D. J. Newham

The consequences of eccentric contractions and their relationship to delayed onset muscle pain

SummaryExercise can cause muscle pain for a number of reasons. Usually the pain is experienced during the exercise and recovers rapidly afterwards. There is one type of muscle pain that has a very different and characteristic time course. In this situation the exercise itself, and the immediate post-exercise period are painfree. The pain is not felt for about eight hours and is maximal 1 or 2 days later. Delayed onset muscle pain occurs after unaccustomed, high force contractions and is particularly associated with eccentric contractions. The concensus of opinion is that the pain is caused by some form of damage, but the mechanism for the pain is not known. This review summarises the literature on the consequences of eccentric contractions and relates them to delayed onset muscle pain. There is clear evidence of damage to the muscle fibres themselves, their membranes and, at a later stage, mononuclear cell infiltration, but all these have very different time courses and none are the same as the pain. Intramuscular pressures are raised in some, but not all, painful compartments and even when raised follow a different time course to the pain. Anti-inflammatory agents do not affect the pain, but due to the incomplete understanding of the action of these drugs, the role of inflammation in delayed onset muscle pain is uncertain.Despite the considerable evidence of damage after eccentric contractions, the cause of delayed onset muscle pain is still unknown.

Skeletal muscle damage: a study of isotope uptake, enzyme efflux and pain after stepping.

SummaryWe have studied the occurrence of skeletal muscle uptake of 99mtechnetium pyrophosphate (Tc-PYP), creatine kinase (CK) release and muscle pain in normal subjects after exercise. Five subjects stepped on and off a high bench in such a way that one leg stepped up and the other down. Pain only developed in the muscles used for descending: quadriceps, adductors and gluteal muscles of one leg and the calf muscle of the other. A large rise in plasma CK occurred in four subjects but no increased Tc-PYP muscle uptake was seen in the quadriceps. In the four subjects with high CK effluxes, increased isotope uptake was seen in the thigh adductors used when stepping down; in the two subjects with the largest CK effluxes there was extensive uptake into the gluteal muscles. Muscle pain preceded and was not well correlated with either the magnitude of the enzyme release or the amount and distribution of increased muscle isotope uptake. We conclude that delayed onset muscle pain, the cause of which remains unknown, is a poor indicator of muscle damage as indicated by circulating muscle enzymes and muscle isotope uptake. Tc-PYP uptake by skeletal muscle can provide useful information about the localisation and time course of muscle damage.

Role of mechanical damage in pathogenesis of proximal myopathy in man

No adequate explanation has as yet been provided for the predominant proximal and symmetrical distribution of skeletal muscle weakness and wasting in human myopathies. One obvious difference between proximal and distal muscles is that in their postural antigravity role the former are involved in eccentric contractions to a much greater extent than are the latter. Recent physiological studies have shown that eccentric contractions produce considerable muscle damage in normal healthy subjects. The damage starts in individual sarcomeres but becomes more extensive over 1-2 days, the progression probably being due to the stronger sarcomeres stretching the weaker, damaged sarcomeres during normal activity and/or to the enzyme degradation of myofibrillar proteins when muscle damage results in Ca++ inflow. As a muscle becomes weaker and unable to meet the functional demands made upon it the likelihood of accidental stretch becomes greater. The vicious circle of weakness, stretch, damage, and further weakness may be the reason why the proximal muscles, which normally function eccentrically to some degree, are the most severely affected in a wide range of myopathic disorders.

Carbonic anhydrase III in Duchenne muscular dystrophy

Plasma carbonic anhydrase III (CAIII) levels determined by radioimmunoassay have been compared, in detail, with creatine kinase (CK) as indices of Duchenne muscular dystrophy (DMD). CAIII levels were markedly elevated in all patients but variability of levels in a number of individual patients was higher than CK.