Decreased secretion rate of salivary markers of mucosal immunity, and in particular salivary immunoglobulin A (s-IgA), have been implicated as risk factors for subsequent episodes of respiratory infection in athletes. IgA is the predominant Ig in mucosal secretions and acts with innate mucosal defences to provide the 'first line of defence' against pathogens and antigens presented at the mucosa. As well as summarising the evidence concerning the effects of acute exercise and longer-term intensive training on these markers of mucosal immunity, this review explores the factors that impact upon salivary responses to exercise, such as method of saliva collection, stimulation of saliva collection and the method of reporting s-IgA data. The influence of adequate hydration and nutritional supplementation during exercise as well as exercising in extreme environmental conditions on salivary responses is also explored. Finally, the possible mechanisms underlying the acute and longer-term of effects of exercise on salivary responses are examined, with particular emphasis on the potential role of the sympathetic nervous system and the expression and mobilisation of the polymeric Ig receptor.

Patients with chronic kidney disease frequently present with chronic elevations in markers of inflammation, a condition that appears to be exacerbated by disease progression and onset of haemodialysis. Systemic inflammation is interlinked with malnutrition and muscle protein wasting and is implicated in a number of morbidities including cardiovascular disease: the most common cause of mortality in this population. Research in the general population and other chronic disease cohorts suggests that an increase in habitual activity levels over a prolonged period may help redress basal increases in systemic inflammation. Furthermore, those populations with the highest baseline levels of systemic inflammation appear to have the greatest improvements from training. On the whole, the activity levels of the chronic kidney disease population reflect a sedentary lifestyle, indicating the potential for increasing physical activity and observing health benefits. This review explores the current literature investigating exercise and inflammatory factors in the chronic kidney disease population and then attempts to explain the contradictory findings and suggests where future research is required.

Curcumin, a natural polyphenol extracted from turmeric, is a potent antioxidant and anti-inflammatory agent. In the past few decades, curcumin’s ability to impact chronic inflammatory conditions such as metabolic syndrome, arthritis, and cancer has been widely researched, along with growing interest in understanding its role in exercise-induced muscle damage (EIMD). EIMD impacts individuals differently depending on the type (resistance exercise, high-intensity interval training, and running), intensity, and duration of the exercise. Exercise disrupts the muscles’ ultrastructure, raises inflammatory cytokine levels, and can cause swelling in the affected limb, a reduction in range of motion (ROM), and a reduction in muscular force-producing capacity. This review focuses on the metabolism, pharmacokinetics of various brands of curcumin supplements, and the effect of curcumin supplementation on EIMD regarding muscle soreness, activity of creatine kinase (CK), and production of inflammatory markers. Curcumin supplementation in the dose range of 90–5000 mg/day can decrease the subjective perception of muscle pain intensity, increase antioxidant capacity, and reduce CK activity, which reduces muscle damage when consumed close to exercise. Consumption of curcumin also improves muscle performance and has an anti-inflammatory effect, downregulating the production of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-8. Curcumin may also improve oxidative capacity without hampering training adaptations in untrained and recreationally active individuals. The optimal curcumin dose to ameliorate EIMD is challenging to assess as its effect depends on the curcumin concentration in the supplement and its bioavailability.

Purpose: The relationship between inflammatory markers and energetic metabolism has been explored. However, the relationship between exercise intensity and fitness status is unclear, and it is necessary to understand this relationship to apply specific exercise guidance. The purpose of the study was to analyze metabolic and inflammatory responses imposed by acute exercise sessions performed at moderate, heavy, and severe intensities and their relationship with the physical fitness status.Methods: Nineteen healthy male volunteers performed three acute exercise sessions until exhaustion or up to 60 minutes on a cycle ergometer at moderate (90% of first ventilatory threshold [VT1]), heavy (midpoint between VT1 and second ventilatory threshold [VT2]), and severe (midpoint between VT2 and maximal aerobic power) intensities. Blood lactate, glucose, NEFA, endotoxin, and cytokines were determined for each exercise session. Peripheral and lipopolysaccharide (LPS)‐stimulated release of tumor necrosis factor alpha (TNF‐α), interleukin (IL)‐6, and IL‐10 was analyzed before, after, and 60 minutes after sessions.Results: In peripheral blood, severe intensity increased lactate, endotoxin, and TNF‐α immediately after exercise and glucose at 60 min after exercise. There was a trend for IL‐10 increase at 60 minutes after exercise in peripheral blood. Immediately after exercise, LPS‐stimulated TNF‐α, IL‐6, IL‐6/IL‐10 ratio, and lactate levels were higher in the severe intensity while nonester fatty acid levels decreased at this time. At 60 minute after exercise, higher concentrations of glucose and a trend for increased IL‐10 were observed in severe intensity. A positive correlation was observed between maximal aerobic power and IL‐10 ( r = 0.513; P = 0.042), and negative correlations between maximal aerobic power and endotoxin ( r = −0.531; P = 0.034) and lactate ( r = −0.538; P = 0.031) in heavy intensity.Conclusion: Our data show a novel finding that higher cytokine responses occur at higher intensities, mainly in severe intensity. However, the anti‐inflammatory (IL‐10) response was physical fitness–dependent.