Skeletal Muscle Energetics and Metabolism

Abstract

IThe following abbreviations will be used: ATP, ADP, AMP, adenosine trio, di-, and monophosphate; IMP, inosine monophosphate; PC, phosphoryl-creatine; F-6-P, fructose-6-phosphate; G-I-P, glucose-I-phosphate; 1,6 FDP, fructose 1,6 diphos phate; FDNB, fl uorodinitrobenzene; IAA, iodoacetate; NADH, reduced nicotin amide adeninedinucleotide; Po, the isometric tetanus tension at maximum thick and thin filament overlap; 10' the muscle length corresponding to maximum thick and thin filament overlap; V max, the maximal shortening velocity. 93

Post-contractile phosphocreatine splitting in muscle as revealed by time-resolved 31P nuclear magnetic resonance.

“…It is most likely that the distribution of myosin and actomyosin intermediates during maintained contraction is very different from that before contraction, and that it takes a long time for these intermediate species to become redistributed to their pre-contractile level after the muscle has relaxed. This has also been suggested to explain the energy balance discrepancy (HoMSHER and KEAN, 1978). A successful kinetic model of the crossbridge cycle should describe the delayed PCr breakdown without concomitant Pi release as was observed in vivo and was reported here.…”

“…One discrepancy (the unexplained heat) relates to the observation that the measured enthalpy production (heat+work) during contraction is considerably greater than that expected on the basis of the changes in the known chemical reactions and the best estimate of the molar enthalpies of these reactions WOLEDGE, 1978, 1979;HOMSHER and KEAN, 1978;GILBERT et al, 1971). The simplest hypothesis to explain this energy imbalance is that a hitherto unidentified exothermic reaction occurs during contraction.…”

“…These changes recover after relaxation, if oxygenation is adequate. This has been revealed by chemical analysis (LUNDSGAARD, 1934;CARLSON and SIGER, 1960;MOMMAERTS, 1969;CURTIN and WOLEDGE, 1978;HOMSHER and KEAN, 1978) and by phosphorus nuclear magnetic resonance (31P NMR) of living muscle (DAWSON et al, 1977). Improved time-resolution of 31P NMR has allowed us to follow the course of changes of the levels of PCr and P; associated with contraction of living muscles in more detail and without the confusing intervention of semi-specific metabolic inhibitors such as iodoacetate (IAA) or fluorodinitrobenzene (FDNB).…”

Interaction Between Troponin and Myosin Enhances Contractile Activity of Myosin in Cardiac Muscle

“…Solution ATPase assays have been widely used to study not only the molecular mechanism of MgATP hydrolysis by myosin (Trentham et al, 1976;Homsher and Kean, 1978;Taylor, 1979;Eisenberg and Greene, 1980), but also to dissect Ca 2þ -dependent molecular interactions within the thin filament that affect myosin's MgATP activity (mATPase) (Trybus and Taylor, 1980;Chalovich et al, 1981;Gordon et al, 2000). Ca 2þ regulation of actomyosin interactions can also be reconstituted for study at the level of single, regulated thin filaments using in vitro motility (IVM) assays.…”

Dependence of shortening heat on sarcomere length in frog muscle and fiber bundles.

“…These results suggest that the shortening heat originates in the shift in the population of cross-bridge states during rapid shortening, and the transition is reversed afterwards, being coupled to ATP splitting. Cross-bridge mechanisms to account for the above findings have been proposed by several authors (CURTIN and WoLEDGE, 1978 ;HOMSHER and KEAN, 1978 ;KODAMA and YAMADA, 1979). According to the independent force-generator theory (GoRDON et al, 1966), shortening heat in rapidly shortening muscles is expected to be directly proportional to the extent of overlap between thick and thin filaments in each half sarcomere.…”