The scientific mechanism and application strategy of EMS in combating sarcopenia
Sarcopenia is characterized by progressive decline in muscle mass, strength, and function, and is a core issue in aging and related diseases such as chronic diseases and long-term bed rest. EMS (Electric Pulse Muscle Stimulation) activates atrophic muscle groups through neuromuscular electrical stimulation, combined with metabolic regulation and regenerative repair mechanisms, becoming an effective tool for combating sarcopenia. The following are its functional path and implementation points:
The core mechanism of EMS in combating sarcopenia
Activate satellite cells to promote muscle fiber regeneration
The Ca ² ⁺ influx induced by electrical pulses activates the Notch signaling pathway, stimulating the proliferation and differentiation of muscle stem cells (satellite cells) into new muscle fibers.
Data: After 8 weeks of EMS intervention, the number of satellite cells in elderly subjects increased by 42% (compared to the control group).
Inhibit protein breakdown and improve synthesis decomposition balance
EMS enhances muscle protein synthesis by activating the mTOR pathway, while reducing MAFbx (muscle atrophy factor) expression by inhibiting the FoxO pathway.
Effect: The muscle ubiquitin proteasome activity in the EMS group decreased by 28% (slowing down catabolism).
Optimize the recruitment of sports units and reshape neural control
High frequency stimulation (80-100Hz) preferentially activates type II muscle fibers, improving the ratio of muscle fiber types (fast/slow).
Clinical evidence: Patients with post-stroke sarcopenia showed a 35% increase in neuromuscular junction transmission efficiency after EMS treatment.
