ANALYSIS OF POST EXERCISE MYALGIA. D.J. Newham* & R.H.T.

Edwards* (SPON: R.O'Neil), Dept of Medicine, University College London School of Medicine, London WC1 655, England.

Aim of investigation: Myalgia after exercise is well

described but poorly understood. We have documented the time course of the

myalgia to see how it compared with indications of muscle fatigueanddamage.

Methods: Normal subjects performed a step test so one quadriceps worked concentrically (stepping up) and the other eccentrically (stepping

down).Before and at intervals after exercise the following were measured;

voluntary force generation, contractile properties, muscle morphology and

circulating plasma levels of creatine kinase (CR). Tenderness - a featureof

this type of myalgia was quantified using a force transducer technique.

Results: Pain and tenderness developed only in the muscles which had worked eccentrically, they were not detectable until approximately eight

hours after exercise and reached peak intensity after 24-48 hours. Muscle

fatigue was maximal at the end of exercise and recovered over 24 hours.

Morphological indications of damage were only seen after eccentric work,

they were present at the end of exercise but were more extensive at the time of peak tenderness. Two time courses were seen for the enzyme efflux; in some subjects peak levels occured 24 hours after exercise whileinothers

they occured after 4-5 days and were of a much greater magnitude. Conclusions: The fact that pain and damage occured only in

eccentrically worked muscles indicates that they are determined by the tension per active fibre and not by metabolic cost. Fatigue followed a completely different time course to the myalgia and so is unlikely to share a common underlying mechanism. Morphological and biochemical indications of muscle damage followed a similar but not identical time course to the myalgia. It would seem that some form of mechanically induced muscle damage is the cause of post exercise myalgia.

THE MAGNITUDE OF ACUTE CARDIAC PAIN IS DEPENDENT ON THE GROWTH RATE OF INFARCTIOtj RUT NOT INFLULNCED BY PITUI@Y ENDORPHINS. A.Pertovaara ’ ,T.Koivula ’ ,J.Leppaluotg , Dept.Physiol.Univ.Helsinkia, Centr.Univ.Hosp.Tampere , Dept.Physiol.Univ.OuluC.

Aim: We tried to determine if acute cardiac pain in humans is depend- ent= the size of acute myocardial infarction (AMI) or on the growth rate of AMI. Moreover, we tried to find out if pituitary endorphins would modulate acute cardiac pain.

Methods: The intensity of chest pain was evaluated verbally with words frominnish Pain Questionnaire (Ketovuori&PGntinen, Pain 11.247), before the blood sampling (and after the administration of 6 rrq of i.v. morphine when required). The growth rate and size of AM1 was determined by a serial analysis of plasma creatine kinase isoenzymes (on admission and 4 h afterwards). Beta-endorphin/beta-lipotropin (BE) and prolactin level in plasma was determined by radioimmunoassay.

Results: A significant positive correlation was found between the growth rate of AM1 and pain, whereas there was a tendency to neqative correlation between AM1 size and pain. A weak tendency to positive corre- lation was found between plasma BE level and pain, and plasma prolactin level and pain. The patients with a low BE level did not have a more effective alleviation of pain by morphine administration than patients with high BE levels,

Conclusions: Small infarctions growing rapidly produce the worst pain. Pituitary endorphins or other stress-induced pituitary mechanisms do not attenuate acute cardiac pain.