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The Bowditch effect is an autoregulation method by which myocardial tension increases with an increase in heart rate. Also known as the Treppe phenomenon, Treppe effect or staircase effect. It was first observed by Henry Pickering Bowditch in 1871.

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.[1]

Alternatively, another mechanism is that the Na+-Ca++ membrane exchanger, which operates continually, has less time to remove the Ca++ that arrives in the cell because of the decreased length of diastole with positive chronotropy. With an increased intracellular Ca++ concentration, there follows a positive inotropy.[2]


  1. ^ Noble, M. I. (1988). An introduction to modern work on the Bowditch phenomenon. Cardiovascular Research, 22(8), 586-586. doi:10.1093/cvr/22.8.586
  2. ^ Physiology at a Glance, Second Edition (2008) — Jeremy Ward & Roger Linden