# Indistinguishable mitochondrial phenotypes after exposure of healthy myoblasts to myalgic encephalomyelitis/chronic fatigue syndrome or control serum

## TL;DR

This study found no evidence that blood from people with ME/chronic fatigue syndrome affects mitochondria in muscle cells differently than blood from healthy people.

## Contribution

A large-scale replication study using pre-registration and a bigger sample size to test mitochondrial effects of ME sera.

## Key findings

- No significant differences in maximal respiratory capacity between ME and control sera treatments.
- Over 1,700 mitochondrial stress tests showed no support for ME serum affecting myoblast mitochondria.
- Results contradict earlier findings suggesting ME serum alters mitochondrial function in vitro.

## Abstract

Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome is a disease of uncertain aetiology that affects up to 400,000 individuals in the UK. Exposure of cultured cells to the sera of people with ME has been proposed to cause phenotypic changes in these cells in vitro when compared to sera from healthy controls. ME serum factors causing these changes could inform the development of diagnostic tests. In this study, we performed a large-scale, pre-registered replication of an experiment from Fluge et al (2016) that reported an increase in maximal respiratory capacity in healthy myoblasts after treatment with serum from people with ME compared to serum from healthy controls. We replicated the original experiment with a larger sample size, using sera from 67 people with ME and 53 controls to treat healthy cultured myoblasts, and generated results from over 1,700 mitochondrial stress tests performed with a Seahorse Bioanalyser. We observed no significant differences between treatment with ME or healthy control sera for our primary outcome of interest, oxygen consumption rate at maximal respiratory capacity. Results from our study provide strong evidence against the hypothesis that ME blood factors differentially affect healthy myoblast mitochondrial phenotypes in vitro.