Kategoriarkiv: Forskning og artikler

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Changes in inflammatory mediators following eccentric exercise of the elbow flexors.

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Nevner hvordan forskjellige inflammasjonsmarkører ikke stemmer nevneverdig godt overens med progresjonen av stølhet. Den nevner også noe veldig interessant om at det er IL-10, som er en anti-inflammatorisk cytokin, som gjør at vi tilpasses treningen siden den øker betraktelig ved «repeated bouts of training».

(Hirose et.al. 2004) http://www.ncbi.nlm.nih.gov/pubmed/15633588

Abstract

The aims of this study were to examine the plasma concentrations of inflammatory mediators including cytokines induced by a single bout of eccentric exercise and again 4 weeks later by a second bout of eccentric exercise of the same muscle group. Ten untrained male subjects performed two bouts of the eccentric exercise involving the elbow flexors (6 sets of 5 repetitions) separated by four weeks. Changes in muscle soreness, swelling, and function following exercise were compared between the bouts. Blood was sampled before, immediately after, 1 h, 3 h, 6 h, 24 h (1 d), 48 h (2 d), 72 h (3 d), 96 h (4 d) following exercise bout to measure plasma creatine kinase (CK) activity, plasma concentrations of myoglobin (Mb), interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1ra), IL-4, IL-6, IL-8, IL-10, IL-12p40, tumor necrosis factor (TNF)-alpha, granulocyte colony-stimulating factor (G-CSF), myeloperoxidase (MPO), prostaglandin E2 (PGE2), heat shock protein (HSP) 60 and 70. After the first bout, muscle soreness increased significantly, and there was also significant increase in upper arm circumference; muscle function decreased and plasma CK activity and Mb concentration increased significantly. These changes were significantly smaller after the second bout compared to the first bout, indicating muscle adaptation to the repeated bouts of the eccentric exercise. Despite the evidence of greater muscle damage after the first bout, the changes in cytokines and other inflammatory mediators were quite minor, and considerably smaller than that following endurance exercise. These results suggest that eccentric exercise-induced muscle damage is not associated with the significant release of cytokines into the systemic circulation. After the first bout, plasma G-CSF concentration showed a small but significant increase, whereas TNF-alpha and IL-8 showed significant decreases compared to the pre-exercise values. After the second bout, there was a significant increase in IL-10, and a significant decrease in IL-8. In conclusion, although there was evidence of severe muscle damage after the eccentric exercise, this muscle damage was not accompanied by any large changes in plasma cytokine concentrations. The minor changes in systemic cytokine concentration found in this study might reflect more rapid clearance from the circulation, or a lack of any significant metabolic or oxidative demands during this particular mode of exercise. In relation to the adaptation to the muscle damage, the anti-inflammatory cytokine IL-10 might work as one of the underlying mechanisms of action.

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The evolutionary origin of form and function

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Spennende studie som nevner at gener har lite med utvikling av organismer å gjøre. Det er heller «the second law of thermodynamics» som styrer det.

In summary, we propose that the life process is based not on genetic variation, but on the second law of thermodynamics (hereinafter the second law) and the principle of least action, as proposed for thermodynamically open systems by De Maupertuis (Ville et al. 2008), which at the most fundamental level say the same thing.

Det som avgjør om en organisme er levedyktig eller ikke er dens evne til å hente energi fra omgivelsene. For oss kan dette peke på jo mer effektiv blodsirkulasjonens distribusjon av oksygen til cellene er, jo mer fri energi har vi tilgjengelig.

In this reformulation form and function, extant and extinct, are the consequence of natural selection acting primarily upon the ability of organisms to extract energy (nutrient) from their environment, as pointed out in 1835, prior to the publication of Origin, by Edward Blyth (Blyth, 1835).

De reformulerer også definisjonen på entropi, som vanligvis er sett på som kaos. Her sier de at det egentlig bør oppfattes som en organisert kompleksitet fordi den bundede energien i lavere livsformer er tilgjengelig som fri energi for høyere livsformer. Det er fullt mulig dette kan forståes i sammenheng med mitokondrias funksjon for oss. Energien som mitokondria skaper blir tilgjengelig som fri energi for oss.

Energy, in the form of nutrient, is consumed, thereby producing entropy, according to the second law in the most efficient way (least action) possible given the conditions. Under these circumstances, explicitly thermodynamically open systems, entropy is maximised in the form of organisation or complexity (Sharma & Annila, 2007) and not, as proposed by Boltzmann, disorder (Sharma & Annila2007). In terms of the food chain, the entropy (bound energy) of lower forms is available as free energy (nutrient) for higher forms.

Gener fungerer bare som en blueprint for de erfaringene molekyler og celler gjør seg med omgivelsene. Genene er notisblokken.

We predicate the current proposal on a metabolism-first origin of life (Baverstock, 2013), in which proteins, free of DNA, were a form of proto-life. Life appeared when these proto-life forms recruited nucleic acids in the form of DNA to act as a template for replication and to code for essential peptides (Annila & Baverstock, 2014) through the process of reverse translation making it possible for true replication to occur.

Sett i lys av dette kan vi innse at gen-mutasjon har lite å gjøre med evolusjon.

In other words mutation of existing coding sequences is unnecessary for evolution to have taken place – that is not to say that evolution has not taken advantage of mutational events, but that genetic variation is not rate limiting.

De forklarer også hvorfor f.eks. en mus og et menneske har nesten helt samme genuttykk, men helt forskjellig form og funksjon.

Thus, for example, mouse and man are phenotypically distinct organisms with closely similar genotypes (Baverstock, 2011), that is, a near identical complement of peptides, which give rise through dissipative information generating processes within the cell, to two distinct information outputs (phenotypes).

De konkluderer med at utvikling skjer ved at en organisme utvikler bedre måter å tilegne seg energi fra omgivelsene på. F.eks. kan mitokontria, respirasjonssystemet, sirkulasjonssystemet og nervesystemet være funksjoner som gir bedre tilegning og utnyttelse av energi i en organisme slik vi er. 

The evolution of multicellular organisms with complex forms and functional abilities can be accounted for based on a fundamental tenet underpinned by the second law of thermodynamics, with natural selection acting on the ability of the organism to transduct energy (nutrient) most efficiently from its ecosystem by deploying that form and those functions.

http://onlinelibrary.wiley.com/enhanced/doi/10.1113/jphysiol.2014.271775/

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RR interval-respiratory signal waveform modeling in human slow paced and spontaneous breathing.

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Enda en bekreftelse på at pusten påvirker vagusnerven, og vagusnerven påvirker betennelser. Og at 0,1Hz (6 pust i minuttet) gir sterkest påvirkning på vagusnerven.

http://www.ncbi.nlm.nih.gov/pubmed/25139803/

Denne studien var en datamodell av hvordan forskjellige elementer av pusten (dybde og hastighet i dette tilfellet) påvirker hjerterytmen, som uttrykker vagusnerven. De fant at pustefrekvensen påvirket mest, altså hastigheten i dette tilfellet. 

The model’s results depended on breathing frequency with the least error occurring during slow paced breathing.

Deres forklaring på hvorfor pusten påvirker hjerterytmen er at strekk-reseptorer i lungene sier ifra om lungevolum som hjernen så bruker til å vurdere kardiovagale (vagusnervens påvirkning på hjertet) signaler.

Assuming that a0 represents slowly adapting pulmonary stretch receptors (SARs) and a1 SARs in coordination with other stretch receptors and central integrative coupling; then pulmonary stretch receptors relaying the instantaneous lung volume are the major factor determining cardiovagal output during inspiration.

De sier at ved forskjellige sykdommer blir det dårligere forbindelse mellom blodstrømning, blodtrykk, hjerterytme og pust, som gir ustabil kardivagal styring.

The role of vagal afferent neurons in cardiorespiratory coupling may relate to neurocardiovascular diseases in which weakened coupling among venous return, arterial pressure, heart rate and respiration produces cardiovagal instability.

Dette kan bidra til saktere, eller manglende, helbredelse av sykdom. Når man lærer å bruke pusten til å styrke vagusnerven er man i det minste én faktor nærmere helbredelse.

 

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Immediate effects of breathing re-education on respiratory function and range of motion in chronic neck pain.

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Å lære seg å bruke riktige pustemuskler gir mindre muskelspenninger og bedre bevegelighet i nakken. Om diafragma, den viktigste pustemuskelen, er svak eller på en eller annen måte ikke blir brukt nok, vil nakkemusker ta over store deler av pustefunksjonen. Dette kan være grunnlag til mange plager i nakken.

I denne studien gjorde 36 mennesker 30 minutter pustetrening. Smertenivåer og muskelspenninger ble redusert, og bevegelse i brystkassen og i nakken ble økt. 

Med enkle øvelser kan man få store resultater. Kun 30 minutter er nok! Om man gjør øvelser hver dag og diafragma blir sterke så trengs det mye mindre tid også.

http://www.ncbi.nlm.nih.gov/pubmed/25141528/

CONCLUSION:

Breathing re-education can change breathing patterns and increase chest expansion. This change leads to an improvement in CROM Positive consequences may result from the improvement in diaphragm contraction or reduced activity of accessory muscles.

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Effect of graded hypoxia on supraspinal contributions to fatigue with unilateral knee-extensor contractions.

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Og denne som nevner at det er hypoxi (lavt oksygennivå) som bidrar mest til «central fatigue», som kalles «supraspinal fatigue» her.

http://www.ncbi.nlm.nih.gov/pubmed/20813979

Abstract

Supraspinal fatigue, defined as an exercise-induced decline in force caused by suboptimal output from the motor cortex, accounts for over one-quarter of the force loss after fatiguing contractions of the knee extensors in normoxia. We tested the hypothesis that the relative contribution of supraspinal fatigue would be elevated with increasing severities of acute hypoxia. On separate days, 11 healthy men performed sets of intermittent, isometric, quadriceps contractions at 60% maximal voluntary contraction to task failure in normoxia (inspired O(2) fraction/arterial O(2) saturation = 0.21/98%), mild hypoxia (0.16/93%), moderate hypoxia (0.13/85%), and severe hypoxia (0.10/74%). Electrical stimulation of the femoral nerve was performed to assess neuromuscular transmission and contractile properties of muscle fibers. Transcranial magnetic stimulation was delivered to the motor cortex to quantify corticospinal excitability and voluntary activation. After 10 min of breathing the test gas, neuromuscular function and cortical voluntary activation prefatigue were unaffected in any condition. The fatigue protocol resulted in ∼ 30% declines in maximal voluntary contraction force in all conditions, despite differences in time-to-task failure (24.7 min in normoxia vs. 15.9 min in severe hypoxia, P < 0.05). Potentiated quadriceps twitch force declined in all conditions, but the decline in severe hypoxia was less than that in normoxia (P < 0.05). Cortical voluntary activation also declined in all conditions, but the deficit in severe hypoxia exceeded that in normoxia (P < 0.05). The additional central fatigue in severe hypoxia was not due to altered corticospinal excitability, as electromyographic responses to transcranial magnetic stimulation were unchanged. Results indicate that peripheral mechanisms of fatigue contribute relatively more to the reduction in force-generating capacity of the knee extensors following submaximal intermittent isometric contractions in normoxia and mild to moderate hypoxia, whereas supraspinal fatigue plays a greater role in severe hypoxia.

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Central and Peripheral Fatigue in Male Cyclists after 4-, 20-, and 40-km Time Trials.

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Nevner at «central fatigue» kommer av lavt oksygennivå, spesielt etter lange treningsøkter. «Peripheral fatigue» kommer etter korte og intense treningøkter.

http://www.ncbi.nlm.nih.gov/pubmed/25051388/

Time to complete 4 km, 20 km and 40 km was 6.0±0.2 min, 31.8±1.0 min and 65.8±2.2 min, at average exercise intensities of 96%, 92% and 87% of VO2max, respectively.

Greater peripheral fatigue was evident after the 4 km (40% reduction in potentiated twitch) compared to the 20 km (31%) and 40 km TTs (29%). In contrast, longer TTs were characterized by more central fatigue, with greater reductions in voluntary activation measured by motor nerve (-11% and -10% for 20 km and 40 km vs. -7% for 4 km) and cortical (-12% and -10% for 20 km and 40 km vs. -6% for 4 km) stimulation.

CONCLUSIONS:

These data demonstrate fatigue after self-paced exercise is task-dependent, with a greater degree of peripheral fatigue after shorter, higher intensity (∼6 min) TTs and more central fatigue after longer, lower intensity TTs (>30 min).

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Sukker + inflammasjon = sant?

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Veldig bra artikkel om norsk forskning som gjøres på forholdet mellom mat og betennelser. Beskriver hvordan urinsyrekrystaller, som kommer fra leverens omdanning av sukker til fett, aktiverer immunceller i blodårene og skaper betennelser. Nevner også at kolesterolkrystaller, som kommer fra kolesteroloppsamling på blodkarveggene, kan gi samme aktivering av immunsystemets betennelsesmekanisme.

http://blog.medisin.ntnu.no/sukker-inflammasjon-sant/

Inflammasjon må reguleres nøye, for dersom immunforsvaret overreagerer kan responsen i seg selv gi mer skade enn selve årsaken. Kronisk inflammasjon kobles blant annet til sykdommer som aterosklerose (åreforkalkning), overvekt, kreft, diabetes (sukkersyke) og demens.

 

Cellene sender da ut et kraftig rop om hjelp, som aktiverer immunforsvaret ytterligere. Dette nødsignalet er tett regulert, for om det skyter over mål får vi en kronisk inflammasjon. Om dette manifesterer seg i et ledd får vi rødme, varme, smerte, og hevelse, kanskje bedre kjent som sykdommen urinsyregikt.

Vi fullfører for tiden et prosjekt hvor vi har sett på om kolesterolkrystaller aktiverer immunforsvaret på samme måte. Også her overreagerer nemlig immunforsvaret, og konsekvensen kan være at selve åreveggen, og ikke krystallene brytes ned. Dette kan gi et sår, som igjen kan gi en blodpropp

 

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Vibration Therapy in Management of Delayed Onset Muscle Soreness (DOMS).

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Svært interessant studie på hvordan vibrasjon (percussor) hjelper mot smerte og stølhet. Den snakker mest om whole-body-vibration, som f.eks. på en Vibroplate. Men de fleste fysiologiske effektene gjelder også for lokal vibrasjon som gis av en Percussor. 

http://www.ncbi.nlm.nih.gov/pubmed/25121012

Hele studien her: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127040/

Abstract

Both athletic and nonathletic population when subjected to any unaccustomed or unfamiliar exercise will experience pain 24-72 hours postexercise. This exercise especially eccentric in nature caused primarily by muscle damage is known as delayed-onset muscle soreness (DOMS). This damage is characterized by muscular pain, decreased muscle force production, reduce range of motion and discomfort experienced. DOMS is due to microscopic muscle fiber tears. The presence of DOMS increases risk of injury. A reduced range of motion may lead to the incapability to efficiently absorb the shock that affect physical activity. Alterations to mechanical motion may increase strain placed on soft tissue structures. Reduced force output may signal compensatory recruitment of muscles, thus leading to unaccustomed stress on musculature. Differences in strength ratios may also cause excessive strain on unaccustomed musculature. A range of interventions aimed at decreasing symptoms of DOMS have been proposed. Although voluminous research has been done in this regard, there is little consensus among the practitioners regarding the most effective way of treating DOMS. Mechanical oscillatory motion provided by vibration therapy. Vibration could represent an effective exercise intervention for enhancing neuromuscular performance in athletes. Vibration has shown effectiveness in flexibility and explosive power. Vibration can apply either local area or whole body vibration. Vibration therapy improves muscular strength, power development, kinesthetic awareness, decreased muscle sore, increased range of motion, and increased blood flow under the skin. VT was effective for reduction of DOMS and regaining full ROM. Application of whole body vibration therapy in postexercise demonstrates less pressure pain threshold, muscle soreness along with less reduction maximal isometric and isokinetic voluntary strength and lower creatine kinase levels in the blood.

 

Cutaneous Receptors Responses: The sensation of pressure and touch is masked during vibration [20], and also postvibration [21]. Some cutaneous mechanoreceptor afferents get aroused for many minutes postvibration [21] and this may be the physiological reason for the tingling sensation often experienced postvibration. On the basis of gate control hypothesis [22] we can infer that vibration strongly impacts affrents discharge from fast adapting mechanoreceptors and muscle spindles and hence become an effective pain reliever.

Pain Perception Responses: Vibration can be used as transcutaneous electrical nerve stimulation (TENS) [23] to reduce the perception of pain [7]. Passive vibration has reduced pain in 70% of patients with acute and chronic musculoskeletal pain [24] and passive 80 Hz vibration has been shown to reduce pain caused by muscle pressure [25]. More recent evidence suggests that pain perception in DOMS depends partly on fast myelinated afferent fibres, which are distinct from those that convey most other types of pain [26].

Lundeberg et al., concluded that vibration relieved pain by activating the large diameter fibres while suppressing the transmission activity in small diameter fibres [24,28].

Vibration therapy leads to increase of skin temperature and blood flow [30].

 

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Flere studier om dehydrering

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Effects of hydration status on cognitive performance and mood. – (2014)

«Current findings in the field suggest that particular cognitive abilities and mood states are positively influenced by water consumption. The impact of dehydration on cognition and mood is particularly relevant for those with poor fluid regulation, such as the elderly and children.» http://www.ncbi.nlm.nih.gov/pubmed/24480458

Influence of progressive fluid restriction on mood and physiological markers of dehydration in women. – (2013)

«The significant effects of FD on mood included decreased alertness and increased sleepiness, fatigue and confusion. The most consistent effects of mild dehydration on mood are on sleep/wake parameters.» http://www.ncbi.nlm.nih.gov/pubmed/22716932

Water consumption, not expectancies about water consumption, affects cognitive performance in adults. – (2013)

«This suggests that water consumption effects on letter cancellation are due to the physiological effects of water, rather than expectancies about the effects of drinking water.» http://www.ncbi.nlm.nih.gov/pubmed/23104227

Effects of drinking supplementary water at school on cognitive performance in children. – (2012)

«…our results showed that a remarkable proportion of children were in a state of mild, voluntary dehydration at the beginning of the school day (84%). We found a significant negative correlation between dehydration and the auditory number span, which indicates a beneficial effect of drinking supplementary water at school on short-term memory. Moreover, there was a positive correlation between dehydration andperformance in the verbal analogy task.» http://www.ncbi.nlm.nih.gov/pubmed/22841529

Mild dehydration affects mood in healthy young women. – (2012)

«In conclusion, degraded mood, increased perception of task difficulty, lower concentration, and headache symptoms resulted from 1.36% dehydration in females. Increased emphasis on optimal hydration is warranted, especially during and after moderate exercise.» http://www.ncbi.nlm.nih.gov/pubmed/22190027

Hydration, morbidity, and mortality in vulnerable populations. – (2012)

«Epidemiological studies have shown an association, although not necessarily a causal one, between a low habitual fluid intake and some chronic diseases, including urolithiasis, constipation, asthma, cardiovascular disease, diabetic hyperglycemia, and some cancers.» http://www.ncbi.nlm.nih.gov/pubmed/23121352

Challenges of linking chronic dehydration and fluid consumption to health outcomes. – (2012)

Og denne som nevner det meste rundt utfordringer med å måle vannintak, noe av årsaken til at det er vanskelig å finne objektive medisinske parametere på det: http://www.ncbi.nlm.nih.gov/pubmed/23121346

Mild dehydration impairs cognitive performance and mood of men. – (2011)

«In conclusion, mild dehydration without hyperthermia in men induced adverse changes in vigilance and working memory, and increased tension/anxiety and fatigue.» http://www.ncbi.nlm.nih.gov/pubmed/21736786

Water, Hydration and Health – (2011)

Review som nevner det meste.

«As with physical functioning, mild to moderate levels of dehydration can impair performance on tasks such as short-term memory, perceptual discrimination, arithmetic ability, visuomotor tracking, and psychomotor skills.53–56» http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2908954/

Hydration and disease. – (2007)

«Avoidance of a high fluid intake as a precautionary measure may be indicated in patients with cardiovascular disorders, pronounced chronic renal failure (III), hypoalbuminemia, endocrinopathies, or in tumor patients with cisplatin therapy (IIb) and menace of water intoxication. Acute systemic mild hypohydration or dehydration may be a pathogenic factor in oligohydramnios (IIa), prolonged labor (IIa), cystic fibrosis (III), hypertonic dehydration (III), and renal toxicity of xenobiotica (Ib). Maintaining good hydration status has been shown to positively affect urolithiasis (Ib) and may be beneficial in treating urinary tract infection (IIb), constipation (III), hypertension (III), venous thromboembolism (III), fatal coronary heart disease (III), stroke (III), dental disease (IV), hyperosmolar hyperglycemic diabetic ketoacidosis (IIb), gallstone disease (III), mitral valve prolapse (IIb), and glaucoma (III). Local mild hypohydration or dehydration may play a critical role in the pathogenesis of several broncho-pulmonary disorders like exercise asthma (IIb) or cystic fibrosis (Ib).» http://www.ncbi.nlm.nih.gov/pubmed/17921462

Human water needs. – (2005)

«A daily water intake of 3.7 L for adult men and 2.7 L for adult women meets the needs of the vast majority of persons. However, strenuous physical exercise and heat stress can greatly increase daily water needs, and the individual variability between athletes can be substantial.» http://www.ncbi.nlm.nih.gov/pubmed/16028570

“Drink at least eight glasses of water a day.” Really? Is there scientific evidence for “8 × 8”? – (2002)

En studie med et klart utgangspunkt i å argumentere mot alle råd om å drikke vann for normale friske mennesker. Sannsynligvis har denne ikke fått med seg noen av studiene jeg har linket til over.

«However, a breakdown of the beverages shows that nearly one-half (47%) of the total drinking fluid was coffee (396 ml), tea (152 ml), soft drinks (179 ml), and alcohol (70 ml),»

«Equally to be emphasized, lest the message of this review be misconstrued, is the fact (based on published evidence) that large intakes of fluid, equal to and greater than 8 x 8, are advisable for the treatment or prevention of some diseases and certainly are called for under special circumstances, such as vigorous work and exercise, especially in hot climates.»

«In summary, this article is concerned with fluid intake forhealthy adults in atemperate climate, performing, at most, mild exercise. Excluded were any special circumstances, such as illnesses, hot climates, and strenuous work or exercise.» http://ajpregu.physiology.org/content/283/5/R993.long