adaptive capacity
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The interval model training has been more recommended to promote aerobic adaptations due to recovery period that enables the execution of elevated intensity and as consequence, higher workload in relation to continuous training. However, the physiological and aerobic capacity adaptations in interval training with identical workload to continuous are still uncertain. The purpose was to characterize the effects of chronic and acute biomarkers adaptations and aerobic capacity in interval and continuous protocols with equivalent load. Fifty Wistar rats were divided in three groups: Continuous training (GTC), interval training (GTI) and control (CG). The running training lasted 8 weeks (wk) and was based at Anaerobic Threshold (AT) velocity. GTI showed glycogen super-compensation (mg/100 mg) 48 h after training session in relation to CG and GTC (GTI red gastrocnemius (RG)=1.41+/-0.16; GTI white gastrocnemius (WG)=1.78+/-0.20; GTI soleus (S)=0.26+/-0.01; GTI liver (L)=2.72+/-0.36; GTC RG=0.42+/-0.17; GTC WG=0.54+/-0.22; GTC S=0.100+/-0.01; GTC L=1.12+/-0.24; CG RG=0.32+/-0.05; CG WG=0.65+/-0.17; CG S=0.14+/-0.01; CG L=2.28+/-0.33). The volume performed by GTI was higher than GTC. The aerobic capacity reduced 11 % after experimental period in GTC when compared to GTI, but this change was insignificant (19.6+/-5.4 m/min; 17.7+/-2.5 m/min, effect size = 0.59). Free fatty acids and glucose concentration did not show statistical differences among the groups. Corticosterone concentration increased in acute condition for GTI and GTC. Testosterone concentration reduced 71 % in GTC immediately after the exercise in comparison to CG. The GTI allowed positive adaptations when compared to GTC in relation to: glycogen super-compensation, training volume performed and anabolic condition. However, the GTI not improved the aerobic performance.
- MeSH
- aerobióza fyziologie MeSH
- anaerobní práh fyziologie MeSH
- běh fyziologie MeSH
- fyziologická adaptace fyziologie MeSH
- glukosa metabolismus MeSH
- glykogen metabolismus MeSH
- játra fyziologie MeSH
- kondiční příprava zvířat fyziologie MeSH
- kortikosteron metabolismus MeSH
- kosterní svaly fyziologie MeSH
- krysa rodu rattus MeSH
- kyseliny mastné neesterifikované metabolismus MeSH
- potkani Wistar MeSH
- tělesná hmotnost fyziologie MeSH
- testosteron metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Warm-blooded animals such as birds and mammals are able to protect stable body temperature due to various thermogenic mechanisms. These processes can be facultative (occurring only under specific conditions, such as acute cold) and adaptive (adjusting their capacity according to long-term needs). They can represent a substantial part of overall energy expenditure and, therefore, affect energy balance. Classical mechanisms of facultative thermogenesis include shivering of skeletal muscles and (in mammals) non-shivering thermogenesis (NST) in brown adipose tissue (BAT), which depends on uncoupling protein 1 (UCP1). Existence of several alternative thermogenic mechanisms has been suggested. However, their relative contribution to overall heat production and the extent to which they are adaptive and facultative still needs to be better defined. Here we focus on comparison of NST in BAT with thermogenesis in skeletal muscles, including shivering and NST. We present indications that muscle NST may be adaptive but not facultative, unlike UCP1-dependent NST. Due to its slow regulation and low energy efficiency, reflecting in part the anatomical location, induction of muscle NST may counteract development of obesity more effectively than UCP1-dependent thermogenesis in BAT.
- MeSH
- chvění * fyziologie MeSH
- energetický metabolismus fyziologie MeSH
- fyziologická adaptace * fyziologie MeSH
- hnědá tuková tkáň * metabolismus MeSH
- kosterní svaly * metabolismus MeSH
- lidé MeSH
- obezita * metabolismus patofyziologie MeSH
- termogeneze * fyziologie MeSH
- uncoupling protein 1 metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
S krátkodobým nedostatkem pohybové aktivity se v průběhu života setká téměř každý. U pravidelně trénujících sportovců je důvodem nejčastěji akutní onemocnění nebo úraz. U nesportující populace souvisí omezení pohybové aktivity v jakémkoliv věku nejčastěji se zdravotními problémy, může však souviset i s nařízenými protipandemickými opatřeními, jak jsme nedávno zažili v souvislosti s celosvětovým bojem s pandemií COVID-19. Jako „detraining“ pak označujeme stav, který s takovýmto mimořádným omezením pohybové aktivity nastává. Projevuje se především úbytkem či ztrátou adaptačních schopností dosažených předchozím tréninkem, příp. předchozí běžnou každodenní pohybovou aktivitou. U sportovců dochází k poklesu výkonnosti, u průměrně zdatných osob k oslabení zdravotního stavu, vyžadujícího rekonvalescenci. U osob, které již dříve trpěly zdravotními potížemi, může „detraining“ vést ke ztrátě samostatnosti a prohloubení jejich křehkosti až k úplné závislosti na okolí. V prevenci těchto negativních důsledků je třeba jednak zkrátit období nutného omezení pohybu na minimum, ve stravě zajistit dostatek bílkovin, minimalizovat čas strávený na lůžku či sedavým způsobem a využívat v praxi online instruktáží, jak si zacvičit i v domácím prostředí. V opačném případě jen několik málo týdnů bez pohybu vede k velmi výraznému snížení tělesné kondice, projevující se zejména velmi významným poklesem kardiorespirační kapacity.
Almost everyone will experience a short-term lack of physical activity during their lifetime. In athletes who train regularly, the reason is most often an acute illness or injury. In the untrained population, restrictions on physical activity at any age are most often linked to health problems, but may also be related to anti-pandemic measures, as we have recently seen in the global fight against the COVID-19 pandemic. As "detraining" we mean a condition that occurs with such an extraordinary reducing of physical activity. It is manifested mainly by a decrease or loss of adaptive abilities, achieved by previous training or previous normal daily physical activity. In athletes there is a decrease in performance, in average fit people there is a weakening of the state of health, which requires convalescence. For people who have previously suffered from health problems, "detraining" can lead to loss of independence and deepening of their frailty to complete dependence on the environment. In the prevention of these negative consequences, it is necessary to reduce the period of restriction of movement to a minimum, ensure sufficient protein in the diet, minimize time spent in bed or sedentary and use online instruction on how to exercise at home. Otherwise, only a few weeks without optimal movement leads to a very significant reduction in physical condition, manifested in particular by a very significant decrease of adaptations earned from training especialy of cardiorespiratory capacity.
- Klíčová slova
- akutní nedostatek pohybu, detraining,
- MeSH
- COVID-19 MeSH
- hospitalizace MeSH
- imobilizace * škodlivé účinky MeSH
- kardiorespirační zdatnost MeSH
- lidé MeSH
- pohybová aktivita MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- přehledy MeSH
γδ T cells are considered to be innate-like lymphocytes that respond rapidly to stress without clonal selection and differentiation. Here we use next-generation sequencing to probe how this paradigm relates to human Vδ2neg T cells, implicated in responses to viral infection and cancer. The prevalent Vδ1 T cell receptor (TCR) repertoire is private and initially unfocused in cord blood, typically becoming strongly focused on a few high-frequency clonotypes by adulthood. Clonal expansions have differentiated from a naive to effector phenotype associated with CD27 downregulation, retaining proliferative capacity and TCR sensitivity, displaying increased cytotoxic markers and altered homing capabilities, and remaining relatively stable over time. Contrastingly, Vδ2+ T cells express semi-invariant TCRs, which are present at birth and shared between individuals. Human Vδ1+ T cells have therefore evolved a distinct biology from the Vδ2+ subset, involving a central, personalized role for the γδ TCR in directing a highly adaptive yet unconventional form of immune surveillance.
- MeSH
- antigeny CD27 metabolismus MeSH
- biologické markery metabolismus MeSH
- buněčná diferenciace MeSH
- buněčné klony cytologie MeSH
- CX3C chemokinový receptor 1 metabolismus MeSH
- cytotoxicita imunologická MeSH
- dárci tkání MeSH
- dospělí MeSH
- fenotyp MeSH
- genetická variace MeSH
- hypervariabilní oblasti genetika MeSH
- imunitní dozor * MeSH
- interleukin-15 farmakologie MeSH
- lidé MeSH
- proliferace buněk MeSH
- receptory antigenů T-buněk gama-delta metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
We are facing a revival of the strategy to counteract obesity and associated metabolic disorders by inducing thermogenesis mediated by mitochondrial uncoupling protein-1 (UCP1). Thus, the main focus is on the adaptive non-shivering thermogenesis occurring both in the typical depots of brown adipose tissue (BAT) and in UCP1-containing cells that could be induced in white adipose tissue (WAT). Because contribution of WAT to resting metabolic rate is relatively small, the possibility to reduce adiposity by enhancing energy expenditure in classical white adipocytes is largely neglected. However, several pieces of evidence support a notion that induction of energy expenditure based on oxidation of fatty acids (FA) in WAT may be beneficial for health, namely: (i) studies in both humans and rodents document negative association between oxidative capacity of mitochondria in WAT and obesity; (ii) pharmacological activation of AMPK in rats as well as cold-acclimation of UCP1-ablated mice results in obesity resistance associated with increased oxidative capacity in WAT; and (iii) combined intervention using long-chain n-3 polyunsaturated FA (omega 3) and mild calorie restriction exerted synergism in the prevention of obesity in mice fed a high-fat diet; this was associated with strong hypolipidemic and insulin-sensitizing effects, as well as prevention of inflammation, and synergistic induction of mitochondrial oxidative phosphorylation (OXPHOS) and FA oxidation, specifically in epididymal WAT. Importantly, these changes occurred without induction of UCP1 and suggested the involvement of: (i) futile substrate cycle in white adipocytes, which is based on lipolysis of intracellular triacylglycerols and re-esterification of FA, in association with the induction of mitochondrial OXPHOS capacity, β-oxidation, and energy expenditure; (ii) endogenous lipid mediators (namely endocannabinoids, eicosanoids, prostanoids, resolvins, and protectins) and their cognate receptors; and (iii) AMP-activated protein kinase in WAT. Quantitatively, the strong induction of FA oxidation in WAT in response to the combined intervention is similar to that observed in the transgenic mice rendered resistant to obesity by ectopic expression of UCP1 in WAT. The induction of UCP1-independent FA oxidation and energy expenditure in WAT in response to the above physiological stimuli could underlie the amelioration of obesity and low-grade WAT inflammation, and it could reduce the release of FA from adipose tissue and counteract harmful consequences of lipid accumulation in other tissues. In this respect, new combination treatments may be designed using naturally occurring micronutrients (e.g. omega 3), reduced calorie intake or pharmaceuticals, exerting synergism in the induction of the mitochondrial OXPHOS capacity and stimulation of lipid catabolism in white adipocytes, and improving metabolic flexibility of WAT. The role of mutual interactions between adipocytes and immune cells contained in WAT in tissue metabolism should be better characterised. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.
- MeSH
- bílá tuková tkáň cytologie metabolismus MeSH
- energetický metabolismus * MeSH
- fenotyp MeSH
- iontové kanály metabolismus MeSH
- krysa rodu rattus MeSH
- lidé MeSH
- metabolismus lipidů * MeSH
- mitochondriální proteiny metabolismus MeSH
- mitochondrie fyziologie MeSH
- myši MeSH
- oxidační stres MeSH
- oxidativní fosforylace * MeSH
- signální transdukce MeSH
- tukové buňky cytologie metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
