High-intensity intermittent exercise increases adenosine hydrolysis in platelets and lymphocytes and promotes platelet aggregation in futsal athletes

Miron, Vanessa Valéria; Baldissarelli, Jucimara; Pranke, Gabriel Ivan; Mânica, Aline; Bonadiman, Beatriz da Silva Rosa; Manfredi, Leandro Henrique; Morsch, Vera Maria; Schetinger, Maria Rosa Chitolina; Cardoso, Andréia Machado

doi:10.1080/09537104.2018.1529299

Cited by 18 publications

(21 citation statements)

References 25 publications

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“…This may be due to the fast removal of RBC-derived microvesicles by the reticulo-endothelial system [33]. However, we observed a significant increase in the concentration of platelet-derived vesicles (Figure 4), supporting the suggestions that exercise may activate platelets and induce platelet precursor mobilization [34][35][36][37]. Platelet activation may be increased by exercise-induced inflammatory responses [8,14].…”

Section: Discussionsupporting

confidence: 80%

Red Blood Cell Aging as a Homeostatic Response to Exercise-Induced Stress

et al. 2019

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Our knowledge on the molecular mechanisms of red blood cell aging is mostly derived from in vitro studies. The Four Days Marches of Nijmegen in the Netherlands, the world’s largest yearly walking event, constitutes a unique possibility to study the effect of mechanical and biochemical stressors occurring during moderate-intensity exercise on red blood cell aging in vivo. Therefore, longitudinal measurements were performed of biophysical, immunological, and functional red blood cell characteristics that are known to change during aging. Our data show that moderate-intensity exercise induces the generation of a functionally improved red blood cell population with a higher deformability and a decreased tendency to aggregate. This is likely to be associated with an early removal of the oldest red blood cells from the circulation, as deduced from the (dis)appearance of removal signals. Thus, the physiological red blood cell aging process maintains homeostasis in times of moderate-intensity exercise-induced stress, probably by accelerated aging and subsequent removal of the oldest, most vulnerable red blood cells.

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Section: Discussionsupporting

confidence: 80%

Red Blood Cell Aging as a Homeostatic Response to Exercise-Induced Stress

et al. 2019

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“…APM has long been known as a specifically selective blocker of SK2 channels [ 27 ]. Ca 2+ /calmodulin-dependent protein kinase II (CaMKII), one of the main downstream targets of Ca 2+ and CaM, is activated by Ca 2+ /CaM [ 29 ]. TNFα is produced in SK2/K Ca 2.2 channel-activated microglia [ 8 ].…”

Section: Resultsmentioning

confidence: 99%

“…SK channels are associated with neuroinflammation in microglia. The CaMKII pathway was found to be significantly activated in LPS-stimulated microphages, with an increase in intracellular Ca 2+ levels and CaMKII phosphorylation [ 29 , 45 ]. APM, a specifically selective blocker of SK channels, decreased LPS-induced SK/K Ca 2.2 and pCaMKII expression in BV2 and rat primary microglial cells.…”

Section: Discussionmentioning

confidence: 99%

Apamin Suppresses LPS-Induced Neuroinflammatory Responses by Regulating SK Channels and TLR4-Mediated Signaling Pathways

Park

Jang

Park

2020

IJMS

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Neuroinflammation plays a vital role in neurodegenerative conditions. Microglia are a key component of the neuroinflammatory response. There is a growing interest in developing drugs to target microglia and thereby control neuroinflammatory processes. Apamin (APM) is a specifically selective antagonist of small conductance calcium-activated potassium (SK) channels. However, its effect on neuroinflammation is largely unknown. We examine the effects of APM on lipopolysaccharide (LPS)-stimulated BV2 and rat primary microglial cells. Regarding the molecular mechanism by which APM significantly inhibits proinflammatory cytokine production and microglial cell activation, we found that APM does so by reducing the expression of phosphorylated CaMKII and toll-like receptor (TLR4). In particular, APM potently suppressed the translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)/signal transducer and activator of transcription (STAT)3 and phosphorylated mitogen-activated protein kinases (MAPK)-extracellular signal-regulated kinase (ERK). In addition, the correlation of NF-κB/STAT3 and MAPK-ERK in the neuroinflammatory response was verified through inhibitors. The literature and our findings suggest that APM is a promising candidate for an anti-neuroinflammatory agent and can potentially be used for the prevention and treatment of various neurological disorders.

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“…This data reinforces the well-known role of A 1 R in hypothermia 81 . Circulating adenosine levels increase during exercise 30 , 31 , and global A 2A R KO imbalance appears to increase the A 1 R role, signaling hypothermia even after exercise. These results are limited to the use of infrared temperature, as we have not measured rectal temperature due to interference (vaginal manipulation) in the evaluation of the estrous cycle of females.…”

Section: Discussionmentioning

confidence: 99%

“…Adenosine can act as an inhibitory modulator of the Central Nervous System (CNS) associated with tiredness and drowsiness 24 – 29 . During exercise, circulating ADP/AMP/adenosine levels increase due to ATP hydrolysis 30 , 31 . However, there is still no substantial evidence on the role of adenosine in exercise-induced fatigue.…”

Section: Introductionmentioning

confidence: 99%

Neuronal adenosine A2A receptors signal ergogenic effects of caffeine

Aguiar

Speck

Canas

et al. 2020

Sci Rep

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Caffeine is one of the most used ergogenic aid for physical exercise and sports. However, its mechanism of action is still controversial. The adenosinergic hypothesis is promising due to the pharmacology of caffeine, a nonselective antagonist of adenosine A 1 and A 2A receptors. We now investigated A 2A R as a possible ergogenic mechanism through pharmacological and genetic inactivation. Forty-two adult females (20.0 ± 0.2 g) and 40 male mice (23.9 ± 0.4 g) from a global and forebrain A 2A R knockout (KO) colony ran an incremental exercise test with indirect calorimetry (Vȯ 2 and RER). We administered caffeine (15 mg/kg, i.p., nonselective) and SCH 58261 (1 mg/kg, i.p., selective A 2A R antagonist) 15 min before the open field and exercise tests. We also evaluated the estrous cycle and infrared temperature immediately at the end of the exercise test. Caffeine and SCH 58621 were psychostimulant. Moreover, Caffeine and SCH 58621 were ergogenic, that is, they increased Vȯ 2 max, running power, and critical power, showing that A 2A R antagonism is ergogenic. Furthermore, the ergogenic effects of caffeine were abrogated in global and forebrain A 2A R KO mice, showing that the antagonism of A 2A R in forebrain neurons is responsible for the ergogenic action of caffeine. Furthermore, caffeine modified the exercising metabolism in an A 2A R-dependent manner, and A 2A R was paramount for exercise thermoregulation. The natural plant alkaloid caffeine (1,3,7-trimethylxantine) is one of the most common ergogenic substances for physical activity practitioners and athletes 1-10. Caffeine increases endurance 1,8-12 , intermittent 7,13,14 and resistance 4,15 exercise in humans. In rodents, its ergogenic effects are conserved because caffeine increases running time on the treadmill at constant 16,17 and accelerated speeds 18,19. Sports sciences promote nonselective phosphodiesterase (PDE) inhibition 7,8 and increased calcium mobilization 2,7,8 as mechanisms for these ergogenic effects. However, the primary pharmacological effect of caffeine is the nonselective antagonism of adenosine A 1 and A 2A receptors (A 1 R, A 2A R) 20-23. Adenosine can act as an inhibitory modulator of the Central Nervous System (CNS) associated with tiredness and drowsiness 24-29. During exercise, circulating ADP/AMP/adenosine levels increase due to ATP hydrolysis 30,31. However, there is still no substantial evidence on the role of adenosine in exercise-induced fatigue. It is just known that the nonselective A 1 R and A 2A R agonist 5′-(N-ethylcarboxamido)adenosine (NECA), injected into the rat brain, abolishes the ergogenic effects of caffeine 16. Since there is increasing evidence that the adenosine modulation system critically controls allostasis 29 and A 2A R have a crucial role in the ability of caffeine to normalize brain function 30, we hypothesized that caffeine decreases fatigue during exercise through antagonism of A 2A R in the CNS. We combined the use of pharmacology (SCH 58261 and caffeine) and transgenic mice with tissue-selective deletion ...

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High-intensity intermittent exercise increases adenosine hydrolysis in platelets and lymphocytes and promotes platelet aggregation in futsal athletes

Cited by 18 publications

References 25 publications

Red Blood Cell Aging as a Homeostatic Response to Exercise-Induced Stress

Red Blood Cell Aging as a Homeostatic Response to Exercise-Induced Stress

Apamin Suppresses LPS-Induced Neuroinflammatory Responses by Regulating SK Channels and TLR4-Mediated Signaling Pathways

Neuronal adenosine A2A receptors signal ergogenic effects of caffeine

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