SUMMARY1. Healthy subjects actually performed and mentally simulated a leg exercise at two levels of work (15 and 19 kg loads). Heart rate, respiration rate and end-tidal PCO were measured in both conditions. In addition, muscular metabolism was simultaneously measured using 31P nuclear magnetic resonance (NMR) spectroscopy.2. During actual exercise, heart and respiration rates increased, first abruptly and then gradually in relation to the level of work. End-tidal Pco was unaltered.NMR spectra showed a drop in phosphocreatine (PCr) and an increase in inorganic phosphate (Pi) concentrations. Intracellular pH fell to 6-65 at maximal effort with a 19 kg load. 3. During mental simulation, both heart and ventilatory rate increased immediately after mental exercise was begun. This increase was proportional to the amount of simulated exercise. Heart rate remained about 25 % below the level observed during actual exercise. The increase in respiration rate, by contrast, was more marked than during actual exercise. Finally, end-tidal Pco decreased progressively to about 18 % of the resting value.4. During mental simulation, NMR spectra were unchanged with respect to the resting values.

Calf muscle metabolism of six patients with end-stage chronic renal failure undergoing maintenance hemodialysis and of six control subjects was studied using 31P nuclear magnetic resonance spectroscopy at 4.7 Tesla. Spectra were obtained at rest, during exercise and recovery. At rest, the inorganic phosphate, ATP and phosphocreatine concentrations, and the intracellular pH were similar in both groups of subjects. In the patients, the maximum workload achieved at the end of exercise led to a 84% and 46% depletion of phosphocreatine and ATP, respectively; under this condition, the intracellular pH fell to 6.50 +/- 0.09. In control subjects, a maximum workload caused no change in ATP concentration at the end of exercise, but a phosphocreatine depletion and an intracellular pH fall similar to those observed in the patients. Although the rate of phosphocreatine depletion during exercise was not different in the two groups of subjects, the decrease in intracellular pH was more rapid in the patients than in control subjects. At the end of maximum exercise, the rates of recovery of both phosphocreatine and intracellular pH were significantly reduced in the muscle of hemodialysis patients when compared to normal subjects. These results suggest that, in the calf muscle of hemodialysis patients, energy production via oxidative metabolism is impaired and compensated for by an increase in anaerobic glycolysis.

Recent reports have indicated that 48-72 h of fasting, Type 1 diabetes and high-protein feeding induce gluconeogenesis in the small intestine of adult rats in vivo. Since this would (i) represent a dramatic revision of the prevailing view that only the liver and the kidneys are gluconeogenic and (ii) have major consequences in the metabolism, nutrition and diabetes fields, we have thoroughly re-examined this question in the situation reported to induce the highest rate of gluconeogenesis. For this, metabolically viable small intestinal segments from 72 h-fasted adult rats were incubated with [3-13C]glutamine as substrate. After incubation, substrate utilization and product accumulation were measured by enzymatic and NMR spectroscopic methods. Although the segments utilized [13C]glutamine at high rates and accumulated 13C-labelled products linearly for 30 min in vitro, no substantial glucose synthesis could be detected. This was not due to the re-utilization of [13C]glucose initially synthesized from [13C]glutamine. Arteriovenous metabolite concentration difference measurements across the portal vein-drained viscera of 72 h-fasted Wistar and Sprague-Dawley rats clearly indicated that glutamine, the main if not the only gluconeogenic precursor taken up, could not give rise to detectable glucose production in vivo. Therefore we challenge the view that the small intestine of the adult rat is a gluconeogenic organ.