A Preliminary Examination of Cryotherapy and Secondary Injury in Skeletal Muscle.

A Preliminary Examination of Cryotherapy and Secondary Injury in Skeletal Muscle Merrick MA, Rankin JM, Andres FA, Hinm CL (Athletic Training Department, Indiana State University, Terre Haute, Ind; Departments of Health Promotion & Human Performance and Medicinal and Biological Chemistry, The University of Toledo, Toledo, Ohio; Movement Science Department, Grand Valley State University, Grand Rapids, Mich), Med Sci Sports Exerc. 1999;31:1516-1521.

This study investigated the use of cryotherapy in the treatment of acute musculoskeletal injury. The authors based their study on the secondary injury model, which hypothesizes that a period of posttraumatic hypoxia results from the hemodynamic changes induced by a primary musculoskeletal injury. The application of cold is believed to modify the secondary injury process by reducing metabolic demand or reducing the rate of chemical reactions that damage the tissue. The study, therefore, sought to verify the presence of secondary injury in skeletal muscle, measure it, and determine whether acute cryotherapy alters it.

Nineteen Sprague-Dawley rats were randomly assigned to either a cryotherapy (n = 10) or control group (n = 9). Injury was induced in the cryotherapy group by use of a Kelly hemostatic forceps on the right triceps surae muscle. The left uninjured calf was used as a control. After injury, the cryotherapy group received a crushed ice pack applied to the injured calf using elastic tape for 5 hours. The triceps surae muscle from both groups were then excised bilaterally and analyzed by assay for mitochondrial function through the reduction of triphenyltetrazolium chloride (TTC) to triphenylformazan (formazan red). An ANCOVA was used to evaluate the comparison of ice and no-ice groups.

The results showed that injured tissues (both treated and untreated) had less TTC reduction (6.59 [+ or -] 1.01 [micro]g/mg/h and 4.48 [+ or -] 0.79 [micro]g/mg/h, respectively) than uninjured control tissues (ice group: 7.94 [+ or -] 1.49 [micro]g/mg/h, no-ice group: 6.62 [+ or -] 0.75 [micro]g/mg/h). According to the researchers, the no-ice TTC reduction was only two thirds that of the ice group, suggesting that cooling tissues with ice initiates some mechanism by which mitochondrial damage is retarded. The presence of secondary injury was revealed by the differences between the TTC reduction in the injured and noninjured control groups subsequent to the initial injury.

The authors concluded that secondary injury occurred following primary crush injury in this animal model and that the extent of secondary injury may be reduced if cold is applied continuously for 5 hours immediately following the primary injury. The authors acknowledged certain limitations of this study, and they indicated that additional research will be needed before the clinical implications of this information can be fully appreciated.

Elaine Filusch Betts, PT, PhD Central Michigan University Mt Pleasant, Mich