ICE MASSAGE INEFFECTIVE IN RECOVERY FROM MUSCLE DAMAGE
Howatson, G., van Someren, D. A., Hortobagyi, T. (2006). Ice massage does not attenuate reductions in muscle function following maximal lengthening contractions. Medicine and Science in Sports and Exercise, 38(5), Supplement abstract 2121.
"Ice massage is a commonly used method of cryotherapy in the treatment of muscle soreness after exercise; however the empirical evidence that supports its use is somewhat limited and equivocal". This investigation examined the efficacy of ice massage for reducing markers of muscle damage and soreness following maximal lengthening contractions. Male subjects (N = 12) were randomly assigned to an ice massage or placebo treatment. The protocol was designed to induce muscle damage to the forearm flexors using an isokinetic dynamometer and consisted of 3 x 10 sets of maximal lengthening contractions at 30°/s. Treatments were administered immediately post-exercise and at 24 and 48 hours post-exercise. The ice massage consisted of a 15-minute treatment and the placebo was a five-minute sham ultrasound treatment. Variables monitored were creatine kinase, delayed onset muscle soreness, limb girth, maximal voluntary isometric torque and maximal voluntary isokinetic torque at 60°/s and 210°/s. Measurements were taken pre-exercise, immediately after, and at 24, 48, 72, and 96 hours post-exercise (but before the post-exercise 24 and 48 hours treatments with ice).
A significant time main effect for all six variables indicated the occurrence of muscle damage. Of these six variables, only creatine kinase showed a significant treatment x time interaction with lower levels at 96 hours after ice massage compared with the placebo.
Implication. Ice massage failed to reduce muscle soreness, limb girth, and the decrement in torque production, suggesting that it was ineffective in promoting muscle function recovery following exercise-induced muscle damage. The reduction in creatine kinase efflux at 96 hours suggests that ice massage may have attenuated secondary cellular damage resulting from the lengthening contractions.