Eccentric contractions, characterized by the lengthening of the muscle-tendon complex, present several unique features compared with other types of contractions, which may lead to unique adaptations. Due to its specific physiological and mechanical properties, there is an increasing interest in employing eccentric muscle work for rehabilitation and clinical purposes. However, unaccustomed eccentric exercise is known to cause muscle damage and delayed pain, commonly defined as “Delayed-Onset Muscular Soreness” (DOMS). To date, the most useful preventive strategy to avoid these adverse effects consists of repeating sessions involving submaximal eccentric contractions whose intensity is progressively increased over the training. Despite an increased number of investigations focusing on the eccentric contraction, a significant gap still remains in our understanding of the cellular and molecular mechanisms underlying the initial damage response and subsequent adaptations to eccentric exercise. Yet, unraveling the molecular basis of exercise-related muscle damage and soreness might help uncover the mechanistic basis of pathological conditions as myalgia or neuromuscular diseases. In addition, a better insight into the mechanisms governing eccentric training adaptations should provide invaluable information for designing therapeutic interventions and identifying potential therapeutic targets.

These findings suggest that the eccentric training resulted in a switch to oxidative metabolism, which may be associated with protection from DOMS.

Unaccustomed eccentric exercise may cause skeletal muscle damage with an increase in plasma creatine kinase (CK) activity. Although the wide variability among individuals in CK response to standardized lengthening contractions has been well described, the reasons underlying this phenomenon have not yet been understood. Therefore, this study investigated a possible correlation of the changes in muscle damage indirect markers after an eccentric exercise with the decline in muscle performance during the exercise. Twenty-seven healthy untrained male subjects performed three sets of 30 maximal isokinetic eccentric contractions of the knee extensors. The muscular work was recorded using an isokinetic dynamometer to assess muscle fatigue by means of various fatigue indices. Plasma CK activity, muscle soreness, and stiffness were measured before (pre) and one day after (post) exercise. The eccentric exercise bout induced significant changes of the three muscle damage indirect markers. Large inter-subject variability was observed for all criteria measured. More interestingly, the log (CK(post) /CK(pre)) and muscle stiffness appeared to be closely correlated with the relative work decrease (r = 0.84, r(2)  = 0.70 and r = 0.75, r(2)  = 0.56, respectively). This is the first study to propose that the muscle fatigue profile during maximal eccentric protocol could predict the magnitude of the symptoms associated with muscle damage in humans.

Our data suggest that the eccentrically biased contractions in mice induced specific adaptations in protein expression and muscle fiber composition, which may reflect a more oxidative muscle phenotype. The differences in stress placed on the muscle between both trainings may be responsible for some unique adaptations resulting from the eccentrically biased training.

The aims of this study were first to compare the response of dominant and non-dominant legs to eccentric exercise and second, to examine whether there is an effect of exercise order on the magnitude of symptoms associated with intense eccentric protocols. Eighteen young men performed three sets of 30 maximal eccentric isokinetic (60° s(-1)) contractions of the knee extensors (range of motion, ROM: 0°-100°, 0 = full extension) using either dominant or non-dominant leg. They repeated a similar eccentric bout using the contralateral leg 6 weeks later. The sequence of leg's use was allocated to create equally balanced groups. Four indirect markers of muscle damage including subjective pain intensity, maximal isometric strength, muscle stiffness and plasma creatine kinase (CK) activity were measured before and 24 h after exercise. All markers changed significantly following the eccentric bout performed either by dominant or non-dominant legs, but no significant difference was observed between legs. Interestingly, the comparison between the first and second eccentric bouts revealed that muscle soreness (-42%, P<0.001), CK activity (-62%, P<0.05) and strength loss (-54%, P<0.01) were significantly lower after the second bout. This study suggests that leg dominance does not influence the magnitude of exercise-induced muscle damage and supports for the first time the existence of a contralateral protection against exercise-induced muscle damage in the lower limbs.