Enhanced plasma IL-6 and IL-1ra responses to repeated vs. single bouts of prolonged cycling in elite athletes

2002 ◽  
Vol 92 (6) ◽  
pp. 2547-2553 ◽  
Author(s):  
Ola Ronsen ◽  
Tor Lea ◽  
Roald Bahr ◽  
Bente Klarlund Pedersen

The impact of repeated bouts of exercise on plasma levels of interleukin (IL)-6 and IL-1 receptor antagonist (IL-1ra) was examined. Nine well-trained men participated in four different 24-h trials: Long [two bouts of exercise, at 0800–0915 and afternoon exercise (Ex-A), separated by 6 h]; Short (two bouts, at 1100–1215 and Ex-A, separated by 3 h); One (single bout performed at the same Ex-A as second bout in prior trials); and Rest (no exercise). All exercise bouts were performed on a cycle ergometer at 75% of maximal O2uptake and lasted 75 min. Peak IL-6 observed at the end of Ex-A was significantly higher in Short (8.8 ± 1.3 pg/ml) than One (5.2 ± 0.7 pg/ml) but not compared with Long (5.9 ± 1.2 pg/ml). Peak IL-1ra observed 1 h postexercise was significantly higher in Short (1,774 ± 373 pg/ml) than One (302 ± 53 pg/ml) but not compared with Long (1,276 ± 451 pg/ml). We conclude that, when a second bout of endurance exercise is performed after only 3 h of recovery, IL-6 and IL-1ra responses are elevated. This may be linked to muscle glycogen depletion.

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S349
Author(s):  
Thomas B. Adolpho ◽  
Patr??cia Lopes Campos ◽  
Bruno Gualano ◽  
Josilene Carla Gomes ◽  
Fernanda Baeza Scagliusi ◽  
...  

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S349
Author(s):  
Thomas B. Adolpho ◽  
Patrícia Lopes Campos ◽  
Bruno Gualano ◽  
Josilene Carla Gomes ◽  
Fernanda Baeza Scagliusi ◽  
...  

2019 ◽  
Vol 15 (4) ◽  
pp. 243-251
Author(s):  
C. Giacomet ◽  
D. Pochmann ◽  
P.K. Peccin ◽  
M.C. Boeira ◽  
C. Dani ◽  
...  

Recent clinical studies demonstrated that single bouts of exercise including high intensity interval training (HIIT) protocols are able to modulate muscle damage and epigenetic markers as well as brain-derived neurotrophic factor (BDNF) levels in different populations, however, this relationship is lacking in obese women. To evaluate the impact of a single bout of HIIT on creatine kinase (CK), BDNF and global histone H3 and H4 acetylation levels in obese postmenopausal women. The sample consisted of 10 volunteers with a body mass index of 27 to 39.9 kg / m2 that were submitted to a single session of HIIT on a cycle ergometer for 60 s (separated by 75 s of active recovery). In order to measure the biomarkers, blood samples (15 ml) were collected immediately before and immediately after the intervention. Our protocol did not modify any biomarkers (P>0.05), although a negative correlation between fat mass and global histone H3 levels (P=0.022) and between oxygen consumption and global histone H4 levels (P=0.003) were found. A single bout of HIIT on a cycle ergometer is not an effective strategy to modulate histone acetylation status, CK and BDNF levels in postmenopausal obese women. Future studies considering different exercise protocols should be done in order to elucidate this issue.


2001 ◽  
Vol 91 (1) ◽  
pp. 425-434 ◽  
Author(s):  
Ola Ronsen ◽  
Bente Klarlund Pedersen ◽  
Tone Rasmussen Øritsland ◽  
Roald Bahr ◽  
Jens Kjeldsen-Kragh

This study compared leukocyte counts and lymphocyte responsiveness during and after a second bout of high-intensity endurance exercise on the same day with the response to a similar but single bout of exercise. Nine athletes participated in three 24-h trials: 1) rest in bed (Rest); 2) one bout of exercise (One); and 3) two bouts of exercise (Two). All bouts consisted of 75 min at ∼75% of maximal O2uptake on a cycle ergometer. Lymphocytes in whole blood were stimulated with monoclonal antibodies against CD2 and assessed by flow cytometry for expression of the early activation molecule CD69. The second bout of exercise in the Two trial was associated with significantly increased concentrations of total leukocytes, neutrophils, lymphocytes, CD4+, CD8+, and CD56+cells and a significantly decreased percentage of CD56+cells expressing CD69 compared with a single bout. Additionally, there was a significantly decreased CD69 fluorescence in CD56+cells postexercise. These differences suggest a “carry-over” effect in the immune system from a first to a second bout of exercise on the same day.


2014 ◽  
Vol 63 (4) ◽  
pp. 401-408 ◽  
Author(s):  
Keisuke Shiose ◽  
Takuro Tobina ◽  
Yasuki Higaki ◽  
Akira Kiyonaga ◽  
Hiroaki Tanaka

2016 ◽  
Vol 116 (12) ◽  
pp. 2053-2065 ◽  
Author(s):  
Kurt A. Escobar ◽  
Trisha A. VanDusseldorp ◽  
Chad M. Kerksick

AbstractSubstantial research has been completed examining the impact of carbohydrate (CHO) intake on endurance exercise, whereas its role in resistance-based exercise performance, adaptation and cell signalling has yet to be fully characterised. This empirical shortcoming has precluded the ability to establish specific CHO recommendations for resistance exercise. This results in recommendations largely stemming from findings based on endurance exercise and/or anecdotal evidence despite the distinct energetic demands and molecular responses mediating adaptation from endurance- and resistance-based exercise. Moreover, the topic of CHO and exercise has become one of polarising nature with divergent views – some substantiated, others lacking evidence. Current literature suggests a moderately high daily CHO intake (3–7 g/kg per d) for resistance training, which is thought to prevent glycogen depletion and facilitate performance and adaptation. However, contemporary investigation, along with an emerging understanding of the molecular underpinnings of resistance exercise adaptation, may suggest that such an intake may not be necessary. In addition to the low likelihood of true glycogen depletion occurring in response to resistance exercise, a diet restrictive in CHO may not be detrimental to acute resistance exercise performance or the cellular signalling activity responsible for adaptation, even when muscle glycogen stores are reduced. Current evidence suggests that signalling of the mammalian target of rapamycin complex 1, the key regulatory kinase for gene translation (protein synthesis), is unaffected by CHO restriction or low muscular glycogen concentrations. Such findings may call into question the current view and subsequent recommendations of CHO intake with regard to resistance-based exercise.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thomas Duflot ◽  
Charlotte Laurent ◽  
Anne Soudey ◽  
Xavier Fonrose ◽  
Mouad Hamzaoui ◽  
...  

AbstractThis study addressed the hypothesis that epoxyeicosatrienoic acids (EETs) synthesized by CYP450 and catabolized by soluble epoxide hydrolase (sEH) are involved in the maintenance of renal allograft function, either directly or through modulation of cardiovascular function. The impact of single nucleotide polymorphisms (SNPs) in the sEH gene EPHX2 and CYP450 on renal and vascular function, plasma levels of EETs and peripheral blood monuclear cell sEH activity was assessed in 79 kidney transplant recipients explored at least one year after transplantation. Additional experiments in a mouse model mimicking the ischemia–reperfusion (I/R) injury suffered by the transplanted kidney evaluated the cardiovascular and renal effects of the sEH inhibitor t-AUCB administered in drinking water (10 mg/l) during 28 days after surgery. There was a long-term protective effect of the sEH SNP rs6558004, which increased EET plasma levels, on renal allograft function and a deleterious effect of K55R, which increased sEH activity. Surprisingly, the loss-of-function CYP2C9*3 was associated with a better renal function without affecting EET levels. R287Q SNP, which decreased sEH activity, was protective against vascular dysfunction while CYP2C8*3 and 2C9*2 loss-of-function SNP, altered endothelial function by reducing flow-induced EET release. In I/R mice, sEH inhibition reduced kidney lesions, prevented cardiac fibrosis and dysfunction as well as preserved endothelial function. The preservation of EET bioavailability may prevent allograft dysfunction and improve cardiovascular disease in kidney transplant recipients. Inhibition of sEH appears thus as a novel therapeutic option but its impact on other epoxyfatty acids should be carefully evaluated.


Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 906
Author(s):  
Agnieszka Mikłosz ◽  
Bartłomiej Łukaszuk ◽  
Adrian Chabowski ◽  
Jan Górski

Endothelial lipase (EL) is an enzyme capable of HDL phospholipids hydrolysis. Its action leads to a reduction in the serum high-density lipoprotein concentration, and thus, it exerts a pro-atherogenic effect. This study examines the impact of a single bout exercise on the gene and protein expression of the EL in skeletal muscles composed of different fiber types (the soleus—mainly type I, the red gastrocnemius—mostly IIA, and the white gastrocnemius—predominantly IIX fibers), as well as the diaphragm, and the heart. Wistar rats were subjected to a treadmill run: 1) t = 30 [min], V = 18 [m/min]; 2) t = 30 [min], V = 28 [m/min]; 3) t = 120 [min], V = 18 [m/min] (designated: M30, F30, and M120, respectively). We established EL expression in the total muscle homogenates in sedentary animals. Resting values could be ordered with the decreasing EL protein expression as follows: endothelium of left ventricle > diaphragm > red gastrocnemius > right ventricle > soleus > white gastrocnemius. Furthermore, we observed that even a single bout of exercise was capable of inducing changes in the mRNA and protein level of EL, with a clearer pattern observed for the former. After 30 min of running at either exercise intensity, the expression of EL transcript in all the cardiovascular components of muscles tested, except the soleus, was reduced in comparison to the respective sedentary control. The protein content of EL varied with the intensity and/or duration of the run in the studied whole tissue homogenates. The observed differences between EL expression in vascular beds of muscles may indicate the muscle-specific role of the lipase.


Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2555 ◽  
Author(s):  
Takahashi ◽  
Matsunaga ◽  
Banjo ◽  
Takahashi ◽  
Sato ◽  
...  

We investigated the effects of nutrient intake timing on glycogen accumulation and its related signals in skeletal muscle after an exercise that did not induce large glycogen depletion. Male ICR mice ran on a treadmill at 25 m/min for 60 min under a fed condition. Mice were orally administered a solution containing 1.2 mg/g carbohydrate and 0.4 mg/g protein or water either immediately (early nutrient, EN) or 180 min (late nutrient, LN) after the exercise. Tissues were harvested at 30 min after the oral administration. No significant difference in blood glucose or plasma insulin concentrations was found between the EN and LN groups. The plantaris muscle glycogen concentration was significantly (p < 0.05) higher in the EN group—but not in the LN group—compared to the respective time-matched control group. Akt Ser473 phosphorylation was significantly higher in the EN group than in the time-matched control group (p < 0.01), while LN had no effect. Positive main effects of time were found for the phosphorylations in Akt substrate of 160 kDa (AS160) Thr642 (p < 0.05), 5'-AMP-activated protein kinase (AMPK) Thr172 (p < 0.01), and acetyl-CoA carboxylase Ser79 (p < 0.01); however, no effect of nutrient intake was found for these. We showed that delayed nutrient intake could not increase muscle glycogen after endurance exercise which did not induce large glycogen depletion. The results also suggest that post-exercise muscle glycogen accumulation after nutrient intake might be partly influenced by Akt activation. Meanwhile, increased AS160 and AMPK activation by post-exercise fasting might not lead to glycogen accumulation.


Author(s):  
Pablo A. Scacchi Bernasconi ◽  
Nancy P. Cardoso ◽  
Roxana Reynoso ◽  
Pablo Scacchi ◽  
Daniel P. Cardinali

AbstractCombinations of fructose- and fat-rich diets in experimental animals can model the human metabolic syndrome (MS). In rats, the increase in blood pressure (BP) after diet manipulation is sex related and highly dependent on testosterone secretion. However, the extent of the impact of diet on rodent hypophysial-testicular axis remains undefined. In the present study, rats drinking a 10% fructose solution or fed a high-fat (35%) diet for 10 weeks had higher plasma levels of luteinizing hormone (LH) and lower plasma levels of testosterone, without significant changes in circulating follicle-stimulating hormone or the weight of most reproductive organs. Diet manipulation brought about a significant increase in body weight, systolic BP, area under the curve (AUC) of glycemia after an intraperitoneal glucose tolerance test (IPGTT), and plasma low-density lipoprotein cholesterol, cholesterol, triglycerides, and uric acid levels. The concomitant administration of melatonin (25 μg/mL of drinking water) normalized the abnormally high LH levels but did not affect the inhibited testosterone secretion found in fructose- or high-fat-fed rats. Rather, melatonin per se inhibited testosterone secretion. Melatonin significantly blunted the body weight and systolic BP increase, the increase in the AUC of glycemia after an IPGTT, and the changes in circulating lipid profile and uric acid found in both MS models. The results are compatible with a primary inhibition of testicular function in diet-induced MS in rats and with the partial effectiveness of melatonin to counteract the metabolic but not the testicular sequelae of rodent MS.


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