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¹ Institute of Membrane and Systems Biology, University of Leeds, Leeds, LS2 9JT, UK
² Faculty of Life Sciences, 2.18c Core Technology Facility, University of Manchester, Manchester, M13 9NT, UK

Correspondence to Holly Shiels: holly.shiels{at}manchester.ac.uk

During vertebrate evolution there has been a shift in the way in which the heart varies cardiac output (the product of heart rate and stroke volume). While mammals, birds, and amphibians increase cardiac output through large increases in heart rate and only modest increases (30%) in stroke volume, fish and some reptiles use modest increases in heart rate and very large increases in stroke volume (up to 300%). The cellular mechanisms underlying these fundamentally different approaches to cardiac output modulation are unknown. We hypothesized that the divergence between volume modulation and frequency modulation lies in the response of different vertebrate myocardium to stretch. We tested this by progressively stretching individual cardiac myocytes from the fish heart while measuring sarcomere length (SL), developed tension, and intracellular Ca²⁺ ([Ca²⁺]_i) transients. We show that in fish cardiac myocytes, active tension increases at SLs greater than those previously demonstrated for intact mammalian myocytes, representing a twofold increase in the functional ascending limb of the length–tension relationship. The mechanism of action is a length-dependent increase in myofilament Ca²⁺ sensitivity, rather than changes in the [Ca²⁺]_i transient or actin filament length in the fish cell. The capacity for greater sarcomere extension in fish myocardium may be linked to the low resting tension that is developed during stretch. These adaptations allow the fish heart to volume modulate and thus underpin the fundamental difference between the way fish and higher vertebrates vary cardiac output.

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