Adaptation to lengthening contractions is independent of voluntary muscle recruitment but relies on inflammation.

Lengthening contractions trigger an adaptive response decreasing the susceptibility to exercise-induced muscle damage (EIMD). We hypothesized that 1) this adaptation can be observed when voluntary muscle recruitment is bypassed and 2) inflammation repression lessens the adaptive response. Rat ankle dorsiflexors were submitted to two bouts of elicited lengthening contractions 14 days apart; in vitro force production and macrophage concentrations were obtained before and 2 days after each bout in rats treated or not for 2 or 7 days with diclofenac. The first bout caused a 45% force deficit in the placebo group vs. 25% in the diclofenac group, whereas the ED1+ macrophage concentration increased by 10- and 5-fold, respectively. After the second bout, only diclofenac-treated rats (2 or 7 days) presented significant force deficits and increases in ED1+ and ED2+ macrophage concentrations, but this was more pronounced in the 7-day group. We conclude that adaptation to lengthening contractions does not depend on neural components but is likely mediated by strengthening of muscle structural/cellular elements and that inflammation is important for this process.