A linear model of muscle respiration explains monoexponential phosphocreatine changes

Abstract

Phosphocreatine (PCr) content was measured by phosphorus nuclear magnetic resonance spectroscopy in the gastrocnemius muscles of pentobarbital-anesthetized rats during and after twitch stimulation at rates up to 0.75 Hz. The monoexponential time constant for PCr changes was similar at the onset of vs. during recovery after stimulation and was not significantly different for different stimulation rates (mean time constant 1.44 min). Steady-state PCr level during stimulation was linearly related to the product of stimulation rate times peak twitch force. These results are shown to be consistent with a simple first-order electrical analog model of oxidative metabolism that is applicable at submaximal oxidative rates. The model assumes equilibrium of the creatine kinase reaction, which is modeled as a chemical capacitor, with capacitance proportional to the total creatine level, and PCr level proportional to the cytosolic free energy of ATP hydrolysis.

Skeletal muscle oxidative metabolism in sedentary humans: 31P-MRS assessment of O2 supply and demand limitations

“…PCr recovery is a useful measure of skeletal muscle oxidative capacity and is dependent on mitochondrial respiratory function (3,11). A further advantage of the measure is that PCr recovery does not require a correction for active muscle mass (10,16) and is independent of the work level (17), provided that muscle intracellular pH does not fall severely (2). Thus the measurement of PCr recovery has proven useful in determining the oxidative capacity of skeletal muscle in a variety of conditions (12,15,30,32).…”

“…The supply of O 2 and its utilization by skeletal muscle is a tightly interwoven process that cannot easily be assessed by a single measurement. Although 31 P-magnetic resonance spectroscopy (MRS) measurements of phosphocreatine (PCr) recovery provide an accurate measure of skeletal muscle oxidative metabolism (2,11,15,17), alone this methodology is unable to discern limitation caused by O 2 supply from that of mitochondrial O 2 demand.However, the combination of PCr recovery measurement under conditions of altered O 2 availability, manipulated by varying the inspired O 2 fraction (FI O 2 ), has been utilized to demonstrate that, in exercise-trained humans, under normoxic conditions, O 2 availability limits maximal oxidative rate (7). The practical implication of these data is that PCr recovery measurements alone should be interpreted with caution because differences in PCr recovery between subjects may not be due to metabolic limitations (1, 5, 19) but rather to limitations in O 2 supply (30).…”

“…The supply of O 2 and its utilization by skeletal muscle is a tightly interwoven process that cannot easily be assessed by a single measurement. Although 31 P-magnetic resonance spectroscopy (MRS) measurements of phosphocreatine (PCr) recovery provide an accurate measure of skeletal muscle oxidative metabolism (2,11,15,17), alone this methodology is unable to discern limitation caused by O 2 supply from that of mitochondrial O 2 demand.…”

Comparison of measuring energy metabolism by different 31P‐magnetic resonance spectroscopy techniques in resting, ischemic, and exercising muscle

“…2c). The maximal oxidative flux (Q max ) was also calculated according to the ADP based model (23) and according to the linear model (24).…”

The Rate of Phosphocreatine Hydrolysis and Resynthesis in Exercising Muscle in Humans using 31P-MRS.

“…Consequently, a continuous and highly time-resolved, kinetic evaluation of high energy phosphorus compounds in human muscle during exercise was determined by 31-phosphorus nuclear magnetic resonance spectroscopy ( 31 P-MRS) (Binzoni et al, 1992;Kiessling et al, 1971;Kushmerick and Meyer, 1985;Meyer 1988;Mizuno et al, 1994;Mole et al, 1985;Yoshida and Watari, 1994;Yoshida and Watari, 1997;Yoshida et al, 1996). During exercise, however, both anaerobic and aerobic pathways are activated, making it difficult to measure the ATP production resulting from the more complex pathways of PCr hydrolysis, glycolysis, and oxidative phosphorylation (Gollnick and Hermansen, 1973;Henriksson, 1977;Holloszy, 1973;Saltin and Gollnick, 1983).…”