The Bowditch effect is an autoregulation mechanism in the field of medicine and science. It is the effect by which tension increases in the muscles of the heart with an increase in heart rate. The effect is also known as the Treppe phenomenon, the Treppe effect, or the Staircase effect.

The Bowditch effect was first observed by Henry Pickering Bowditch in 1871. Henry was an American soldier, a physician, a physiologist, and the dean of the Harvard School of Medicine.

A series of vigorous contractions take place increasingly in the muscles of the heart. These contractions take place when a corresponding series of stimuli is applied to any rested muscle. Due to these increasing series of contractions, this effect is called as staircase effect or staircase phenomenon.

Cause of Bowditch effect

The main underlying cause of this effect is an increase in the calcium levels in the sarcoplasmic reticulum. As the calcium level increases in the cardiac cells, it is further released into the sarcoplasm. The sarcoplasmic reticulum (SR) is a membrane-bound structure found in muscle cells. It is just similar to the endoplasmic reticulum. The main function of the SR is to store calcium ions.

Another mechanism for the effect could be the sodium-calcium membrane exchanger. This operates in a continuous manner, hence, has less time to remove the Ca++ that arrives in the cell. This is because of the decreased length of diastole and increase in the heart rate. With an increase in intracellular Ca++ concentration, the heart rate also increases.

An increase in heart rate increases the force of contraction generated by the myocardial cells. The concept of a frequency-based positive inotropic response of the heart was first explained in 1871 by Henry Pickering Bowditch. An inotrope is an agent that changes the force of muscular contractions. Negatively inotropic means a weak force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction.

Changes in inotropy are an important feature of cardiac muscle. This is because unlike skeletal muscle, cardiac muscle cannot change its force generation through changes in the motor nerve. When the heart muscle contracts, all the muscle fibers are activated. At this point, the only mechanisms that can alter force generation are changes in the length of the fiber. Another factor that can alter the force generation is the change in inotropy.

Detailed description bowditch effect

Bowditch found this after he stimulated a resting frog’s ventricular muscles. The basis of the phenomenon that he found, had associations with calcium ion handling and mishandling in cardiac cells. It involved proteins that participate in the excitation and contraction coupling.

Loss of internal muscle strength resulted from impaired Bowditch effect has sone involvement in conditions like cardiomyopathy, ischemia, and heart failure. It also leads to systolic dysfunction. The Bowditch phenomenon is often absent or even reversed in some observed cases of heart failure.

Sometimes a condition of heart failure arises due to the heart’s inability to provide the required blood circulation for energy. This is due to the impaired actin-myosin interaction process. An impaired actin-myosin function may lead to heart failure even during low-stress exercise. This is described as a null or inverse staircase phenomenon.

The Bowditch effect has mainly been studied in the muscles of the heart. It is considered to be a major contributor to the internal myocardial reserve and responsible for 40% of the increase in cardiac output.

Bodily functions

A similar staircase effect/ Bowditch effect also has implications in skeletal muscle. A progressive increase in muscle tension during an early phase of exercise may cause an increase in calcium concentrations in the myocyte’s sarcoplasm.

Bowditch effect is essential in understanding the dynamics of a failing heart. A healthy heart can cause a positive Bowditch effect due to its increase in sarcoplasmic endoplasmic reticulum Ca load. Whereas, a negative Bowditch effect is pathological. This negative Bowditch effect occurs from a reduced expression of the SERCA protein (sarcoplasmic endoplasmic reticulum calcium).

An increased muscular contraction (inotropy) results in increased active tension. Furthermore, the inotropic property of cardiac muscle is displayed in the force-velocity relationship. The force and velocity relationship is based on the change in velocity of fiber shortening at zero loads. The increased velocity of fiber shortening (which occurs with increased inotropy) increases the rate of ventricular pressure.

Sodium-Calcium Exchange

The hypothetical exchange process of sodium and calcium is situated in the sarcolemma. It couples sodium efflux to calcium influx and responds to increases in intracellular sodium concentration. Calcium inflow across the sarcolemmal membrane of the myocardium is very essential for the maintenance of contractility.

The sarcolemma is not freely permeable to calcium. The influx related to contraction is a function only at specific systems or pathways of this membrane. There is evidence that suggests that at least two components are present that allows calcium movement across the sarcolemma.

Reuter has demonstrated the existence of a slow inward calcium current. He told that inward calcium flow was slow when membrane depolarization was done. He suggested that this flow is the experimental analog of the phenomenon.

It is reasonable to assume that the interaction of calcium with sarcolemmal sites depends on the concentration of free calcium. In addition to this, Langer and his colleagues have even shown that myocardial contractility depends on a pool of calcium. This pool of calcium rapidly exchanges with extracellular calcium and is displaced by lanthanum.

For many years, the concept of the Bowditch effect, that is, increasing heart rate to enhance inotropy, was exploited to study closely about heart failure.

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