Richard H. T. Edwards

Electron spin resonance studies of intact mammalian skeletal muscle

Samples of skeletal muscle from mice, rats and man have been examined by conventional electron spin resonance techniques. One major free-radical signal with g value 2.0036-2.004 was detected in all intact muscle samples and homogenates at 77 K whereas this signal was not seen at room temperature. Other less prominant signals were also detected. Thirty minutes of excessive contractile activity of rat hind limb muscles was found to result in a leakage of intracellular creatine kinase enzyme into the blood plasma and also produced an average 70% increase in the amplitude of the major electron spin resonance signal. These data support the hypothesis that increased free-radical activity may play some role in muscle damage caused by extensive muscular activity.

Unbiased estimation of human body composition by the Cavalieri method using magnetic resonance imaging.

The classical methods for estimating the volume of human body compartments in vivo (e.g. skin‐fold thickness for fat, radioisotope counting for different compartments, etc.) are generally indirect and rely on essentially empirical relationships — hence they are biased to unknown degrees. The advent of modern non‐invasive scanning techniques, such as X‐ray computed tomography (CT) and magnetic resonance imaging (MRI) is now widening the scope of volume quantification, especially in combination with stereological methods. Apart from its superior soft tissue contrast, MRI enjoys the distinct advantage of not using ionizing radiations.

In vivo model of muscle pain: Quantification of intramuscular chemical, electrical, and pressure changes associated with saline-induced muscle pain in humans

Abstract Intramuscular injection of hypertonic saline is a good model to study human muscle pain (Kellgren 1938). The present study concerns the intramuscular (i.m.) pain mediators in saline‐induced muscle pain. In experiment 1, the diffusion of infused hypertonic and isotonic saline (0.5 ml) in m. tibialis anterior was illustrated by magnetic resonance imaging (MRI) in one subject. In experiment 2, six volunteers received four sequential infusions (0.5 ml given at 5 min intervals) of isotonic saline and thereafter four sequential infusions (0.5 ml given at 5 min intervals) of hypertonic saline into m. tibialis anterior. The isotonic and hypertonic saline infusions were computer‐controlled and separated by 20 min. The muscle pain intensity was assessed by continuous recordings on a visual analogue scale (VAS). One microdialysis probe was inserted 1 cm from the infusion needle in m. tibialis anterior and another probe in the other m. tibialis anterior. Concentrations of the i.m. sodium, potassium, magnesium, and prostaglandin E2 (PGE2) were assessed from the dialysates. Intramuscular electromyography (EMG) and pressure were assessed in the area of the infused saline. In experiment 1, the infusion of hypertonic and isotonic saline created a visible saline‐pool on the MRI scans. These saline‐pool volumes were stable and not correlated to the pain scores. In experiment 2, infusion of isotonic saline produced little pain compared to infusion of hypertonic saline. Maximal pain was reported after the first infusion of hypertonic saline and thereafter the pain gradually decreased with subsequent infusions of hypertonic saline. During infusion of hypertonic saline the i.m. sodium and potassium concentrations increased significantly, i.m. magnesium concentration tended to be increased, and the i.m. PGE2 concentration tended to be decreased although these changes were not significant. The i.m. EMG was smaller during and after infusions of hypertonic saline compared with isotonic saline. The i.m. pressure was not different during the infusions of hypertonic and isotonic saline but was increased between the infusions of hypertonic saline. This study has shown that i.m. infusion of hypertonic saline produced a saline‐pool, causing the i.m. pressure to increase. Possibly, pain activation and cessation are related to increased intramuscular sodium and potassium content respectively.

Hypotheses of peripheral and central mechanisms underlying occupational muscle pain and injury

SummaryIn an overview of the problem of occupational muscle pain the evidence indicates that injury is more common the greater the load and the worse the posture in which the work is performed. The commonest are backstrains or ligament or joint damage due to overuse. Fatigue is associated with alterations in energy metabolites in muscle while pain is often due to microscopical damage to the cellular architecture. The progress of pathological changes in muscle following occupational injury may be similar to those seen in primary fibromyalgia (fibrositis) because of a final common pathway involving calcium-induced secondary damage.Occupational muscle pain frequently occurs in the muscles supporting the upper limb girdle and head in workers engaged in repetitively performing skilled manipulations or activities requiring high or sustained mental concentration. It is suggested that both occupational myalgia of this kind may be due to an imbalance in the use of muscles for postural activity (holding or supporting fine movements) compared to phasic use in dynamic work. While there are undoubtedly muscular indications of damage these may be secondary to alterations in (unconscious) central motor control mechanisms.

Exercise induced activation of the branched-chain 2-oxo acid dehydrogenase in human muscle

SummaryThe present study was conducted to investigate the metabolic regulation of the oxidation of branched-chain amino acids (BCAA) by exercise in human skeletal muscle. Five trained male volunteers were exercised on a cycle ergometer at 70%±10% (mean±SD) of their maximal oxygen consumption % MathType!MTEF!2!1!+-% feaafiart1ev1aaatCvAUfeBSjuyZL2yd9gzLbvyNv2CaerbuLwBLn% hiov2DGi1BTfMBaeXatLxBI9gBaerbd9wDYLwzYbItLDharqqtubsr% 4rNCHbGeaGqiVu0Jf9qqqrpepC0xf9qiW7rqqrFfpeea0xe9LqFf0x% c9q8qqaqFn0dXdir-xcvk9pIe9q8qqaq-xir-f0-yqaqVeLsFr0-vr% 0-vr0xc8meaabaqaciGacaGaaeqabaWaaeaaeaaakeaacaGGOaGabm% OvayaacaWaaSbaaSqaaGqaaiacCb4FpbWaaSbaaWqaaiaa-jdacaWF% TbGaa8xyaiaa-HhaaeqaaaWcbeaakiaacMcaaaa!41C5!

How does dystrophin deficiency lead to muscle degeneration?--evidence from the mdx mouse.

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Objective quantification of muscle and fat in human dystrophic muscle by magnetic resonance image analysis

. Percutaneous quadriceps muscle biopsies were obtained under local anaesthesia at rest and after 30 and 120 min of exercise. In the muscle samples the active and total amount of the branched-chain 2-oxo acid dehydrogenase complex (BC-complex), the regulatory enzyme in the oxidative pathway of the BCAA, were measured. Glycogen content and activity of mitochondrial marker enzymes were also measured. Blood samples were obtained every 20 min for the measurement of metabolites. Heart rate and rated perceived exertion on the Borg scale were recorded every 10 min. At rest 4.0%±2.5% of the BC complex was active, after 30 min of exercise 9.9%±9.0% and after 120 min 17.5%±8.5% (mean±SD). Exercise did not change the total activity. The largest activation was seen in two of the subjects who developed higher blood lactates early on during exercise and decreased their muscle glycogen more (indications of anaerobic metabolism). These data demonstrate that in trained individuals significant increases in the activity of the BC-complex occur only after prolonged intense exercise. In spite of the 4-fold activation, the data support the classical view that amino acids and protein do not contribute substantially as an energy source during exercise, since % MathType!MTEF!2!1!+-% feaafiart1ev1aaatCvAUfeBSjuyZL2yd9gzLbvyNv2CaerbuLwBLn% hiov2DGi1BTfMBaeXatLxBI9gBaerbd9wDYLwzYbItLDharqqtubsr% 4rNCHbGeaGqiVu0Jf9qqqrpepC0xf9qiW7rqqrFfpeea0xe9LqFf0x% c9q8qqaqFn0dXdir-xcvk9pIe9q8qqaq-xir-f0-yqaqVeLsFr0-vr% 0-vr0xc8meaabaqaciGacaGaaeqabaWaaeaaeaaakeaaceWGwbGbai% aadaWgaaWcbaacbaGaiWfG-9eadaWgaaadbaGaa8Nmaaqabaaaleqa% aaaa!3D99!