Introduction

The first line of defense of an organism against an acid load is the available endogenous buffering of its body fluids. These buffers bind most of the protons and greatly minimize the fall in pH. Conventional descriptions in vertebrates generally define two major buffering compartments, the extracellular fluid and the intracellular fluid. Extracellular fluid buffering is dominated by bicarbonate, with a minor contribution from plasma proteins; whereas in the intracellular compartment, non-bicarbonate buffers such as proteins and phosphates predominate.

Often neglected in a consideration of body buffers is the skeleton, even though this structure, with its rich reservoir of mineral phosphates and carbonates, is potentially the major source of buffering power in the body. Skeletal contribution to routine buffering, however, is often less important because of slow exchange kinetics with the extracellular fluid and because of inaccessibility of much of the bone mineral. Under certain circumstances, though, bone can play a central role in acid–base balance. In clinical cases of chronic nonrespiratory acidosis, skeletal buffers are heavily recruited and this response has led to extensive investigations of the role of bone in acid–base function in humans and other mammals. Normal stresses of animals can also produce acidotic states that involve skeletal buffers as, for example, in crustaceans in which hypoxic states can lead to lactate retention and dissolution of CaCO3 from their exoskeletons.

A dramatic and ecologically relevant example of bone involvement in acid buffering is the contribution of the shell of the freshwater turtle in neutralizing lactic acid produced during prolonged anoxic submergence by these animals.