scholarly journals Statins Attenuate the Increase in P-Selectin Produced by Prolonged Exercise

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Amanda Zaleski ◽  
Jeffrey Capizzi ◽  
Kevin D. Ballard ◽  
Christopher Troyanos ◽  
Aaron Baggish ◽  
...  

Strenuous endurance exercise increases inflammatory markers and acutely increases cardiovascular risk; however, statins may mitigate this response. We measured serum levels of p-selectin in 37 runners treated with statins and in 43 nonstatin treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) as well as within 1 hour after (FINISH) and 24 hours after (POST) the race. The increase in p-selectin immediately after exercise was lower in statin users (PRE to FINISH: 20.5 ± 19.4 ng/mL) than controls (PRE to FINISH: 30.9 ± 27.1 ng/mL;P<0.001). The increase in p-selectin 24 hours after exercise was also lower in statin users (PRE to POST: 21.5 ± 26.6 ng/mL) than controls (PRE to POST: 29.3 ± 31.9 ng/mL;P<0.001). Furthermore, LDL-C was positively correlated with p-selectin at FINISH and POST (P<0.01andP<0.05, resp.), irrespective of drug treatment, suggesting that lower levels of LDL-C are associated with a reduced inflammatory response to exercise. We conclude that statins blunt the exercise-induced increase in p-selectin following a marathon and that the inflammatory response to a marathon varies directly with LDL-C levels.

2006 ◽  
Vol 101 (4) ◽  
pp. 1222-1227 ◽  
Author(s):  
Martin Whitham ◽  
Gary J. Walker ◽  
Nicolette C. Bishop

The stimulus for the release of 72-kDa heat shock protein (HSP72) during exercise in humans is currently unclear. Recent evidence in an animal model is suggestive of an involvement of catecholamines. The present study, therefore, investigated the effect of caffeine supplementation, a known stimulator of sympathetic activity, on the extracellular (e)HSP72 response to prolonged exercise. Ten healthy male endurance-trained cyclists were recruited (age: 21 ± 1 yr, maximum O2 uptake 61.1 ± 1.7 ml·kg−1·min−1, mean ± SE). Each subject was randomly assigned to ingest either 6 mg/kg body mass of caffeine (Caff) or placebo (Pla) 60 min before one of two 90-min bouts of cycling at 74 ± 1% maximum O2 uptake. Trials were performed at least 7 days apart in a counterbalanced design. Venous blood samples were collected by venepuncture at pretreatment, preexercise, postexercise, and 1 h postexercise. Serum caffeine and plasma catecholamines were determined using a spectrophotometric assay and high-performance liquid chromatography, respectively. Plasma HSP72 and cortisol were determined by ELISA. Serum caffeine concentrations were significantly increased throughout Caff, while no increases were detected in Pla. Caffeine supplementation and exercise was associated with a greater eHSP72 response than exercise alone (postexercise Caff 8.6 ± 1.3 ng/ml; Pla 5.9 ± 0.9 ng/ml). This greater eHSP72 response was associated with a greater epinephrine response to exercise in Caff. There was a significant increase in norepinephrine and cortisol, with no intertrial differences. The present data suggest that, in humans, catecholamines may be an important mediator of the exercise-induced increase in eHSP72 concentration.


1999 ◽  
Vol 87 (6) ◽  
pp. 2157-2167 ◽  
Author(s):  
Michael I. Lindinger ◽  
Peggy L. Horn ◽  
Simon P. Grudzien

The hypothesis was tested that exercise-induced changes in plasma composition stimulate unidirectional K+ transport ( J inK) in human red blood cells (RBCs). Ten men performed two 30-s high-intensity leg-cycling tests separated by 4 min of rest. Antecubital venous blood was sampled before exercise and at the end of the second exercise bout. RBCs were separated from true exercise plasma,42K was added to plasma, and RBC K+ transport was studied in vitro at 37°C. In the second part of the study, blood from nine healthy men studied in vitro at 37°C was used to test the hypothesis that exercise-simulated (ES) plasma stimulates net K+ transport and J inK (measured using 86Rb) in human RBCs. The J inK of resting RBCs added to true exercise plasma was 1,574 ± 200 (SE) μmol ⋅ h−1 ⋅ l−1vs. 1,236 ± 256 μmol ⋅ h−1 ⋅ l−1in true resting plasma at 2 min (controls). In true exercise and ES plasma, J inK was increased through activation of the ouabain-sensitive Na+-K+pump and the bumetanide-sensitive Na+-K+-2Cl−cotransporter. Increases in plasma osmolality and K+, H+, and epinephrine concentrations independently and in combination stimulated K+ transport into human RBCs. In a third series of experiments, in which ES plasma K+ concentration was continuously measured during the first 5 min of incubation of RBCs, a 1.6 ± 0.3 mmol/l decrease in plasma K+concentration occurred during the first 2 min. It is concluded that RBCs transport K+ at elevated rates in response to exercise-induced changes in plasma composition.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1129-1129
Author(s):  
Alwine Kardinaal ◽  
Min Young Park ◽  
Jong Eun Jeon ◽  
Hee Jung Choi ◽  
Ji Yeon Kim ◽  
...  

Abstract Objectives The aim was to develop a human challenge model in which modulation of immune and inflammatory response by food ingredients can be evaluated. We hypothesized that oral cholera vaccination, in addition to inducing a specific antibody response, induces a significant increase in gut inflammatory response. Methods Twenty healthy men (age 30.6 ± 1.8 y; BMI 24.9 ± 0.6) were enrolled in the study. Fecal and blood samples were collected at baseline. After a 2-week run-in period (D0-D14), subjects were vaccinated with oral cholera vaccine Dukoral (D15). After a period of 2 weeks, a second vaccination was administered (D29). Fecal samples were collected the day before (D14; D28) and the days (D16/D17; D30/D31) after each vaccination, as well as on D42. Blood samples were collected before vaccination (D15; D29), and on D16 and D17/D31, on D43. Primary outcome was fecal calprotectin concentration, secondary outcomes were serum levels of cholera toxin (CTB)-specific IgA and IgG. Other markers of local and systemic inflammatory response included beta-defensins, IP-10, IL-1 ra and hsCRP. Changes over time were tested by means of a linear mixed model. Outliers were identified with the 1.5xIQR rule and excluded from analysis. Results Fecal calprotectin did not increase after the first vaccination. After the second vaccination, a significant increase was observed: from 12.8 ± 2.5 μg/g feces (mean ± SEM) on day 29 to 18.0 ± 2.9 μg/g on day 31 (P = 0.017). Plasma CTB-specific IgA and IgG were strongly increased after the first vaccination, with a further increase after the second vaccination. Plasma CRP slightly decreased on D17, compared to D15 (P = 0.016). IL-1ra significantly decreased 2 days after the first vaccination (P = 0.011), whereas no change was observed after the second vaccination. Beta-defensin was significantly increased at D31 compared to D29 (from 42.7 ± 7.0 to 80.7 ± 16.1 (P = 0.014)). IP-10 did not show any response to vaccination. Conclusions In addition to the expected antibody response, oral cholera vaccination induces an increase in fecal calprotectin and beta defensin, pointing to vaccine induced intestinal inflammation. These readouts may be added to intervention studies with dietary compounds to evaluate the potential for modulating immune responsiveness. Funding Sources Bio&Medical Technol Developm Program of the Natl Res Foundation, Min Science & ICT of Rep Korea.


2020 ◽  
Author(s):  
Diego Viasus ◽  
Antonella F Simonetti ◽  
Andres Estupiñan-Bohorquez ◽  
Jordi Carratalà

Abstract Background: Studies have suggested that an inappropriate inflammatory response is a major cause of treatment failure and mortality in patients with community-acquired pneumonia (CAP). We aimed to determine the effect of comorbidities and age on serum inflammatory markers in CAP.Methods: We performed a prospective cohort study of adults hospitalized with CAP. For the purposes of this study, we compared patients according to comorbidities and age. Inflammatory markers were measured at hospital admission, focusing on acute phase proteins, cytokines, and monocyte human leukocyte antigen DR (mHLA-DR) expression.Results: In patients with chronic pulmonary disease (COPD), serum cytokines had significantly decreased levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and mHLA-DR expression, as well as the C-reactive protein (CRP), compared with patients who had no comorbidities. Similarly, patients with chronic heart disease had a significantly reduced CRP levels and mHLA-DR expression, whereas patients with chronic kidney disease had significantly higher serum levels of procalcitonin and TNF-α. Lower procalcitonin, IL-6, and IL-10 levels, as well as mHLA-DR expression, were documented in older patients, but with no significant differences compared to younger patients. Multimorbidity in older patients was associated with significant lower levels of CRP and mHLA-DR expression.Conclusions: The circulating inflammatory markers to CAP have profiles that differ with age and underlying comorbidities. Multimorbidity in the elderly is also associated with lower serum levels of some inflammatory markers. These findings suggest that age and comorbidities have much more of an impact than to simply reduce physiological reserve and can cause variations in the inflammatory response in CAP.


1991 ◽  
Vol 70 (3) ◽  
pp. 979-987 ◽  
Author(s):  
H. Perrault ◽  
M. Cantin ◽  
G. Thibault ◽  
G. R. Brisson ◽  
G. Brisson ◽  
...  

The exercise-induced increase in plasma atriopeptin (ANP) has been related to exercise intensity. The independent effect of duration on the ANP response to dynamic exercise remains incompletely documented. The purpose of this study was to describe the time course of plasma ANP concentration during a 90-min cycling exercise protocol and to examine this in light of concurrent variations in plasma arginine vasopressin (AVP), aldosterone (ALD), and catecholamine (norepinephrine and epinephrine) concentrations as well as plasma renin activity (PRA). Seven male and four female healthy college students (23 +/- 2 yr) completed a prolonged exercise protocol on a cycle ergometer at an intensity of 67% of maximal O2 uptake. Venous blood was sampled through an indwelling catheter at rest, after 15, 30, 45, 60, and 90 min of exercise, and after 30 min of passive upright recovery. Results (means +/- SE) indicate an increase in ANP from rest (22 +/- 2.6 pg/ml) at 15 min of exercise (45.3 +/- 7.4 pg/ml) with a further increase at 30 min (59.4 +/- 9.8 pg/ml) and a leveling-off thereafter until completion of the exercise protocol (51.7 +/- 10.7 pg/ml). In plasma ALD and PRA, a significant increase was found from rest (ALD, 21.4 +/- 6.4 ng/dl), PRA, 2.5 +/- 0.5 ng.ml-1.h-1 after 30 min of cycling, which continued to increase until completion of the exercise (ALD 46.6 +/- 8.7 ng/dl, PRA 9.5 +/- 0.9 ng.ml-1.h-1.(ABSTRACT TRUNCATED AT 250 WORDS)


1998 ◽  
Vol 274 (4) ◽  
pp. R894-R902 ◽  
Author(s):  
L. Maureen Odland ◽  
George J. F. Heigenhauser ◽  
Denis Wong ◽  
Melanie G. Hollidge-Horvat ◽  
Lawrence L. Spriet

The study examined the existence and regulation of fat-carbohydrate interaction during low- and moderate-intensity exercise. Eight males cycled for 10 min at 40% and 60 min at 65% maximal O2 uptake (V˙o 2 max) while infused with either Intralipid and heparin (Int) or saline (Con). Before exercise, plasma arterial free fatty acid (FFA) was 0.69 ± 0.04 mM (Int) vs. 0.25 ± 0.04 mM (Con). Muscle biopsies were taken at rest and at 10, 20, and 70 min of exercise. Arterial and femoral venous blood samples and expired gases were collected simultaneously throughout exercise, and blood flow was estimated from pulmonary O2 uptake and the leg arterial-venous O2 difference. Respiratory exchange ratio was higher in Con (0.94 ± 0.01) compared with Int (0.91 ± 0.01). Mean net leg FFA uptake was higher in Int (0.16 ± 0.03 vs. 0.04 ± 0.01 mmol/min), and net lactate efflux was reduced (Int, 1.55 ± 0.36 vs. Con, 3.07 ± 0.47 mmol/min). Leg net glucose uptake was unaffected by Int. Muscle glycogen degradation was 23% lower in Int [230 ± 29 vs. 297 ± 36 mmol glucosyl units/kg dry muscle (dm)]. Pyruvate dehydrogenase activity in the a form (PDH a) was lower during Int (1.61 ± 0.17 vs. 2.22 ± 0.24 mmol ⋅ min−1 ⋅ kg wet muscle−1), and muscle citrate was higher (0.59 ± 0.04 vs. 0.48 ± 0.04 mmol/kg dm). Muscle lactate, phosphocreatine, ATP, acetyl-CoA, acetyl-carnitine, and Pi were unaffected by Int. Calculated free AMP was significantly lower in Int compared with Con at 70 min of exercise (3.3 ± 0.8 vs. 1.5 ± 0.3 μmol/kg dm). The high FFA-induced reduction in glycogenolysis and carbohydrate oxidation at 65% V˙o 2 maxappears to be due to regulation at several sites. The reduced flux through phosphorylase and phosphofructokinase during Int may have been due to reduced free AMP accumulation and increased cytoplasmic citrate. The mechanism for reduced PDH transformation to the a form is unknown but suggests reduced flux through PDH.


2021 ◽  
pp. 5-8

Objectives: Exercise is an important tool to stimulate oxidative stress and metabolic demands. We intended to evaluate impact of aerobic exercise on oxidative stress parameters and their relationships between irisin and nesfatin-1 levels. Material and Method: Total of ten healthy sedentary female subjects exercise for a 30 min of aerobic running exercise work intensity corresponded to associated their anaerobic threshold. Venous blood samples were taken before and at the end of the exercise. Serum irisin nesfatin-1 and TAS and TOS levels were analyzed using ELISA methods. Results: Exercise caused increase of irisin (11%) and nesfatin-1 (12%) levels. During exercise a decrease in TAS (-11%) and increased in TOS (29%) levels were observed. There was a significant correlation between changes of irisin and TAS levels (R=-0.67594, p=0.03). Conclusion: Consequently, exercise induced skeletal muscle activity may cause increase in oxidative stress, irisin and nesfatin-1 levels. Irisin hormone may be a secreted against to increased exercise-induced increased oxidative stress muscle activity.


2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Ismail Biyik ◽  
Fatma Nihan Turhan Caglar ◽  
Nilgun Isiksacan ◽  
Nursel Kocamaz ◽  
Pınar Kasapoglu ◽  
...  

Introduction. Hypertension (HT) is a common serious condition associated with cardiovascular morbidity and mortality. The pathogenesis of HT is multifactorial and has been widely investigated. Besides the vascular, hormonal, and neurological factors, inflammation plays a crucial role in HT. Many inflammatory markers such as C-reactive protein, cytokines, and adhesion molecules have been studied in HT, which supported the role of inflammation in the pathogenesis of HT. Presepsin (PSP) is a novel biomarker of inflammation. Therefore, the potential relationship between PSP and HT was investigated in this study. Methods. Forty-eight patients with controlled HT and 48 controls without HT were included in our study. Besides routine clinical and laboratory data, PSP levels were measured in peripheral venous blood samples from all the participants. Results. PSP levels were significantly lower in patients with HT than in controls (144.98±75.98 versus 176.67±48.12 pg/mL, p=0.011). PSP levels were positively correlated with hsCRP among both the patient and the control groups (p=0.015 and p=0.009, resp.). However, PSP levels were not correlated with WBC among both groups (p=0.09 and p=0.67, resp.). Conclusions. PSP levels are not elevated in patients with well-controlled HT compared to controls. This result may be associated with anti-inflammatory effects of antihypertensive medicines.


1990 ◽  
Vol 68 (1) ◽  
pp. 44-47 ◽  
Author(s):  
R. K. Hetzler ◽  
R. G. Knowlton ◽  
S. M. Somani ◽  
D. D. Brown ◽  
R. M. Perkins

Because it has previously been shown that it takes much more caffeine to cause fat mobilization in vitro than in vivo, it has been suggested that there may be an active metabolite working with caffeine causing an increase in lipolysis in vivo. To determine the relationship between the appearance of paraxanthine (caffeine's major dimethylxanthine metabolite) and free fatty acid (FFA) mobilization after intravenous caffeine administration, 10 men were studied at rest after receiving a dose of 4 mg/kg lean body mass. Venous blood samples were obtained before dosing and at minutes 5, 10, 15, 30, 45, 60, 90, 120, 150, and 180. Serum levels of FFA, glycerol, caffeine, and paraxanthine were determined in duplicate. Concentrations of FFA and glycerol were corrected for plasma volume changes. A high negative correlation was seen between decreases in caffeine and increases in FFA (r = -0.90) and a high positive correlation was seen between the appearance of paraxanthine and FFA (r = 0.93). It was concluded that paraxanthine may play a role in increased lipolysis after caffeine administration in humans.


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