Bird cardiomyocytes are long, thin and lack t-tubules, similar to ectothermic non-avian reptiles. Yet, birds achieve greater contractile rates and developed pressures than mammals, whose wide cardiomyocytes contain a dense transverse (t)-tubular network allowing for uniform excitation-contraction coupling and strong contractile force. To address this apparent contradiction, this talk will  link recent electrophysiological studies on bird cardiomyocytes with ultrastructure measurements and computational approaches.  Data will show that the strong transsarcolemmal Ca²⁺ influx via the L-type Ca²⁺ current (I_CaL) and the high gain of Ca²⁺-induced Ca²⁺ release (CICR) from the sarcoplasmic reticulum (SR), coupled with the internal SR Ca²⁺ release relay system, facilitates the strong fast contractions in the long thin bird cardiomyocytes, without the need for t-tubules.  The significance of this in relation to the evolution of the vertebrate heart and the evolution of endothermy will be discussed.