Key result
Active stretching of isolated rabbit muscle myofibrils increased sarcomere length non-uniformity compared to isometric contractions (0.9 vs 0.7 µm), but this did not correlate with residual force enhancement.
Sarcomere length non-uniformity does not appear to contribute to residual force enhancement following active stretching of isolated skeletal muscle myofibrils, challenging the widely accepted sarcomere length non-uniformity theory.
Challenges sarcomere non-uniformity theory of RFE in isolated myofibrils; leaves open its role in intact muscle and clinical relevance.
The sarcomere length non-uniformity theory (SLNT) is a widely accepted explanation for residual force enhancement (RFE). RFE is the increase in steady-state isometric force following active muscle stretching. The SLNT predicts that active stretching of a muscle causes sarcomere lengths (SL) to become non-uniform, with some sarcomeres stretched beyond actin-myosin filament overlap (popping), causing RFE. Despite being widely known, this theory has never been directly tested. We performed experiments on isolated rabbit muscle myofibrils (n = 12) comparing SL non-uniformities for purely isometric reference contractions (I-state) and contractions following active stretch producing RFE (FE-state). Myofibrils were activated isometrically along the descending limb of the force-length relationship (mean ± 1 standard deviation (SD) = 2.8 ± 0.3 µm sarcomere(-1)). Once the I-state was reached, myofibrils were shortened to an SL on the plateau of the force-length relationship (2.4 µm sarcomere(-1)), and then were actively stretched to the reference length (2.9 ± 0.3 µm sarcomere(-1)). We observed RFE in all myofibrils (39 ± 15%), and saw varying amounts of non-uniformity (1 SD = 0.9 ± 0.5 µm) that was not significantly correlated with the amount of RFE, but through pairwise comparisons was found to be significantly greater than the non-uniformity measured for the I-state (0.7 ± 0.4 µm). Three myofibrils exhibited no increase in non-uniformity. Active stretching was accompanied by sarcomere popping in four myofibrils, and seven had popped sarcomeres in the I-state. These results suggest that, while non-uniformities are present with RFE, they are also present in the I-state. Furthermore, non-uniformity is not associated with the magnitude of RFE, and myofibrils that had no increase in non-uniformity with stretch still showed normal RFE. Therefore, it appears that SL non-uniformity is a normal associate of muscle contraction, but does not contribute to RFE following active stretching of isolated skeletal muscle myofibrils.
No takes yet. Share an insight, caveat, or question.
Johnston et al. (2016) studied Isolated rabbit muscle myofibrils (n=12). Active stretch vs. Isometric reference contractions was evaluated on Sarcomere length non-uniformities. Active stretching of isolated rabbit muscle myofibrils increased sarcomere length non-uniformity compared to isometric contractions (0.9 vs 0.7 µm), but this did not correlate with residual force enhancement.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: