Electrochemical principles indicate how living membranes may regulate the rate of a bioelectrochemical reaction. If this reaction is the rate limiting biochemical link in an electrogenic metabolic pathway, to regulate its rate is to regulate the pathway. This metabolic regulation is called the Bioelectrochemical throttle of metabolism. The throttle concept is employed to interpret propagated action potentials, excitation-contraction coupling in muscle, and very briefly, other instances of metabolic regulation. For the propagated action potential, there is feedback in an electrogenic metabolic pathway, between the rates of a bioelectrochemical and a non-bioelectrochemical reaction. For excitation-contraction coupling, there is the change in state of constituents of this pathway as its rate changes, constituents which regulate tonus. And there are other instances to which the throttle applies, in which the bioelectrochemical reaction may occur in different biological membranes, and in different electrogenic metabolic pathways. Section 1. If a metabolic reaction proceeds as an electric current, regulating this current could regulate not only the rate of this reaction itself, but other, rate-linked metabolic reactions. Selected electrochemical principles indicate how living membranes may regulate metabolism by regulating bioelectric currents. Section 2. By applying the bioelectrochemical throttle to feedback between rate changes of a non-bioelectrochemical reaction in an electrogenic metabolic pathway, and of the bioelectrochemical reaction, I have developed a metabolic interpretation of electric excitation: o (1) the rate of all reactions of an electrogenic metabolic pathway is slow in the resting, steady-state membrane; (2) an action potential is initiated when the rate of a non-bioelectrochemical link in this pathway increases to a threshold value, in a given area of the membrane; (3) this alters the state of its reaction constituents in this area. Since these are also membrane constituents, it alters the state of the membrane; (4) bioelectric current flows between the altered area of the membrane and unaltered area, or in other words, the rate of the bioelectrochemical link in the metabolic pathway increases; (5) the bioelectrochemical reaction rate increase is coupled to further rate increase of the non-bioelectrochemical reaction, etc., until neither reaction is rate limiting; in the excited membrane; (6) the pathway subsequently slows to the resting rate, and the pathway constituents return to the pre-excitation steady state; (7) metabolic potassium extrusion is suggested as the bioelectrochemical reaction, and metabolic calcium release from its carrier as the non-bioelectrochemical one. Section 3. biochemical reaction rate changes of a propagated action potential alter the states of biochemical reaction constituents in a muscle fiber, and these constituents regulate tonus. It is pointed out that to avoid negative electrostatic charge build up in the myoplasm when there is net potassium extrusion, net electron transfer from myoplasmic oxidation-reduction couples to membrane couples would be necessary. The potassium extrusion rate increase, part and parcel of electric excitation, therefore shifts the oxidation-reduction potential of myoplasmic couples toward the oxidizing direction, and contraction occurs as a result. Experimental evidence is presented according to which oxidized muscle does in fact contract; reduced muscle relaxes. Section 4. The throttle concept is applicable for metabolic regulations in which all-or-none bioelectric changes do not occur.