Search PubMed⌕ Search

PubMed · 6117420

Human muscle function and fatigue.

Abstract

Fatigue is defined as a failure to maintain the required or expected force. The force of a voluntary contraction is graded according to both the tension generated in each muscle fibre and the number of fibres recruited. The same is true of fatigue. Percutaneous electrical stimulation of a muscle via its motor nerve allows the contractile function to be measured independently of volition. Studies have been made of the forces generated isometrically at different stimulation frequencies (frequency: force curve), and of fatiguability (tendency to lose force in a given time at specified stimulation frequencies), in the quadriceps and adductor pollicis muscles. Electrical stimulation recordings of the programmed stimulation myograms distinguish forms of muscle fatigue. Low frequency fatigue which implies impaired excitation-contraction coupling is long-lasting, whereas high frequency fatigue which represents impaired muscle membrane excitation recovers rapidly. Electromyographic (EMG) indicators of fatigue are well recognized but their use is limited because they cannot alone indicate whether alterations in excitation-contraction coupling underlie fatigue. Alterations in the power spectrum of the EMG precede (force) fatigue in sustained maximum voluntary contractions. Fatigue may ultimately be due to a failure of the rate of energy supply to meet demand, but the precise expression of this defect may vary, such that failure of excitation or of activation may predominate over failure of the energy supply.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R H Edwards. 1981. Human muscle function and fatigue.. https://doi.org/10.1002/9780470715420.ch1

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Impact of maternal nutrition and metabolism on health of the offspring.

Since the original publication of the theory of the fetal origins of adult diseases more than 15 years ago, extensive epidemiological studies have linked the environment in utero to adult health. Maternal nutrition and metabolism are major mechanisms by which the intrauterine environment programs the health of the offspring. Both growth-restricted and overgrown fetuses are at risk for postnatal disease. This paper summarizes the nutritional and metabolic causes of both these conditions and also reviews the interventions that have been tested to mitigate these effects.

Energy Metabolism↗

The regulation of energy generating metabolic pathways by p53.

The function of p53 as a tumor suppressor remains undisputed. p53 has a central role in cellular stress responses as well as affecting cancer development and progression. The word "central", however, is becoming increasingly more of an understatement as the list of p53-regulated pathways and processes is ever expanding. Although much focus continues to center on p53-mediated signaling cascades that control cell growth arrest and/or apoptosis, recent work has begun to define a role for p53 in the regulation of metabolic pathways typically thought of as essential for maintaining life. With the first potential link between p53 and glycolysis reported nearly ten years ago, the topic has gained a renewed interest. Recent studies now demonstrate the ability of p53 to regulate the expression of several novel genes including PGM (phosphoglycerate mutase), TIGAR (TP53-induced glycolysis and apoptosis regulator) and, SCO2 (synthesis of cytochrome c oxidase 2), each intimately linked to the processes of glycolysis and oxidative phosphorylation. With this discovery, yet another novel means by which p53 carries out its tumor suppressor function is brought into light.

Energy Metabolism↗

Bringing metabolic networks to life: convenience rate law and thermodynamic constraints.

BACKGROUND: Translating a known metabolic network into a dynamic model requires rate laws for all chemical reactions. The mathematical expressions depend on the underlying enzymatic mechanism; they can become quite involved and may contain a large number of parameters. Rate laws and enzyme parameters are still unknown for most enzymes. RESULTS: We introduce a simple and general rate law called "convenience kinetics". It can be derived from a simple random-order enzyme mechanism. Thermodynamic laws can impose dependencies on the kinetic parameters. Hence, to facilitate model fitting and parameter optimisation for large networks, we introduce thermodynamically independent system parameters: their values can be varied independently, without violating thermodynamical constraints. We achieve this by expressing the equilibrium constants either by Gibbs free energies of formation or by a set of independent equilibrium constants. The remaining system parameters are mean turnover rates, generalised Michaelis-Menten constants, and constants for inhibition and activation. All parameters correspond to molecular energies, for instance, binding energies between reactants and enzyme. CONCLUSION: Convenience kinetics can be used to translate a biochemical network--manually or automatically--into a dynamical model with plausible biological properties. It implements enzyme saturation and regulation by activators and inhibitors, covers all possible reaction stoichiometries, and can be specified by a small number of parameters. Its mathematical form makes it especially suitable for parameter estimation and optimisation. Parameter estimates can be easily computed from a least-squares fit to Michaelis-Menten values, turnover rates, equilibrium constants, and other quantities that are routinely measured in enzyme assays and stored in kinetic databases.

Energy Metabolism↗