Chronic muscle tissue infiltration by inflammatory cells (e.g., leukocytes, neutrophils, and monocytes) activates oxidative and inflammatory signaling cascades that degrade cellular structures and promote necrosis such as inducible nitric oxide synthase (iNOS) and NF-kB [90,101,115]. CAPE and high levels (200 and 300 mg/kg) of crude and processed bee pollen reduced inflammatory cell infiltration into the gastrocnemius muscle of rats with muscle injury induced by eccentric exercise and ischemia reperfusion [90,101,102]. This effect was revealed by lower activity of myeloperoxidase, an indicator of neutrophil sequestration [101,102]. As such, CAPE and bee pollen not only suppressed lipid peroxidation (lower levels of malondialdehyde, MDA) but also inhibited the activity of myostatin and the production of muscle depleting cytokines and chemokines such as IL-1β, α2-macroglobulin, and monocyte chemotactic protein 1 (MCP-1) [36,38,90,101]. The underlying mechanism entailed downregulation of nuclear p65NF-κB and blockage of its consensus binding sites in skeletal muscle [101]. As a result, bee products increased muscle mass both in sarcopenic obese rat and malnourished old rats [36] and restored the structure of myofibers (despite the persistence of necrosis) compared with untreated eccentric exercising animals, which demonstrated necrotic and fragmented myofibers [90].