The Truth About Exercise

Dokumentar om høy-intensitetstrening:

Mer om HIIT (Peak 8) fra Dr.Mercola her:

Introvideo til Peak 8 prinsippet for trening: http://youtu.be/BT5hRYXmxSE
Artikkel om Peak8 treningen: http://fitness.mercola.com/sites/fitness/archive/2012/02/10/phil-campbell-interview.aspx
Les artikkelen og se den nederste videoen for å få et inntrykk av hvor intenst treningen skal være de 30sek som intervallene varer.

Relationship between daily physical activity level and low back pain in young, female desk-job workers.

For mye trening og for lite trening gir ryggsmerter. Akkurat passe mye trening er best.

http://www.ncbi.nlm.nih.gov/pubmed/25261333

Abstract

OBJECTIVES:

The purpose of this study was to investigate the relationship between daily physical activity (PA) level and low back pain (LBP) in young women.

MATERIAL AND METHODS:

Two hundred forty three female, desk-job workers aged 20-40 voluntarily participated in the study. The participants were assessed by the use of Oswestry Disability Index for measuring LBP disability and by the use of the short version of the International Physical Activity Questionnaire for PA assessment. The 1-way ANOVA test was used for comparing the mean values according to the physical activity level groups. Correlations between the average LBP disability score and all the other variables were obtained using Pearson’s correlation analysis. The level of statistical significance was p < 0.05.

RESULTS:

Significant differences were found for LBP disability score between the results of 3 different PA groups (p < 0.05) (low, moderate and high PA groups). The correlation between the average LBP disability score and body weight (r = 0.187, p < 0.01), body mass index (r = 0.165, p < 0.01), vigorous MET score (r = 0.247, p < 0.01) and total PA MET score (r = 0.131, p < 0.01) were significant.

CONCLUSIONS:

The main finding of this study is that there is a U-shaped relationship between PA and LBP disability score in young women. A moderate level of daily physical activity and preventing body weight and fat gain should be recommended in young, female desk-job workers in order to prevent and manage low back pain.

Melatonin prevents mitochondrial dysfunction and insulin resistance in rat skeletal muscle.

Om hvordan melatonin beskytter mitokondriene i muskler og insulin resistens.

Teodore et.al. 2014. http://www.ncbi.nlm.nih.gov/pubmed/24981026

Abstract

Melatonin has a number of beneficial metabolic actions and reduced levels of melatonin may contribute to type 2 diabetes. The present study investigated the metabolic pathways involved in the effects of melatonin on mitochondrial function and insulin resistance in rat skeletal muscle. The effect of melatonin was tested both in vitro in isolated rats skeletal muscle cells and in vivo using pinealectomized rats (PNX). Insulin resistance was induced in vitro by treating primary rat skeletal muscle cells with palmitic acid for 24 hr. Insulin-stimulated glucose uptake was reduced by palmitic acid followed by decreased phosphorylation of AKT which was prevented my melatonin. Palmitic acid reduced mitochondrial respiration, genes involved in mitochondrial biogenesis and the levels of tricarboxylic acid cycle intermediates whereas melatonin counteracted all these parameters in insulin-resistant cells. Melatonin treatment increases CAMKII and p-CREB but had no effect on p-AMPK. Silencing of CREB protein by siRNA reduced mitochondrial respiration mimicking the effect of palmitic acid and prevented melatonin-induced increase in p-AKT in palmitic acid-treated cells. PNX rats exhibited mild glucose intolerance, decreased energy expenditure and decreased p-AKT, mitochondrial respiration, and p-CREB and PGC-1 alpha levels in skeletal muscle which were restored by melatonin treatment in PNX rats. In summary, we showed that melatonin could prevent mitochondrial dysfunction and insulin resistance via activation of CREB-PGC-1 alpha pathway. Thus, the present work shows that melatonin play an important role in skeletal muscle mitochondrial function which could explain some of the beneficial effects of melatonin in insulin resistance states.

An acid-sensing ion channel that detects ischemic pain

Nevner mange interessante ting om hvordan lav pH som følge av CO2 ikke er det samme som lav pH som følge av f.eks. melkesyre(laktic acid). De sier at melkesyre og ATP må være sammen for å gjøre pH-sensitive nerver aktive. Noe som skjer ved hard trening hvor ATP lekker ut fra muskel cellene. Laktat aktiverer ASICs umiddelbart, mens ATP er «treg» og det skjer i løpet av 30-60 sekunder. Kanskje denne overaskelsen i nervesystemet er utgangspunktet for sentralsensiteringen som skjer ved DOMS?

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2005001100001

Paradox number 2 answered: coincident detection of lactate, ATP and acid

We are left with a seemingly more profound paradox: how can acid be relevant to ischemic pain if no pain is caused by metabolic events such as hypercapnia that can cause the same kind of pH change that occurs during a heart attack? Pan et al. (13) demonstrated the paradox most convincingly. They measured the pH on the surface of the heart when a coronary artery was blocked and found that it dropped from pH 7.4 to 7.0. Then they reperfused the artery and had the animal breathe carbon dioxide until the resulting hypercapnia dropped the pH of the heart to 7.0. The blockade of the artery caused increased firing of sensory axons that innervate the heart, but the hypercapnia did not. How can this observation be reconciled with their other result (see above) that buffering extracellular pH greatly diminishes axon firing during artery occlusion? The simple interpretation is that protons must be necessary to activate the sensory axons, but cannot by themselves be sufficient. In other words, something must act together with protons to activate the axons.

We searched for compounds released during ischemia that might act together with protons to activate ASIC3. We found two: lactate and adenosine 5′-triphosphate (ATP). When the channel is activated by pH 7.0 in the presence of 15 mM lactate, the resulting current is 80% greater than when lactate is absent (Figure 6). These are physiological values. Under resting conditions, extracellular lactate is about 1 mM in skeletal muscle; after extreme ischemic exercise it rises to 15-30 mM (26). The increased current in the presence of lactate makes the channel better at sensing the lactic acidosis that occurs in ischemia than other kinds of acidosis such as the carbonic acidosis when an animal breathes CO2.

Extracellular ATP rises to >10 µM when a muscle contracts without blood flow (27). We find that a transient appearance of such extracellular ATP can greatly increase ASIC3 current even for minutes after the ATP is removed (Figure 7).

Though they both increase ASIC3 current, lactate and ATP have qualitatively different effects. Lactate acts immediately and must be present for the ASIC current to be enhanced. ATP increases the current slowly – a peak is reached between 15 s and 1 min after ATP is applied – and the effect persists for minutes after ATP is removed. Also, lactate acts on every cell that expresses ASIC3 whereas ATP acts on some cells but not others. We find that lactate acts by altering the basic gating of the channel, which, surprisingly, involves binding of calcium in addition to protons (28). In contrast, the ATP binding site must not be the ASIC3 channel itself; there are a variety of purinergic receptors, some of which are ion channels and some of which are G-protein-coupled receptors. We are presently asking if any of these known receptors might mediate ATP modulation of ASIC3.

Oxygen regulation and limitation to cellular respiration in mouse skeletal muscle in vivo

Denen Studien sier noe ekstremt viktig: Oksygen, mye eller lite, har ingen ting med regulering av cellerespirasjon å gjøre annet enn å være tilgjengelig som et substrat (altså noe cellene kan leve på). De nevner at oksygen bare blir et problem om det går under 2-3 mmHg. Og at blodceller virker som enn buffer ved at de slipper av oxygen for å holde det ovenfor

Marcinek et.al. 2003. Oxygen regulation and limitation to cellular respiration in mouse skeletal muscle in vivo.

http://ajpheart.physiology.org/content/285/5/H1900.full

Therefore, we reject a regulatory role for oxygen in cellular respiration and conclude that oxygen acts as a simple substrate for respiration under physiological conditions.

LOW OXYGEN TENSIONS are characteristic of active muscle. During maximal aerobic exercise, intracellular PO2 in skeletal muscle falls to as low as 2–3 mmHg based on an average myoglobin (Mb) saturation of ∼50% (2427). The intracellular oxygen tension at the maximal rate of sustained exercise sets the lower end of the range of physiologically relevant intracellular PO2 values. These values are just above the threshold where isolated mitochondria (12,29), isolated cells (3940), and intact muscle (28) begin to become oxygen limited. Thus the intracellular PO2 reached during heavy muscle exercise may approach the threshold for limiting cellular respiration in vivo.

Experiments in isolated mitochondria and cells have shown that the respiration rate remains relatively constant over the physiological PO2 range (1236), with a clear reduction occurring only at PO2 below 2–3 mmHg.

Our in vivo results from the mouse hindlimb indicate that until a threshold PO2 is reached (2–3 mmHg), there is no effect of oxygen tension on the phosphorylation state of the cell.

In mouse skeletal muscle in vivo, oxygen tension in the physiological range had no significant effect on cellular respiration over a threefold range of baseline rates of oxygen consumption. This is the expected outcome if oxygen is acting as a simple substrate with no significant regulatory role under physiological conditions.

Thus we found no evidence for a change in the relationship between respiration rate and intracellular PO2 with a greater than threefold increase in the fully oxygenated respiration rate. This leads us to conclude that oxygen is not limiting to cellular oxygen consumption and, therefore, does not play a significant role in regulating cellular respiration in vivo under these conditions.

Studies on exercising human muscle support the conclusion that oxygen tension in skeletal muscle does not fall to levels low enough to significantly inhibit cellular respiration except under extreme physiological conditions [i.e., maximum oxygen consumption (V̇O2 max) in trained individuals]. These studies indicate that Mb saturations at the aerobic capacity of human skeletal muscle are ∼50% in vivo (2.4 mmHg) (2427). Our results indicate that above this intracellular PO2, there is little effect of oxygen tension on the cellular respiration rate over the range tested in the present study.

Decreasing the capacity for oxygen delivery by breathing hypoxic air was found to drop Mb saturation below the 50% level and to reduce oxygen consumption during exercise (26). In contrast, supplementing oxygen by breathing of hyperoxic air during a maximum oxygen consumption test either did not effect or resulted in a small increase (∼10%) in V̇O2 max (625).

The transition between oxygen-independent and oxygen-dependent respiration in vivo also occurs in this range of intracellular oxygen tensions (2–3 mmHg). Therefore, an important role of Mb in skeletal muscle may be as an oxygen buffer to help maintain intracellular PO2 above the point at which it becomes limiting to cellular respiration.

In conclusion, the findings of the present study lead us to reject the hypothesis that oxygen plays a regulatory role in cellular respiration over the physiological range of intracellular oxygen tensions. This conclusion is based on the absence of interaction between [PCr], pH (and therefore phosphorylation state), oxygen consumption, and PO2 above 3 mmHg over a greater than threefold range in oxygen consumption rates. These results are consistent with the hypothesis that oxygen acts as a simple substrate for cellular respiration over the physiological range of oxygen tensions.

One-set resistance training elevates energy expenditure for 72 h similar to three sets.

Denen Studien nevner mange interessante ting om Resting Energy Expenditure, altså energien kroppen bruker til å reparere seg etter trening. Vanligvis bruker kroppen 60-75% av energien bare på å opprettholde en fysiologiske funksjoner under hvile, mens i 72t etter trening kan den økes med 6%, eller ca. 420 kJ. Denne studien viste at det var lite ekstra økning om man gjorde en enkelt 15 min økt, eller om man gjorde det 3 ganger.

Heden et.al. 2011. One-set resistance training elevates energy expenditure for 72 h similar to three sets.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3071293/

Resting energy expenditure (REE) accounts for approximately 60–75% of an individual’s daily energy expenditure (Dolezal and Potteiger 1998Hunter et al. 2000Lemmer et al. 2001Pratley et al. 1994). Determining modalities that increase REE is important as small perturbations in REE can have a significant impact on the regulation and maintenance of body weight (Dolezal and Potteiger 1998Hunter et al. 2000Lemmer et al. 2001Pratley et al. 1994). Unlike aerobic exercise, which results in significant increases in energy expenditure during, and for a short time following cessation of the activity, the energy expenditure during resistance training (RT) is relatively low (Melby et al. 1993Phillips and Ziuraitis 2003), but the increase in energy expenditure after the cessation of the activity and between RT session may be elevated (Dolezal et al. 2000Melby et al. 1993Taaffe et al. 1995).

The REE also corresponds pretty good to the progression of DOMS. But is also, as anything else we have looked at, not correlated to the intensity of DOMS.

 

Results indicated that both the RT protocols elevated REE by ~ 420 kJ (6%) after 24 h in absolute and relative to fat-free mass and this elevation was maintained in both protocols for 72 h post RT bout.

 

The results of this investigation support the current ACSM recommendation for RT, which is one set of eight to ten exercises focusing on the major muscle groups (Haskell et al. 2007). Although this recommendation is most often cited for overall muscular fitness, the fact that a single set can elevate REE for 72 h may be an important modality for weight management.

 

The importance of increasing REE may be with the interaction between REE and energy balance. Increasing REE sufficiently could possibly result in a negative energy balance that could prevent an increase in fat mass.

 

These factors include elevated body temperature, resynthesis of glycogen from lactate, ion redistribution, replenishment of oxygen stores in blood and muscle, resynthesis of adenosine triphosphate and creatine phosphate, circulation and ventilation, and residual hormone effects (Bahr 1992Bangsbo et al. 1990Borsheim and Bahr 2003). However, it seems that these processes are associated with temporary elevations and do not explain prolonged REE elevations observed beyond 24 h post exercise (Bahr 1992Bangsbo et al. 1990Borsheim and Bahr 2003).

 

For, example, although not measured in this study, myofibrillar protein turnover (Kim et al. 2005) could increase REE and has been shown to account for as much as 20% of REE (Welle and Nair 1990). In addition, sympathetic nervous system activity may be related to changes in REE. For example, low volume RT has been shown to increase muscle sympathetic nerve activity (Pratley et al. 1994) and to elevate rates of muscle protein synthesis and breakdown up to 48-h post-exercise. Finally, changes in insulin or IGF-1 may contribute to alterations in the repair and resynthesis of skeletal muscle that may contribute to an elevation in REE beyond 24 h (Nindl et al. 2009).

ACE ID genotype affects blood creatine kinase response to eccentric exercise

Hvordan genetiske forskjeller gir økt disponering from CK respons fra trening.

http://jap.physiology.org/content/103/6/2057

Unaccustomed exercise may cause muscle breakdown with marked increase in serum creatine kinase (CK) activity. The skeletal muscle renin-angiotensin system (RAS) plays an important role in exercise metabolism and tissue injury. A functional insertion (I)/deletion (D) polymorphism in the angiotensin I-converting enzyme (ACE) gene (rs4646994) has been associated with ACE activity. We hypothesized that ACE ID genotype may contribute to the wide variability in individuals’ CK response to a given exercise. Young individuals performed maximal eccentric contractions of the elbow flexor muscles. Pre- and postexercise CK activity was determined. ACE genotype was significantly associated with postexercise CK increase and peak CK activity. Individuals harboring one or more of the I allele had a greater increase and higher peak CK values than individuals with the DD genotype. This response was dose-dependent (mean ± SE U/L: II, 8,882 ± 2,362; ID, 4,454 ± 1,105; DD, 2,937 ± 753, ANOVA, P = 0.02; P = 0.009 for linear trend). Multivariate stepwise regression analysis, which included age, sex, body mass index, and genotype subtypes, revealed that ACE genotype was the most powerful independent determinant of peak CK activity (adjusted odds ratio 1.3, 95% confidence interval 1.03–1.64, P = 0.02). In conclusion, we indicate a positive association of the ACE ID genotype with CK response to strenuous exercise. We suggest that the IIgenotype imposes increased risk for developing muscle damage, whereas the DD genotype may have protective effects. These findings support the role of local RAS in the regulation of exertional muscle injury.