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. 2018 Mar;102(3):287-295.
doi: 10.1007/s00223-017-0354-4. Epub 2017 Nov 3.

Relationships Between Markers of Inflammation and Muscle Mass, Strength and Function: Findings from the Hertfordshire Cohort Study

Affiliations

Relationships Between Markers of Inflammation and Muscle Mass, Strength and Function: Findings from the Hertfordshire Cohort Study

L D Westbury et al. Calcif Tissue Int. 2018 Mar.

Abstract

We investigated the longitudinal relationships between inflammation markers and the following outcomes in a UK cohort study: appendicular lean mass (ALM); walking speed; level and change in grip strength; and sarcopenia defined by the European Working Group on Sarcopenia in Older People. Analyses were based on 336 community-dwelling older men and women (aged 59-70 years) who participated in the Hertfordshire Cohort Study (HCS). Inflammation markers were ascertained at baseline using enzyme-linked immunosorbent assay techniques and Bio-Plex Pro Assays. Grip strength was measured at baseline and follow-up [median follow-up time: 10.8 years (inter-quartile range 10.2-11.6)] and change in grip strength was ascertained using a residual change approach. At follow-up, ALM was ascertained using dual-energy X-ray absorptiometry, customary walking speed was measured and sarcopenia status was ascertained. Gender-adjusted linear and Poisson regression was used to examine the associations between inflammation markers and outcomes with and without adjustment for anthropometric and lifestyle factors. Higher C-reactive protein was associated (p < 0.04) with lower grip strength and accelerated decline in grip strength from baseline to follow-up. Higher cortisol was associated with lower ALM (p < 0.05). Higher interleukin-8 (IL-8) was associated with lower ALM (p < 0.05) and increased risk of sarcopenia [fully-adjusted relative risk per SD increase in IL-8: 1.37 (95% CI 1.10, 1.71), p = 0.005]. All associations were robust in fully-adjusted analyses. Inflammation markers were associated with measures of muscle mass, strength and function in HCS. Further work is required to replicate these associations and to delineate the underlying mechanisms.

Keywords: Adipokine; Inflammation; Interleukin; Muscle; Sarcopenia; Strength.

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Conflict of interest statement

Conflict of interest

L. D. Westbury, N. R. Fuggle, H. E. Syddall, N. A. Duggal, S. C. Shaw, K. Maslin, E. M. Dennison, J. M. Lord and C. Cooper declare that they have no conflict of interest.

Ethical Approval

The baseline Hertfordshire Cohort Study had ethical approval from the Hertfordshire and Bedfordshire Local Research Ethics Committee and the follow-up had ethical approval from the East and North Hertfordshire Ethical Committees.

Human and Animal Rights

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed Consent

All participants gave signed consent to participate in the study and for their health records to be accessed in the future.

Figures

Fig. 1
Fig. 1
Flow diagram for the Hertfordshire Cohort Study analysis sample
Fig. 2
Fig. 2
SD difference (95% CI) in outcomes per SD increase in inflammatory predictors. Ad:lep adiponectin:leptin ratio. Regression models adjusted for the following characteristics at baseline: gender, age, follow-up time, height, weight-for-height residual, smoking history (ever vs never), alcohol consumption, diet quality and physical activity. Poisson regression models with robust variance estimation were used for EWGSOP sarcopenia status to yield relative risks (RR). Models for ALM were not adjusted for weight-for-height residual and models for change in grip were not adjusted for follow-up time (follow-up time was already used to derive the grip change measure). Adjusted p values are presented. Change in grip strength from HCS baseline to follow-up was obtained using a residual change method to ensure grip change measure was independent of baseline grip level. A positive estimate illustrates that a higher level of the inflammatory marker was associated with reduced loss of grip strength and a negative estimate reflects accelerated loss. Apart from IL-8, all inflammatory markers were log-transformed prior to standardising

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