Abstract

Burmese pythons (Python molurus) and American alligators (Alligator mississippiensis) utilize intermittent feeding strategies, with prolonged fasts punctuated by bouts of voracious feeding. Both species exhibit large increases in postprandial oxygen consumption (V̇O2). Presumably in response to increased O2 demand, P. molurus has been shown to exhibit postprandial cardiac hypertrophy (PCH) of up to 40%. By contrast, alligators exhibit no significant PCH. The “triggers” and universality (both within and between species) of this response therefore remain unclear. Notably, maximal V̇O2 in digesting Burmese pythons may exceed V̇O2 during maximal activity, whereas the opposite is true in alligators. We hypothesize that an O2 supply‐demand mismatch triggers PCH, which was tested in both species by halving hematocrit values (inducing anemia) and feeding animals large meals. Within 48 hours after feeding, normoxic and anemic pythons exhibited heart rates 78% and 126% higher, respectively, than fasted controls. While no PCH was found in fed normoxic animals, fed anemic animals exhibited 38% more massive hearts. Similar cardiovascular responses and hypertrophies occurred in fed anemic alligators. These findings support our hypothesis that an oxygen supply‐demand mismatch is the upstream stimulant of PCH, a phenomenon now known to exist across at least two taxa of reptiles. Funding provided by the Danish Research Council to TW and NSF grant IOS 0922756 to JWH. CES received support from an NSF GRF and a SICB FGST.

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