The Neuroendocrinology of Stress: A Never Ending Story

Journal of Neuroendocrinology, Journal Year: 2008, Volume and Issue: 20(6), P. 880 - 884

Published: June 1, 2008

Evolutionary success depends on our ability to adapt changing circumstances. The neuroendocrine response stress is an excellent example of a plastic system that responds threats homeostasis and alters its output meet current expected future demands. At the level hypothalamus, corticotroph secretagogues corticotrophin‐releasing hormone (CRH) arginine vasopressin (AVP) respond rapidly acute stressor but, following chronic stress, they with reduction CRH but major increase in AVP. release AVP activates pro‐opiomelanocortin anterior pituitary cells adrenocorticotrophic into peripheral blood from where it targets receptors adrenal cortex glucocorticoid hormones. These hormones (i.e. corticosterone rat cortisol man) are released pulsatile ultradian pattern which defines normal circadian rhythm. frequency pulses increased under states rats genetically determined hyper‐responsiveness hypothalamic‐pituitary‐adrenal axis. Interestingly, neonatal influences can also programme alterations rhythmicity, implicating epigenetic factors regulation. tissue receptors, alteration rhythm has differential effects mineralocorticoid receptor (GR) binding DNA offers mechanism for specific responses altered dynamics. experience not only seen at GR regulation, evident behavioural responsiveness brain stem serotonergic pathways, as measured by tryptophan hydroxylase mRNA stem.

Language: Английский

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Muscle fatigue: what, why and how it influences muscle function

The Journal of Physiology, Journal Year: 2007, Volume and Issue: 586(1), P. 11 - 23

Published: Aug. 17, 2007

Much is known about the physiological impairments that can cause muscle fatigue. It fatigue be caused by many different mechanisms, ranging from accumulation of metabolites within fibres to generation an inadequate motor command in cortex, and there no global mechanism responsible for Rather, mechanisms are specific task being performed. The development typically quantified as a decline maximal force or power capacity muscle, which means submaximal contractions sustained after onset There even evidence duration some tasks not limited principal muscles. Here we review experimental approaches focus on identifying limit failure rather than those Selected comparisons tasks, groups individuals interventions with task-failure approach provide insight into rate-limiting adjustments constrain function during fatiguing contractions.

Language: Английский

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Mental fatigue impairs physical performance in humans

Journal of Applied Physiology, Journal Year: 2009, Volume and Issue: 106(3), P. 857 - 864

Published: Jan. 9, 2009

Mental fatigue is a psychobiological state caused by prolonged periods of demanding cognitive activity. Although the impact mental on and skilled performance well known, its effect physical has not been thoroughly investigated. In this randomized crossover study, 16 subjects cycled to exhaustion at 80% their peak power output after 90 min task (mental fatigue) or watching emotionally neutral documentaries (control). After experimental treatment, mood questionnaire revealed (P = 0.005) that significantly reduced time (640 +/- 316 s) compared with control condition (754 339 0.003). This negative was mediated cardiorespiratory musculoenergetic factors as physiological responses intense exercise remained largely unaffected. Self-reported success intrinsic motivation related were also unaffected prior However, mentally fatigued rated perception effort during be higher 0.007). As ratings perceived exertion increased similarly over in both conditions < 0.001), reached maximal level disengaged from earlier than condition. conclusion, our study provides evidence limits tolerance humans through rather mechanisms. Future research area should investigate common neurocognitive resources shared

Language: Английский

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Physical and metabolic demands of training and match-play in the elite football player

Journal of Sports Sciences, Journal Year: 2006, Volume and Issue: 24(7), P. 665 - 674

Published: May 5, 2006

In soccer, the players perform intermittent work. Despite performing low-intensity activities for more than 70% of game, heart rate and body temperature measurements suggest that average oxygen uptake elite soccer is around maximum (VO(2max). This may be partly explained by 150 - 250 brief intense actions a top-class player performs during which also indicates rates creatine phosphate (CP) utilization glycolysis are frequently high game. Muscle glycogen probably most important substrate energy production, fatigue towards end game related to depletion in some muscle fibres. Blood free-fatty acids (FFAs) increase progressively compensating progressive lowering glycogen. Fatigue occurs temporarily matches, but it still unclear what causes reduced ability maximally. There major individual differences physical demands capacity tactical role team. These should taken into account when planning training nutritional strategies players, who require significant intake week.

Language: Английский

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Exertional Heat Illness during Training and Competition

Medicine & Science in Sports & Exercise, Journal Year: 2007, Volume and Issue: 39(3), P. 556 - 572

Published: March 1, 2007

SUMMARY Exertional heat illness can affect athletes during high-intensity or long-duration exercise and result in withdrawal from activity collapse soon after activity. These maladies include associated muscle cramping, exhaustion, exertional heatstroke. While certain individuals are more prone to exhaustion the (i.e., not acclimatized, using medications, dehydrated, recently ill), heatstroke (EHS) seemingly healthy even when environment is relatively cool. EHS defined as a rectal temperature greater than 40°C accompanied by symptoms signs of organ system failure, most frequently central nervous dysfunction. Early recognition rapid cooling reduce both morbidity mortality with EHS. The clinical changes be subtle easy miss if coaches, medical personnel, do maintain high level awareness monitor at-risk closely. Fatigue occur rapidly stress increases common causes hot conditions. When conditions, term often applied. In some cases, only discernable difference between severe on-site evaluations. Heat will generally resolve symptomatic care oral fluid support. Exercise cramping exhaustive work any range, but appears prevalent humid Muscle usually responds rest replacement salt (sodium). Prevention strategies essential reducing incidence EHS, cramping. INTRODUCTION This document replaces, part, 1996 Position Stand titled "Heat Cold Illnesses Distance Running" (9) considers selected related conditions (EHS, cramping) that may active people warm environments. recommendations intended heat-related physical activity, individual physiologic responses daily health status variable, so compliance these guarantee protection. occurs world wide prolonged intense almost every venue (e.g., cycling, running races, American football, soccer). (1,27,62,64,65,109,132,154,160,164) (54,71,149,150) hot-humid cool (133). cramps typically involve excessive hyperthermia, rather fatigue, body water and/or electrolyte depletion, regulatory fail face exhaustion. address recognition, treatment, reduction for does anesthesia-induced malignant sunburn, anhidrotic sweat gland disorders classified other disease categories, because solely exposure. Hyponatremia also intake addressed ACSM Fluid Replacement Stand. Evidence statements this based on strength scientific evidence regard outcomes. Because research ethics preclude use human subjects study illnesses, employs following criteria: A, recommendation consistent good-quality patient- subject-oriented evidence; B, inconsistent limited-quality C, consensus, usual practice, opinion, disease-oriented evidence, case series studies diagnosis, prevention, screening. General Background: Exhaustion, Hyperthermia, Dehydration Exhaustion response inability continue heavy exertion all ranges. As ambient beyond 20°C (68°F) rises, time decreases (58). From perspective it difficult distinguish those who must stopped due likely triggered combination hyperthermia-induced peripheral activation decreased (brain fatigue) (110,118), hydration level, effect hyperthermia depletion energy stores, imbalance, factors. Some central, spinal cord, factor into etiology activity; exact mechanisms have yet explained (90,114-116,171). exercise-related an extension phenomenon, pronounced, stores faster hotter especially acclimatized (71). results collapse, syndrome referred environments, postexercise postural hypotension leg elevation less 30 min. There several variables including duration intensity exercise, environmental acclimatization exercise-heat stress, innate capacity (V˙O2max), conditioning, status, personal factors like supplements, sleep, recent illness. at fixed load, groups show decrease (time exhaustion) increase perceived relative humidity total decreases. combined effects dehydration performance degree either alone. Compared moderate athlete slow pace avoid risk before task completed. statement. reduces endurance performance, storage (11,12,16,41,57,141). category A. core above (104°F) (71,85,86,149,150), athletic recreational influenced intensity, clothing, equipment, Hyperthermia muscle-generated accumulates dissipates via increased sweating skin blood flow (3). production 15-20 times rest, raise 1°C (1.8°F) 5 min no removed (105). Prolonged lead life-threatening condition rate promptly recognized treated cooling. removal controlled (CNS) centers hypothalamus organs. functional requires gradient shell. If remains constant, augmenting removal. shell rises internal production, lost dissipation) increases. Wide variations tolerance exist among athletes. extent which elevated below diminishes contributes (110) unknown, there considerable attrition temperatures reach 39-40°C (144). laboratory studies, precooling extend preheating shorten circumstances tend terminate fatigue about (61). years, importance has been investigated. shown brain always higher hyperthermic compared control (119). Also, 37 cerebral maximal voluntary muscular force output concurrent wave (110,118). Brain explain why exercising while others able override controls push themselves strenuously develop It unusual experience without noticeable impairment, competition. Elevated up 41.9°C (107.4°F) noted soccer players, football lineman, road runners, marathoners (21,42,46,98,125,129,130,132,161,165,176). significant tolerate well widely accepted threshold >40°C obvious sequelae (71,85,86,104,149,150). environments participants lose considerably replaced (3,72,126). deficits exceed 3-5% weight, begin decline (19) dissipation. Water 6-10% weight weather, clinically losses sodium (Na+) chloride (Cl−) (25,45,71,100,102,155,173) decreasing cardiac output, (12,41,57,71,101,141,142). direct cramps) indirect heatstroke) (10). Excessive loss, implicated loss hyponatremia (>8 h) events heat. one illustrating cumulative affects male soldier (32 yr, 180 cm, 110.47 kg, 41.4 mL·kg−1·min−1) participating monitored, multiday, regimen 41.2°C (106.0°F), 39% RH was asymptomatic 38.3-38.9°C days 3-7 (16). morning day 8, he 5.4 kg (4.8%) had baseline heart rate, 6 7. On developed weakness, abdominal cramps, vomiting 39.6°C (103.3°F). His endorphin cortisol levels were 2 greater, respectively, indicating intolerance. Thirteen males maintained near their prestudy completed protocol incident. day-to-day tolerance, should monitored humans levels, splanchnic skeletal provide plasma glucose, remove heat, metabolic products working muscles (70). distribution increase, compensatory vasoconstriction vascular resistance worsens insufficiency (71,84). reproduced rat model supports assertion plays role (70,73,84). mechanism partially explains where cool, vasoconstricted helps filling mean arterial pressure, prolongs How evolve, what sequence, completely understood (106). dehydration, unaffected, discontinue stressful path leads assumed pass through however anecdotal data seem refute notion fresh 30-60 racing hot, real then transition very short. protective that, once stopped, developing stroke reduced exercise-induced dissipation A program prudent along acclimatization, improved cardiorespiratory fitness, reasonable problems. field changes. B. EXERTIONAL HEAT ILLNESSES Heatstroke Etiology. (core >40°C) disturbances multiple failure. produced outpaces transfer surroundings, disrupt function. Almost patients exhibit sweat-soaked pale opposed dry, flushed described presentation non-exertion-related (classic) (162). Predisposing Although strenuous environment, lack poor fitness primary leading highly trained heat-acclimatized inadequate (18,34,71). greatest exists wet bulb globe (WBGT) exceeds 28°C (82°F) (20,81,156) (>75% V˙O2max) lasts longer 1 h outlined "Monitoring Environment." (8-18°C [45-65°F]) (18-28°C [65-82°F]) (14,56,132,133), suggesting susceptibility (14,22,55,56,66) incomplete temporary viral medications (81,133). Ten 14 training improve C. substantially stressors such sudden training, lengthy initial exposure vapor barrier sleep deprivation (14), hydration, nutrition. previous raises overnight (14,168). Over-the-counter drugs nutritional supplements containing ephedrine, synephrine, ma huang sympathomimetic compounds (23,121), require verification cause trials. Appropriate ingestion minimizes (46,60). However, absence fast generates (18,34,165). Skin miliaria rubra), alcohol use, drug abuse ecstasy), antidepressant (69), obesity, age >40 genetic predisposition history linked (14,55,85,150). Athletes they fever, respiratory infection, diarrhea, (14,81). 179 casualties 14-km race over 9 yr showed 23% reported gastrointestinal (128). similar 10 military three fever six recalled least warning sign impending prior (14). 4 d preseason players takes place hottest summer fit. emphasizes gradually introducing induce carefully monitoring behavior practices, selectively modifying duration, periods) high-risk Three influence early season players: (a) failure coaches adjust practice current advice sports medicine staff; (b) unfit unacclimatized practicing intensely heat; (c) equipment introduced acclimatization. One cases (14) eight incidents occurred group 12.1-13.8 km·h−1 ≥25°C (77°F), host altered occurred. lowest aerobic power V˙O2max ≤ 40 (14,64,96). To group, fit function intensities group's end run V˙O2max. Air runners pack. More reports males, hypotheses advanced First, men simply situations combat football). Second, predisposed gender-specific hormonal, physiological, psychological, morphological mass, surface area-to-mass ratio) differences. Women, however, immune disorder, number women rise participation sports. EHS: low deprivation, dysfunction, illness, medications. Physical Pathophysiology. underlying pathophysiology tissue critical cell membranes damaged, systems disrupted, giving characteristic (56,149). heated its thermal 40°C), cascade disrupts volume, metabolism, acid-base balance, membrane permeability initially dysfunction finally death (71,91,175). complex variable onset brain, cardiac, renal, gastrointestinal, hematologic, patients. multisystem directly area degree-minutes under vs. graph length required organs <40°C (14,20,47,48). Tissue thresholds elevation, peak temperature, determine injury (72). initiated cognitive return normal range within hour symptoms, recover fully (47,48). victims cooled immediately theoretically 60°C·min (120°F·min; curve) 40.5°C lasting (see Fig. 1). Conversely, go unrecognized quickly, 40.5°C, mortality. Outcomes 20 "light" 16 "severe" (150) coma brief light limited <1 h, despite involvement confirmed serum liver enzymes (74,172). Severe moribund admission died evident damage (150). initiation therapy (14,20,47,48).FIGURE 1: Cooling curves late interventions. intervention curve (the dashed line) approximately 60 (cooling 50 min) >145. prognosis poor. delayed stoke evaluation transported initiated. arrow marks start intervention.Hyperthermia suppresses function, reversible cooling, demonstrated echocardiography Cardiac oxygen delivery tissues, transport deep tissues skin. accelerates hypoxia, acidosis heating begins hypothalamic disrupting regulation pressure flow. Interestingly, "lifesaving," stopping allows triggers therapy. stimulates muscle. During effort, example, 80-85% distributed (139). thermoregulatory vasodilatation cutaneous beds augment regulates intestinal limits exchange gut promotes bowel ischemia. Gut breakdown lipopolysaccharide fragments gram-negative bacteria leak systemic circulation, increasing endotoxic shock. accentuate GI tract speed process. Rhabdomyolysis, fibers, 40°C). eccentric concentric overuse rhabdomyolysis, earlier (71,74). decomposes membranes, myoglobin released renal tubular toxicity obstruction inadequate. Intracellular potassium extracellular space, potentially inducing arrhythmias. Heating suppress acute worsened sustained hypotension, crystallization myoglobin, disseminated intravascular coagulation, (31,70,153). Incidence. varies event rising humidity. Limited regarding activities. fatal outcomes press, reporting non unless involves profile rare strikes "at random" four 350,000 1995 2002 (131). Fatal air 26-30°C (78-86°F) 50-80% (87). observed activities continuous, exercise. Twin Cities Marathon, averages per 10,000 finishers (136); WBGT rises. contrast, popular 11.5-km race, staged (WBGT 21-27°C), 10-20 entrants (18,34). same course, (A Crago, M.D., communication). Such burdens suggests scheduled safest runners. Recognition. Immediate paramount survival (68). appearance depends (14,48,71,81,150). nonspecific disorientation, confusion, dizziness, irrational behavior, inappropriate comments, irritability, headache, walk, balance resulting profound hyperventilation, vomiting, delirium, seizures, coma. Thus, change personality trigger assessment collision mistaken concussion; nonathletes, misdiagnosed psychosis. estimate vital establishing measured collapses exhibits Ear (aural canal tympanic membrane), oral, temporal artery, axillary measurements used diagnose spuriously lowered air, skin, liquids contact (18,134,135). Oral affected swallowing, cold liquids, fanning (33,151). At systolic <100 mm Hg, tachycardia, shocklike sweaty, skin) common. aural), temporal, clumsiness, stumbling, nausea, apathy, impairment consciousness (71,85,149,161). Treatment. emergency immediate whole satisfactory outcome (14,44,48,72,82,85,120,132,149). and, complications, evacuation hospita

Language: Английский

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Neurobiology of Exercise

Obesity, Journal Year: 2006, Volume and Issue: 14(3), P. 345 - 356

Published: March 1, 2006

Abstract Voluntary physical activity and exercise training can favorably influence brain plasticity by facilitating neurogenerative, neuroadaptive, neuroprotective processes. At least some of the processes are mediated neurotrophic factors. Motor skill regular enhance executive functions cognition types learning, including motor learning in spinal cord. These adaptations central nervous system have implications for prevention treatment obesity, cancer, depression, decline associated with aging, neurological disorders such as Parkinson's disease, Alzheimer's dementia, ischemic stroke, head cord injury. Chronic voluntary also attenuates neural responses to stress circuits responsible regulating peripheral sympathetic activity, suggesting constraint on that could plausibly contribute reductions clinical hypertension, heart failure, oxidative stress, suppression immunity. Mechanisms explaining these not yet known, but metabolic neurochemical pathways among skeletal muscle, cord, offer plausible, testable mechanisms might help explain effects system.

Language: Английский

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Monocarboxylate transporters in the central nervous system: distribution, regulation and function

Journal of Neurochemistry, Journal Year: 2005, Volume and Issue: 94(1), P. 1 - 14

Published: June 10, 2005

Abstract Monocarboxylate transporters (MCTs) are proton‐linked membrane carriers involved in the transport of monocarboxylates such as lactate, pyruvate, well ketone bodies. They belong to a larger family composed 14 members mammals based on sequence homologies. MCTs found various tissues including brain where three isoforms, MCT1, MCT2 and MCT4, have been described. Each these isoforms exhibits distinct regional cellular distribution rodent brain. At level, MCT1 is expressed by endothelial cells microvessels, ependymocytes astrocytes. MCT4 expression appears be specific for By contrast, predominant neuronal monocarboxylate transporter MCT2. Interestingly, part immunoreactivity located at postsynaptic sites, suggesting particular role their synaptic transmission. In addition variation during development upon nutritional modifications, new data indicate that MCT regulated translational level neurotransmitters. Understanding how could importance not only neuroenergetics but also areas functional imaging, regulation food intake glucose homeostasis, or central nervous system disorders ischaemia neurodegenerative diseases.

Language: Английский

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Climate Econometrics

Annual Review of Resource Economics, Journal Year: 2016, Volume and Issue: 8(1), P. 43 - 75

Published: Aug. 19, 2016

Identifying the effect of climate on societies is central to understanding historical economic development, designing modern policies that react climatic events, and managing future global change. Here, I review, synthesize, interpret recent advances in methods used measure effects social outcomes. Because weather variation plays a large role progress, formalize relationship between from an econometric perspective discuss use these two factors as identifying variation, highlighting trade-offs key assumptions different research designs deriving conditions when exactly identifies climate. then describe advances, such parameterization variables perspective, nonlinear models with spatial temporal displacement, characterization uncertainty, measurement adaptation, cross-study comparison, empirical estimates project impact conclude by discussing remaining methodological challenges.

Language: Английский

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Central Fatigue

Sports Medicine, Journal Year: 2006, Volume and Issue: 36(10), P. 881 - 909

Published: Jan. 1, 2006

Language: Английский

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Opioid‐mediated muscle afferents inhibit central motor drive and limit peripheral muscle fatigue development in humans

The Journal of Physiology, Journal Year: 2008, Volume and Issue: 587(1), P. 271 - 283

Published: Nov. 18, 2008

We investigated the role of somatosensory feedback from locomotor muscles on central motor drive (CMD) and development peripheral fatigue during high-intensity endurance exercise. In a double-blind, placebo-controlled design, eight cyclists randomly performed three 5 km time trials: control, interspinous ligament injection saline (5K(Plac), L3-L4) or intrathecal fentanyl (5K(Fent), to impair cortical projection opioid-mediated muscle afferents. Peripheral quadriceps was assessed via changes in force output pre- versus postexercise response supramaximal magnetic femoral nerve stimulation (DeltaQ(tw)). The CMD trials estimated electromyogram (iEMG). Fentanyl had no effect strength. Impairment neural increased iEMG first 2.5 5K(Fent) 5K(Plac) by 12 +/- 3% (P < 0.05); second km, similar between trials. Power also 6 2% higher 11 lower (both P 0.05). Capillary blood lactate (16.3 0.5 12.6 1.0%) arterial haemoglobin O(2) saturation (89 1 94 1%) 5K(Plac). Exercise-induced DeltaQ(tw) greater following (-46 2 -33 2%, 0.001). Our results emphasize critical working centrally mediated determination CMD. Attenuated afferent exercising an overshoot power normally chosen athlete, thereby causing rate accumulation metabolites excessive fatigue.

Language: Английский

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