Multiple Cryotherapy Attenuates Oxi-Inflammatory Response Following Skeletal Muscle Injury.
Agnieszka Zembroń-ŁacnyBarbara MorawinEdyta Wawrzyniak-GramackaJaroslaw GramackiPawel JarmuzekDariusz KotlegaEwa ZiemannPublished in: International journal of environmental research and public health (2020)
The oxi-inflammatory response is part of the natural process mobilizing leukocytes and satellite cells that contribute to clearance and regeneration of damaged muscle tissue. In sports medicine, a number of post-injury recovery strategies, such as whole-body cryotherapy (WBC), are used to improve skeletal muscle regeneration often without scientific evidence of their benefits. The study was designed to assess the impact of WBC on circulating mediators of skeletal muscle regeneration. Twenty elite athletes were randomized to WBC group (3-min exposure to -120 °C, twice a day for 7 days) and control group. Blood samples were collected before the first WBC session and 1 day after the last cryotherapy exposure. WBC did not affect the indirect markers of muscle damage but significantly reduced the generation of reactive oxygen and nitrogen species (H2O2 and NO) as well as the concentrations of serum interleukin 1β (IL-1β) and C-reactive protein (CRP). The changes in circulating growth factors, hepatocyte growth factor (HGF), insulin-like growth factor (IGF-1), platelet-derived growth factor (PDGFBB), vascular endothelial growth factor (VEGF), and brain-derived neurotrophic factor (BDNF), were also reduced by WBC exposure. The study demonstrated that WBC attenuates the cascade of injury-repair-regeneration of skeletal muscles whereby it may delay skeletal muscle regeneration.
Keyphrases
- skeletal muscle
- growth factor
- stem cells
- inflammatory response
- vascular endothelial growth factor
- insulin resistance
- wound healing
- endothelial cells
- induced apoptosis
- lipopolysaccharide induced
- oxidative stress
- lps induced
- toll like receptor
- open label
- body composition
- type diabetes
- signaling pathway
- phase iii
- high intensity
- phase ii
- cell death
- liver injury