# Interaction of pulsed low frequency electromagnetic field (PEMF) with mitochondria

## TL;DR

This study explores how pulsed electromagnetic fields affect mitochondria, finding that they influence ATP-synthesis-linked respiration but not NO-inhibited respiration.

## Contribution

The study introduces a novel investigation into how PEMF interacts with mitochondrial function and ATP synthesis.

## Key findings

- PEMF selectively stimulates respiration linked to ATP-synthesis.
- PEMF does not restore mitochondrial respiration inhibited by NO.
- Blue light can restore NO-inhibited mitochondrial respiration.

## Abstract

Pulsed electromagnetic field (PEMF) therapy is a non-invasive treatment that delivers electric and magnetic fields to tissues via inductive coils inducing salutary effects. Previously PEMF was reported to accelerate gas transport in the liquid phase. Drawing analogies from electrical elements, we hypothesized that PEMF can modulate transmembrane potential of biological membranes. Given that mitochondria interact with gaseous molecules such as oxygen and nitric oxide (NO) and contain voltage-sensitive channels, this study focused on the effects of a single PEMF device with a low input-energy and a 1ms, 30 kHz sine wave duty cycle per pulse on mitochondrial function. Experiments were conducted using cell cultures, tissue homogenates, and isolated mitochondria. We assessed mitochondrial membrane potential, NO levels, and mitochondrial respiration. We found no evidence that PEMF restores mitochondrial respiration inhibited by NO, but it can be restored by exposure of mitochondria to blue light. Our findings show that PEMF selectively stimulates respiration linked to ATP-synthesis affecting less uncoupled respiration. This suggests that changes in ATP-synthesis underlies the primary beneficial effects observed here. The underlying mechanisms may include interaction of PEMF with mitochondrial transport systems or activity of mitochondrial complexes. The exact mechanisms still should be investigated.

The online version contains supplementary material available at 10.1038/s41598-026-37527-6.