Preliminary studies on muscle tissue metabolism were made in a series of 18 patients treated in an intensive care unit. In acutely ill patients with circulatory or respiratory insufficiency, there was an increase in muscle lactate content, a decrease in the phosphorylcreatine stores as well as decreased in adenosine triphosphate (ATP) and total adenine (TA) contents. These findings could partly be explained by a relative hypoxia in the muscle but acute hypoxia alone would not account for the decrease in ATP or TA. These changes in the adenylate pool were still more pronounced in patients with prolonged diseases. In this series the ATP content was only 50% of the normal, despite normal lactate content. The reason for the low adenine nucleotide level in muscle tissue is thought to be due primarily to an increased formation and deamination of adenosine monophosphate during hypoxia in combination with a decreased rate of purine synthesis in the liver and/or a decreased capacity for "purine salvage" in the muscle. This itself might, in turn, be mediated by a low energy state in muscle or liver or be due to other metabolic disturbances or tissue damage. It was found that prolonged immobilization without metabolic disturbances did not change the TA content in muscle, while short-lasting severe metabolic acidosis decreased the TA content. A correction of the metabolic disturbance immediately increased the TA content in muscle. A low energy charge potential was found in patients with prolonged diseases, possibly being the cellular expression for the concept of the post-traumatic catabolic state.