one of the explanations is the inability of the na/k-atpase to keep up with influx of sodium at higher heart rates. when a higher heart rate occurs, for example due to adrenergic stimulation, the l type calcium channel has increased activity. the 3na/ca exchanger (which allows 3 na to flow down its gradient in exchange for 1 ca ion to flow out of the cell) works to decrease the levels of intracellular calcium. as the heart rate becomes more robust and the length of diastole decreases, the na/k-atpase, which removes the na brought into the cell by the na/ca exchanger, does not keep up with the rate of na influx. this leads to a less efficient na/ca exchange since the gradient is decreasing for sodium and the driving force behind calcium transport is actually the concentration gradient of sodium, therefore ca builds up within the cell. this results in an accumulation of calcium in the myocardial cell via the sodium calcium exchanger and leads to a greater state of inotropism, a mechanism which is also seen with cardiac glycosides.