Evaluation of mitochondrial function in chronic myofascial trigger points - a prospective cohort pilot study using high-resolution respirometry

Abstract

Background: Myofascial trigger points (MTrPs) are hyperirritable areas in the fascia of the affected muscle, possibly related to mitochondrial impairment. They can result in pain and hypoxic areas within the muscle. This pilot study established a minimally invasive biopsy technique to obtain high-quality MTrP tissue samples to evaluate mitochondrial function via high-resolution respirometry. Secondary objectives included the feasibility and safety of the biopsy procedure.

Methods: Twenty healthy males participated in this study, 10 with a diagnosis of myofascial pain in the musculus (m.) trapezius MTrP (TTP group) and 10 with a diagnosis of myofascial pain in the m. gluteus medius (GTP group). Each participant had 2 muscle biopsies taken in one session. The affected muscle was biopsied followed by a biopsy from the m. vastus lateralis to be used as a control. Measurements of oxygen consumption were carried out using high-resolution respirometry.

Results: Mitochondrial respiration was highest in the GTP group compared to the TTP group and the control muscle whereas no differences were observed between the GTP and the control muscle. When normalizing respiration to an internal reference state, there were no differences between muscle groups. None of the participants had hematomas or reported surgical complications. Patient-reported pain was minimal for all 3 groups. All participants reported a low procedural burden.

Conclusions: This pilot study used a safe and minimally invasive technique for obtaining biopsies from MTrPs suitable for high-resolution respirometry analysis of mitochondrial function. The results suggest that there are no qualitative differences in mitochondrial function of MTrPs of the trapezius and gluteus medius muscles compared to the vastus lateralis control muscle, implying that alterations of mitochondrial function do not appear to have a role in the development of MTrPs.

Trial registration: Registered as No. 20131128-850 at the Coordinating Center for Clinical Studies of the Medical University of Innsbruck, trial registration date: 28th November 2013 and retrospectively registered on 11th of October 2018 at ClinicalTrials.gov with the ID NCT03704311 .

Keywords: High-resolution respirometry; Mitochondria; Mitochondrial function; Muscle biopsy; Myofascial trigger points.

Conflict of interest statement

Ethics approval and consent to participate

The study was approved by the Ethical Committee of the Medical University Innsbruck (AN4859 318/4.9) in accordance with the current version (2013) of the Declaration of Helsinki, and it was registered as No. 20131128–850 by the Coordinating Center for Clinical Studies of the Medical University Innsbruck and retrospectively registered on 11th of October 2018 at Consent for publication

Not applicable.

Competing interests

The authors declare that there are no competing interests.

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Figures

Fig. 1

High-resolution respirometry with permeabilized fibers from a muscle biopsy sample. Oxygen flux (JO2) is displayed as pmol O2.s− 1.mg− 1 wet weight and changes in response to application of the following substrate-uncoupler-inhibitor titration protocol: mitochondrial leak state without adenylates (LN) after addition of glutamate (G) and malate (M), complex I-supported oxidative phosphorylation capacity (OXPHOS) after addition of ADP (D), pyruvate (P) and cytochrome c (c), complex I-supported electron transfer capacity (ETC) after addition of an uncoupler (U), and succinate-supported ETC after addition of succinate (S), followed by titration of rotenone (Rot); at the end of the protocol, malonic acid (Mna) and antimycin A were added. Abbreviations: CIP = complex I-supported oxidative phosphorylation capacity; CIE = complex I-supported ETC; CIIE = ETC of CII; CI + IIE = maximal ETC of CI and CII; ETC = electron transfer capacity; OXPHOS = oxidative phosphorylation; LN = leak state without adenylates

Fig. 2

Differences in mass-specific mitochondrial respiration among the different muscle groups. Mass-specific mitochondrial respiration among different muscle groups affected by a myofascial trigger point (m. gluteus medius and m. trapezius) and the unaffected control muscle (m. vastus lateralis) after initiating mitochondrial leak state without adenylates (LN), complex I-supported oxidative phosphorylation capacity (CIP), complex I-supported electron transfer capacity (ETC) of CI (CIE), maximal ETC of CI and CII (CI + IIE) and ETC of CII (CIIE). Abbreviations: TrP M. glut. Med. = musculus gluteus medius trigger point; TrP M. trapezius = musculus trapezius trigger point; CTR M. vast. Lat. = musculus vastus lateralis control muscle; see Fig. 1 for additional abbreviations

Fig. 3

Respiratory states normalized for the internal reference state of electron transfer capacity (ETC). Normalizing respiration for ETC of CI and CII (CI + IIE) results in flux control ratios, which reflect important mitochondrial qualitative alterations in mitochondrial function. The leak state without adenylates (LN), complex I-supported oxidative phosphorylation capacity (CIP), complex I-supported ETC (CIE), and ETC of CII (CIIE) are displayed, and all states are normalized to maximal ETC of CI and CII (CI + IIE). Abbreviations: TrP M. glut. Med. = musculus gluteus medius trigger point; TrP M. trapezius = musculus trapezius trigger point; CTR M. vast. Lat. = musculus vastus lateralis control muscle; see Fig. 1 for additional abbreviations