The time course of the latency relaxation as a function of the sarcomere length in frog and mammalian muscle

Abstract

In a comparative study the isometric twitch tension and the latency relaxation were correlated to the sarcomere length in frog and mammalian muscle, the latter only in the length range from 2.4 to 3.1 μm since at higher degrees of stretch the sarcomere lengths became increasingly non‐uniform along the fibres. The location of the triads in mammalian muscle fibres was examined by means of electron microscopy. During stretch the location of the triads was gradually changed from the overlap zone at sarcomere lengths below 2.6 to 2.7 jim to the I‐band at sarcomere lengths above 3.0 to 3.1 μm, their centres (T‐tubules) being equally distributed between the overlap zone and the I‐band at sarcomere lengths around 2.9 μm. In both types of muscle the maximum amplitude of the latency relaxation (of about equal relative size) occurred at a sarcomere length of about 3.1 μm; and both twitch tension and latency relaxation were dependent upon the presence of a zone of overlap between the thin and thick filaments. In neither of the two types of muscles did the time, t1, from stimulation to the onset of tension drop depend upon the sarcomere length. At room temperature (22oC) t1 was about 1 ms in mammalian muscle and 2 ms in frog muscle. In mammalian muscle the time, t2, from the stimulus to the maximum drop in tension and the time, t3, to positive tension development were both substantially uninfluenced by changes in sarcomere length in the range 2.4 to 2.9 μm, whereas in frog muscle both t2 and t3 increased linearly with increasing sarcomere length in the above range. These findings are discussed in the light of the different locations of the triads in frog and mammalian muscle. It is concluded that the theory of Sandow (1966)–extended by Mulieri (1972)–and that of Haugen & Sten‐Knudsen (1976), which both have the virtue of being able to account for the increase of the latent period with stretch in frog muscle, also would be applicable to mammalian muscle provided that a time lag of 0.5 to 1.0 ms exists from the time of the binding of Ca2+‐ions to the troponin molecules inside the zone of overlap until the attached cross bridges start to move and develop tension.