The heart of a turtle is an organ enabling these reptiles to endure environments lethal for many other vertebrates. It possesses unique features that allow for prolonged underwater dives and extended periods without oxygen.
Anatomy of the Turtle Heart
The turtle heart, like that of most reptiles, is structured with three chambers: two atria and a single ventricle. This configuration differs from the four-chambered hearts found in mammals and birds, which have two atria and two fully separated ventricles. In the turtle, the right atrium receives deoxygenated blood from the body, while the left atrium collects oxygenated blood returning from the lungs. Both atria then empty into the single ventricle.
A distinguishing characteristic of the turtle’s ventricle is its partial division by muscular ridges and incomplete septa. These internal structures, sometimes described as three interconnected sub-chambers (cavum venosum, cavum arteriosum, and cavum pulmonale), help to reduce the mixing of oxygenated and deoxygenated blood. This partial partitioning allows for flexible blood flow control. The presence of a sinus venosus, a thin-walled sac that receives deoxygenated blood before it enters the right atrium, also contributes to the heart’s overall structure and function.
How the Turtle Heart Adapts to Extreme Conditions
The turtle heart’s three-chambered anatomy facilitates physiological adaptations for surviving low oxygen or prolonged dives. One adaptation is the ability to selectively shunt blood, meaning the heart can redirect blood flow away from or towards the lungs. During a dive or when oxygen is scarce, the heart can perform a right-to-left shunt, where deoxygenated blood bypasses the lungs and is pumped directly back into the systemic circulation. This mechanism conserves energy by not sending blood to non-functional lungs and prioritizes oxygen delivery to vital organs.
Conversely, when the turtle is breathing air, a left-to-right shunt can occur, directing oxygenated blood from the systemic side back towards the lungs. Accompanying these blood flow changes is the diving reflex, a physiological response that includes a slowing of the heart rate, known as bradycardia. A turtle’s heart rate can decrease dramatically, from around 20-40 beats per minute to as low as 1-2 beats per minute in cold, oxygen-deprived conditions.
Bradycardia, combined with peripheral vasoconstriction, redistributes blood flow to prioritize essential organs like the brain and heart, while reducing supply to less critical tissues. The control of these cardiovascular changes is largely mediated by the parasympathetic nervous system.
Surviving Without Oxygen: Cellular Resilience
Beyond circulatory adjustments, turtle heart cells possess biochemical toughness that allows them to function for extended periods without oxygen, a state known as anoxia. This cellular resilience is separate from the blood flow adaptations. A key mechanism is metabolic depression, where the cells drastically reduce their energy demand. This allows the turtle’s heart to maintain function even with lower ATP turnover rates, with studies showing a reduction of up to 50% at 15°C and even more at colder temperatures.
Turtle heart cells can efficiently switch to anaerobic metabolism, producing energy without oxygen. While anaerobic metabolism typically leads to the rapid accumulation of harmful byproducts like lactate in other animals, turtle cells have mechanisms to manage these substances. They limit the buildup of succinate and maintain adenosine triphosphate (ATP) and adenosine diphosphate (ADP) levels, which helps prevent oxidative damage upon reintroduction of oxygen.
Furthermore, turtle heart tissue is adept at preventing cell damage during the reintroduction of oxygen, a phenomenon known as reperfusion injury. In mammals, restoring blood flow after oxygen deprivation can cause damage due to the sudden influx of oxygen and reactive oxygen species. Turtle cells are protected by their ability to maintain mitochondrial integrity and by mechanisms that limit the driving force for reactive oxygen species production. This allows their mitochondria to quickly resume normal function upon reoxygenation, preventing cellular harm.