The role of pH on the thermodynamics and kinetics of muscle biochemistry: an in vivo study by (31)P-MRS in patients with myo-phosphorylase deficiency

In this study we assessed ΔG'(ATP) hydrolysis, cytosolic [ADP], and the rate of phosphocreatine recovery using Phosphorus Magnetic Resonance Spectroscopy in the calf muscle of a group of patients affected by glycogen myo-phosphorylase deficiency (McArdle disease). The goal was to ascertain whether and to what extent the deficit of the glycogenolytic pathway would affect the muscle energy balance. A typical feature of this pathology is the lack of intracellular acidosis. Therefore we posed the question of whether, in the absence of pH decrease, the rate of phosphocreatine recovery depends on the amount of phosphocreatine consumed during exercise. Results showed that at the end of exercise both [ADP] and ΔG'(ATP) of patients were significantly higher than those of matched control groups reaching comparable levels of phosphocreatine concentration. Furthermore, in these patients we found that the rate of phosphocreatine recovery is not influenced by the amount of phosphocreatine consumed during exercise. These outcomes provide experimental evidence that: i) the intracellular acidification occurring in exercising skeletal muscle is a protective factor for the energy consumption; and ii) the influence of pH on the phosphocreatine recovery rate is at least in part related to the kinetic mechanisms of mitochondrial creatine kinase enzyme.     

Skeletal muscle phosphocreatine recovery in exercise-trained humans is dependent on O2 availability.

In skeletal muscle, phosphocreatine (PCr) recovery from submaximal exercise has become a reliable and accepted measure of muscle oxidative capacity. During exercise, O2 availability plays a role in determining maximal oxidative metabolism, but the relationship between O2 availability and oxidative metabolism measured by 31P-magnetic resonance spectroscopy (MRS) during recovery from exercise has never been studied. We used 31P-MRS to study exercising human gastrocnemius muscle under conditions of varied fractions of inspired O2 (FIO2) to test the hypothesis that varied O2 availability modulates PCr recovery from submaximal exercise. Six male subjects performed three bouts of 5-min steady-state submaximal plantar flexion exercise followed by 5 min of recovery in a 1.5-T magnet while breathing three different FIO2 concentrations (0.10, 0. 21, and 1.00). Under each FIO2 treatment, the PCr recovery time constants were significantly different, being longer in hypoxia [33. 5 +/- 4.1 s (SE)] and shorter in hyperoxia (20.0 +/- 1.8 s) than in normoxia (25.0 +/- 2.7 s) (P 相似文献   

The physiological response of diploid and triploid brook trout to exhaustive exercise

Using triploidy as an experimental model, we examined whether cell size limits the post-exercise recovery process in fish. Because triploids generally possess larger cells, which could affect many physiological and biochemical processes, we hypothesized that triploids would take longer to recover from exhaustive exercise compared to diploids. To test this, we measured plasma lactate, glucose and osmolality, and white muscle energy stores (glycogen, phosphocreatine and ATP) and lactate before and immediately following exhaustive exercise and during recovery at 2 and 4 h post-exercise. In addition, oxygen consumption and ammonia excretion rates were determined before and after exhaustive exercise. Overall, diploid and triploid brook trout showed similar metabolic responses exercise, but plasma osmolality, white muscle lactate, white muscle ATP and post-exercise oxygen consumption rates recovered earlier in triploids compared to diploids. The results of this study suggest that the characteristic larger cell size of triploidy does not limit the physiological response to, or recovery from, exhaustive exercise.     

The effects of an acute temperature change on the metabolic recovery from exhaustive exercise in luvenile Atlantic salmon (Salmo salar)

This research examined the influence of acute changes of water temperature on the recovery processes following exhaustive exercise in juvenile Atlantic salmon (Salmo salar). White muscle phosphocreatine (PCr), ATP, lactate, glycogen, glucose, pyruvate, plasma lactate, and plasma osmolality were measured during rest and at 0, 1, 2, and 4 h following exhaustive exercise in fish acclimated and exercised at 12 degrees C and acutely exposed to either 6 degrees C or 18 degrees C water during recovery. An acute exposure to 6 degrees C water during the recovery period resulted in a severe reduction of metabolic recovery in salmon. However, metabolites such as muscle PCr and ATP and plasma lactate recovered very quickly (2-4 h) in fish acutely exposed to 18 degrees C during recovery. Overall, differences exist when postexercise metabolite levels are compared between acclimated fish and those fish acutely exposed to different water temperatures (either higher or lower). Taken together, the findings of the acute experiments suggest that at some point following exercise fish may seek warmer environments to speed the recovery process. However, the relationship between behavioural thermoregulation and recovery following exhaustive exercise in fish is not well understood.     

MITOCHONDRIA: Investigation of in vivo muscle mitochondrial function by 31P magnetic resonance spectroscopy

The most important function of mitochondria is the production of energy in the form of ATP. The socio-economic impact of human diseases that affect skeletal muscle mitochondrial function is growing, and improving their clinical management critically depends on the development of non-invasive assays to assess mitochondrial function and monitor the effects of interventions. ³¹P magnetic resonance spectroscopy provides two approaches that have been used to assess in vivo ATP synthesis in skeletal muscle: measuring P_i ⟶ ATP exchange flux using saturation transfer in resting muscle, and measuring phosphocreatine recovery kinetics after exercise. However, P_i ⟶ ATP exchange does not represent net mitochondrial ATP synthesis flux and has no simple relationship with mitochondrial function. Post-exercise phosphocreatine recovery kinetics, on the other hand, yield reliable measures of muscle mitochondrial capacity in vivo, whose ability to define the site of functional defects is enhanced by combination with other non-invasive techniques.     

Muscle metabolism in older subjects using 31P magnetic resonance spectroscopy.

We used phosphorus magnetic resonance spectroscopy to study the calf muscles of elderly normal (mean +/- SD) (80.0 +/- 5.12 years), elderly impaired (80.7 +/- 0.58 years), old normal (66.8 +/- 1.92 years), and young normal people (24.6 +/- 4.72 years). Relative levels of inorganic phosphate (Pi), phosphocreatine (PCr), and adenosine triphosphate were measured with a 1.9-tesla, 30-cm bore magnet at rest and following plantra flexon exercise. No differences were found at rest or during recovery from exercise in the elderly normal subjects with respect to gender or the presence of stable medical problems treated with medication. At rest there was an age-related decrease in the ratio of PCr/Pi. After exercise, the time constant of PCr recovery increased with age. A mild 7-week exercise regimen consisting of plantar flexion had no effect on time constant of PCr recovery in the elderly subjects. Four elderly impaired subjects had lower PCr/Pi ratios at rest and slower time constant of PCr recovery after exercise than normal elderly subjects. We conclude that gender and the presence of stable medical problems had no effect on muscle metabolism in the elderly and that the elderly recovered slower than young controls. This slower recovery was not corrected with a mild exercise program.     

Increase of free Mg<Superscript>2+</Superscript>in the skeletal muscle of chronic fatigue syndrome patients

In a previous study we evaluated muscle blood flow and muscle metabolism in patients diagnosed with chronic fatigue syndrome (CFS). To better understand muscle metabolism in CFS, we re-evaluated our data to calculate free Magnesium levels in skeletal muscle. Magnesium is an essential cofactor in a number of cell processes. A total of 20 CFS patients and 11 controls were evaluated. Phosphorus magnetic resonance spectroscopy from the medial gastrocnemius muscle was used to calculate free Mg²⁺ from the concentrations and chemical shifts of Pi, PCr, and beta ATP peaks. CFS patients had higher magnesium levels in their muscles relative to controls (0.47 + 0.07 vs 0.36 + 0.06 mM, P < 0.01), although there was no difference in the rate of phosphocreatine recovery in these subjects, as reported earlier. This finding was not associated with abnormal oxidative metabolism as measured by the rate of recovery of phosphocreatine after exercise. In summary, calculation of free Mg²⁺ levels from previous data showed CFS patients had higher resting free Mg²⁺ levels compared to sedentary controls.     

Phosphocreatine recovery kinetics following low- and high-intensity exercise in human triceps surae and rat posterior hindlimb muscles

Previous studies have suggested the recovery of phosphocreatine (PCr) after exercise is at least second-order in some conditions. Possible explanations for higher-order PCr recovery kinetics include heterogeneity of oxidative capacity among skeletal muscle fibers and ATP production via glycolysis contributing to PCr resynthesis. Ten human subjects (28 +/- 3 yr; mean +/- SE) performed gated plantar flexion exercise bouts consisting of one contraction every 3 s for 90 s (low-intensity) and three contractions every 3 s for 30 s (high-intensity). In a parallel gated study, the sciatic nerve of 15 adult male Sprague-Dawley rats was electrically stimulated at 0.75 Hz for 5.7 min (low intensity) or 5 Hz for 2.1 min (high intensity) to produce isometric contractions of the posterior hindlimb muscles. [(31)P]-MRS was used to measure relative [PCr] changes, and nonnegative least-squares analysis was utilized to resolve the number and magnitude of exponential components of PCr recovery. Following low-intensity exercise, PCr recovered in a monoexponential pattern in humans, but a higher-order pattern was typically observed in rats. Following high-intensity exercise, higher-order PCr recovery kinetics were observed in both humans and rats with an initial fast component (tau < 15 s) resolved in the majority of humans (6/10) and rats (5/8). These findings suggest that heterogeneity of oxidative capacity among skeletal muscle fibers contributes to a higher-order pattern of PCr recovery in rat hindlimb muscles but not in human triceps surae muscles. In addition, the observation of a fast component following high-intensity exercise is consistent with the notion that glycolytic ATP production contributes to PCr resynthesis during the initial stage of recovery.     

The reproducibility of measurements of intramuscular magnesium concentrations and muscle oxidative capacity using <Superscript>31</Superscript>P MRS

³¹P magnetic resonance spectroscopy (³¹P MRS) has been used to measure intramuscular magnesium concentrations and muscle metabolism. Abnormal intramuscular magnesium has been reported in several patient populations with suspected metabolic disorders. The purpose of this study was to evaluate our ability to measure intramuscular magnesium and muscle metabolism in the quadriceps muscles of healthy subjects, and to test whether these measurements were influenced by prior exercise. Twelve normal, healthy male volunteers were tested in a 3 Tesla magnet on four separate days. Resting [Mg²⁺] was calculated from the heights and frequency shifts of the phosphate, phosphocreatine and ATP peaks. Phosphocreatine (PCr) recovery kinetics were measured after 30-39 second bouts of isometric exercise. Thirty minutes prior to the 3^rd test session the subjects completed a 2 hour treadmill walk at 40-60% of heart rate reserve. Resting [Mg²⁺] averaged 0.388 mM and had an interclass correlation coefficient between days (ICC) of 0.352. The mean end exercise PCr was 47.6% and the mean end exercise pH was 6.97. PCr recovery averaged 39 seconds (p = 0.892) and had an ICC of 0.819. Prior long duration exercise did not produce significant alterations in either PCr recovery kinetics or intracellular magnesium levels (p = 0.440). In conclusion, the reproducibility of Resting [Mg²⁺] was less than that of PCr recovery measurements, and may reflect the sensitivity of these measurements to phasing errors. In addition, prior exercise is unlikely to alter measurements of resting metabolites or muscle metabolism suggesting that rigorous control of physical activity prior to metabolic testing is unnecessary.     

Some factors determining the PCr recovery overshoot in skeletal muscle

It has been proposed recently that the phosphocreatine (PCr) overshoot (increase above the resting level) during muscle recovery after exercise is caused by a slow decay during this recovery of the direct activation of oxidative phosphorylation taking place during muscle work. In the present article the factors determining the appearance and size of the PCr overshoot are studied using the computer model of oxidative phosphorylation in intact skeletal muscle developed previously. It is demonstrated that the appearance and duration of this overshoot is positively correlated with the value of the characteristic decay time of the direct activation of oxidative phosphorylation. It is also shown that the size of PCr overshoot is increased by low resting PCr/Cr ratio (what is confirmed by our unpublished experimental data), by high intensity of the direct activation of oxidative phosphorylation, by high muscle work intensity and by low rate of the return of cytosolic pH to the resting value during muscle recovery.     

Exercise testing as a diagnostic entity in mitochondrial myopathies

Exercise intolerance is one of the most common symptoms in patients with mitochondrial myopathies (MM). At the whole body level, this is characterized by a reduction in maximal oxygen consumption (VO2max) with an excessive carbon dioxide production (VCO2), increased rating of perceived exertion and a hyperdynamic circulatory response at a given exercise intensity. Fewer patients with MM display overt muscle atrophy and weakness even in the absence of a peripheral neuropathy. At the level of the skeletal muscle, the abnormal exercise response in MM patients is characterized by an increase in; delivery of oxygen relative to extraction (reduced myoglobin or hemoglobin desaturation), lactate production, phosphocreatine hydrolysis and time of post-exercise PCr and ADP recovery. Classically, the characterization of exercise intolerance is performed using cycle ergometry with measurements of VO2, VCO2, respiratory exchange ratio (RER = VCO2/VO2), heart rate, minute ventilation, rating of perceived exertion, and cardiac output (where available). Exercise protocols to maximum or for a given time period at a set workload can differentiate MM from controls with a sensitivity of 0.63-0.75 and a specificity of 0.70-0.90. Modified hand-grip exercise protocols, especially if coupled with simultaneous measurements of myoglobin/hemoglobin desaturation (near infra-red spectroscopy) or venous oxygenation, can achieve similar or higher levels of sensitivity and specificity. Similarly, exercise coupled with muscle phosphocreatine/Pi ratios, PCr, pH or ADP recovery kinetics, determined using magnetic resonance spectroscopy are useful in differentiating MM, but are limited by availability, experience and cost. In summary, aerobic exercise testing with some measurement of oxygen consumption can be performed in most institutions and can provide valuable information in the both the work-up of patients with suspected MM as well as in the monitoring of therapy in such patients.     

Failure of low-velocity swimming to enhance recovery from exhaustive exercise in largemouth bass (Micropterus salmoides)

This study was intended to discover whether forcing largemouth bass (Micropterus salmoides) to swim at 0.5 body lengths/second following exercise would expedite recovery relative to fish recovered in static water. Exercise resulted in a suite of physiological disturbances for largemouth bass that included a depletion of anaerobic energy stores, an accumulation of lactate, and increased cardiac output. At 1 h following exercise, exhaustively exercised largemouth bass forced to swim exhibited expedited recovery relative to fish in static water, evidenced by lower concentrations of lactate in white muscle, elevated concentrations of phosphocreatine in white muscle, and reduced concentrations of glucose in plasma. By 4 h postexercise, largemouth bass forced to swim during recovery exhibited signs of physiological disturbance that were absent in fish recovered in static water. These signs of disturbance included a loss of osmotically active particles from plasma, elevated lactate in plasma, reductions of phospocreatine in white muscle, and increased cardiac output. These results are discussed in relation to the body of work with salmonid fishes showing physiological benefits to recovering fish in flowing water.     

Exercise-induced splitting of the inorganic phosphate peak: investigation by time-resolved 31P-nuclear magnetic resonance spectroscopy

To investigate the splitting of the inorganic phosphate (Pi) peak during exercise and recovery, a time-resolved ³¹phosphorus nuclear magnetic resonance spectroscopy (³¹P-MRS) technique was used. Seven healthy young sedentary male subjects performed knee flexion exercise in the prone position inside a 2.1-T magnet, with the surface coil for ³¹P-MRS being placed on the biceps femoris muscle. After a 1-min warm-up without loading, the exercise intensity was increased by 0.41 W at 15-s intervals until exhaustion, followed by a 5-min recovery period. The ³¹P-MRS were recorded every 5 s during the rest-exercise-recovery sequence. Computer-aided contour analysis and pixel imaging of the Pi and phosphocreatine peaks were performed. Five of the seven subjects showed two distinct Pi peaks during exercise, suggesting two different pH distributions in exercising muscle (high pH and low pH region). In these five subjects, the high-pH increased rapidly just after the onset of exercise, while the low-pH peak increased gradually approximately 60 s after the onset of exercise. During recovery, the disappearance of the high-pH peak was more rapid than that of the low-pH peak. These findings suggest that our method ³¹P-MRS provides a simple approach for studying the kinetics of the Pi peak and intramuscular pH during exercise and recovery.     

Altered Energetics of Exercise Explain Risk of Rhabdomyolysis in Very Long-Chain Acyl-CoA Dehydrogenase Deficiency

Rhabdomyolysis is common in very long-chain acyl-CoA dehydrogenase deficiency (VLCADD) and other metabolic myopathies, but its pathogenic basis is poorly understood. Here, we show that prolonged bicycling exercise against a standardized moderate workload in VLCADD patients is associated with threefold bigger changes in phosphocreatine (PCr) and inorganic phosphate (Pi) concentrations in quadriceps muscle and twofold lower changes in plasma acetyl-carnitine levels than in healthy subjects. This result is consistent with the hypothesis that muscle ATP homeostasis during exercise is compromised in VLCADD. However, the measured rates of PCr and Pi recovery post-exercise showed that the mitochondrial capacity for ATP synthesis in VLCADD muscle was normal. Mathematical modeling of oxidative ATP metabolism in muscle composed of three different fiber types indicated that the observed altered energy balance during submaximal exercise in VLCADD patients may be explained by a slow-to-fast shift in quadriceps fiber-type composition corresponding to 30% of the slow-twitch fiber-type pool in healthy quadriceps muscle. This study demonstrates for the first time that quadriceps energy balance during exercise in VLCADD patients is altered but not because of failing mitochondrial function. Our findings provide new clues to understanding the risk of rhabdomyolysis following exercise in human VLCADD.     

Phosphocreatine and pH recovery without restoration of mechanical function during prolonged activity of rat gastrocnemius muscle: an in vivo 31P NMR study

Metabolic impairment in skeletal muscle was suggested to be involved in the development of local mechanical fatigue but until now results have dealt with short activity periods whereas little data on exhaustive and prolonged exercises are available. Stimulations of rat leg muscle lasting 45 min were induced by tetanic trains delivered via sciatic nerve at five different rhythms. Energy metabolism of the stimulated gastrocnemius muscle was followed by 31P NMR spectroscopy using surface coil while mechanical function was recorded. Our data showed a decrease in the force level to very low values a few minutes after exercise onset. This mechanical impairment only induced a transient metabolic failure followed by rapid restoration of high phosphocreatine (PCr) values and intracellular pH, without mechanical recovery. In addition, at the end of exercise, the PCr content was proportional to the fatigue level. As these experiments could not have impaired neuromuscular junction, the data would indicate that fatigue was maintained by a mechanism which does not appear to depend directly on muscle cell energy stores.     

Continuous, graded steady-state muscle work in rats studied by in vivo 31P-NMR

Theoretical consideration and experimental findings of 31P nuclear magnetic resonance spectroscopy (NMR) studies of exercising human muscle suggest that a graded, steady-state work protocol is highly suitable for performance evaluation in health and disease. We describe a similar rat model for repeated 31P-NMR studies that follows many of the 31P-NMR features observed in normal human controls. Calf muscles of rats anesthetized with chloral hydrate were indirectly stimulated at four frequencies (0.25, 0.5, 1.0, and 2.0 Hz). It was found that 1) several steady states can be briefly maintained in this model; 2) work-induced phosphocreatine (PCr) fall and inorganic phosphate (Pi) rise is stoichiometric; 3) a linear relationship between stimulation rate and Pi/PCr was obtained, with a slope of 2.01 +/- 0.4 (+/- 2SD, n = 15); 4) no significant drop in ATP was observed, allowing the estimation of phosphorylation potential (PP) changes during this range of muscle work (PP at rest was 61,603 +/- 25,100 M-1 and fell to 6,700 +/- 900 M-1 at the end of exercise); and 5) poststimulation recovery was rapid, with a rate of 2.27 +/- 0.5 PCr/Pi U/min. This simple model can be used for prolonged studies of chronic animal muscle disorders.     

On the kinetics of anaerobic power

ABSTRACT: BACKGROUND: This study investigated two different mathematical models for the kinetics of anaerobic power. Model 1 assumes that the work power is linear with the work rate, while model 2 assumes a linear relationship between the alactic anaerobic power and the rate of change of the aerobic power. In order to test these models, a cross country skier ran with poles on a treadmill at different exercise intensities. The aerobic power, based on the measured oxygen uptake, was used as input to the models, whereas the simulated blood lactate concentration was compared with experimental results. Thereafter, the metabolic rate from phosphocreatine break down was calculated theoretically. Finally, the models were used to compare phosphocreatine break down during continuous and interval exercises. RESULTS: Good similarity was found between experimental and simulated blood lactate concentration during steady state exercise intensities. The measured blood lactate concentrations were lower than simulated for intensities above the lactate threshold, but higher than simulated during recovery after high intensity exercise when the simulated lactate concentration was averaged over the whole lactate space. This fit was improved when the simulated lactate concentration was separated into two compartments; muscles + internal organs and blood. Model 2 gave a better behavior of alactic energy than Model 1 when compared against invasive measurements presented in the literature. During continuous exercise, model 2 showed that the alactic energy storage decreased with time, whereas model 1 showed a minimum value when steady state aerobic conditions were achieved. During interval exercise the two models showed similar patterns of alactic energy. CONCLUSIONS: The current study provides useful insight on the kinetics of anaerobic power. Overall, our data indicates that blood lactate levels can be accurately modeled during steady state, and suggests a linear relationship between the alactic anaerobic power and the rate of change of the aerobic power.     

Effects of high-intensity training on muscle lactate transporters and postexercise recovery of muscle lactate and hydrogen ions in women

The purpose of this study was to investigate the effects of high-intensity interval training (3 days/wk for 5 wk), provoking large changes in muscle lactate and pH, on changes in intracellular buffer capacity (betam(in vitro)), monocarboxylate transporters (MCTs), and the decrease in muscle lactate and hydrogen ions (H+) after exercise in women. Before and after training, biopsies of the vastus lateralis were obtained at rest and immediately after and 60 s after 45 s of exercise at 190% of maximal O2 uptake. Muscle samples were analyzed for ATP, phosphocreatine (PCr), lactate, and H+; MCT1 and MCT4 relative abundance and betam(in vitro) were also determined in resting muscle only. Training provoked a large decrease in postexercise muscle pH (pH 6.81). After training, there was a significant decrease in betam(in vitro) (-11%) and no significant change in relative abundance of MCT1 (96 +/- 12%) or MCT4 (120 +/- 21%). During the 60-s recovery after exercise, training was associated with no change in the decrease in muscle lactate, a significantly smaller decrease in muscle H+, and increased PCr resynthesis. These results suggest that increases in betam(in vitro) and MCT relative abundance are not linked to the degree of muscle lactate and H+ accumulation during training. Furthermore, training that is very intense may actually lead to decreases in betam(in vitro). The smaller postexercise decrease in muscle H+ after training is a further novel finding and suggests that training that results in a decrease in H+ accumulation and an increase in PCr resynthesis can actually reduce the decrease in muscle H+ during the recovery from supramaximal exercise.     

Effect of creatine supplementation on sprint exercise performance and muscle metabolism

The aim of thepresent study was to examine the effect of creatine supplementation(CrS) on sprint exercise performance and skeletal muscle anaerobicmetabolism during and after sprint exercise. Eight active, untrainedmen performed a 20-s maximal sprint on an air-braked cycle ergometerafter 5 days of CrS [30 g creatine (Cr) + 30 g dextrose perday] or placebo (30 g dextrose per day). The trials wereseparated by 4 wk, and a double-blind crossover design was used. Muscleand blood samples were obtained at rest, immediately after exercise,and after 2 min of passive recovery. CrS increased the muscle total Crcontent (9.5 ± 2.0%, P < 0.05, mean ± SE); however, 20-s sprint performance was not improved byCrS. Similarly, the magnitude of the degradation or accumulation ofmuscle (e.g., adenine nucleotides, phosphocreatine, inosine 5'-monophosphate, lactate, and glycogen) and plasma metabolites (e.g., lactate, hypoxanthine, and ammonia/ammonium) were also unaffected by CrS during exercise or recovery. These data demonstrated that CrS increased muscle total Cr content, but the increase did notinduce an improved sprint exercise performance or alterations inanaerobic muscle metabolism.

     

31P-NMR spectroscopy and the metabolic properties of different muscle fibers

To study the in vivo recruitment of different fiber types and their metabolic properties, 31P-nuclear magnetic resonance spectroscopy (31P-NMRS) of the human calf muscle was performed in seven normal sedentary subjects. In the exhaustive exercise protocol used, the work load was increased every minute during 5 min. This resulted in a prominent split of the Pi resonance in all subjects, indicating pH compartmentation in the muscles studied. From the chemical shift of the Pi peaks relative to phosphocreatine (PCr) at the end of the exercise, intracellular pH (pHi) averaged 6.92 +/- 0.05 (SD) in compartment 1 and 6.23 +/- 0.15 in compartment 2. The recovery of both Pi resonances after exercise could be followed easily in five of these subjects. The recovery rate of the Pi peak is a good estimate of the oxidative metabolism at the end of the exercise. A monoexponential regression analysis showed that the mean initial recovery rate S0 was 2.49 +/- 0.17%/s in compartment 1 and only 0.87 +/- 0.12%/s in compartment 2, indicating aerobic function three times higher in compartment 1 at the end of exercise. The mean relative ATP fraction dropped significantly (P less than 0.001), from 20.0 +/- 1.0% of the total 31P signal integral before exercise to 14.0 +/- 1.6% at the end of exercise. The simultaneous visualization of two compartments, in good order, one with high pHi and fast recovery and another with low pHi and slow recovery, is rationalized by the different metabolic behavior of type I and II fibers in human calf muscle in response to exhaustive exercise. This study demonstrates that 31P-NMRS is an excellent noninvasive procedure to quantify aerobic metabolism in both fiber types simultaneously.