing fish is likely only a minor inefficiency.

 

Developmental hypoxia has profound and persistent effects on the vertebrate cardiovascular system, but the nature, magnitude, and long-term outcome of the hypoxic consequences are species specific. Here we aim to identify common and novel cardiovascular responses among vertebrates that encounter developmental hypoxia, and we discuss the possible medical and ecological implications. 

Developmental oxygen is a powerful stressor that can induce morphological and functional changes in the cardiovascular systems of embryonic and juvenile vertebrates. This plasticity has been ascribed, at least in part, to the unique status of the developing cardiovascular system, which undergoes organogenesis while meeting the tissue oxygen demands of the embryo. We have previously reported an array of functional and morphological changes in embryonic American alligators that persist into juvenile life. Most notably, cardiac enlargement as well as functional parameters of anesthetized juvenile alligators remains after embryonic hypoxic exposure. Because the effects of developmental oxygen in crocodilians have only been investigated in anesthetized animals, we explored the pressure dynamics of both ventricles as well as systemic pressure in response to stressors of acute hypoxia and swimming. Our current findings demonstrate that developmental programming of cardiac function (intraventricular pressure and heart rate) does persist into juvenile life, but it is chamber-specific and depends on the experimental manipulation. Acute hypoxic exposure revealed that juvenile alligators that had experienced 10% O 2 as embryos maintain right ventricle function and increase left ventricle function during exposure. Finally, the data indicate blood flow in the left aorta must originate from the left ventricle during acute hypoxia and swimming. 

Most animals elevate cardiac output during exercise through a rise in heart rate ( f H ), whereas stroke volume (V S ) remains relatively unchanged. Cardiac pacing reveals that elevating f H alone does not alter cardiac output, which is instead largely regulated by the peripheral vasculature. In terms of myocardial oxygen demand, an increase in f H is more costly than that which would incur if V S instead were to increase. We hypothesized that f H must increase because any substantial rise in V S would be constrained by the pericardium. To investigate this hypothesis, we explored the effects of pharmacologically induced bradycardia, with ivabradine treatment, on V S at rest and during exercise in the common snapping turtle ( Chelydra serpentina) with intact or opened pericardium. We first showed that, in isolated myocardial preparations, ivabradine exerted a pronounced positive inotropic effect on atrial tissue but only minor effects on ventricle. Ivabradine reduced f H in vivo, such that exercise tachycardia was attenuated. Pulmonary and systemic V S rose in response to ivabradine. The rise in pulmonary V S largely compensated for the bradycardia at rest, leaving total pulmonary flow unchanged by ivabradine, although ivabradine reduced pulmonary blood flow during swimming (exercise × ivabradine interaction, P < 0.05). Although systemic V S increased, systemic blood flow was reduced by ivabradine both at rest and during exercise, despite ivabradine’s potential to increase cardiac contractility. Opening the pericardium had no effect on f H , V S , or blood flows before or after ivabradine, indicating that the pericardium does not constrain VS in turtles, even during pharmacologically induced bradycardia.