Junctophilins (JP1 & JP2) are expressed in skeletal muscle and are the primary proteins involved in transverse (T)-tubule and sarcoplasmic reticulum (SR) membrane apposition. During the performance of eccentric contractions, the apposition of T-tubule and SR membranes may be disrupted, resulting in excitation-contraction (EC) coupling failure and thus reduced force-producing capacity. In this study, we made three primary observations: 1) Through the first three days after the performance of 50 eccentric contractions in vivo by the left hindlimb anterior crural muscles of female mice, both JP1 and JP2 were significantly reduced by ~50 and 35%, respectively, while no reductions were observed after the performance of non-fatiguing concentric contractions; 2) following the performance of a repeated bout 50 eccentric contractions in vivo, only JP1 was immediately reduced (~30%) but recovered by 3d post-injury in tandem with the recovery of strength and EC coupling; and 3) following the performance of 10 eccentric contractions at either 15 or 35˚C by isolated mouse EDL muscle, isometric force, EC coupling, and JP1 and JP2 were only reduced after the 35˚C eccentric contractions. Regression analysis of JP1 and JP2 content in TA and EDL muscles from each set of experiments indicated that JP damage is significantly associated with early (0 – 3d) strength deficits after performing eccentric contractions (R = 0.49; P < 0.001). As a whole, the results of this study indicate that JP damage plays in role in early force deficits due to EC coupling failure following the performance of eccentric contractions.

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