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Key Points Physical inactivity increases the risk of type 2 diabetes, cardiovascular diseases, chronic obstructive pulmonary disease, colon cancer, breast cancer, dementia and depression. Physical inactivity leads to the accumulation of visceral fat and consequently the activation of a network of inflammatory pathways. Chronic inflammation promotes the development of insulin resistance, atherosclerosis, neurodegeneration and tumour growth, and subsequently the development of a number of diseases associated with physical inactivity. The protective effect of exercise against chronic inflammation-associated diseases may, to some extent, be ascribed to an anti-inflammatory effect of regular exercise. The anti-inflammatory effect of regular exercise may be mediated by a reduction in visceral fat mass (with a subsequent decreased release of adipokines from adipose tissue) and/or by the induction of an anti-inflammatory environment with each bout of exercise. Possible mechanisms by which exercise exerts its anti-inflammatory effect include: release of interleukin-6 (IL-6) into the circulation from contracting muscle fibres and subsequent increases in circulating levels of IL-10 and IL-1 receptor antagonist; increased circulating numbers of IL-10-secreting regulatory T cells; downregulation of Toll-like receptor expression on monocytes and inhibition of downstream responses (such as pro-inflammatory cytokine production, antigen presentation and co-stimulatory molecule expression); reduction in the circulating numbers of pro-inflammatory monocytes; and inhibition of monocyte and/or macrophage infiltration into adipose tissue. Although regular moderate exercise is associated with a reduced incidence of infection compared with a completely sedentary state, the long hours of hard training undertaken by elite athletes appear to make these individuals more susceptible to infections. This is also probably attributable to the anti-inflammatory effects of exercise inducing a degree of immunosuppression. Important remaining questions on the anti-inflammatory effects of exercise include: what is the independent contribution of an exercise-induced reduction in visceral fat versus other exercise-induced anti-inflammatory mechanisms? What is the relative importance of the different anti-inflammatory mechanisms? What modes, intensities and durations of exercise are required to optimize the anti-inflammatory effects of exercise? The beneficial impact of exercise on health is indisputable. Here, the authors review the direct and indirect anti-inflammatory effects of exercise and discuss the potential mechanisms involved. Regular exercise reduces the risk of chronic metabolic and cardiorespiratory diseases, in part because exercise exerts anti-inflammatory effects. However, these effects are also likely to be responsible for the suppressed immunity that makes elite athletes more susceptible to infections. The anti-inflammatory effects of regular exercise may be mediated via both a reduction in visceral fat mass (with a subsequent decreased release of adipokines) and the induction of an anti-inflammatory environment with each bout of exercise. In this Review, we focus on the known mechanisms by which exercise — both acute and chronic — exerts its anti-inflammatory effects, and we discuss the implications of these effects for the prevention and treatment of disease.

Understanding exercise metabolism and the relationship with volatile organic compounds (VOCs) holds potential in both health care and sports performance. Exercise metabolism can be investigated using whole body exercise testing (in vivo) or through the culture and subsequent electrical pulse stimulation (EPS) of myotubes (in vitro). This research investigates the novel headspace (HS) analysis of EPS skeletal muscle myotubes. An in vitro system was built to investigate the effect of EPS on the volatile constituents in the HS above EPS skeletal muscle. The C2C12 immortalised cell line was chosen. EPS was applied to the system to induce myotube contraction. The in vitro system was applied to the analysis of VOCs using thermal desorption (TD) sampling. Samples were collected under four conditions: environmental samples (enviro), acellular media HS samples (blank), skeletal muscle myotubes without stimulation HS samples (baseline) and EPS of skeletal muscle myotube HS samples (stim). TD sampling combined with gas-chromatography mass spectrometry (GC-MS) detected two compounds that, after multivariate and univariate statistical analysis, were identified as changing due to EPS (p < 0.05). These compounds were tentatively assigned as 1,4-Dioxane-2,5-dione, 3,6-dimethyl- and 1-pentene. The former is a known lactide and the latter has been reported as a marker of oxidative stress. Further research should focus on improvements to the EPS system, including the use of more relevant cell lines, quantification of myotube contractions, and the application of targeted analysis, metabolic assays and media analysis.

Asthma is one of the most common and prevalent problems worldwide affecting over 300 million individuals. There is some evidence from observational and intervention studies to suggest a beneficial effect of n-3 PUFA in inflammatory diseases, specifically asthma. Marine-based n-3 PUFA have therefore been proposed as a possible complementary/alternative therapy for asthma. The proposed anti-inflammatory effects of n-3 fatty acids may be linked to a change in cell membrane composition. This altered membrane composition following n-3 fatty acid supplementation (primarily EPA and DHA) can modify lipid mediator generation via the production of eicosanoids with a reduced inflammatory potential/impact. A recently identified group of lipid mediators derived from EPA including E-series resolvins are proposed to be important in the resolution of inflammation. Reduced inflammation attenuates the severity of asthma including symptoms (dyspnoea) and exerts a bronchodilatory effect. There have been no major health side effects reported with the dietary supplementation of n-3 fatty acids or their mediators; consequently supplementing with n-3 fatty acids is an attractive non-pharmacological intervention which may benefit asthma.

Both honey and fish oil have been historically used in medicine and identified as having antimicrobial properties. Although analyses of the substances have identified different components within them, it is not fully understood how these components interact and contribute to the observed effect. With the increase in multi-drug resistant strains of bacteria found in infections, new treatment options are needed. This study aimed to assess the antimicrobial abilities of fish oil components, including docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and derived resolvins (RvE1, RvD2, and RvD3), as well as two varieties of manuka honey, against a panel of medically relevant microorganisms and antimicrobial resistant organisms, such as Methicillin Resistant Staphylococcus aureus (MRSA) and carbapenem-resistant Escherichia coli. Minimum inhibitory concentrations (MIC) and minimum bactericidal concentrations (MBC) were identified; further minimum biofilm eradication concentrations (MBEC) were investigated for responsive organisms, including S. aureus, E. coli, Staphylococcus epidermidis, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Concurrent with the existing literature, manuka honey was found to be a broad-spectrum antimicrobial with varied potency according to methylglyoxal content. DHA and EPA were both effective against Gram-positive and negative bacteria, but some drug-resistant strains or pathogens were not protected by a capsule. Only E. coli was inhibited by the resolvins.

Chronic wounds are becoming an increasing burden on healthcare services, as they have extended healing times and are susceptible to infection, with many failing to heal, which can lead ultimately to amputation. Due to the additional rise in antimicrobial resistance and emergence of difficult-to-treat Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter spp. (ESKAPE pathogens), novel treatments will soon be required asides from traditional antibiotics. Many natural substances have been identified as having the potential to aid in both preventing infection and increasing the speed of wound closure processes. Manuka honey is already in some cases used as a topical treatment in the form of ointments, which in conjunction with dressings and fish skin grafts are an existing US Food and Drug Administration-approved treatment option. These existing treatment options indicate that fatty acids from fish oil and manuka honey are well tolerated by the body, and if the active components of the treatments were better understood, they could make valuable additions to topical treatment options. This review considers two prominent natural substances with established manufacturing and global distribution—marine based fatty acids (including their metabolites) and manuka honey—their function as antimicrobials and how they can aid in wound repair, two important aspects leading to resolution of chronic wounds.

Exhaled volatile organic compounds (VOCs) are of interest due to their minimally invasive sampling procedure. Previous studies have investigated the impact of exercise, with evidence suggesting that breath VOCs reflect exercise-induced metabolic activity. However, these studies have yet to investigate the impact of maximal exercise to exhaustion on breath VOCs, which was the main aim of this study. Two-litre breath samples were collected onto thermal desorption tubes using a portable breath collection unit. Samples were collected pre-exercise, and at 10 and 60 min following a maximal exercise test (VO2MAX). Breath VOCs were analysed by thermal desorption-gas chromatography-mass spectrometry using a non-targeted approach. Data showed a tendency for reduced isoprene in samples at 10 min post-exercise, with a return to baseline by 60 min. However, inter-individual variation meant differences between baseline and 10 min could not be confirmed, although the 10 and 60 min timepoints were different (p = 0.041). In addition, baseline samples showed a tendency for both acetone and isoprene to be reduced in those with higher absolute VO2MAX scores (mL(O2)/min), although with restricted statistical power. Baseline samples could not differentiate between relative VO2MAX scores (mL(O2)/kg/min). In conclusion, these data support that isoprene levels are dynamic in response to exercise.

Previous research has demonstrated that fish oil supplementation has a protective effect on exercise-induced bronchoconstriction (EIB) in elite athletes, which may be attributed to its antiinflammatory properties. Since EIB in asthma involves proinflammatory mediator release, it is feasible that fish oil supplementation may reduce the severity of EIB in asthmatic subjects. To determine the efficacy of fish oil supplementation on severity of EIB in subjects with asthma. Randomized, double-blind, crossover study. Lung function and exercise testing in a university research laboratory. Sixteen asthmatic patients with documented EIB entered the study on their normal diet and then received either fish oil capsules containing 3.2 g of eicosapentaenoic acid and 2.0 g of docohexaenoic acid (fish oil diet, n = 8) or placebo capsules (placebo diet, n = 8) daily for 3 weeks. At the beginning of the study (normal diet) and at the end of each treatment phase, the following pre-exercise and postexercise measures were assessed: (1) pulmonary function; (2) induced sputum differential cell count percentage and proinflammatory eicosanoid metabolite (leukotriene C4 [LTC4]-leukotriene E4 [LTE4] and prostaglandin D2 [PGD2]) and cytokine (interleukin [IL]-1β and tumor necrosis factor [TNF]-α) concentrations; and (3) eicosanoid metabolites leukotriene B4 (LTB4) and leukotriene B5 (LTB5) generation from activated polymorphonuclear leukocytes (PMNLs). On the normal and placebo diet, subjects exhibited EIB. However, the fish oil diet improved pulmonary function to below the diagnostic EIB threshold, with a concurrent reduction in bronchodilator use. Induced sputum differential cell count percentage and concentrations of LTC4-LTE4, PGD2, IL-1β, and TNF-α were significantly reduced before and following exercise on the fish oil diet compared to the normal and placebo diets. There was a significant reduction in LTB4 and a significant increase in LTB5 generation from activated PMNLs on the fish oil diet compared to the normal and placebo diets. Our data suggest that fish oil supplementation may represent a potentially beneficial nonpharmacologic intervention for asthmatic subjects with EIB.

Background Inspiratory muscle training has been shown to improve performance in elite swimmers, when used as part of routine training, but its use as a respiratory warm-up has yet to be investigated. Aim To determine the influence of inspiratory muscle exercise (IME) as a respiratory muscle warm-up in a randomised controlled cross-over trial. Methods A total of 15 elite swimmers were assigned to four different warm-up protocols and the effects of IME on 100 m freestyle swimming times were assessed.Each swimmer completed four different IME warm-up protocols across four separate study visits: swimming-only warm-up; swimming warm-up plus IME warm-up (2 sets of 30 breaths with a 40% maximum inspiratory mouth pressure load using the Powerbreathe inspiratory muscle trainer); swimming warm-up plus sham IME warm-up (2 sets of 30 breaths with a 15% maximum inspiratory mouth pressure load using the Powerbreathe inspiratory muscle trainer); and IME-only warm-up. Swimmers performed a series of physiological tests and scales of perception (rate of perceived exertion and dyspnoea) at three time points (pre warm-up, post warm-up and post time trial). Results The combined standard swimming warm-up and IME warm-up were the fastest of the four protocols with a 100 m time of 57.05 s. This was significantly faster than the IME-only warm-up (mean difference=1.18 s, 95% CI 0.44 to 1.92, p<0.01) and the swim-only warm-up (mean difference=0.62 s, 95% CI 0.001 to 1.23, p=0.05). Conclusions Using IME combined with a standard swimming warm-up significantly improves 100 m freestyle swimming performance in elite swimmers.

Abstract In elite athletes, exercise-induced bronchoconstriction (EIB) may respond to dietary modification, thereby reducing the need for pharmacologic treatment. Ten elite athletes with EIB and 10 elite athletes without EIB (control subjects) participated in a randomized, double-blind crossover study. Subjects entered the study on their normal diet, and then received either fish oil capsules containing 3.2 g eicosapentaenoic acid and 2.2 g docohexaenoic acid (n-3 polyunsaturated fatty acid [PUFA] diet; n = 5) or placebo capsules containing olive oil (placebo diet; n = 5) taken daily for 3 weeks. Diet had no effect on preexercise pulmonary function in either group or on postexercise pulmonary function in control subjects. However, in subjects with EIB, the n-3 PUFA diet improved postexercise pulmonary function compared with the normal and placebo diets. FEV1 decreased by 3 ± 2% on n-3 PUFA diet, 14.5 ± 5% on placebo diet, and 17.3 ± 6% on normal diet at 15 minutes postexercise. Leukotriene (LT)E4, 9α, 11β-prostaglandin F2, LTB4, tumor necrosis factor–α, and interleukin-1β, all significantly decreased on the n-3 PUFA diet compared with normal and placebo diets and after the exercise challenge. These data suggest that dietary fish oil supplementation has a markedly protective effect in suppressing EIB in elite athletes, and this may be attributed to their antiinflammatory properties.

Because the anomalous respiratory characteristics of competitive swimmers have been suggested to be due to inspiratory muscle work, the respiratory muscle and pulmonary function of 30 competitively trained swimmers was assessed at the beginning and end of an intensive 12-week swim training (ST) program. Swimmers ( n  = 10) combined ST with either inspiratory muscle training (IMT) set at 80% sustained maximal inspiratory pressure (SMIP) with progressively increased work–rest ratios until task failure for 3-days per week (ST + IMT) or ST with sham-IMT (ST + SHAM-IMT, n  = 10), or acted as controls (ST only, ST, n  = 10). Measures of respiratory and pulmonary function were assessed at the beginning and end of the 12 week study period. There were no significant differences ( P  > 0.05) in respiratory and pulmonary function between groups (ST + IMT, ST + SHAM-IMT and ST) at baseline and at the end of the 12 week study period. However, within all groups significant increases ( P  < 0.05) were observed in a number of respiratory and pulmonary function variables at the end of the 12 week study, such as maximal inspiratory and expiratory pressure, inspiratory power output, forced vital capacity, forced expiratory and inspiratory volume in 1-s, total lung capacity and diffusion capacity of the lung. This study has demonstrated that there are no appreciable differences in terms of respiratory changes between elite swimmers undergoing a competitive ST program and those undergoing respiratory muscle training using the flow-resistive IMT device employed in the present study; as yet, the causal mechanisms involved are undefined.