Highlights from the literature.

Question: What causes early muscle (myofib-rillar) fatigue in intact muscle fibers, and how does temperature affect these results? Background: When muscles are activated by motoneurons, they respond by generating tension in the muscle fibers. This process requires the hydrolysis of ATP, which results in an accumulation of metabolic products. The accumulation of metabolic products is a primary factor associated with a decline in muscle force (fatigue). The mechanisms involved in fatigue have been studied using a variety of intensities, durations, and variations in the mechanics of the contractions involved, but they have typically been performed under artificial conditions, such as at room temperature. Observations: In these experiments, Roots et al. utilized isolated, small bundles of fast fibers from rat muscle and looked at their performance at a range of temperatures. Additionally, they used shortening contractions instead of isometric contractions, which do not show the same temporal decline in force as is associated with myofib-rillar fatigue. One interesting finding was that in shortening mode (i.e., when the muscle shortened during part of the contraction) the fatigue of force was greater than in isometric mode. In addition, and perhaps surprisingly, they found that, as the temperature increased, the extent of fatigue decreased. Significance: These findings suggest that, in an experimental design that more closely resembles physiological conditions, the force fatigue arises through the action of actin and myosin cross-bridge cycling and thus the accumulation of metabolites. Indeed, their finding that fatigue is less at high temperatures than at low temperatures is consistent with the idea that accumulation of products of ATP hydrolysis is the main cause of fatigue. Although earlier studies have reported faster fatigue at higher temperatures using different experimental conditions, the authors suggest that the sensitivity of force production to metabolites decreases as temperature increases. Additional experiments will be required to sort this out. Nonetheless, this report adds a valuable step toward elucidating the underlying molecular mechanisms that cause deterioration of muscle performance under normal physiological conditions. Intracellular sodium regulates proteolyt-ic activation of the epithelial sodium channel. Question: What is the mechanism that underlies regulation of the epithelial sodium channel? Background: The apical membranes of some organs, such as the lungs and kidneys, express the epithelial sodium (Na +) channel (ENaC), which functions to maintain home-ostasis of Na +. This constitutively active ion channel regulates intracellular Na + concentrations via a negative feedback mechanism. Thus, when the intracellular concentration of …