Effects Of Chronic Exercise Research Articles

The Association Between Endurance Training and Heart Rate Variability: The Confounding Role of Heart Rate.

Heart rate variability (HRV) is a widely used marker of cardiac autonomic nervous activity (CANA). Changes in HRV with exercise training have often been interpreted as increases in vagal activity. HRV is strongly associated with heart rate, which in turn, is associated with heart size. There is strong evidence from basic studies that lower heart rate in response to exercise training is caused by morphological and electrical remodeling of the heart. In a cross-sectional study in participants of a 10 mile race, we investigated the influence of endurance exercise on HRV parameters independently of heart size and heart rate. One-hundred-and-seventy-two runners (52 females and 120 males) ranging from novice runners with a first participation to an endurance event to highly trained runners, with up to 15 h of training per week, were included in the analysis. R-R intervals were recorded by electrocardiography over 24 h. Left ventricular end diastolic volume indexed to body surface area (LVEDVI) was assessed by transthoracic echocardiography and peak oxygen consumption (VO2peak) by cardiopulmonary exercise testing. Exercise was quantified by VO2peak, training volume, and race performance. HRV was determined during deep sleep. HRV markers of vagal activity were moderately associated with exercise variables (standardized β = 0.28–0.40, all p < 0.01). These associations disappeared when controlling for heart rate and LVEDVI. Due to the intrinsic association between heart rate and HRV, conclusions based on HRV parameters do not necessarily reflect differences in CANA. Based on current evidence, we discourage the use of HRV as a marker of CANA when measuring the effect of chronic exercise.

Effect of chronic exercise on fluoride metabolism in fluorosis-susceptible mice exposed to high fluoride

The present study investigated the effect of chronic exercise on fluoride (F) metabolism in fluorosis-susceptible mice exposed to high-F and explored the relationship between F concentrations in bone and plasma. Thirty male mice were randomised into three groups: Group I (No-F, No-Exercise), Group II (50 ppmF, No-Exercise), Group III (50 ppmF, Exercise). Body weight and physical performance of all mice were measured at baseline and end of experiment. F concentrations of plasma and bone were measured at the end of experiment. Mean plasma F concentration was significantly higher (p < 0.001) in Groups II and III compared with Group I. Mean bone F concentration was also significantly higher (p < 0.01) in Groups II and III compared with Group I. There was a significant correlation (p = 0.01, r = 0.54) between F concentration of plasma and bone. Mean body weight of Group I mice was significantly higher than Group II (p < 0.001) and Group III (p = 0.001) mice at the end of the experiment. This study, which provides the first data on the effect of chronic exercise on F metabolism in fluorosis-susceptible mice, suggests no effect of chronic exercise on F in plasma and bone. However, exposure to high-F resulted in lower body weight and exercise capacity in mice.

Effect of Chronic Exercise on Irisin Plasma Level and Browning of White Adipose Tissue in Rat Models with Obesity or Type 2 Diabetes Mellitus

Objective: To study the effect of swimming exercise training on plasma irisin level and browning of white adipose tissue in rats models with obesity or type 2 diabetes mellitus (T2DM). Methods: 60 male rats were divided into 4 groups, I) Control group, II) Exercise trained group, III) Obese group: includes 2 subgroups; subgroup A received high-fat diet and subgroup B received high-fat diet associated with daily exercise training and IV) Type 2 diabetic group: includes 2 subgroups; subgroup A and B. Both subgroups have T2DM. Subgroup B, in addition, was associated with daily exercise training after induction of T2DM.

Chronic effects of exercise implemented during school-break time on neurophysiological indices of inhibitory control in adolescents

Abstract Objection The present study investigated the effects of an exercise intervention, which was implemented during school-break time, on the P300 component of event-related potentials and inhibitory control. Methods Adolescents aged 12–15 years were allocated to an exercise and control group. The exercise group performed 20 min of aerobic and coordinative exercise per school day over a period of 8 weeks. Before and after the intervention, stimulus-locked event-related potentials were recorded during a Stroop task using electroencephalography. Cluster-based permutation testing revealed a greater increase of the P300 amplitude in the exercise compared to the control group, most pronounced for the parieto-occipital region. Additionally, increases in P300 amplitude were associated with decreases in incompatible reaction time on the Stroop task. Conclusion An exercise program implemented during school-break time enhances adolescents' inhibitory control. This benefit seems to be due to an improved allocation of attentional resources towards the cognitive task.

PH recovery from a proton load in rat cardiomyocytes: effects of chronic exercise.

The ability of cardiomyocytes to recover from a proton load was examined in the hearts of exercise-trained and sedentary control rats in CO2/[Formula: see text]-free media. Acidosis was created by the NH4Cl prepulse technique, and intracellular pH (pHi) was determined using fluorescence microscopy on carboxy-SNARF-1 AM-loaded isolated cardiomyocytes. CO2-independent pHi buffering capacity (βi) was measured by incrementally reducing the extracellular NH4Cl concentration in steps of 50% from 20 to 1.25 mM. βi increased as pHi decreased in both exercise-trained and sedentary control groups. However, the magnitude of increase in βi as a function of pHi was found to be significantly ( P < 0.001) greater in the exercise-trained group compared with the sedentary control group. The rate of pHi recovery from an imposed proton load was found to not be different between the exercise-trained and control groups. The Na+/H+ exchanger-dependent H+ extrusion rate during the recovery from an imposed proton load, however, was found to be significantly greater in the exercise-trained group compared with the control group. By increasing βi and subsequently the Na+/H+ exchanger-dependent H+ extrusion rate, exercise training may provide cardiomyocytes with the ability to better handle an intracellular excess of H+ generated during hypoxia/ischemic insults and may serve in a cardioprotective role. These data may be predictive of two positive outcomes: 1) increased exercise tolerance by the heart and 2) a protective mechanism that limits the degree of myocardial acidosis and subsequent damage that accompanies ischemia-reperfusion stress. NEW & NOTEWORTHY The enhanced ability to deal with acidosis conferred by exercise training is likely to improve exercise tolerance and outcomes in response to myocardial ischemia-reperfusion injury.

Effect of Exercise on Inflammatory Profile of Older Persons: Systematic Review and Meta-Analyses.

Inflammatory cytokines and acute phase proteins increase with aging, promoting a chronic low-grade inflammation. Studies have shown a positive effect of exercise on inflammatory markers in older persons. Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) are the main biomarkers investigated. However, it is unclear if exercise could decrease all these biomarkers. The aim was to analyze the effect of chronic exercise on IL-6, TNF-α, and CRP levels in older persons. Preferred Reporting Items in Systematic Reviews and Meta-analyses guidelines were adopted. Original articles that investigated the effect of chronic exercise on inflammatory profile of the elderly persons were eligible for this review. The databases PubMed, PEDro, EBSCO, and BioMed Central were searched. Three reviewers evaluated each publication for reducing bias. Data about IL-6, TNF-α, and CRP were collected and analyzed. A standardized mean difference based on estimated pooled effect size was calculated considering heterogeneity index (I2) and random effect. Seventy-six studies were retrieved from databases, and 8 of them were analyzed. IL-6 and CRP levels decreased after chronic exercise (overall effect P < .05). Regular exercise decreases IL-6 and CRP levels in older persons. The effect of exercise on TNF-α remains unclear.

The effects of aerobic exercise on depression-like, anxiety-like, and cognition-like behaviours over the healthy adult lifespan of C57BL/6 mice

Preclinical studies have demonstrated exercise improves various types of behaviours such as anxiety-like, depression-like, and cognition-like behaviours. However, these findings were largely conducted in studies utilising short-term exercise protocols, and the effects of lifetime exercise on these behaviours remain unknown. This study investigates the behavioural effects of lifetime exercise in normal healthy ageing C57BL/6 mice over the adult lifespan. 12 week-old C57BL/6 mice were randomly assigned to voluntary wheel running or non-exercise (control) groups. Exercise commenced at aged 3 months and behaviours were assessed in young adult (Y), early middle age (M), and old (O) mice (n=11–17/group). The open field and elevated zero maze examined anxiety-like behaviours, depression-like behaviours were quantified with the forced swim test, and the Y maze and Barnes maze investigated cognition-like behaviours. The effects of lifetime exercise were not simply an extension of the effects of chronic exercise on anxiety-like, depression-like, and cognition-like behaviours. Exercise tended to reduce overt anxiety-like behaviours with ageing, and improved recognition memory and spatial learning in M mice as was expected. However, exercise also increased anxiety behaviours including greater freezing behaviour that extended spatial learning latencies in Y female mice in particular, while reduced distances travelled contributed to longer spatial memory and cognitive flexibility latencies in Y and O mice. Lifetime exercise may increase neurogenesis-associated anxiety. This could be an evolutionary conserved adaptation that nevertheless has adverse impacts on cognition-like function, with particularly pronounced effects in Y female mice with intact sex hormones. These issues require careful investigation in future rodent studies.

Acute and chronic effects of exercise on mRNA expression in the skeletal muscle of two mouse models of peripheral artery disease.

Endurance exercise improves walking performance in patients with peripheral artery disease (PAD), which is characterized by skeletal muscle dysfunction caused by lower extremity ischemia. Although transcriptional analyses of exercise-induced changes in normal animals and healthy volunteers have been reported, no detailed study has explored exercise-induced alterations in gene expression in PAD animal models. Here, we determined the acute and chronic effects of exercise on mRNA expression in the skeletal muscles of two mouse models of PAD. Three particular gene categories were investigated: known exercise-responsive genes (Pgc1a, Il6, Nr4a1, Nr4a2, and Nr4a3); myogenic and muscle regeneration-related genes (Myf5, Myogenin, Myomaker, and Myh3); and Gpr56 and its ligand Col3a1. PAD was induced by bilateral femoral artery ligation in normal C57BL/6 and diabetic KK-Ay mice. From 1 week after surgery, repetitive twice-weekly 30-min treadmill endurance exercise sessions were applied. Altered mRNA expression in the soleus muscles was measured in both the acute and chronic phases. In the acute phase, transcript levels of exercise-inducible genes showed significant increases in both C57BL/6 and diabetic KK-Ay PAD mice; levels of regeneration-related genes showed little alteration, and those of Gpr56 increased immediately and significantly after exercise in both models. In the chronic phase, transcript levels of Pgc1a, Myf5, Myogenin, Myomaker, Myh3, Gpr56, and Col3a1 were upregulated significantly in sedentary C57BL/6 PAD mice compared with that in sham-operated mice. Exercise training inhibited the upregulation of Col3a1, Myf5, and Myogenin significantly. In KK-Ay PAD mice, only Gpr56 mRNA levels increased significantly compared with those in sham-operated mice. RNA sequence analysis revealed 33 and 166 differentially upregulated, and 363 and 99 downregulated, genes after exercise training in C57BL/6 PAD and KK-Ay PAD mice, respectively. In summary, we detected significant alterations of skeletal muscle genes after exercise in PAD mouse models and characterized their expression patterns.

A chronic physical activity treatment in obese rats normalizes the contributions of ET-1 and NO to insulin-mediated posterior cerebral artery vasodilation.

This study tested the hypotheses that obesity-induced decrements in insulin-stimulated cerebrovascular vasodilation would be normalized with acute endothelin-1a receptor antagonism and that treatment with a physical activity intervention restores vasoreactivity to insulin through augmented nitric oxide synthase (NOS)-dependent dilation. Otsuka Long-Evans Tokushima Fatty rats were divided into the following groups: 20 wk old food controlled (CON-20); 20 wk old free food access (model of obesity, OB-20); 40 wk old food controlled (CON-40); 40 wk old free food access (OB-40); and 40 wk old free food access+RUN (RUN-40; wheel-running access from 20 to 40 wk). Rats underwent Barnes maze testing and a euglycemic hyperinsulinemic clamp (EHC). In the 40-wk cohort, cerebellum and hippocampus blood flow (BF) were examined (microsphere infusion). Vasomotor responses (pressurized myography) to insulin were assessed in untreated, endothelin-1a receptor antagonism, and NOS inhibition conditions in posterior cerebral arteries. Insulin-stimulated vasodilation was attenuated in the OB vs. CON and RUN groups (P ≤ 0.04). Dilation to insulin was normalized with endothelin-1a receptor antagonism in the OB groups (between groups, P ≥ 0.56), and insulin-stimulated NOS-mediated dilation was greater in the RUN-40 vs. OB-40 group (P < 0.01). At 40 wk of age, cerebellum BF decreased during EHC in the OB-40 group (P = 0.02) but not CON or RUN groups (P ≥ 0.36). Barnes maze testing revealed increased entry errors and latencies in the RUN-40 vs. CON and OB groups (P < 0.01). These findings indicate that obesity-induced impairments in vasoreactivity to insulin involve increased endothelin-1 and decreased nitric oxide signaling. Chronic spontaneous physical activity, initiated after disease onset, reversed impaired vasodilation to insulin and decreased Barnes maze performance, possibly because of increased exploratory behavior.NEW & NOTEWORTHY The new and noteworthy findings are that 1) in rodents, obesity-related deficits in insulin-mediated vasodilation are associated with increased influence of insulin-stimulated ET-1 and depressed influence of insulin-stimulated NOS and 2) a physical activity intervention, initiated after the onset of disease, restores insulin-mediated vasodilation, likely by normalizing insulin-stimulated ET-1 and NOS balance. These data demonstrate that the treatment effects of chronic exercise on insulin-mediated vasodilation extend beyond active skeletal muscle vasculature and include the cerebrovasculature.

Acute and Chronic Effects of Exercise on Cardiovascular System

Cardiovascular rehabilitation through exercise is of great interest since cardiovascular disease is one of the main cause of mortality worldwide. Exercise presents benefic effects on the reduction of cardiovascular disorders development. Previous studies analyzed the influence of aerobic exercise in improving cardiovascular function through physiological mechanism[. In this special number of the Journal of Cardiology and Therapy we discuss the acute and chronic effects of exercise on cardiovascular system.

The importance of animal studies in Exercise Science

Abstract — The validity and relevance of research with animals for the development of knowledge in Exercise Science have for long been discussed. Given the complexity of the biological systems, the use of animal models offers a significant contribution to uncover new findings about acute and chronic effects of exercise, particularly when these studies in humans have limitations and ethical implications. There have been notable findings using experimental animals either in basic sciences or in clinical studies involving physiology, pharmacology, genetic, biochemistry, urology, endocrinology and cancer. This article presents a brief review of scientific research using animal models with a focus on exercise training as an effective tool for the prophylaxis and treatment of different pathological processes, which are the basis of many concepts taught and used in undergraduate courses and graduate programs, as well as in new researches showed in scientific conference meetings in numerous areas of science.Keywords:

Structural, Contractile and Electrophysiological Adaptations of Cardiomyocytes to Chronic Exercise.

Cardiac beneficial effects of chronic exercise is well admitted. These effects mainly studied at the organ and organism integrated levels find their origin in cardiomyocyte adaptation. This chapter try to highlight the main trends of the data related to the different parameters subject to such adaptations. This is addressed through cardiomyocytes size and structure, calcium and contractile properties, and finally electrophysiological alterations induced by training as they transpire from the literature. Despite the clarifications needed to decipher healthy cardiomyocyte remodeling, this overview clearly show that cardiac cell plasticity ensure the cardiac adaptation to exercise training and offers an interesting mean of action to counteract physiological disturbances induced by cardiac pathologies.

Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

ABSTRACTThe function and morphology of β-cells is largely dependent on insulin demand. As β-cells cover a bigger cell proportion in pancreas islets, changes of insulin producer cells affect the whole pancreatic islet morphology. Growth factors as the neurotrophins regulate the pancreas physiology, besides; physical exercise increases insulin sensitivity, and further modifies brain derived neurotrophic factor (BDNF) concentration in plasma. The aim of this study was to investigate the effects of chronic exercise (running in a treadmill for 8 weeks) intensity on pancreatic islet morphometry in healthy state. The BDNF receptor effect on the pancreatic islet morphometry was also evaluated. Adult male Wistar rats were divided in 6 groups: Control (C); moderate intensity training (MIT); high intensity training (HIT) did not treat with BDNF receptor inhibitor (K252a), and C, MIT and HIT treated with K252a. The results shown that chronic exercise induces β-cells hypertrophy without BDNF receptor participation. On the other hand, the moderate exercise increases the number of β cells per islet; the last effect does not require TrkB participation. In sedentary conditions, the K252a treatment reduced the β-cell density. Exercise intensity has differential effects on pancreas islet morphometry in healthy model; furthermore, BDNF receptor plays a role to maintain the amount of β-cells in sedentary state.

Using event-related potentials to study the effects of chronic exercise on cognitive function

In recent years, advancements in neuroscientific methods have led to considerable progress with regard to the nature of the relationship between exercise and cognitive function. This review focuses on several components of the event-related potential (ERP) and how they can be successfully used to better understand subtle aspects of cognition that may be influenced by regular exercise participation. A select review of research that has incorporated ERPs to study the relationship between chronic exercise participation or cardiorespiratory fitness and cognitive function is presented followed by a brief overview of important methodological considerations when using the ERP technique. Future directions for the application of ERPs to achieve a more comprehensive understanding of the effects of chronic exercise on cognitive function are offered.

Exercise training and high-fat diet elicit endocannabinoid system modifications in the rat hypothalamus and hippocampus.

The purpose of the present study was to examine the effect of chronic exercise on the hypothalamus and hippocampus levels of the endocannabinoids (eCBs) anandamide (AEA) and 2-arachidonoylglycerol (2-AG) and of two AEA congeners and on the expression of genes coding for CB1, CB2 receptors (Cnr1 and Cnr2, respectively), and the enzymes responsible for eCB biosynthesis and degradation, in rats fed with a standard or high-fat diet. Male Wistar rats (n=28) were placed on a 12-week high-fat (HFD) or standard diet period, followed by 12weeks of exercise training for half of each group. Tissue levels of eCBs and related lipids were measured by liquid chromatography mass spectrometry, and expression of genes coding for CB1 and CB2 receptors and eCB metabolic enzymes was measured by quantitative real-time polymerase chain reaction (qPCR). HFD induced a significant increase in 2-AG (p<0.01) in hypothalamus. High-fat diet paired with exercise training had no effect on AEA, 2-AG, and AEA congener levels in the hypothalamus and hippocampus. Cnr1 expression levels were significantly increased in the hippocampus in response to HFD, exercise, and the combination of both (p<0.05). Our results indicate that eCB signaling in the CNS is sensitive to diet and/or exercise.

Effects of chronic exercise on the endocannabinoid system in Wistar rats with high-fat diet-induced obesity

The endocannabinoid system is dysregulated during obesity in tissues involved in the control of food intake and energy metabolism. We examined the effect of chronic exercise on the tissue levels of endocannabinoids (eCBs) and on the expression of genes coding for cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2) (Cnr1 and Cnr2, respectively) in the subcutaneous (SAT) and visceral adipose tissues and in the soleus and extensor digitorim longus (EDL) muscles, in rats fed with standard or high-fat diet. Twenty-eight male Wistar rats were placed on high-fat diet or standard diet (HFD and Ctl groups, respectively) during 12weeks whereafter half of each group was submitted to an exercise training period of 12weeks (HFD + training and Ctl + training). Tissue levels of eCBs were measured by LC-MS while expressions of genes coding for CB1 and CB2 receptors were investigated by qPCR. High-fat diet induced an increase in anandamide (AEA) levels in soleus and EDL (p < 0.02). In soleus of the HFD group, these changes were accompanied by elevated Cnr1 messenger RNA (mRNA) levels (p < 0.05). In EDL, exercise training allowed to reduce significantly this diet-induced AEA increase (p < 0.005). 2-Arachidonoylglycerol (2-AG) levels were decreased and increased by high-fat diet in SAT and EDL, respectively (p < 0.04), but not affected by exercise training. Unlike the HFD + training group, 2-AG levels in soleus were also decreased in the HFD group compared to Ctl (p < 0.04). The levels of eCBs and Cnr1 expression are altered in a tissue-specific manner following a high-fat diet, and chronic exercise reverses some of these alterations.

Impact of physical exercise on catechol-O-methyltransferase activity in depressive patients: A preliminary communication

BackgroundCatechol-O-methyltransferase (COMT) is a catabolic enzyme involved in the degradation of bioactive molecules including the neurotransmitters epinephrine, norepinephrine, and dopamine. Higher COMT activity in depressive patients in comparison to non-depressed individuals has been reported. The effect of aerobic exercise on depressive patients has been studied and a number of researchers and clinicians believe it to be effective in the treatment of depression and to be involved in several molecular underlying mechanisms. However, the effect of physical exercise on this enzyme activity is unknown, and it remains to be elucidated if chronic exercise changes COMT activity. This randomized control trial evaluates the effects of chronic exercise on peripheral COMT (S-COMT) activity in women with depressive disorder. MethodsFourteen women (aged: 51.4±10.5 years) diagnosed with depression (according to International Classification of Diseases-10) were randomized to one of two groups: pharmacotherapy plus physical exercise (n=7) or only pharmacotherapy (n=7). The aerobic exercise program was supervised, lasting between 45–50min/session, three times/week for 16 weeks. Erythrocyte soluble COMT were assessed prior to and after the exercise program. ResultsExercise group when compared to a control group presented a significant decrease (p=0.02, r=−0.535) in S-COMT activity between baseline and post-intervention. LimitationsThese data are preliminary outcomes from a small sample and should be replicated. ConclusionsChronic exercise therapy combined with pharmacotherapy leads to significant decrease in S-COMT activity. Our results provide evidence that exercise interferes with S-COMT activity, a molecular mechanism involved in depression.

Understanding How Exercise Promotes Cognitive Integrity in the Aging Brain.

Alterations in the structure and organization of the aging central nervous system (CNS), and associated functional deficits, result in cognitive decline and increase susceptibility to neurodegeneration. Age-related changes to the neurovascular unit (NVU), and their consequences for cerebrovascular function, are implicated as driving cognitive impairment during aging as well as in neurodegenerative disease. The molecular events underlying these effects are incompletely characterized. Similarly, the mechanisms underlying effects of factors that reduce the impact of aging on the brain, such as physical exercise, are also opaque. A study in this issue of PLOS Biology links the NVU to cognitive decline in the aging brain and suggests a potential underlying molecular mechanism. Notably, the study further links the protective effects of chronic exercise on cognition to neurovascular integrity during aging.

Diet-induced increases in chemerin are attenuated by exercise and mediate the effect of diet on insulin and HOMA-IR.

Chemerin concentrations are elevated in obesity and associated with inflammation and insulin resistance. Exercise improves insulin sensitivity, which may be facilitated by changes in chemerin. We explored the effects of chronic exercise on chemerin levels in diet-induced obese mice. We divided 40 mice into 4 groups: high-fat diet/exercise, high-fat diet/sedentary, normal diet/exercise, and normal diet/sedentary. A 9-week dietary intervention was followed by a 12-week exercise intervention (treadmill run: 11 m/min for 30 min, 3×/week). We analyzed blood samples before and after the exercise intervention. We used t-tests and linear regression to examine changes in chemerin, insulin resistance, and inflammatory markers, and associations between changes in chemerin and all other biomarkers. Chemerin increased significantly across all mice over the 12-week intervention (mean ± SD = 40.7 ± 77.8%, p = 0.01), and this increase was smaller in the exercise versus sedentary mice (27.2 ± 83.9% versus 54.9 ± 70.5%, p = 0.29). The increase among the high-fat diet/exercise mice was ~44% lower than the increase among the high-fat diet/sedentary mice (55.7 ± 54.9% versus 99.8 ± 57.7%, p = 0.12). The high-fat diet mice showed significant increases in insulin (773.5 ± 1286.6%, p < 0.0001) and homeostatic model assessment of insulin resistance (HOMA-IR; 846.5 ± 1723.3%, p < 0.01). Mediation analyses showed that increases in chemerin explained a substantial amount of the diet-induced increases in insulin and HOMA-IR. Chronic exercise may attenuate diet-driven increases in circulating chemerin, and the insulin resistance associated with a high-fat diet may be mediated by diet-induced increases in chemerin.

Optimal Vitamin D Status is Associated with Healthier Immune Indices in Untrained, but not Trained Females

The anti‐inflammatory effects of chronic exercise are well established; less is known about immune changes associated with vitamin D. This study explored the relationship between inflammatory indices in exercise trained (TR) and untrained (UN) individuals with 25‐hydroxyvitamin D (25OHD) concentrations either above (HD) or below (LD) optimal concentrations. Subjects (n=63, 19‐35 years) were evaluated for body composition and maximal aerobic capacity (VO2peak). 25OHD levels, lipopolysaccharide (LPS)‐stimulated interleukin‐6 (IL‐6) production, and inflammatory monocytes and toll like receptor 4 (TLR4) expression were determined in whole blood. TR (n=30) had higher 25OHD levels (p=0.015) and VO2peak (p&lt;0.0001), lower body weight (p=0.039) and percent body fat (p=0.011), and lower LPS‐stimulated IL‐6 production (p=0.0163) compared to UN (n=33). UN with HD had lower numbers of total monocytes, CD14+CD16‐ cells, and lower TLR4 expression on CD14+CD16+ cells compared to UN with LD. Exercise was related to increased 25OHD, improved body composition, and decreased inflammation. Additionally, vitamin D may mediate inflammation in those who do not exercise.