Differences in serum IL-6 response after 1°C rise in core body temperature in individuals with spinal cord injury and cervical spinal cord injury during local heat stress

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 9 with CSCI, 10 with thoracic and lumbar spinal cord injury (TLSCI) and 8 able-bodied (AB) subjects. Time since injury was 16.4±4.1 years in TLSCI and 16.1±3.4 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, tumor 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. Conclusion: 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

The effect of acute and chronic exercise on inflammatory markers in SCI

A spinal cord injury (SCI) is associated with an increased prevalence of physical inactivity and obesity, conditions linked to illnesses with inflammatory etiology, such as diabetes or cardiovascular disease. This may at least partly explain the elevated inflammatory risk marker profile and the higher occurrence of the associated diseases found in individuals with SCI. In able-bodied populations, exercise helps to improve this risk marker profile prompting the question whether exercise can mitigate some of the SCI related risk through acute disturbances of the inflammatory environment. Despite a smaller active muscle mass during upper body activities, a similar acute inflammatory response has been observed with this modality when compared with lower body exercise. This supports the use of upper body exercise interventions to combat disease linked to inflammation in individuals not able to participate in other exercise activities. However, more dramatic reductions in active muscle mass and/or sympathetic dysfunction found in those with cervical SCI can result in an absent or blunted acute inflammatory response. Nonetheless, intervention strategies like exercise, functional electrical stimulation or passive elevation of core temperature induce some modest positive acute responses even in individuals with high level SCI. The evidence base for chronic interventions is small but suggests that long term exercise can indeed improve the inflammatory risk marker profile in individuals with thoracic and, to a lesser extent, with cervical SCI. Future challenges include defining disability-specific minimal exercise or temperature stimuli required to induce meaningful chronic changes in inflammatory markers