response to exercise during chronic exposure to altitude. The results from some of these studies have shown that the lower lactate is not due ro a greater oxidative capacity of the muscle, an improved capillary-to-fiber ratio, or an improvement in oxygen delivery (50, 107). Instead, the reduction in lactate seems to be associated with a lower plasma epinephrine concentration which, as we know from chap. 5, would provide less stimulation of glycogenolysis via -adrenergic receptor stimulation (85, 107). Evidence supporting this proposition comes from a study in which propranolol (a -adrenergic receptor blocking drug) was shown to reduce the lactate response to acute hypoxia to a level seen only after chronic hypoxia (107). However, the changes in epinephrine with acclimatization to altitude cannot entirely explain the lower lactate response (85). The lower lactate response may also bedue to muscular adaptations resulting in tighter metabolic control such that the ADP concentration does not increase as much during exercise, this results in less stimulation of glycolysis (50). Consequently, the lactate paradox may be the result of both hormonal (epinephrine) and intracellular (lower [ADP]) adaptations that occur with chronic exposure to hypoxia. A recent attempt to explain the lactate paradox is found in a “viewpoint” by Noakes (88), with commentaries by other authors and Noakes’ rebuttal (89). This explanation focuses on the brain’s need to protect oxygen delivery to itself by limiting muscle recruitment when exercise is done under chronic exposure to hypoxia. If the brain limits the recruitment of muscle fibers, less carbohydrate is metabolized and less lactate will be produce. However, commentaries (26) from various authors, including the authors of the principal paper cited by Noakes, argued against that hypothesis.