Direct assessment of leukocyte signalling and cytokine secretion reveals exercise intensity-dependent reductions in anti-inflammatory cytokine action.

Circulating interleukin (IL)-6 and IL-10 concentrations are widely used to evaluate the anti-inflammatory effects of exercise but do not capture cytokine action at the cellular level. Whether and how acute exercise impacts anti-inflammatory cytokine action in humans is unknown. To determine how exercise intensity and pattern impact IL-6 and IL-10 action in blood leukocytes, 16 active adults (eight males/eight females; age: 30 ± 3 years; body mass index: 22.8 ± 2.3 kg/m2; V ̇ O 2 peak ${{\dot{V}}_{{{{\mathrm{O}}}_{\mathrm{2}}}{\mathrm{peak}}}}$ : 51 ± 6 mL/kg/min) completed a no-exercise control condition (CTL) or isocaloric bouts of cycling performed below (moderate continuous exercise; MCE) or above (heavy continuous or heavy intermittent exercise; HCE or HIE, respectively) lactate threshold. Venous blood (before, after, 30 min after and 90 min after exercise) was analysed for immune cell subpopulations, plasma cytokine concentrations, anti-inflammatory cytokine action and monocyte phenotype. Exercise induced rapid leukocytosis (P < 0.001) and increased plasma IL-6 (P < 0.001), IL-10 (P = 0.0145) and tumour necrosis factor-⍺ (TNF-⍺) (P = 0.0338) concentrations in an intensity-dependent manner (HCE and/or HIE vs. CTL). These systemic changes coincided with a diminished ability of IL-10/6 to phosphorylate STAT3 (P < 0.001) and inhibit TNF-⍺ secretion (P = 0.0238) in blood leukocytes following HCE and HIE. Monocyte polarization experiments revealed lower CD80 [MCE (P = 0.0933) and HIE (P = 0.0187) vs. CTL] and a tendency for higher CD163 expression (HCE vs. CTL, P = 0.0985), suggesting that hyporesponsiveness to anti-inflammatory cytokine action does not impede the ability of exercise to promote an anti-inflammatory monocyte phenotype. These findings provide novel insights into the immunomodulatory effects of exercise in humans and highlight the importance of directly measuring cellular cytokine action when evaluating the anti-inflammatory effects of exercise. KEY POINTS: Circulating cytokine concentrations are frequently used to evaluate the anti-inflammatory effects of exercise but may not capture changes in cytokine action occurring at the cellular level. We directly assessed anti-inflammatory cytokine action - measured using a combination of intracellular signalling and cytokine secretion ex vivo - in distinct immune cell subpopulations after acute calorie-matched exercise bouts differing in intensity and pattern. Anti-inflammatory cytokine action was blunted following higher intensity exercise despite corresponding increases in circulating cytokine concentrations and immune cell counts. Changes in cytokine action were not explained by changes in cytokine receptor expression on circulating immune cells. Our findings provide new insights into the immunomodulatory effects of exercise in humans and highlight the importance of directly measuring cellular cytokine action when evaluating the anti-inflammatory effects of exercise.

Costly immunometabolic remodelling in disused muscle buildup through physical exercise.

The mechanisms underlying the immunometabolic disturbances during skeletal muscle atrophy caused by a plethora of circumstances ranging from hospitalization to spaceflight missions remain unknown. Here, we outline the possible pathways that might be dysregulated in such conditions and assess the potential of physical exercise to mitigate and promote the recovery of muscle morphology, metabolism and function after intervals of disuse. Studies applying exercise to attenuate disuse-induced muscle atrophy have shown a pivotal role of circulating myokines in the activation of anabolic signalling pathways. These muscle-derived factors induce accretion of contractile proteins in the myofibers, and at the same time decrease protein breakdown and loss. Regular exercise plays a crucial role in re-establishing adequate immunometabolism and increasing the migration and presence in the muscle of macrophages with an anti-inflammatory phenotype (M2) and T regulatory cells (Tregs) after disease-induced muscle loss. Additionally, the switch in metabolic pathways (glycolysis to oxidative phosphorylation [OXPHOS]) is important for achieving rapid metabolic homeostasis during muscle regeneration. In this review, we discuss the molecular aspects of the immunometabolic response elicited by exercise during skeletal muscle regeneration. There is not, nevertheless, consensus on a single optimal intensity of exercise required to improve muscle strength, mass and functional capacity owing to the wide range of exercise protocols studied so far. Despite the absence of agreement on the specific strategy, physical exercise appears as a powerful complementary strategy to attenuate the harmful effects of muscle disuse in different scenarios.

Assessment of aerobic fitness in individuals with and without nonspecific chronic low back pain: a pilot study.

Aerobic fitness assessment in patients with low back pain (LBP) may help clinicians to plan how to progress the aerobic training. This was a pilot study designed to evaluate the performance of people with LBP on two different aerobic fitness tests performed on a treadmill and to compare the measure of aerobic fitness between people with LBP and healthy individuals. Ten people with LBP and 10 healthy individuals underwent two aerobic fitness protocols, the modified Bruce and maximum incremental test protocols, performed on a treadmill. Data collected during the protocols were: oxygen consumption, heart rate (HR), blood lactate concentration, respiratory quotient, rating of perceived exertion response, and pain intensity. Independent t-test and two-way analysis of variance were used respectively to assess difference between groups characteristics and physiological responses to the protocols. Our results showed that both groups were similar with regards to age (P = 0.839) or HRrest (P = 0.730) but the LBP group showed higher BMI compared to the healthy group (P = 0.031). Regarding the performance of both groups on the aerobic fitness tests, the only significant difference was reported for respiratory quotient which showed a main effect of test (P = 0.015) with higher values favoring the modified Bruce over the incremental test. Our study showed that most people with LBP are able to perform and tolerate both aerobic fitness tests but no significant differences between people with LBP and healthy individuals on both protocols were reported.

Relationship between Health Costs and Inflammatory Profile in Public Health.

INTRODUCTION: The association between obesity and physical activity level is well established in the literature, as well as its consequences that lead to chronic noncommunicable diseases. In addition, it is also possible to obtain the immunometabolic mechanism that explains the pathway of associations between obesity, chronic noncommunicable diseases and the level of physical activity. It also seems clear that treating illnesses has a financial impact on healthcare systems around the world, so it seems important to assess the financial impact on the healthcare system of individuals with immunometabolic dysfunction. AIM: This study aimed to assess whether there is a correlation between metabolic and inflammatory markers and healthcare costs according to body adiposity and habitual physical activity (HPA). METHODS: This is a cross-sectional study, where the sample includes men and women aged over 50. Participants underwent evaluations that included the following variables: i) immunometabolic markers, ii) healthcare costs, iii) obesity, iv) habitual physical activity, and v) history of personal illness. Statistical significance was set at values lower than 5% and the software used was BioEstat. RESULTS: The correlation between metabolic and inflammatory markers and healthcare costs demonstrated a positive and significant relationship, adjusted for obesity and HPA, between glucose concentrations and exam costs (r = 0.343, p-value = 0.007) and total cost (r = 261; p-value = 0.043); HOMA index and cost of exams (r = 0.267; pvalue = 0.038); and IL-10 and cost of medical consultation (r = 0.297; p-value = 0.020). CONCLUSION: Metabolic and inflammatory markers may be related to the costs of consultations and examinations, independent of obesity and HPA.

Is Oxygen Uptake Measurement Enough to Estimate Energy Expenditure During High-Intensity Intermittent Exercise? Quantification of Anaerobic Contribution by Different Methods.

Purpose: The aim of the present study was to compare the contributions of the anaerobic pathway as determined by two different methods and energy expenditure during a typical high-intensity intermittent exercise (HIIE) protocol. Methods: A descriptive research design was utilized in which thirteen physically active men performed six experimental sessions consisting of an incremental test (session 1), submaximal tests at 40, 50, 60, 70, 75, 80, 85, 90% of velocity associated with maximum oxygen uptake (v V˙ O2max) with two intensities per session (sessions 2-5), and the HIIE protocol (session 6; 10 efforts of 1 min at v V˙ O2max interspersed by 1 min of passive recovery). The estimation of anaerobic energy system contribution was calculated by: (a) the excess post-exercise oxygen consumption plus delta lactate method and (b) the accumulated oxygen deficit method using the difference between predicted oxygen demand from the submaximal tests of varying intensities and accumulated oxygen uptake during HIIE. Estimation of aerobic energy system contribution was calculated through the measurement of oxygen consumption during activity. Total EE during the entire HIIE protocol (efforts + recovery) and for the efforts only were calculated from each method. Results: For efforts + recovery and efforts only, anaerobic contribution was similar for both methods, and consequently total EE was also equivalent (p = 0.230 for both comparisons). During efforts + recovery, aerobic:anaerobic energy system contribution was (68 ± 4%: 32 ± 4%), while efforts only was (54 ± 5%: 46 ± 5%) with both situations demonstrating greater aerobic than anaerobic contribution (p < 0.001 for both). Conclusion: Anaerobic contribution seems to be relevant during HIIE and must to be taken into account during total EE estimation; however, the type of method employed did not change the anaerobic contribution or total EE estimates.

Acute high-intensity exercise with low energy expenditure reduced LDL-c and total cholesterol in men.

A reduction in LDL cholesterol and an increase in HDL cholesterol levels are clinically relevant parameters for the treatment of dyslipidaemia, and exercise is often recommended as an intervention. This study aimed to examine the effects of acute, high-intensity exercise ( approximately 90% VO(2max)) and varying carbohydrate levels (control, low and high) on the blood lipid profile. Six male subjects were distributed randomly into exercise groups, based on the carbohydrate diets (control, low and high) to which the subjects were restricted before each exercise session. The lipid profile (triglycerides, VLDL, HDL cholesterol, LDL cholesterol and total cholesterol) was determined at rest, and immediately and 1 h after exercise bouts. There were no changes in the time exhaustion (8.00 +/- 1.83; 7.82 +/- 2.66; and 9.09 +/- 3.51 min) and energy expenditure (496.0 +/- 224.8; 411.5 +/- 223.1; and 592.1 +/- 369.9 kJ) parameters with the three varying carbohydrate intake (control, low and high). Glucose and insulin levels did not show time-dependent changes under the different conditions (P > 0.05). Total cholesterol and LDL cholesterol were reduced after the exhaustion and 1 h recovery periods when compared with rest periods only in the control carbohydrate intake group (P < 0.05), although this relation failed when the diet was manipulated. These results indicate that acute, high-intensity exercise with low energy expenditure induces changes in the cholesterol profile, and that influences of carbohydrate level corresponding to these modifications fail when carbohydrate (low and high) intake is manipulated.