Force enhancement extended the relaxation phase in active stretched cardiac papillary muscle

Rapid active stretching the muscle induced a peak passive tension. The muscle was tolerated an isometric static stretch after the active stretch, and presented a subsequent relaxation phase with the passive tension attenuation. A myogenic spontaneous contraction may generated in this phase. The spontaneous contraction relative force enhancement may interrupt the relaxation process in cardiac muscle. In this study, we investigated the spontaneous contraction occurrence and its force enhancement properties in relaxation phase of excessive stretched cardiac muscle. The cardiac papillary muscle was isolated from the Kunming mice cardiac ventricle, primarily stabled in Ringer’s solution. The preparations were lengthening to 20% of its initial length to obtain a low preload. A single active stretch carried out under this low preload. The preparation further lengthening to 40% of its low preload length to be in a high preload condition. Muscle was continuously excessively active stretched twice under the high preload condition. The excessive static stretch induced spontaneous force amplitude (AIFE), force enhancement extensive time in 1st and 2nd stretch (t1 and t2) and velocity increases % of time in 2nd stretch were analysed. The results indicated that a significant spontaneous force arose under the high preload condition. However, the amplitude and extensive duration were depending on the strengthening of excessive load. 1) Muscle force enhancement time (t2) was significantly prolonged because of bearing the 2nd excessive load under high preload condition, however the Ca2+ concentration not significantly affect t2. The t2 prolongation existed both in intact muscles and shed muscles (117.42±34.80 msec and 260.20±34.50 msec). 2) The spontaneous force amplitude (AIFE) in 2nd excessive load surpassed its passive tension maximum (PTmax) in Ca2+ rich solutions (6327.49±524.52 mg to 4576.96±435.80 mg, 2062.10±287.59 mg to 1132.13±98.25 mg, in Ringer’s solution and 3% CaCl2-modified Ringer’s solution respectively), however, no surpass observed in Ca2+ lacking solutions and in CfTX-1 shed muscle (1121.76±320.25 mg to 1868.87±119.59 mg respectively). 3) In 2nd excessive load, force enhancement maximum tension–time integral (TTImax) was not depending on Ca2+ concentration, however the force enhancement velocity maximum (dT/dtmax) was significant increasing in high Ca2+ solution and shed preparations. We concluded that the excessive load facilitated the force enhancement generation during cardiac muscle relaxation. The significant myogenic spontaneous contraction relative force enhancement interrupted the cardiac muscle relaxation process, prolonged cardiac diastolic phase. CfTX-1 peptide was the compound prolonged the cardiac muscle relaxation process by reducing the AIFE and extending the t. This study is useful from further developing the study of the contraction-relaxation cycle interruption in overload heart.*Joint first authors; #Correspondence autho