Carnivorous reptiles exhibit a massive increase in oxygen demand following a meal to meet the increased metabolic demands associated with digestion. Inherently, this increase in oxygen demand places an extra demand on the cardiovascular system; the heart needs to work harder to transport more oxygen to the metabolically active digestive organs. Pythons appear to deal with this increased cardiac demand by substantially increasing the mass of their heart(cardiac hypertrophy) within two days of feeding. But just how do these snakes manage to pump up their heart's mass?

Andersen and colleagues at the University of California, Irvine, were interested in determining the cause of the cardiac hypertrophy following feeding in the python (Python molurus). They wanted to know if the increase in heart mass was due to increased protein synthesis (i.e. formation of new heart muscle) or a water shift between extracellular and intracellular compartments, leading to increased fluid content of the heart tissues. In order to investigate this, Andersen and colleagues obtained ventricles from three groups of pythons: (1) fasting (these snakes had been fasted for 28 days); (2) digesting (these animals had digested a large meal 2 days earlier);and (3) post-digestive (these pythons had digested a large meal 28 days earlier). For each of these groups, the team measured ventricular dry/wet mass ratio, the ventricle's total protein, RNA and myofibrillar protein concentrations on a mass-specific basis, and the expression of messenger RNA for heavy-chain cardiac myosin, a contractile element of the heart.

As they expected, the team observed a 40% increase in pythons' ventricular mass during digestion. They identified several clues that this hypertrophy was due to de novo protein synthesis and not increased fluid content of the heart. Primarily, the team found that the expression of messenger RNA for heavy-chain cardiac myosin increased significantly 2 days after feeding,indicating that digesting snakes synthesise myosin. Further, they discovered that the hearts' mass-specific total protein, RNA and myofibrillar protein concentrations did not change during digestion. In other words, as the pythons' hearts increased in mass after feeding, the ratio of protein to heart mass remained the same, indicating that new protein was being formed as the hearts expanded. This finding also ruled out increased water content as an explanation for the cardiac hypertrophy; if the increased heart mass was due to an increase in fluid content, these mass-specific protein concentrations would have decreased. Finally, they found that ventricular dry/wet mass ratio did not differ between fasted and fed snakes, providing further evidence that the larger hearts were not due to increased water content. The team concluded that the cardiac hypertrophy observed in digesting pythons is due to the synthesis of new contractile protein.

Additionally, the team showed that the increase in heart mass during digestion was a fully reversible process. The mass of post-digestive snakes'hearts was similar to the mass of fasted snakes' hearts. Thus, following a meal, a python can rapidly increase its heart size by 40% and then decrease it again within 28 days. In comparison with mammalian species, in which comparable increments in ventricular size take weeks to develop, this cardiac remodelling occurs very rapidly. As such, Andersen and colleagues stress that this natural, rapidly occurring and fully reversible cardiac hypertrophy could provide a useful model for investigating the mechanisms that lead to cardiac remodelling and growth in other animals.

Andersen, J. B., Rourke, B. C., Caiozzo, V. J., Bennet, A. E. and Hicks, J. W. (
). Postprandial cardiac hypertrophy in pythons.