Kihlström M, Salminen A, Vihko V
Department of Cell Biology, University of Jyväskylä, Finland.
Eur J Appl Physiol Occup Physiol. 1988;57(2):177-80. doi: 10.1007/BF00640659.
Strenuous prolonged running causes muscle fibre necrosis in skeletal muscles. The muscle injury is associated with inflammation and a strong increase in the total activities of certain acid hydrolases a few days after exertion. The activity changes of acid hydrolases quantitatively well reflect the severity of histopathological changes during the myopathy (for review see Salminen, Acta Physiol Scand [Suppl 539] 1985). In this study male NMRI-mice were exposed to a protocol of fasting and refeeding together with or without a 6 h run on a treadmill at 13.5 m.min-1. The animals were killed 4 days after the exercise and samples from the red part of quadriceps femoris were analyzed for arylsulfatase (ASase) and beta-glucuronidase (GUase) activities. Starvation protocols did not affect ASase or GUase. Running caused a 3.2-fold increase in ASase and a 5.1-fold increase in GUase. If mice were exercised in the fasted condition a normal exercise response occurred in both activities, but when mice were exercised 2 days after the finish of fasting the exercise response was greatly diminished. Thus food deprivation followed by 2 days refeeding induces a protection against exercise myopathy in mice. The protection greatly resembles that induced by regular endurance training preceding strenuous prolonged exertion.
