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Age- and sex-specific effects in paravertebral surface electromyographic back extensor muscle fatigue in chronic low back pain.

ABSTRACT: The impact of aging on the back muscles is not well understood, yet may hold clues to both normal aging and chronic low back pain (cLBP). This study sought to investigate whether the median frequency (MF) surface electromyographic (SEMG) back muscle fatigue method-a proxy for glycolytic muscle metabolism-would be able to detect age- and sex-specific differences in neuromuscular and muscle metabolic functions in individuals with cLBP in a reliable way, and whether it would be as sensitive as when used on healthy individuals. With participants seated on a dynamometer (20° trunk anteflexion), paraspinal SEMG activity was recorded bilaterally from the multifidus (L5), longissimus (L2), and iliolumbalis (L1) muscles during isometric, sustained back extensions loaded at 80% of maximum from 117 younger (58 females) and 112 older (56 female) cLBP individuals. Tests were repeated after 1-2 days and 6 weeks. Median frequency, the SEMG variable indicating neuromuscular fatigue, was analyzed. Maximum back extensor strength was comparable between younger and older participants. Significantly less MF-SEMG back muscle fatigue was observed in older as compared to younger, and in older female as compared to older male cLBP individuals. Relative reliability was excellent, but absolute reliability appeared large for this SEMG-fatigue measure. Findings suggest that cLBP likely does not mask the age-specific diagnostic potential of the MF-SEMG back extensor fatigue method. Thus, this method possesses a great potential to be further developed into a valuable biomarker capable of detecting back muscle function at risk of sarcopenia at very early stages.

SUBMITTER: Ebenbichler G

PROVIDER: S-EPMC7031171 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionChronic low back pain (CLBP) is the leading cause of disability worldwide. However, there is no consensus in the literature regarding optimal management. Exercise intervention is the most widely used treatment as it likely influences contributing factors such as physical and psychological. Literature evaluating the effects of exercise on CLBP is often generalised, non-specific and employs inconsistent outcome measures. Moreover, the mechanisms behind exercise-related improvements are poorly understood. Recently, research has emerged identifying associations between neuromuscular-biomechanical impairments and CLBP-related disability. This information can be used as the basis for more specific and, potentially more efficacious exercise interventions for CLBP patients.Methods and analysisNinety-four participants (including both males and females) with CLBP aged 18-65 who present for treatment to a Melbourne-based private physiotherapy practice will be recruited and randomised into one of two treatment groups. Following baseline assessment, participants will be randomly allocated to receive either: (i) strengthening exercises in combination with lumbar force accuracy training exercises or (ii) strengthening exercises alone. Participants will attend exercise sessions twice a week for 12 weeks, with assessments conducted at baseline, midway (ie, 6 weeks into the trial) and at trial completion. All exercise interventions will be supervised by a qualified physiotherapist trained in the intervention protocol. The primary outcome will be functional disability measured using the Oswestry Disability Index. Other psychosocial and mechanistic parameters will also be measured.Ethics and disseminationThis study was given approval by the University of Melbourne Behavioural and Social Sciences Human Ethics Sub-Committee on 8 August 2017, reference number 1?749?845. Results of the randomised controlled trial will be published in peer-reviewed journals.Trial registration numberACTRN12618000894291.

Project description:What is the central question of this study? Can physiological concentrations of metabolite combinations evoke sensations of fatigue and pain when injected into skeletal muscle? If so, what sensations are evoked? What is the main finding and its importance? Low concentrations of protons, lactate and ATP evoked sensations related to fatigue. Higher concentrations of these metabolites evoked pain. Single metabolites evoked no sensations. This suggests that the combination of an ASIC receptor and a purinergic P2X receptor is required for signalling fatigue and pain. The results also suggest that two types of sensory neurons encode metabolites; one detects low concentrations of metabolites and signals sensations of fatigue, whereas the other detects higher levels of metabolites and signals ache and hot. The perception of fatigue is common in many disease states; however, the mechanisms of sensory muscle fatigue are not understood. In mice, rats and cats, muscle afferents signal metabolite production in skeletal muscle using a complex of ASIC, P2X and TRPV1 receptors. Endogenous muscle agonists for these receptors are combinations of protons, lactate and ATP. Here we applied physiological concentrations of these agonists to muscle interstitium in human subjects to determine whether this combination could activate sensations and, if so, to determine how the subjects described these sensations. Ten volunteers received infusions (0.2 ml over 30 s) containing protons, lactate and ATP under the fascia of a thumb muscle, abductor pollicis brevis. Infusion of individual metabolites at maximal amounts evoked no fatigue or pain. Metabolite combinations found in resting muscles (pH 7.4 + 300 nm ATP + 1 mm lactate) also evoked no sensation. The infusion of a metabolite combination found in muscle during moderate endurance exercise (pH 7.3 + 400 nm ATP + 5 mm lactate) produced significant fatigue sensations. Infusion of a metabolite combination associated with vigorous exercise (pH 7.2 + 500 nm ATP + 10 mm lactate) produced stronger sensations of fatigue and some ache. Higher levels of metabolites (as found with ischaemic exercise) caused more ache but no additional fatigue sensation. Thus, in a dose-dependent manner, intramuscular infusion of combinations of protons, lactate and ATP leads to fatigue sensation and eventually pain, probably through activation of ASIC, P2X and TRPV1 receptors. This is the first demonstration in humans that metabolites normally produced by exercise act in combination to activate sensory neurons that signal sensations of fatigue and muscle pain.

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Age- and sex-specific effects in paravertebral surface electromyographic back extensor muscle fatigue in chronic low back pain.

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