Being physically active and undertaking exercise on a regular basis are critical lifestyle behaviours which protect against the development of numerous chronic metabolic conditions. One of the key mechanisms by which physical activity exerts favourable health effects appears to be due to its capacity to reduce chronic low-grade inflammation. Single bouts of exercise have a potent anti-inflammatory influence with recent advances describing important effects of acute exercise on inflammatory mediators produced within skeletal muscle (myokines), adipose tissue (adipokines) and leucocytes. The accumulated effects of physical activity or exercise training on systemic inflammation have been studied widely within epidemiological research; however, information from intervention trials is still emerging. Current data suggest that the most marked improvements in the inflammatory profile are conferred with exercise performed at higher intensities, with combined aerobic and resistance exercise training potentially providing the greatest benefit. The purpose of this review is to describe recent advances in our understanding surrounding the acute and chronic effects of physical activity on key mediators of inflammation. Within this, particular attention is given to the interleukin-6 system owing to its apparent centrality in mediating the anti-inflammatory effects of exercise.

This study aimed to determine whether 2 wk of high-intensity intermittent training (HIIT) altered inflammatory status in plasma and adipose tissue in overweight and obese males. Twelve participants [mean (SD): age 23.7 (5.2) yr, body mass 91.0 (8.0) kg, body mass index 29.1 (3.1) kg/m2] undertook six HIIT sessions over 2 wk. Resting blood and subcutaneous abdominal adipose tissue samples were collected and insulin sensitivity determined, pre- and posttraining. Inflammatory proteins were quantified in plasma and adipose tissue. There was a significant decrease in soluble interleukin-6 receptor (sIL-6R; P = 0.050), monocyte chemotactic protein-1 (MCP-1, P = 0.047), and adiponectin (P = 0.041) in plasma posttraining. Plasma IL-6, intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), IL-10, and insulin sensitivity did not change. In adipose tissue, IL-6 significantly decreased (P = 0.036) and IL-6R increased (P = 0.037), while adiponectin tended to decrease (P = 0.056), with no change in ICAM-1 posttraining. TNF-α, MCP-1, and IL-10 were not detectable in adipose tissue. Adipose tissue homogenates were then resolved using one-dimensional gel electrophoresis, and major changes in the adipose tissue proteome, as a consequence of HIIT, were evaluated. This proteomic approach identified significant reductions in annexin A2 (P = 0.046) and fatty acid synthase (P = 0.016) as a response to HIIT. The present investigation suggests 2 wk of HIIT is sufficient to induce beneficial alterations in the resting inflammatory profile and adipose tissue proteome of an overweight and obese male cohort.

In young adults with T2DM, diabetes duration and aortic distensibility were associated with diastolic dysfunction. Interventional studies are required to assess whether cardiac dysfunction can be reversed in this phenotype of patients.

As interleukin-6 (IL-6), its soluble receptor (sIL-6R), and the IL-6/sIL-6R complex is transiently elevated in response to prolonged moderate-intensity exercise, this study investigated how these levels would be modulated by an acute bout of high-intensity intermittent (HIIT) exercise in comparison to continuous moderate-intensity exercise (MOD). This study also investigated the expression of the differentially spliced sIL-6R (DS-sIL-6R) in response to exercise. Eleven healthy males completed two exercise trials matched for external work done (582±82 kJ). During MOD, participants cycled at 61.8 (2.6)% VO 2peak for 58.7 (1.9) min, while HIIT consisted of ten 4-min intervals cycling at 87.5 (3.4)% : V O 2peak separated by 2-min rest. Blood samples were collected pre-exercise, post-exercise, and 1.5, 6, and 23 h post-exercise. Plasma IL-6, sIL-6R, IL-6/sIL-6R complex, and DS-sIL-6R levels were measured by enzyme-linked immunosorbent assay. HIIT caused a significantly greater increase in IL-6 than MOD (P= 0.018). Both MOD and HIIT resulted in an increase in sIL-6R and IL-6/sIL-6R complex (P<0.001), however, this was not significantly different between trials. Soluble IL-6R peaked at 6 h post-exercise in both trials. DS-sIL-6R increased significantly with exercise (P=0.02), representing 0.49% of the total sIL-6R increase. This investigation has demonstrated that the IL-6 response is greater after intermittent high-intensity exercise than comparable moderate-intensity exercise; however, increased IL-6/sIL-6R complex nor sIL-6R was different between HIIT and MOD. The current study has shown for the first time that elevated sIL-6R after HIIT exercise is derived from both proteolytic cleavage and differential splicing.

It has been suggested that circulating hormones and cytokines are important in the adaptive response to low-load resistance training (LLRT) with blood flow restriction (BFR); however, their response following this type of training in older men is unclear. Seven healthy older men (age 71.0 ± 6.5 year, height 1.77 ± 0.05 m, body mass 80.0 ± 7.5 kg; mean ± SD) performed five sets of unilateral LLRT knee extensions (20 % 1-RM) of both limbs, with or without BFR in a counterbalanced order. For the BFR condition, a pressure cuff was applied on the upper thigh and inflated to ~110 mmHg. Venous blood samples were taken at rest and 30-, 60- and 120-min post-exercise and measured for plasma concentrations of growth hormone (GH), insulin-like growth factor 1 (IGF-1), vascular endothelial growth factor (VEGF), cortisol and interleukin-6 (IL-6). GH increased (P < 0.05) from rest to 30-min post-exercise and was greater (P < 0.05) during LLRT with BFR than without. VEGF was significantly (P < 0.05) elevated from resting levels at 30-, 60- and 120-min post-exercise following LLRT with BFR with no change seen following LLRT without BFR. IL-6 increased (P < 0.05) from 30- to 60-min post-exercise and remained elevated at 120-min post-exercise in both conditions. Cortisol and IGF-1 were unaffected following exercise. In conclusion, a single bout of LLRT with BFR increases the circulating concentrations of GH and VEGF in older men and may explain the skeletal muscle and peripheral vascular adaptations observed following training with BFR.