Effects of a 4-week training with voluntary hypoventilation carried out at low pulmonary volumes

november 8, 2013 av Marius

Spennende studie som viser hvordan lav pustefrekvens i selve trening påvirker restitusjonen etterpå. F.eks. hvordan bikarbonat/natron (HCO3-) påvirker melkesyreterskel. Teknikken bestod i å holde pusten 4 sekunder etter utpust, i bolker a 5minutter i løpet av treningsperioden. Det gir spesielt lite oksygen i blodet, som gir mange positive resultater.

http://www.sciencedirect.com/science/article/pii/S1569904807002327

Helle studien her: http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CCsQFjAA&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F5689789_Effects_of_a_4-week_training_with_voluntary_hypoventilation_carried_out_at_low_pulmonary_volumes%2Ffile%2F79e41509ccd387b0f9.pdf&ei=pM58UpS3IIKF4ATU24D4CA&usg=AFQjCNFVh6Yl8e_ScphKf6HTFiLp1CWKsw&sig2=B9Zq9u_LuDDzGru14OKsLQ&bvm=bv.56146854,d.bGE

This study investigated the effects of training with voluntary hypoventilation (VH) at low pulmonary volumes. Two groups of moderately trained runners, one using hypoventilation (HYPO, n = 7) and one control group (CONT, n = 8), were constituted. The training consisted in performing 12 sessions of 55 min within 4 weeks. In each session, HYPO ran 24 min at 70% of maximal O₂ consumption () with a breath holding at functional residual capacity whereas CONT breathed normally. A and a time to exhaustion test (TE) were performed before (PRE) and after (POST) the training period. There was no change in , lactate threshold or TE in both groups at POST vs. PRE. At maximal exercise, blood lactate concentration was lower in CONT after the training period and remained unchanged in HYPO. At 90% of maximal heart rate, in HYPO only, both pH (7.36 ± 0.04 vs. 7.33 ± 0.06; p < 0.05) and bicarbonate concentration (20.4 ± 2.9 mmol L⁻¹ vs. 19.4 ± 3.5; p < 0.05) were higher at POST vs. PRE. The results of this study demonstrate that VH training did not improve endurance performance but could modify the glycolytic metabolism. The reduced exercise-induced blood acidosis in HYPO could be due to an improvement in muscle buffer capacity. This phenomenon may have a significant positive impact on anaerobic performance.

Muscle Pain: Mechanisms and Clinical Significance

september 28, 2013 av Marius

En studie til fra Siegfried Mense, om muskelsmerter. Han har ikke fått med seg at trykksensitive nerver kun finnes i huden. Og han har misforstått litt i forskjellene mellom hud-smerter og muskel-smerter siden han sier at hud-smerter ikke kan ha utstrålende effekt. Han har tydeligvis ikke ikke inkludert subcutane nerver i sin vurdering.

Men mye interessant i denne studien likevel. Spesielt vektleggingen av at lav pH er den viktigste bidragsyteren til muskelsmerter.

Han nevner at input fra muskel-nociceptorer har større relevans i ryggmargen enn input fra huden. Derfor er betennelser og lav pH de viktigste drivkreftene i kroniske smerter.

Nevner også at smerter henger sammen, f.eks. at trapezius kan stramme seg for å beskytte brachialis, slik at smerten kjennes i trapezius, mens problemet egentlig sitter i brachialis.

Beskriver også triggerpunkter, men sier at det foreløpig er veldig mange ubesvarte spørsmål om denne teorien.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696782

Muscle pain is a major medical problem: in, the majority (60% to 85%) of the population has had (nonspecific) back pain of muscular origin at some time or other (lifetime prevalence) (1). Pain evoked by myofascial trigger points has a point prevalence of approximately 30% (2). More than 7% of all women aged 70 to 80 years suffer from the fibromyalgia syndrome (e1). In an Italian study, musculoskeletal pain was found to be the most common reason that patients consulted a doctor (3). Thus, treating physicians should be aware of the mechanisms of muscle pain, insofar as they are currently understood.

Subjective differences between muscle pain and cutaneous pain

Muscle pain	Cutaneous pain
Electrical nerve stimulation induces only one pain	Electrical nerve stimulation induces a first pain and a second pain
Poorly localizable	Well-localized
Tearing, cramping, pressing quality	Stabbing, burning, cutting quality
Marked tendency toward referral of pain	No tendency toward referral of pain
Affective aspect: difficult to tolerate	Affective aspect: easier to tolerate

Muscle pain is produced by the activation of specific receptors (so-called nociceptors): these receptors are specialized for the detection of stimuli that are objectively capable of damaging tissue and that are subjectively perceived as painful. They consist of free nerve endings and are connected to the central nervous system (CNS) by way of unmyelinated (group IV) or thinly myelinated (group III) fibers. They can be sensitized and activated by strong mechanical stimuli, such as trauma or mechanical overloading, as well as by endogenous inflammatory mediators including bradykinin (BK), serotonin, and prostaglandin E2 (PGE2).

Two activating chemical substances are particularly important for the generation of muscle pain: adenosine triphosphate (ATP) and protons (H+ ions).

ATP activates muscle nociceptors mainly by binding to the P2X3 receptor molecule, H+ mainly by binding to the receptor molecules TRPV1 (transient receptor potential vanilloid 1) and ASICs (acid-sensing ion channels) (4).

ATP is found in all cells of the body and is released whenever bodily tissues of any type are injured.

A drop in pH is probably one of the main activators of peripheral nociceptors, as many painful disturbances of muscle are associated with low pH in muscle tissue.

Nerve growth factor (NGF) also has a connection to muscle pain: NGF is synthesized in muscle and activates muscle nociceptors (e2). NGF synthesis is increased when a muscle is inflamed (e3).

Acidic tissue pH is one of the main activating factors leading to muscle pain. Practically all pathological and pathophysiological changes of skeletal muscle are accompanied by a drop in pH, among them

chronic ischemic states,
tonic contractions or spasms,
myofascial trigger points,
(occupationally induced) postural abnormalities, and
myositides.

The neuropeptides stored in muscle nociceptors are released not only when peripheral stimuli activate the nerve endings, but also when spinal nerves are compressed. In this type of neuropathic pain, action potentials are generated at the site of compression and spread not only centripetally, i.e., toward the central nervous system, but also centrifugally, i.e., toward the nociceptive endings, where they induce the release of vasoactive neuropeptides. In this way, neurogenic inflammation comes about, characterized by hyperemia, edema, and the release of inflammatory mediators (8). The inflammatory mediators sensitize the muscle nociceptors and thereby increase neuropathic pain.

The sensitization of the muscle nociceptors by endogenous mediators such as BK and PGE2 is one of the reasons why patients with muscle lesions suffer from tenderness to pressure on the muscle, and from pain on movement or exercise. It is also the reason why many types of muscle pain respond well to the administration of non-steroidal anti-inflammatory drugs (NSAID), which block prostaglandin synthesis.

An influx of nervous impulses from muscle nociceptors into the spinal cord increases the excitability of posterior horn neurons to a greater extent than one from cutaneous nociceptors (9).

Two main mechanisms underlie the overexcitability of spinal nociceptive neurons:

A structural change of ion channels, rendering them more permeable to Na+ and Ca2+, is the short-term result of an influx of nociceptive impulses into the spinal cord. Among other effects, this causes originally ineffective («silent» or «dormant») synapses to become effective.

A change of gene transcription in the neuronal nucleus, leading to a modification of synthetic processes, causes new ion channels to be synthesized and incorporated into the nerve cell membrane. The long-term result of central sensitization is a nociceptive cell whose membrane contains a higher density of ion channels that are also more permeable to ions. This explains the hyperexcitability of the cell. Glial cells, too, particularly microglia, can contribute to the sensitization of central neurons by secreting substances such as tumor necrosis factor a (TNF-a) (8).

The increased excitability of spinal neurons and the spread of excitation within the CNS are the first steps in the process of chronification of muscle pain. The endpoint of chronification consists of structural remodeling processes in the CNS that open up new pathways for nociceptive information and cause pain to persist over the long term. Patients with chronic muscle pain are difficult to treat, because the functional and structural changes in the CNS need time to regress. The fact that not all muscle pain becomes chronic implies that chronification requires not only the mechanisms just discussed, but also other ones, e.g., a genetic predisposition.

Pain arising in muscle is more likely to be referred pain than pain arising in the skin. Referred pain is pain that is felt not (only) at its site of origin, but at another site some distance away. A possible mechanism of referred pain is the spread, within the spinal cord, of excitation due to the muscle lesion (9) (figures 2 and and3).3). As soon as the excitation reaches sensory posterior horn neurons that innervate an area beyond the site of the original muscle lesion, the patient feels referred pain in that area, even though none of the nociceptors in it are activated (13).

An example is shown in figure 3: a stimulus delivered to the myofascial trigger point (MTrP) in the soleus muscle causes only mild local pain, while the patient feels more severe (referred) pain in the sacroiliac joint. No conclusive answers are yet available to the questions of why muscle pain is more likely than cutaneous pain to be referred, why it is usually not referred to both proximal and distal sites, and why pain referral is often discontinuous. There is, however, a well-known discontinuity of spinal topography between the C4 and T2 dermatomes.

The main reason why pain arises in muscle spasm is muscle ischemia, which leads to a drop in pH and the release of pain-producing substances such as bradykinin, ATP, and H+.

The vicious-circle concept of muscle spasm – muscle pain causes spasm, which causes more pain, etc. – should now be considered obsolete. Most studies have shown that muscle pain lowers the excitability of the α-motor neurons innervating the painful muscle (14) (a «pain adaptation» model) (15).

Muscle spasm can be precipitated by, among other things, pain in another muscle. Thus, a spasm-like increase EMG activity in the trapezius muscle has been described in response to painful stimulation of the biceps brachii muscle (16). Another source of muscle spasms is pathological changes in a neighboring joint. These sources of pain must be deliberately sought.

In a widespread hypothesis on the origin of MTrP’s (19), it is supposed that a muscular lesion damages the neuromuscular endplate so that it secretes an excessive amount of acetylcholine. The ensuing depolarization of the muscle cell membrane produces a contraction knot that compresses the neighboring capillaries, causing local ischemia. Ischemia, in turn, leads to the release of substances into the tissue that sensitize nociceptors, accounting for the tenderness of MTrP’s to pressure. Substances of this type have been found to be present within the MTrP’s of these patients (20). This supposed mechanism leaves many questions unanswered but is currently the only comprehensive hypothesis on the origin of MTrP’s.

Patients with MTrP’s often have pain in three locations:

at the site of the MTrP itself,
at the origin or insertion of the affected muscle, because of pulling by the muscle fibers that have been stretched by the contraction knots,
and referred pain outside the MTrP (figure 3).

Because the MTrP is cut off from its blood supply by compression of the local microcirculation, oral NSAID’s are not very effective against TrP pain.

Functional Anatomy of Muscle – Muscle, Nociceptors and Afferent Fibers

september 27, 2013 av Marius

Svært mye interessant om nervesystemets rolle i muskler og smerte.

Spesielt at det er ingen frie nerveender i muskelcellene, men bare i blodkarene i musklene. Derfor reagerer vi med smerte på betennelser og lav pH i blodet, mens trykksensitiviteten kun sitter i huden.

Den nevner at pH sensibiliteten er den viktigste smertebidraget fordi pH synker i de fleste patologiske tilstander, f.eks. hard trening eller skade.

Den nevner at det er mer SP (Substans P, som er relatert til smerte) i huden enn i muskler.

Nevner at frie nerveender ikke går til kapillærer eller muskelceller, bare til arterioler og venuler.

Nevner også innervering av bindevev, og at dette feltet foreløpig er lite studert og oversett. Spesielt viser de til at Toracolumbar Facia (i korsryggen) har størst innervasjon av C-fiber nociceptorer(som inneholder SP) under huden, og litt i multifidene.

En nociceptor er ikke bare en passiv mottaker av impulser, men er også en aktiv deltaker i vevets tilstand når det gjelder betennelser og blodsirkulasjon for de sender nevropetider ut fra doresalhornet til vevet (antidromiske impulser). Altså motsatt vei av reseptor-signalretningen.

CGRP virker vasodilerende, mens SP gjør at blodkarveggenes permeabilitet øker. Når permeabiliteten øker siver det ut proteiner og stoffer som egentlig ikke skal være i vevet, og da økes betennelser og immunsystemets aktivitet. Så det er SP vi ønsker å dempe først og fremst.

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&cad=rja&ved=0CCsQFjAA&url=http%3A%2F%2Fwww.springer.com%2Fcda%2Fcontent%2Fdocument%2Fcda_downloaddocument%2F9783540850205-c1.pdf%3FSGWID%3D0-0-45-935848-p173845615&ei=_GJEUqyUOevn4QSBl4HQDg&usg=AFQjCNEpyWrolHywvUNyw_Cwa8yWTiEUnw&sig2=OJLZ3XrnTalCUUqE-uhCeQ&bvm=bv.53217764,d.bGE

The predominant location of free nerve endings supplied by group IV fibers was the adventitia of arterioles and venules. Surprisingly, muscle fibers themselves did not receive direct innervation by free nerve endings. Group III afferents generated not only free nerve endings but also paciniform corpuscles, whereas group IV fibers terminated exclusively in free nerve endings.The high sensitivity of the free nerve endings to chemical stimuli, particularly to those accompanying inflammatory lesions or disturbances of the microcirculation, may be related to their location on or in the walls of the blood vessels. The finding that the muscle fibers proper are not supplied by free nerve endings (Reinert et al. 1998) may relate to the clinical experience that muscle cell death is usually not painful, at least not if it occurs slowly, as for instance during muscular dystrophy, polymyositis, or dermatomyositis. A different situation is tearing of a muscle fiber bundle, which can be extremely painful. In this condi- tion, many muscle cells are destroyed simultaneously and release their contents (e.g., K+ ions and ATP) in the interstitial space, from where they can diffuse to the next nociceptive endings.

In skeletal muscle, the free nerve endings appear to be distributed quite evenly in the proximodistal direction. At least, in a quantitative evaluation of the inner- vation density by neuropeptide-(SP- and CGRP-) containing fibers, no difference between the proximal and distal portions of the rat gastrocnemius–soleus (GS) muscle was found (Reinert et al. 1998). Therefore, a higher innervation density at the transition zone between muscle and tendon is not a probable explanation for the frequent pain in this region.

However, in the same study the nerve fiber density in the peritendineum (the connective tissue around a tendon) of the rat calcaneal tendon was found to be several times higher than that in the GS muscle. In contrast, the collagen fiber bundles of the tendon tissue proper were almost free of free nerve endings. The high fiber density in the peritendineum may explain the high prevalence of tenderness or pain in the tissue around the tendon and the insertion site. The scarcity of nerve endings in the center of the tendon may relate to the clinical observation that (incomplete) ruptures of the tendon may occur without pain.

Judging from their respon- siveness to pain-producing agents, the following receptor molecules are likely to be relevant for muscle pain and tenderness (Mense and Meyer 1985; Caterina and David 1999; McCleskey and Gold 1999; Mense 2007):

Bradykinin (BKN) receptors (B1 and B2). BKN is cleaved from blood plasma proteins when a blood vessel breaks or increases its permeability so that plasma proteins enter the interstitial space. In intact tissue, BKN excites nerve endings by the activation of the BKN receptor molecule B2, whereas under pathological conditions (e.g., inflammation) the receptor B1 is the predominant one (Perkins and Kelly 1993; for a review of receptor molecules mediating the effects of classic inflammatory (pain-producing or algesic) substances, see Kumazawa 1996).
Serotonin receptors (particularly 5-HT3). Serotonin (5-hydroxytryptamin, 5-HT) is released from blood platelets during blood clotting. The stimulating effects of serotonin on nociceptive terminals in the body periphery are predomi- nantly mediated by the 5-HT3 receptor (at present, more than 15 different 5-HT receptors are known in the CNS). The serotonin concentrations released in the tissue are usually not sufficient to excite nociceptors directly, but they can sen- sitize them, i.e., make them more sensitive to other pain-producing agents such as BKN.
Prostaglandins, particularly prostaglandin E2 (PGE2). Prostaglandins (PGs) are released in a pathologically altered muscle by the enzymatic action of cycloox- igenases. PGE2 binds to a G protein-coupled prostanoid receptor (EP2) in the membrane of the nociceptive ending. Similarly to serotonin, PGE2 sensitizes nociceptors rather than exciting them under (patho)physiological circumstances (Mense 1981).
Acid-sensing ion channels (ASICs). ASICs constitute a family of receptor molecules that are sensitive to a drop in pH and open at various pH values. The channel proteins react already to small pH changes, for instance from pH 7.4 to 7.1. This receptor family (for instance ASIC1 and ASIC3) is particularly impor- tant for muscle pain, because almost all pathologic changes in muscle are accom- panied by a drop in tissue pH, e.g., exhausting exercise, ischemia, and inflammation (Immke and McCleskey 2003). In these conditions, the pH of the muscle tissue can drop to 5–6. The proton-sensitive nociceptors may also be of importance for the induction of chronic muscle pain. Repeated intramuscular injections of acidic solutions have been reported to induce a long-lasting hyper- algesia (Sluka et al. 2001).
P2X3 receptors. This receptor is a subtype of the purinergic receptors that are activated by ATP and its derivatives (Burnstock 2007; Ding et al. 2000). ATP is the energy-carrying molecule in all cells of the body; accordingly, it is present in every tissue cell. It is released from all tissues during trauma and other pathologic changes that are associated with cell death. For this reason, ATP has been considered a general signal substance for tissue trauma and pain (Cook and McCleskey 2002). ATP is particularly important for muscle pain, because it is present in muscle cells in high concentration (Stewart et al. 1994). When injected into human muscle, ATP causes pain (Mo ̈rk et al. 2003).
Transient receptor potential receptor subtype 1 (TRPV1) formerly called VR1. This receptor is one of the most important molecules for the induction of pain. The natural stimulant for the TRPV1 receptor is Capsaicin, the active ingredient of chilli peppers (Caterina and Julius 2001). The receptor is also sensitive to an increase in H+-concentration and to heat, with a threshold of approximately 39C. Its endoge- nous ligands are H+-ions.
Other TRP receptors. TRPV4 is a mechanosensitive ion channel that is sensitive to both weak and strong (noxious) intensities of local pressure (Liedtke 2005). It may be the receptor for mediating pain evoked by pinching and squeezing.
Tyrosine kinase A (TrkA) receptor. The ligand of this receptor is NGF (Caterina and David 1999). NGF is well-known for its sensitizing action on nociceptors in the body periphery and neurons in the CNS; it is synthesized in muscle, and its synthesis is increased during pathophysiological changes of the muscle (e.g., inflammation, Menetrey et al. 2000; Pezet and McMahon 2006).
Glutamate receptors. There is evidence indicating that the NMDA receptor (one of the receptors for glutamate) is present on nociceptive endings in masticatory muscles. Injections of glutamate into the masseter muscle in human subjects induced a reduction in pressure pain threshold which was attenuated by coinjection with ketamine, an NMDA receptor antagonist (Cairns et al. 2006).

Substances exciting muscle nociceptors independent of membrane receptors.

Hypertonic saline: injections of NaCl solutions (4.5–6.0%) have long been and still are used to elicit pain from deep somatic tissues (Kellgren 1938; for review, see Graven-Nielsen 2006).
Potassium ions: The most likely explanation for the excitatory action of high concentrations of extracellular potassium ions is a depolarization of the membrane potential due to a reduction of the inside–outside potassium gradient (usually the potassium concentration inside the axon is much higher).

DRG cells projecting in a cutaneous nerve have been reported to contain SP, CGRP, and somatostatin (SOM).

In comparison to skin nerves, muscle nerves appear to contain less SP. This finding makes sense, because the vasodilatation and plasma extrava- sation caused by the release of SP and CGRP from free nerve endings (see below) would be dangerous for skeletal muscles, since many of them are surrounded by a tight fascia. Therefore, an SP-induced muscle edema would result in a high increase in interstitial pressure, and could cause muscle necrosis.

In a study on functionally identified DRG cells employing a combination of electrophysiological and immunohistochemical techniques, Lawson et al.(1997) reported that cells terminating in cutaneous nociceptive endings showed a strong tendency to express SP, particularly if they had a slow conduction velocity or a small soma in the DRG.

The peptides are synthesized in the somas of the DRG or in ganglion cells of cranial nerves. They are transported to both the central and the peripheral terminal of the primary afferent unit.

In a quantitative evaluation of neuropeptide-containing free nerve endings and preterminal axons (both characterized by varicosities) in the GS muscle of the rat, most endings were found around small blood vessels (arterioles or venules), whereas capillaries and the muscle cells proper were not contacted by these end- ings.

Efferent or motor fibers conduct action potentials from the CNS to the periphery; their soma is located in the spinal cord or brainstem and the fibers leave the CNS via the ventral root or cranial nerve motor roots. An exception are postganglionic sympathetic fibers whose cell bodies are mostly located in the sympathetic trunk (e.g., vasomotor fibers that constrict blood vessels).

The nerve to a locomotor muscle in the cat (the lateral GS) is composed of approximately one-third myelinated (720) and two-thirds unmyelinated (2,480) fibers (Table 2.2; Mitchell and Schmidt 1983; Stacey 1969). Nearly one quarter of the myelinated (group III) fibers had nociceptive properties in neurophysio- logical experiments (Mense and Meyer 1985). Of the unmyelinated fibers, 50% are sensory (group IV), and of these, approximately 55% have been found to be nociceptive in the rat (Hoheisel et al. 2005).

Data obtained from one muscle nerve cannot be transferred directly to other muscle nerves, because considerable differences exist between different muscles. For instance, neck muscle nerves of the cat contain unusually high numbers of sensory group III receptors (Abrahams et al. 1984). One possible explanation for these differences is that the muscles have different functions and environmental conditions: in contrast to the neck muscles, which must register the orientation of the head in relation to the body in fine detail, the locomotor hindlimb muscles often have to contract with maximal strength and under ischemic conditions.

In addition to nociceptors, there are other muscle receptors whose function is essential for the understanding of muscle pain:

Muscle spindles are complex receptive structures that consist of several specialized muscle fibers (the so-called intrafusal muscle fibers; the name is derived from their location inside the spindle-shaped connective tissue sheath. Accordingly, all the “normal” muscle fibers outside the spindle are “extrafusal” fibers). Muscle spindles measure the length and the rate of length changes of the muscle, i.e., their discharge rate increases with increasing muscle length and with increasing velocity of the length change.
Golgi (tendon) organs measure the tension of the muscle. They are arranged in series with the extrafusal muscle fibers; their location is the transition zone between muscle and tendon. The supplying fiber is the Ib afferent, whose structure is identical to the Ia fiber (thick myelin sheath and high conduction velocity). The receptor has a much simpler structure than the muscle spindle; it consists of receptive endings that are interwoven between the collagen fiber bundles of the tendon.
Muscle spindles and Golgi organs are proprioceptors, i.e., they measure the internal state of the body.
Pacinian corpuscles (PC) and paciniform corpuscles. These receptors do not respond to static pressure; they require dynamically changing mechanical stimuli, and are best excited by vibrations of relatively high frequency (close to 300 Hz; Kandel et al. 2000). The receptive ending is formed like a rod, and covered by several concentric membranes which give the receptor an onion-like appearance in cross-sections.

At present, little information is available about the innervation of fascia. This is an important gap in our knowledge, because fascia is an important component of the musculoskeletal system and likely to contribute to many forms of pain that are subsumed under the label “muscle” pain. One example is low back pain: The thoracolumbar fascia (TF) plays an essential role in body posture and trunk move- ments (Bogduk and Macintosh 1984). It is not only a passive transmitter of mechanical forces of the low back and abdominal muscles but also contractile by itself (Schleip et al. 2005).

In the connective tissue around the superficial lamina of the TF we found many CGRP- and SP-containing free nerve endings. The majority of the fibers were located in the subcutaneous layer, as well as between the fascia and the surface of the multifidus muscle (Fig. 2.8). The SP-positive endings are of particular interest, because they are thought to be nociceptors.

The loose connective tissue around the TF is probably deformed during any trunk movement, and therefore the free nerve endings are strategically situated to sense any disorders in these movements. It is conceivable that overload of the fascia puts mechanical stress and irritation on the endings, and thus may contribute to low back pain.

SP then releases histamine from mast cells, and together with CGRP these agents cause vasodilatation and an increase in vascular permeability of the blood vessels around the active ending. The result is a shift of blood plasma from the intravascular to the interstitial space. Outside the blood vessel, BKN is cleaved from the plasma protein kallidin, serotonin (5-HT) is set free from platelets, and PGs (particularly PGE2) from endothelial and other tissue cells. All these substances sensitize nociceptors. Thus, the main tissue alteration induced by a nondestructive noxious mechanical stimulus is a localized region of vasodilatation, edema, and sensitized nociceptors.

A nociceptor is not a passive sensor of tissue-threatening stimuli; it actively influences the microcirculation and chemical composition of the intersti- tial space around it.

If a noxious stimulus activates only one part of the ending, the action potentials originating in that region of the ending can invade antidromically (against the normal direction of propagation) those branches of the ending that were not excited by the stimulus. These antidromic action potentials release neuropeptides from the unstimulated branches. The whole process is called the axon reflex. It is assumed to be the reason for the visible wheal and flare around a cutaneous lesion.

The vascular permeability is increased mainly by SP (and by the neurokinins A and B; Gamse and Saria 1985), whereas CGRP is assumed to act primarily as a vasodilator. There is evidence showing that CGRP enhances the plasma extravasation induced by SP and neurokinins A and B, but reduces the vasodilatory action of SP by desensitizing muscle arterioles to the peptide (O ̈ hle ́n et al. 1988).

The area of wheal and flare after a localized damage to the skin – for instance around a needle prick – could be an indicator of the extent of the excited nocicep- tive ending.

The size of the receptive fields (RFs) of cutaneous polymodal nociceptors was found to be less than 2 mm in cat (Bessou and Perl 1969) and 6–32 mm in rabbit (Kenins 1988). A receptive field is that region of the body from which a receptive ending (or a central sensory neuron) can be excited. The above figures are larger than the reported length of the branches of a nociceptor ending (a few hundred mm; Stacey 1969).

The release of SP, CGRP, neurokinin A, and other agents from nociceptors is the central factor in the cascade of events that lead to neurogenic inflammation in the periphery (Lembeck and Holzer 1979). Neurogenic inflammation is characterized by tissue edema and infiltration by immune cells, i.e., it exhibits the major histo- logical signs of a (sterile) inflammation. It develops whenever action potentials are generated not at the receptive ending but somewhere along the course of primary afferent units (spinal nerve or dorsal root). The action potentials propagate both to the CNS (causing pain) and to the peripheral ending (causing release of neuropep- tides and neurogenic inflammation). The published data indicate that vasodilatation can be elicited by antidromic stimulation of both Ad- and C fibers, but increase in vascular permeability and plasma extravasation by stimulation of C fibers only.

Neuropathies and radiculopathies and other pathological conditions that are asso- ciated with antidromic activity in sensory nerve fibers are examples of such events (Marchand et al. 2005). Neurogenic inflammation is likely to increase the dysesthe- sia and pain of patients suffering from neuropathies.

Inflammatory disorders are usually accompanied by sensitization of peri- pheral nociceptors, which is one source of inflammatory pain (for details, see Chap. 3).

Alterations in Cortical and Cerebellar Motor Processing in Subclinical Neck Pain Patients Following Spinal Manipulation.

september 19, 2013 av Marius

Interessant studie som nevner at personer med kronisk smerte (i nakken) får endret aktivitet i lillehjernen, som styrer våre bevegelsesmønstre. Med manipulering etterfulgt av 20 minutter motorisk trening blir lillehjernens aktivitet lik de som ikke har smerte. Studien nevner manipulering av ryggraden, men sannsynligvis vil også percussor eller en hvilken som helst annen behandling gi samme effekten.

http://www.ncbi.nlm.nih.gov/pubmed/24035521

Subclinical neck pain patients have altered CBI when compared with healthy controls, and spinal manipulation before a motor sequence learning task changes the CBI pattern to one similar to healthy controls.

The fascia of the limbs and back – a review

august 24, 2013 av Marius

Never det meste rundt bindevev: tensegritet, subcutan hud, skinligaments, stretching, ligamenter, nerver, m.m.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2667913/

Fasciae probably hold many of the keys for understanding muscle action and musculoskeletal pain, and maybe of pivotal importance in understanding the basis of acupuncture and a wide range of alternative therapies (Langevin et al. 2001, 2002, 2006a; Langevin & Yandow, 2002; Iatridis et al. 2003). Intriguingly, Langevin et al. (2007) have shown that subtle differences in the way that acupuncture needles are manipulated can change how the cells in fascia respond. The continuum of connective tissue throughout the body, the mechanical role of fascia and the ability of fibroblasts to communicate with each other via gap junctions, mean that fascia is likely to serve as a body-wide mechanosensitive signaling system with an integrating function analogous to that of the nervous system (Langevin et al. 2004; Langevin, 2006). It is indeed a key component of a tensegrity system that operates at various levels throughout the body and which has been considered in detail by Lindsay (2008) in the context of fascia.

Anatomists have long distinguished between superficial and deep fascia (Fig. 1), although to many surgeons, ‘fascia’ is simply ‘deep fascia’. The superficial fascia is traditionally regarded as a layer of areolar connective or adipose tissue immediately beneath the skin, whereas deep fascia is a tougher, dense connective tissue continuous with it.

A diagrammatic representation of a transverse section through the upper part of the leg showing the relative positions of the superficial (SF) and deep fascia (DF) in relation to the skin (S) and muscles. Note how the deep fascia, in association with the bones [tibia (T) and fibula (F)] and intermuscular septa (IS) forms a series of osteofascial compartments housing the extensor, peroneal (PER) and flexor muscles. If pressure builds up within a compartment because of an acute or overuse injury, then the vascular supply to the muscles within it can be compromised and ischaemia results. ANT, anterior compartment; IM, interosseous membrane.

The presence of a significant layer of fat in the superficial fascia is a distinctive human trait (thepanniculus adiposus), compensating for the paucity of body hair. It thus plays an important role in heat insulation. In hairy mammals, the same fascia is typically an areolar tissue that allows the skin to be readily stripped from the underlying tissues (Le Gros Clark, 1945). Where fat is prominent in the superficial fascia (as in man), it may be organized into distinctive layers, or laminae (Johnston & Whillis, 1950), although Gardner et al. (1960) caution that these may sometimes be a characteristic of embalmed cadavers and not evident in the living person. Furthermore, Le Gros Clark (1945) also argues that fascial planes can be artefactually created by dissection. Conversely, however, some layers of deep fascia are more easily defined in fresh than in fixed cadavers (Lytle, 1979).

The superficial fascia conveys blood vessels and nerves to and from the skin and often promotes movement between the integument and underlying structures.

Skin mobility protects both the integument and the structures deep to it from physical damage. Mobility is promoted by multiple sheets of collagen fibres coupled with the presence of elastin (Kawamata et al. 2003). The relative independence of the collagen sheets from each other promotes skin sliding and further stretching is afforded by a re-alignment of collagen fibres within the lamellae. The skin is brought back to its original shape and position by elastic recoil when the deforming forces are removed. As Kawamata et al. (2003)point out, one of the consequences of the movement-promoting characteristics of the superficial fascia is that the blood vessels and nerves within it must run a tortuous route so that they can adapt to an altered position of the skin, relative to the deeper structures.

Although deep fascia elsewhere in the limbs is often not so tightly bound to the skin, nevertheless cutaneous ligaments extending from deep fascia to anchor the integument are much more widespread than generally recognized and serve to resist a wide variety of forces, including gravitational influences (Nash et al. 2004).

According to Bouffard et al. (2008), brief stretching decreases TGF-β1-mediated fibrillogenesis, which may be pertinent to the deployment of manual therapy techniques for reducing the risk of scarring/fibrosis after an injury. As Langevin et al. (2005) point out, such striking cell responses to mechanical load suggest changes in cell signaling, gene expression and cell-matrix adhesion.

In contrast, Schleip et al. (2007) have reported myofibroblasts in the rat lumbar fascia (a dense connective tissue). The cells can contract in vitro andSchleip et al. (2007) speculate that similar contractions in vivo may be strong enough to influence lower back mechanics. Although this is an intriguing suggestion that is worthy of further exploration, it should be noted that tendon cells immunolabel just as strongly for actin stress fibres as do fascial cells and this may be associated with tendon recovery from passive stretch (Ralphs et al. 2002). Finally, the reader should also note that true muscle fibres (both smooth and skeletal) can sometimes be found in fascia. Smooth muscle fibres form the dartos muscle in the superficial fascia of the scrotum and skeletal muscle fibres form the muscles of fascial expression in the superficial fascia of the head and neck.

Consequently, entheses are designed to reduce this stress concentration, and the anatomical adaptations for so doing are evident at the gross, histological and molecular levels. Thus many tendons and ligaments flare out at their attachment site to gain a wide grip on the bone and commonly have fascial expansions linking them with neighbouring structures. Perhaps the best known of these is the bicipital aponeurosis that extends from the tendon of the short head of biceps brachii to encircle the forearm flexor muscles and blend with the antebrachial deep fascia (Fig. 6). Eames et al. (2007) have suggested that this aponeurosis may stabilize the tendon of biceps brachii distally. In doing so, it reduces movement near the enthesis and thus stress concentration at that site.

The bicipital aponeurosis (BA) is a classic example of a fascial expansion which arises from a tendon (T) and dissipates some of the load away from its enthesis (E). It originates from that part of the tendon associated with the short head of biceps brachii (SHB) and blends with the deep fascia (DF) covering the muscles of the forearm. The presence of such an expansion at one end of the muscle only, means that the force transmitted through the proximal and distal tendons cannot be equal. LHB, long head of biceps brachii. Photograph courtesy of S. Milz and E. Kaiser.

Several reports suggest that fascia is richly innervated, and abundant free and encapsulated nerve endings (including Ruffini and Pacinian corpuscles) have been described at a number of sites, including the thoracolumbar fascia, the bicipital aponeurosis and various retinacula (Stilwell, 1957; Tanaka & Ito, 1977; Palmieri et al. 1986; Yahia et al. 1992; Sanchis-Alfonso & Rosello-Sastre, 2000; Stecco et al. 2007a).

Changes in innervation can occur pathologically in fascia, and Sanchis-Alfonso & Rosello-Sastre (2000) report the ingrowth of nociceptive fibres, immunoreactive to substance P, into the lateral knee retinaculum of patients with patello-femoral malignment problems.

Stecco et al. (2008) argue that the innervation of deep fascia should be considered in relation to its association with muscle. They point out, as others have as well (see below in ‘Functions of fascia’) that many muscles transfer their pull to fascial expansions as well as to tendons. By such means, parts of a particular fascia may be tensioned selectively so that a specific pattern of proprioceptors is activated.

It is worth noting therefore that Hagert et al. (2007) distinguish between ligaments at the wrist that are mechanically important yet poorly innervated, and ligaments with a key role in sensory perception that are richly innervated. There is a corresponding histological difference, with the sensory ligaments having more conspicuous loose connective tissue in their outer regions (in which the nerves are located). Comparable studies are not available for deep fascia, although Stecco et al. (2007a) report that the bicipital aponeurosis and the tendinous expansion of pectoralis major are both less heavily innervated than the fascia with which they fuse. Where nerves are abundant in ligaments, blood vessels are also prominent (Hagert et al. 2005). One would anticipate similar findings in deep fascia.

Some of the nerve fibres associated with fascia are adrenergic and likely to be involved in controlling local blood flow, but others may have a proprioceptive role. Curiously, however, Bednar et al. (1995)failed to find any nerve fibres in thoracolumbar fascia taken at surgery from patients with low back pain.

The unyielding character of the deep fascia enables it to serve as a means of containing and separating groups of muscles into relatively well-defined spaces called ‘compartments’.

One of the most influential anatomists of the 20th century, Professor Frederic Wood Jones, coined the term ‘ectoskeleton’ to capture the idea that fascia could serve as a significant site of muscle attachment – a ‘soft tissue skeleton’ complementing that created by the bones themselves (Wood Jones, 1944). It is clearly related to the modern-day concept of ‘myofascia’ that is popular with manual therapists and to the idea of myofascial force transmission within skeletal muscle, i.e. the view that force generated by skeletal muscle fibres is transmitted not only directly to the tendon, but also to connective tissue elements inside and outside the skeletal muscle itself (Huijing et al. 1998; Huijing, 1999).

One can even extend this idea to embrace the concept that agonists and antagonists are mechanically coupled via fascia (Huijing, 2007). Thus Huijing (2007) argues that forces generated within a prime mover may be exerted at the tendon of an antagonistic muscle and indeed that myofascial force transmission can occur between all muscles of a particular limb segment.

Wood Jones (1944) was particularly intrigued by the ectoskeletal function of fascia in the lower limb. He related this to man’s upright stance and thus to the importance of certain muscles gaining a generalized attachment to the lower limb when it is viewed as a whole weight-supporting column, rather than a series of levers promoting movement. He singled out gluteus maximus and tensor fascia latae as examples of muscles that attach predominantly to deep fascia rather than bone (Wood Jones, 1944).

They have argued that a common attachment to the thoracolumbar fascia means that the latter has an important role in integrating load transfer between different regions. In particular, Vleeming et al. (1995) have proposed that gluteus maximus and latissimus dorsi (two of the largest muscles of the body) contribute to co-ordinating the contralateral pendulum like motions of the upper and lower limbs that characterize running or swimming. They suggest that the muscles do so because of a shared attachment to the posterior layer of the thoracolumbar fascia. Others, too, have been attracted by the concept of muscle-integrating properties of fascia. Thus Barker et al. (2007) have argued for a mechanical link between transversus abdominis and movement in the segmental neutral zone of the back, via the thoracolumbar fascia. They feel that the existence of such fascial links gives an anatomical/biomechanical foundation to the practice in manual therapy of recommending exercises that provoke a submaximal contraction of transversus abdominis in the treatment of certain forms of low back pain.

An important function of deep fascia in the limbs is to act as a restraining envelope for muscles lying deep to them. When these muscles contract against a tough, thick and resistant fascia, the thin-walled veins and lymphatics within the muscles are squeezed and their unidirectional valves ensure that blood and lymph are directed towards the heart. Wood Jones (1944) contests that the importance of muscle pumping for venous and lymphatic return is one of the reasons why the deep fascia in the lower limb is generally more prominent than in the upper – because of the distance of the leg and foot below the heart.

In certain regions of the body, fascia has a protective function. Thus, the bicipital aponeurosis (lacertus fibrosus), a fascial expansion arising from the tendon of the short head of biceps brachii (Athwal et al. 2007), protects the underlying vessels. It also has mechanical influences on force transmission and stabilizes the tendon itself distally (Eames et al. 2007).

Om Natron

august 15, 2013 av Marius

Natron, norges billigste kosttilskudd, fåes kjøpt i butikken som helt rent natriumbikarbonat. Bikarbonat er et av de viktigste mineralene i kroppen fordi det hjelper oss å holde en stor pH-buffer kapasitet. Blodets pH holdes innenfor en liten ramme på 7,35-7,45. Hvis pH kommer langt nok utenfor denne rammen kan det være livsfarlig og vi kan gå i koma eller få permanente skader. Med stor nok buffer kan vi tåle store svigninger uten at det trenger å gå på bekostning av andre funksjoner i kroppen. Jeg anbefaler vanligvis 1 ts 2-4x daglig, som er 10-20g, i perioder når man trenger det.

Maten vi spiser og vår moderne livsstil gir kroppen en stor syre-utforing og mange mennesker går rundt med en mild acidose. Det gjelder spesielt om man har et kosthold med mye korn og lite grønnsaker. Bikarbonatinnholdet i blodet går ned, nyrene kompenserer og sjelettet utskiller mineraler. Natron fyller opp bikarbonatlagrene igjen slik at kroppen ikke trenger å kompensere med andre funksjoner.

I denne studien fra 2010 blir kostens påvirkning på surhetsgraden i kroppen gjennomgått. Den nevner bl.a. hvordan selv en mild acidose gjør at muskelene blir insulinresistente. http://www.ncbi.nlm.nih.gov/pubmed/21481501

En studie fra 2001 så på forskjellen mellom et syrefremmende kosthold og et basefremmende kosthold. Selv blodets pH ble minimalt endret, men det gikk på bekostning av andre funksjoner. Ved et surt kosthold henter kroppen basedannende mineraler fra skjelettet. Kalsiumutskillelsen økte med 74% hos de sure og kan være et bidrag til osteoporose. Den basiske gruppen fikk bl.a. bikarbonat å drikke. http://www.ncbi.nlm.nih.gov/pubmed/11446566

Svært interessant studie fra 2009 som viser hvordan bikarbonat øker mitokondrienes aktivitet og respirasjon hos mus fordi H+ i musklene dempes. Musene fikk 0,05g/kg bikarbonat og kom opp i en pH på 7,5 som holdt seg der i mer en enn time etterpå. http://ajpendo.physiology.org/content/299/2/E225

Studie fra 1991 som viser at bikarbonat er essensielt for DNA aktivitet, gjort på in vitro (på celler). pH er optimal mellom 7,5-8. http://www.ncbi.nlm.nih.gov/pubmed/1890072

Studie fra 1990 som viser at natriumklorid (salt) øker kalsium utskillelse, mens natriumbikarbonat (natron) gjør det ikke. Denne studien viser også at tilførsel av bikarbonat faktisk senker blodtrykk etter bare 7 dager. http://www.ncbi.nlm.nih.gov/pubmed/2168457

Denne studien fra 1996 viser også at natriumklorid demper den negative effekten av for mye salt i maten. Det senker blodtrykket. http://www.ncbi.nlm.nih.gov/pubmed/12013486

Denne studien viser at det er klorid-delen av salt, ikke natrium-delen, som skaper høyt blodtrykk og problemene vi hører om ang for mye salt i maten. Natrium som kommer fra natriumbikarbonat regnes som helt ufarlig. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927202/

Studie fra 2012 som viser at å drikke bikarbonat minker faren for hjerte/kar problemer hos unge mennesker med høyt kolesterol. Etter 4 uker sank totalt kolesterol med 6%, LDL med 10%, men CRP og andre faktorer ble ikke påvirket. http://www.ncbi.nlm.nih.gov/pubmed/19954956

TRENING

Bikarbonat brukes til å øke prestasjon og utholdenhet i trening, spesielt i kort-distanse og høy-intensitet øvelser. I intense aktiviteter synker pH i blod, og dette gjør at kroppen må hyperventilere for å fjerne CO2 raskt nok og holde blodet i riktig pH-ramme. Man tilfører bikarbonat for å gi kroppen større bufferkapasitet også under trening.

En studie fra 2010 gjenomgikk hvilke doser og til hvilke tider det bør inntas før treningen. De kom frem til at om man tar 0,2g/kg bør man ta det 40-50min før, og om man tar 0,3g/kg bør man ta det 60min før. http://www.ncbi.nlm.nih.gov/pubmed/20040895

En studie fra 2009 viste at 0,3g/kg ga en mye raske innhenting av pustefrekvens og CO2 etter høy-intensitet trening. Deltakerne fikk 6 doser med 10min mellomrom (fikk pH opp i 7,51) og utførte treningen 1t etter det igjen. De nevner at ved høyere bikarbonat konsentrasjoner konsumeres mer H+ og dermed også produserer mer CO2. http://www.biomed.cas.cz/physiolres/pdf/58/58_537.pdf

En studie fra 2004 så på hvordan bikarbonat påvirker muskel-pH under og etter gjentatte sprinter. pH ble 7,50, men i musklene var det ingen forskjell hverken i pH, melkesyre eller bufferkapsitet. Likevel presterte deltakerene med bikarbonat bedre i sprint 3, 4 og 5 enn kontrollgruppen. Etter trening hadde bikarbonatgruppen mye mer laktat i musklene, noe som innebærer at anaerobisk energi blir lettere tilgjengelig når blodet er mer basisk. Dette forklarerer større utholdenhet. http://www.ncbi.nlm.nih.gov/pubmed/15126714

I en studie fra 2011 ble det vist at det er ingen sammenheng mellom bikarbonat inntak og melkesyre i musklene under høy-intensitet intervaller. http://www.ncbi.nlm.nih.gov/pubmed/21197542

En studie fra 2011 undersøkte hvordan de vanlige høye dosene som anbefales for atleter (0,3g/kg) påvirker mage/tarm symptomer. For noen kan det gi diare. Studien viste at pH ble høyest og mage/tarm problemer minst når det inntas sammen med mat. Og symptomene var værst 90 minutter etter inntak. De konkluderer med at det bør inntas 2-2,5t før trening om man vil unngå mage/tarm symptomer. http://www.ncbi.nlm.nih.gov/pubmed/21719899

En studie fra 2013 viste at ved bikarbonat doser på 0,3g/kg kan det blir mage/tarm symptomer. 91% fikk diarre, 64% ble oppblåst og tørste, 45% ble kvalme. http://www.ncbi.nlm.nih.gov/m/pubmed/23746564

En ny studie fra 2013 undersøkte hvordan bikarbonat inntak flere dager før en treningsøkt kunne forbedre prestasjon og dempe acidose. De to 0,3g/kg i 5 dager. Tid før utmattelse(Tlim) økte med 23%. Bikarbonat økte også plasmavolum. Av den grunn økte ikke pH selv om bikarbonatinntaket økte. Derfor konkluderer forskerne her med at det holder å ta det dagen i forveien. Eller det viser oss at vi ikke trenger å være redd for en akkumulering av bikarbonat ved langvarig inntak. De viser også til at bikarbonat inntak bidrar til å begrense syre-overskudd i musklene ved at basisk blod trekker H+ ut. Dette øker laktat-aktivitet og dermed utholdenheten. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623762/

En studie fra 2011 nevner at pre-alkalisering med bikarbonat før trening minker effekten av Heat-Shock protiner, altså demper stressreaksjonen etter trening. http://www.ncbi.nlm.nih.gov/pubmed/21498114

En studie fra 2013 nevner at oksidativt stress etter trening minker med inntak av bikarbonat, men at årsaken ikke kommer av økt antioksidantaktivitet, men av økt TBARS og Monicyte expressend heat-shock protein. http://www.ncbi.nlm.nih.gov/pubmed/22610152

Studie fra 2012 som viser at kronisk tilførsel av bikarbonat fungerer like bra som akutt. http://www.ncbi.nlm.nih.gov/m/pubmed/23001395

Studie fra 2013 som viser at bikarbonat oksygenmetningen høy under trening. http://www.ncbi.nlm.nih.gov/m/pubmed/23903526

Studie fra 2008 som nevner at en pre-alkalisering bedrer restitusjonen etter trening, både ved aktiv og ved passiv restitusjon. http://www.ncbi.nlm.nih.gov/m/pubmed/18004683

En studie fra 2011 mener at bikarbonat har ingen effekt på trening. http://www.ncbi.nlm.nih.gov/m/pubmed/21465247

Meta-analyse så på 58 studier, fra 2010 som mener man kan ta 0,3-0,5g/kg for å øke prestansjon med 1,7%. http://www.ncbi.nlm.nih.gov/pubmed/21923200

Studie fra 1999 som forteller at ved sykkelritt opp til 60 minutter vil bikarbonat gjøre at man får større utholdenhet, utmattelse utsettes. http://www.ncbi.nlm.nih.gov/m/pubmed/10367725/

Nettside som forteller om bivirkninger m.m. relatert til bikarbonat mot sure oppstøt. http://www.nlm.nih.gov/medlineplus/druginfo/meds/a682001.html

MEDISIN

En studie fra 2000 nevner at det kan brukes for å dempe metabolsk acidemia, men ikke til å fjerne melkesyre. http://www.ncbi.nlm.nih.gov/pubmed/10631227

I medisin kan det brukes i akutt behandling av f.eks. sjokk hvor kroppen går inn i alvorlig acidose, under 7,15. http://www.ncbi.nlm.nih.gov/pubmed/18614899

En studie fra 2013 nevner at bikarbonatinntak demper nyresteinproduksjon etter bare 3 dager, når det gjelder citrat-relaterte steiner. Men pasienter med rene urinsyresteiner vil nok ikke ha like god effekt. http://www.ncbi.nlm.nih.gov/pubmed/23602798

En studie fra 2013 bekrefter at bikarbonat er nyttig for å forhindre komplikasjoner ved nyresvikt. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3729547/

KREFT

Kreftsvulster har en pH på 6,5-6,8, mens normalt vev har en pH på 7,35-7,45. Det sure mijøet i kreftsvulster gjør at de blir mer resistente mot medisiner.

En studie fra 2010 undersøkte muligheten for å endre pH rundt kreftsvulster for å hemme veksten og spredningen. Nevner at inntak av bikarbonat hos mus gjør dette. http://www.ncbi.nlm.nih.gov/pubmed/21155627

En studie fra 2011 nevner at bikarbonat i kreftbehandling er upålitelig. Av en eller annen grunn klarte ikke forskerene å oppnå alkalose i musene. Selve kreftsvulsten blie ikke særlig påvirket, men spredning ble dempet og overlevelse økte for musene i denne studien. http://www.ncbi.nlm.nih.gov/pubmed/21663677

Denne studien fra 2009 nevner at bikarbonat inntak øker pH i kreftceller og hemmer spredning hos mus. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834485/

Studie fra 2013 nevner at bikarbonatinntak øker pH i kreftcellen, som igjen øker opptaket av askorbinsyre og dermed hemmes HIF-1 og kreftens evne til overlevelse. http://www.ncbi.nlm.nih.gov/pubmed/23916956

Studie fra 2013 som viser hvordan bikarbonat og en systemisk høy pH hindrer kreftspredning. http://www.ncbi.nlm.nih.gov/m/pubmed/23936808

ARTIKLER

http://suppversity.blogspot.no/2011/11/baking-soda-for-stressed-white-blood.html

http://www.collective-evolution.com/2012/05/06/baking-soda-is-proving-to-be-an-effective-treatment-for-cancer/

http://articles.mercola.com/sites/articles/archive/2012/08/27/baking-soda-natural-remedy.aspx

http://en.wikipedia.org/wiki/Sodium_bicarbonate

Full gjennomgang av natriumbikarbonats toksisitet her: http://www.inchem.org/documents/sids/sids/sodbicarb.pdf

«The uptake of sodium, via exposure to sodium bicarbonate, is much less than the uptake of sodium via food. Therefore, sodium bicarbonate is not expected to be systemically available in the body. Furthermore it should be realised that an oral uptake of sodium bicarbonate will result in a neutralisation in the stomach due to the gastric acid. » …viser desverre ikke til noe referanse for dette utsagnet.

Natrium er ca. 1/4 av natriumbikarbonat (NaHCO3), så når vi spiser 4g Natron, får vi i oss ca.1g natrium. Maksimumsgrensen for natrium er 5g, som innbærer 20g Natron. http://www.helsekostopplysningen.no/Innhold/Kost–Kosttilskudd/Vitamniner-og-mineraler/Mineraler-og-sporstoffer-/Natrium-Na–Engelsk-Sodium-/

Denne fra 1984 nevner at natriumbikarbonat (baking soda) kjøpt i butikken er bare 3% av prisen av det vi får kjøpt på apotek, men like trygt og effektivt. http://www.ncbi.nlm.nih.gov/pubmed/6319065

Om man har lite magesyre fra før av kan det gir ubehag når man spiser natron og får enda mindre magesyre. En enkel måte å teste dette på er å ta 1ts natron i et halvt glass før mat om morgenen. Om du raper innen 5 min så har du nok magesyre. Bikarbonatet reagerer med magesyren og gir kullsyre. Og derfor raper du. Med lite magesyre blir det ikke laget nok kullsyre til å stimulere raping.

Multiday acute sodium bicarbonate intake improves endurance capacity and reduces acidosis in men

august 15, 2013 av Marius

«Since during multiday NaHCO3intake, a high amount of Na+ is ingested and absorbed, detrimental effects on endurance performance are possible. In fact, a higher [Na⁺] leads to water retention and thereby results in PV expansion 20. An increase in PV decreases blood ion concentrations, and as such results in a diminished [HCO₃^–], which in turn could counteract the benefits associated with NaHCO3 intake. It is therefore questionable, whether [HCO₃^–] can be increased beyond the concentration reached after the first day of supplementation on all subsequent days of supplementation. Consequently, we hypothesized that PV expands following a high Na+ intake, limiting any further increase in [HCO₃^–], and consequently Tlim, beyond that observed after the first day of supplementation.»

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623762/bin/1550-2783-10-16-2.jpg

«In fact, it has been shown that an increased [HCO₃^–] gradient between the intra- and extramyocellular compartment leads to an amplified H+-efflux from the muscle cell and delays the fall in intramyocellular pH 8,14«

«A fall in intramyocellular [H⁺] is associated with muscle fatigue due to 1) an inhibition of glycogenolysis and glycolysis 8, 2) increased muscular K+ release, 3) lesser contractility of the heart muscle 9, 4) inhibition of the sarcoplasmatic calcium release 10 and 5) inhibition of the actin-myosin interactions 11. Thus, delaying the fall in intramyocellular pH might postpone the fatigue process and prolong intact muscle function. Indeed, our results showed that the ingestion of NaHCO3 induced metabolic alkalosis, which in turn enhanced Tlim at CP and thus improved high-intensity exercise in the range of 10 to 20 min duration.»

«As shown in this study, the NaHCO3 intervention led to an increase in [Na⁺] and plasma osmolality after the first bolus administration. This increase was counteracted by an expansion in PV. The increase in PV was to such an extent that pre-exercise blood [HCO₃^–], pH, and ABE remained constant during the 5 days of testing. «

«In accordance with our results, McNaughton et al.29 found an increase in plasma [Na⁺] after the first of five doses of NaHCO3 but no further increase of plasma [Na⁺] on the following days. «

» Second, the apparent PV expansion in response to the high ion intake (see above) blunted any further increase in [HCO₃^–]. If the same mechanism would be true for the chronic supplementation protocol, the effectiveness of this protocol should be questioned, as it seems that [HCO₃^–] cannot be increased limitlessly, i.e. that it probably reaches a ceiling. «

«A respiratory compensation mechanism is unlikely to have occurred in our study because there were no differences between the NaHCO3 and placebo intervention for CO2 (P = 0.903, data not shown) and RER (P = 0.556, data not shown) during the resting measurements before the constant-load tests.»

The Price of Gold

august 5, 2013 av Marius

Bak scenen i toppidrett. Hva er det de egentlig gjennomgår av smerte og pine?

Stretching before sleep reduces the frequency and severity of nocturnal leg cramps in older adults: a randomised trial.

juli 25, 2013 av Marius

Om at enkel stretching før leggetid gjør at nattlige kramper blir markant mindre.

http://www.ncbi.nlm.nih.gov/m/pubmed/22341378/
Hele studien her: http://ajp.physiotherapy.asn.au/AJP/vol_58/1/Hallegraeff.pdf

t six weeks, the frequency of nocturnal leg cramps decreased significantly more in the experimental group, mean difference 1.2 cramps per night (95% CI 0.6 to 1.8). The severity of the nocturnal leg cramps had also decreased significantly more in the experimental group than in the control group, mean difference 1.3 cm (95% CI 0.9 to 1.7) on the 10-cm visual analogue scale.

CONCLUSION: Nightly stretching before going to sleep reduces the frequency and severity of nocturnal leg cramps in older adults.

http://origin-ars.els-cdn.com/content/image/1-s2.0-S1836955312700681-gr1.jpg

What is already known on this topic: Nocturnal leg cramps are common among the elderly, causing pain and sleep disturbance. The medications used to prevent nocturnal leg cramps have variable efficacy and may have substantial side effects.

What this study adds: Nightly stretching of the calves and hamstrings reduces the frequency of nocturnal leg cramps in older adults. Nightly stretching also lessens the pain associated with any cramps that continue to occur.

The cause of nocturnal leg cramps is unknown. However, several possible causes and precipitating factors have been hypothesised. Abnormal excitability of motor nerves, perhaps due to electrolyte imbalance, may be a contributing mechanism (Monderer et al 2010). Diuretics, steroids, morphine, and lithium are also reported to cause nocturnal cramps, as can repetitive movements during sport (Butler et al 2002, Kanaan and Sawaya 2001, Monderer et al 2010). Conversely, physical inactivity has been proposed as a cause, with inadequate stretching leading to reduced muscle and tendon length (Monderer et al 2010, Sontag and Wanner 1988).

Quinine and hydroquinine are moderately effective in reducing the frequency and severity of nocturnal leg cramps (El-Tawil et al 2010, van Kan et al 2000), perhaps by decreasing the excitability of the motor end plate and thereby increasing the refractory period of a muscle (Vetrugno et al 2007). However, quinine can have important side effects, especially for women, such as: thrombocytopenia, hepatitis, high blood pressure, tinnitus, severe skin rash, and haemolytic uremic syndrome (Aronson 2006, Inan-Arslan et al 2006).

Although other medications have been used to treat nocturnal leg cramps such as magnesium, Vitamin B Complex Forte, calcium, and vitamin E, none of these appears to be effective (Anonymous 2007, Daniell 1979).

Moreover, stretching techniques can foster a resilient attitude toward recovery in patients with nocturnal leg cramps by promoting a ‘bounce back and move on’ behavioural strategy (Norris et al 2008), because they give patients a strategy to seek immediate relief.

Each stretch was performed a total of three times, with 10 seconds of relaxation between each stretch. Stretching of both legs was done within three minutes.

Our results showed that six weeks of nightly stretching of the calf and hamstring muscles significantly reduced the frequency and severity of nocturnal leg cramps in older people. The best estimate of the average effect of stretching on the frequency of cramps was a reduction of about one cramp per night.

The stretches reduced the severity of the pain that occurred with the nocturnal leg cramps by 1.3 cm on a 10-cm visual analogue scale.

C-tactile fibers contribute to cutaneous allodynia after eccentric exercise.

juli 14, 2013 av Marius

Mer om huden og c-fibre i relasjon til smerte. Denne viser at ved stølhet så forsvinner smerten om man bedøver huden. Så selv om smerten oppleves som at den sitter i hele muskelen, så er det nervene helt ytterst i huden som faktisk responderer i smerteopplevelsen.

http://www.ncbi.nlm.nih.gov/pubmed/23562300

In DOMS state, there was no resting pain, but vibration reproducibly evoked pain (allodynia). The blockade of cutaneous C fibers abolished this effect, whereas it persisted during blockade of myelinated fibers. In the clinical subject, without exposure to eccentric exercise, vibration (and brushing) produced a cognate expression of CT-mediated allodynia. These observations attest to a broader role of CTs in pain processing.

This is the first study to demonstrate the contribution of CT fibers to mechanical allodynia in exercise-induced as well as pathological pain states. These findings are of clinical significance, given the crippling effect of sensory impairments on the performance of competing athletes and patients with chronic pain and neurological disorders.

Verkstedet Bodywork & Breathing System

Marius Blomsterviks nettside om forskning og kunnskap relatert til behandling av pust, ryggrad og smerte på Verkstedet Klinikk

Stikkordarkiv: trening