Muscle Contraction Group, School of Physiology & Pharmacology, University of Bristol, Medical Sciences Building, Bristol BS8 1TD, UK.
J Muscle Res Cell Motil. 2012 Oct;33(5):313-25. doi: 10.1007/s10974-012-9307-8. Epub 2012 Jun 16.
The aim of the present study was to examine the temperature dependence of active force in lengthening and shortening muscle. Experiments were done, in vitro, on bundles of intact fibres (fibre length L(0) ~2 mm; sarcomere length ~2.5 μm) isolated from a rat fast muscle (flexor hallucis brevis) and a ramp length change of 5-7% L(0) was applied on the plateau of an isometric tetanic contraction. Ramp lengthening increased and ramp shortening decreased the muscle tension to new approximately steady levels in a velocity-dependent way. The isometric tension and the lower steady tension reached at a given shortening velocity, increased with warming from 10 to 35 °C and the relation between tension and reciprocal absolute temperature was sigmoidal. However, the tension-temperature curve of shortening muscle was sharper and shifted to higher temperature with increased velocity. In contrast, the enhanced steady tension during lengthening at a given velocity was largely temperature-insensitive within the same temperature range; we hypothesize that the tension-temperature curve may be shifted to lower temperatures in lengthening muscle. Consequently, when normalised to the isometric tension at each temperature, the tension during lengthening at a given velocity decreased exponentially with increase of temperature. The residual force enhancement that remains after ramp lengthening showed a similar behaviour and was markedly reduced in warming from 10 to 35 °C. The findings are consistent with the thesis that active force generation in muscle is endothermic and strain-sensitive; during shortening with a faster crossbridge cycle it becomes more pronounced, but during lengthening it becomes depressed as the cycle slows in a velocity-dependent way. The residual force enhancement may be caused by the same process in addition to non-crossbridge mechanism(s).
本研究旨在探讨伸展和缩短肌肉中主动力的温度依赖性。实验在体外进行，使用从大鼠快肌（屈趾短肌）中分离出的完整纤维束（纤维长度 L(0)2mm；肌节长度2.5μm）进行，在等长强直收缩的平台上施加 5-7%L(0)的斜坡长度变化。斜坡伸展以速度依赖的方式增加，而斜坡缩短则降低肌肉张力至新的近似稳定水平。等长张力和在给定缩短速度下达到的较低稳定张力随着从 10°C 到 35°C 的升温而增加，张力与倒数绝对温度之间的关系呈 S 形。然而，缩短肌肉的张力-温度曲线更陡峭，并随着速度的增加向更高的温度移动。相比之下，在给定速度下伸展时增强的稳定张力在相同温度范围内对温度的变化不敏感；我们假设张力-温度曲线可能在伸展肌肉中向更低的温度移动。因此，当以每个温度下的等长张力为基准进行归一化时，在给定速度下伸展时的张力随温度升高呈指数下降。在从 10°C 到 35°C 的升温过程中，斜坡伸展后剩余力增强表现出相似的行为，且显著降低。这些发现与肌肉中主动力产生是吸热和应变敏感的假设一致；在更快的横桥循环的缩短过程中，这种情况更为明显，但在较慢的速度依赖性方式下的伸展过程中，这种情况会受到抑制。剩余力增强可能除了非横桥机制外，还与同一过程有关。
