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MUSCLE TEARS AND THEIR DEPENDENCE ON TEMPERATURE



Abstract

Background: Muscle tears and injuries are a huge problem throughout the world. Ways of reducing these injuries are welcome, with warm-up and stretching of muscles prior to use established methodologies. Forces associated with muscles can be thought of as active (stimulated muscle: actin-myosin) and passive (relaxed muscle: elastic proteins and connective tissue). In muscle tears, the connective tissue component is damaged, but there is very little information in the literature on this component of the muscle.

Objective: To examine passive (elastic) components in muscle during impact loading at differing temperatures. In particular to test the hypothesis that the connective tissue component fails at different loads according to the temperature.

Methods: Gastrocnemius and Soleus were isolated from 36 male rat limbs, clamped and exposed to increasing impact loads, by dropping a known weight from increasing heights. Muscle was given one minute to recover before an increased force was applied. Temperature was varied from 17 C to 42 C (to encompass the physiological range) in 5 C increments. The height of drop causing non-recoverable deformation, and the maximum deceleration of the weight (measured using an accelerometer attached to a picoscope) at a constant height was recorded for each temperature.

Results: The energy to failure, i.e. the point at which non-recoverable deformation occurred was found to increase above 32 C (p < 0.01) and the maximum deceleration at impact found to have a downward trend with increasing temperatures. At 17 C, the energy to failure was 317.7 ± 20 mJ, At 22 C, the energy to failure was 301.8 ± 29 mJ, At 27 C, the energy to failure was 317.7 ± 40 mJ, At 32 C, the energy to failure was 333.5 ± 21.2 mJ, At 37 C, the energy to failure was 460.2 ± 15.8 mJ, At 42 C, the energy to failure was 619.5 ± 21.2 mJ,

Conclusions: Muscle was shown to act in an increasingly elastic nature with temperature. At higher temperatures a larger energy is required to deform the muscle permanently, and the muscle decelerates more slowly, both in keeping with elastic properties. The same energy at a lower temperature causes significant deformation within the muscle. This has numerous clinical implications, as the temperature at which this change occurs is encountered during surgery and also by sportsmen on outdoor pitches. More research is required to look at the passive components within muscles in humans.

Correspondence should be addressed to Miss B.E. Scammell at the Division of Orthopaedic & Accident Surgery, Queen’s Medical Centre, Nottingham, NG7 2UH, England