The influence of fatigue on damage from eccentric contractions in the gastrocnemius muscle of the cat

Eccentric exercise is unique in that it can lead to muscle damage and soreness. Concentric exercise is not accompanied by evidence of damage. There are reports in the literature that muscle fatigue is a factor determining the amount of damage from eccentric exercise. Our theory for the damage process predicts that susceptibility for damage is independent of fatigue. Experiments were carried out to test this prediction as well as to seek other evidence in support of our theory. Comparisons were made between the effects of eccentric and concentric contractions. The nerve supply to the medial gastrocnemius muscle of the anaesthetized cat was divided into three equal portions in terms of the tension they generated. In the first experiment a muscle portion was fatigued by giving it 200 shortening contractions over 12 mm at a shortening speed of 50 mm s(-1). This led to a mean fall in isometric tension (37 +/- 4%) without a significant shift in the optimum length for peak active tension. Giving the fatigued muscle 10 eccentric contractions, active stretches over 6 mm at 50 mm s(-1), beginning from the muscle's optimum length led to a further fall in tension (11% +/- 7%) and a significant shift in optimum length (3.7 mm +/- 0.6 mm) in the direction of longer muscle lengths. The shift in optimum was taken as an indicator of muscle damage. This shift was not significantly different from that seen after eccentric contractions carried out on an unfatigued muscle. After a series of eccentric or concentric contractions, tension at the end of a ramp shortening of 6 mm at 10 mm s-1 fell more than isometric tension, and by near equal amounts for the two kinds of contractions. In an unfatigued muscle, if tension was altered by changing the rate of stimulation, the fall in shortening tension was greater than after either concentric or eccentric contractions. These observations were seen to be consistent with predictions of the proposed mechanism for the damage process.