Muscular fatigue has been studied using 31PNMR to measure the levels and rates of utilisation of several key metabolites and the free-energy change for ATP hydrolysis. Force development is closely correlated with metabolite levels and is proportional to the rate at which ATP is hydrolysed.

SUMMARY1. We have used phosphorus nuclear magnetic resonance (31P NMR) to study muscular fatigue in anaerobic amphibian muscle. In this paper the biochemical and energetic changes that result from a series of tetani are related to the decrease in rate constant (1/r) for the final, exponential, phase of relaxation.2. Using 31P NMR we have measured the concentrations of phosphocreatine (PCr), inorganic phosphate (Pi) and ATP as well as the internal pH. From our measurements we have calculated [creatine], [free ADP], the free-energy change (more precisely, the affinity A = -dG/dg) for ATP hydrolysis and the rates of lactic acid production and of ATP hydrolysis. 3. We have found that 1/, the rate constant of relaxation, is correlated with each of the following, independently of the pattern of stimulation: isometric force production, all of the measured or calculated metabolite levels, pH and dG/dg.4. There is a clear dependence upon the pattern of stimulation of the relation between 1/r and each of the following: total duration of the experiment, number of contractions, rate of lactic acid production and rate of ATP hydrolysis.5. The rate of relaxation is linearly related to [PCr], [creatine], [Pi] and dG/d6. It is nonlinearly related to isometric force, [ATP], [H+] and rate of ATP hydrolysis.6. We conclude that the change in 1/IT, like that of isometric force, depends upon metabolic factors, and not upon any independent changes in the activation or deactivation of contraction. We suggest that 1/ir may depend upon the free-energy change for ATP hydrolysis which in turn may be related to the rate of Ca2+ uptake into the sarcoplasmic reticulum.

Exercise-induced decreases in the 1 H transverse relaxation rate (R 2 ) of muscle have been well documented, but the mechanism remains unclear. In this study, the hypothesis was tested that R 2 decreases could be explained by pH decreases and apparent intracellular volume (V i ) increases. 31 P and 1 H spectroscopy, biexponential R 2 analysis, and imaging were performed prior to and following fatiguing exercise in iodoacetate-treated (IAA, to inhibit glycolysis), NaCN-treated (to inhibit oxidative phosphorylation), and untreated frog gastrocnemii. In all exercised muscles, the apparent intracellular R 2 (R 2i ) and pH decreased, while intracellular osmolytes and V i increased. These effects were larger in NaCN-treated and untreated muscles than in IAAtreated muscles. Multiple regression analysis showed that pH and V i changes explain 70% of the R 2i variance. Separate experiments in unexercised muscles demonstrated causal relationships between pH and R 2i and between V i and R 2i . These data indicate that the R 2 change of exercise is primarily an intracellular phenomenon caused by the accumulation of the end-products of anaerobic metabolism. In the NaCN-treated and untreated muscles, the R 2i change increased as field strength increased, suggesting a role for pH-modulated chemical exchange. Key words: skeletal muscle; exercise; hydrogen-ion concentration; osmolarity; nuclear magnetic resonance Exercise-induced increases in the apparent 1 H transverse relaxation time (T 2 ) of muscle water have been well documented. The amount of T 2 change increases as exercise intensity increases; T 2 plateaus 3-4 min after the onset of exercise (1). Following isometric leg extension to fatigue, T 2 recovery follows an approximately exponential time course and is complete after ϳ35 min. (2). The increase in signal intensity from active muscles in T 2 -weighted images allows muscle activity to be detected reliably and noninvasively, which may aid in the placement of regions of interest or surface coils in spectroscopic studies (2,3). With a full understanding of the mechanism(s) of the T 2 change, this phenomenon may also be useful in functional studies of muscle activation during exercise (e.g., Refs. 4 -6), noninvasive studies of pathologic conditions in which the T 2 response to exercise is altered (e.g., Refs. 7 and 8), and as a means of studying noninvasively those physiological changes that increase T 2 .The most universally offered and best-studied explanation for the T 2 increase during exercise is the concomitant increase in muscle volume. However, the mechanism of the T 2 increase is more complex than total water accumulation. For example, recovery of the muscle's anatomical cross-sectional area is faster than T 2 recovery (2), and enhancement of the extracellular fluid volume increase during exercise is not proportional to the T 2 increase (9). A further complication is that both ex vivo amphibian (10) and in vivo mammalian (11) studies suggest that exchange between the intra-and extracellular spaces in muscle is sl...

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