Abstract

Objectives: Passive rise in core body temperature achieved by head-out hot water immersion (HHWI) results in acute increases in serum interleukin (IL)-6 but no change in plasma adrenaline in patients with cervical spinal cord injury (CSCI). The purpose of the present study was to determine the mechanism of heat stress-induced increase in serum IL-6.Setting: A cross-sectional study.Methods: The study subjects were nine with CSCI, ten with thoracic and lumbar spinal cord injury (TLSCI) and eight able-bodied (AB) subjects. Time since injury was 16.1 ± 3.4 years in TLSCI and 16.4 ± 4.1 years in CSCI. Subjects were subjected to lower-body heat stress (LBH) by wearing a hot water-perfused suit until 1 °C increase in core temperature. The levels of serum IL-6, plasma adrenaline, tumour necrosis factor (TNF)-α, C-reactive protein (CRP), and counts of blood cells were measured at normothermia and after LBH.Results: Serum IL-6 concentrations increased significantly immediately after LBH in all the three groups. ΔIL-6% was lower in CSCI subjects compared with AB subjects. Plasma adrenaline concentrations significantly increased after LBH in AB and TLSCI subjects, but did not change throughout the study in CSCI subjects. Cardiac output and heart rate increased at the end of LBH in all three groups.Conclusions: Under a similar increase in core temperature, ΔIL-6% was lower in the CSCI group compared with the AB group. These findings suggest that the observed rise in IL-6 during hyperthermia is mediated, at least in part, by plasma adrenaline.

Highlights

  • Individuals with cervical spinal cord injury (CSCI) and spinal cord injury (SCI) are often in a state of chronic low-grade inflammation

  • lower-body heat stress (LBH) time was significantly shorter in CSCI than AB and thoracic and lumbar spinal cord injury (TLSCI) (Table 1)

  • Despite the similar increase in core temperature in the three groups, DIL-6% was lower in CSCI subjects compared with AB subjects

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Summary

Introduction

Individuals with cervical spinal cord injury (CSCI) and spinal cord injury (SCI) are often in a state of chronic low-grade inflammation. Interleukin (IL)-6 is known as an inflammatory cytokine but it plays important roles in anti-inflammation, immune responses, and metabolic functions [4]. Apart from IL-6, various other myokines, which are cytokines secreted from contracting muscles, seem to play important roles in protection against diseases, such as chronic systemic low-grade inflammation [8,9,10,11]. The myokine response is governed by various muscle contraction-dependent and sympathetic nervous system-mediated signalling pathways [12]. This may explain the blunted myokine response to exercise in CSCI, given their reduced muscle mass and sympathetic dysfunction [13,14]

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