Svalové křeče asociované s fyzickou zátěží jsou poměrně častým, naštěstí však většinou nezávažným, problémem sportujících jedinců. Dlouho byly přikládány dehydrataci a depleci elektrolytů, nicméně síla důkazů pro toto tvrzení je slabá. V současnosti se odborná veřejnost přiklání k neurogenní etiologii tohoto fenoménu, která ovšem neobjasňuje tento fenomén v celé jeho šíři. Předkládáme přehled současného odborného povědomí o patofyziologii a managementu svalových křečí při fyzické zátěži.
Exercise associated muscle cramps are quite often problem of sporting individuals, fortunately mostly not serious one. Dehydration and electrolyte depletion were considered as the cause for a long time, nevertheless scientific evidence for this etiology is weak. Nowadays the neurogenic nature of exercise associated muscle cramps is widely accepted, but this explanation does not elucidate this phenomenon completely. We present a state of the art in pathophysiology and management of exercise associated muscle cramps.
- MeSH
- lidé MeSH
- sportovci MeSH
- sporty MeSH
- svalové křeče * etiologie patofyziologie prevence a kontrola MeSH
- tělesná námaha MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- přehledy MeSH
Novel strategies are needed that can stimulate endogenous signaling pathways to protect the heart from myocardial infarction. The present study tested the hypothesis that appropriate regimen of cold acclimation (CA) may provide a promising approach for improving myocardial resistance to ischemia/reperfusion (I/R) injury without negative side effects. We evaluated myocardial I/R injury, mitochondrial swelling, and β-adrenergic receptor (β-AR)-adenylyl cyclase-mediated signaling. Male Wistar rats were exposed to CA (8°C, 8 h/day for a week, followed by 4 wk at 8°C for 24 h/day), while the recovery group (CAR) was kept at 24°C for an additional 2 wk. The myocardial infarction induced by coronary occlusion for 20 min followed by 3-h reperfusion was reduced from 56% in controls to 30% and 23% after CA and CAR, respectively. In line, the rate of mitochondrial swelling at 200 μM Ca2+ was decreased in both groups. Acute administration of metoprolol decreased infarction in control group and did not affect the CA-elicited cardiprotection. Accordingly, neither β1-AR-Gsα-adenylyl cyclase signaling, stimulated with specific ligands, nor p-PKA/PKA ratios were affected after CA or CAR. Importantly, Western blot and immunofluorescence analyses revealed β2- and β3-AR protein enrichment in membranes in both experimental groups. We conclude that gradual cold acclimation results in a persisting increase of myocardial resistance to I/R injury without hypertension and hypertrophy. The cardioprotective phenotype is associated with unaltered adenylyl cyclase signaling and increased mitochondrial resistance to Ca2+-overload. The potential role of upregulated β2/β3-AR pathways remains to be elucidated.NEW & NOTEWORTHY We present a new model of mild gradual cold acclimation increasing tolerance to myocardial ischemia/reperfusion injury without hypertension and hypertrophy. Cardioprotective phenotype is accompanied by unaltered adenylyl cyclase signaling and increased mitochondrial resistance to Ca2+-overload. The potential role of upregulated β2/β3-adrenoreceptor activation is considered. These findings may stimulate the development of novel preventive and therapeutic strategies against myocardial ischemia/reperfusion injury.
- Publikační typ
- abstrakt z konference MeSH
