The capabilities of the cardiovascular system of the typical bat are exceptional. Heart rates vary from as few as 10 beats per minute during hibernation up to 7001000 beats per minute during flight (Brunet-Rossinni and Austad, 2004; Pauziene et al., 2000). Given the exceptional longevity of bats, one would expect that a cardiovascular system exposed to such extremes in hemodynamic demand would exhibit a decline in cardiac function over time. One would also expect to observe ischemic cardiomyopathy associated with potentially low availability of oxygen during arousal from hibernation. The mammalian heart is composed of distinct cardiomyocyte lineages that give rise to the various anatomical components such as the atrium, ventricles and conduction systems (Chien and Karsenty, 2005). Examination of the mechanisms responsible for the development and maintenance of these cell lineages using techniques such as cell-fate mapping should help to elucidate the mechanisms by which bats mediate the expected cardiovascular senescent processes seen in other long-lived mammals. For example, humans exhibit a stereotypic reduction in cardiac ventricular ejection fraction, pacemaker function and electrophysiological conduction fidelity over time (Schwartz and Zipes, 2005). A potentially heuristic line of research would be to determine if these same senescent processes are exhibited in old bats. Cell lineage fate mapping may reveal protective mechanisms, potentially at the genetic level, that staves off expected decline in cardiovascular function. For example, Wallace (2001) has proposed that gradual accumulation of mutations in mitochondrial DNA over time might explain observed senescent processes in long-lived organisms. No studies have focused on the burden of mitochondrial DNA mutations in aged bats.
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