Does Icing Therapy Decrease Both Regenerative and Metabolic Capacities Following Skeletal Muscle Injury?

Abstract

Effects of icing treatment following skeletal muscle injury on mitochondrial biogenesis, pain marker, and fibrosis were investigated in male Wistar rats. We also examined the countermeasure for offsetting the negative impact of icing treatment. At 28 days after muscle injury, fibrotic area was increased and protein level of Voltage-dependent anion-selective channel 1 was decreased when an icing treatment (ice pack, 0℃ for 20 min) was applied immediately following the injury. The icing treatment reduced mRNA expression levels of pain markers (bradykinin B2 receptor and microsomal prostaglandin E synthase 1) at 1 day after the injury. On the other hand, the icing-related promotion of fibrosis was significantly attenuated when intermittent heat stress was combined, especially from 1-day after the injury (42℃ for 30 min on every other day until 14 days after the injury). Therefore, these results suggest that an icing treatment immediately after skeletal muscle injury attenuates muscle pain at early phase following the injury but impairs both muscle qualitative and mitochondrial recoveries during the regeneration. Our findings also indicate that the negative impact of icing treatment on fibrosis could be rescued when hyperthermia is combined within 1-day after the injury.