Kategoriarkiv: Forskning og artikler

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Human skeletal muscle intracellular oxygenation: the impact of ambient oxygen availability

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Viktig studie som beskriver alt om hvordan oksygen-nivået synker fra innpust gjennom blodkar og ut til celler, og relasjonen til trening hvor cellene ikke mottar oksygenet pga lav CO2 som følge av hyperventillering.

http://jp.physoc.org/content/571/2/415.full

Intracellular oxygen (O2) availability and the impact of ambient hypoxia have far reaching ramifications in terms of cell signalling and homeostasis; however, in vivo cellular oxygenation has been an elusive variable to assess.

These data are the first to document resting intracellular oxygenation in human skeletal muscle, highlighting the relatively high PiO2 values that contrast markedly with those previously recorded during exercise (∼2–5 mmHg). Additionally, the impact of ambient hypoxia on PiO2 and the relationship between changes in SaO2 and PiO2 stress the importance of the O2 cascade from air to cell that ultimately effects O2 availability and O2 sensing at the cellular level.

Changes in intracellular oxygen availability have far reaching consequences likely involved in such diverse processes as angiogenesis (Richardson et al. 1999c; Wagner, 2001) and hypoxic pulmonary vasoconstriction (Wang et al. 2005; Wolin et al. 2005).

Therefore, although it is known that musclePiO2 falls to very low values of 2–5 mmHg during exercising (Mole et al. 1999;Richardson et al. 2001), the starting point for skeletal muscle oxygenation or resting PiO2is, as of yet, unknown.

Hypoxia is both an important stimulus and a constant threat to the human body and its vital organs throughout life. Environmental changes such as exposure to high altitude reduce ambient O2 availability, while lung, vascular, and sleep disorders can result in hypoxia under normoxic conditions. It is known that hypoxia mediates adaptive changes in metabolism, O2 sensing and gene expression. However, although much research has examined the consequences of experimental hypoxic conditions, data documenting hypoxically mediated changes in cellular oxygenation in humans are sparse, if not non-existent.

Specifically, it was determined that in normoxia Mb was 9 ± 1% deoxygenated and this increased to 13 ± 3% in hypoxia. In our view, any degree of Mb deoxygenation supports the role of Mb as a facilitator of O2 diffusion, and thus the observation that Mb is somewhat desaturated in normoxia and furthermore that Mb desaturation increases in hypoxia is consistent with Mb playing a significant role in O2 transport from blood to cell.

Theoretically, because of the O2 cascade from air to tissue, graded reductions in FIO2 should ultimately alter in vivo O2 availability all the way to the myocyte (Richardson et al. 1995b).

In fact, this hypoxic ventilatory response (HVR) varies widely between individuals, and has been used to distinguish between those who will thrive and those who will perish at high altitude (Bartsch et al. 2001).

50% of the variance in PiO2 could be explained by the change in arterial PO2 (Fig. 4). Hence, the fall in skeletal muscle PiO2was attenuated in those subjects with a brisk HVR, making teleological sense and providing perhaps the first evidence, through arterial O2 saturation, of the importance of human HVR in terms of cellular O2 homeostasis.

Despite an apparently strong HVR in some subjects, the ambient hypoxia of 10% O2significantly reduced the average intracellular Mb saturation by ∼44% and calculated PiO2by ∼33%. Although the complete ramifications of such a change within resting muscle cells are unknown (cell signalling and growth factor responses) it is clear that such a perturbation, although relatively large, still leaves the cells far above the suggested ‘critical PO2’ (between 0.1 and 0.5 mmHg) below which muscle metabolism is compromised (Chance & Quistorff, 1978; Wilson et al. 1979; Richmond et al. 1999).

Taken together these data reinforce the concept that O2 availability and metabolism are more tightly coupled during exercise when PiO2 falls to low levels than at rest when there is a relative abundance of O2.

Specifically, in the current study a reduction in the ambient O2 to 10% resulted in an ∼11 mmHg change in PiO2 at rest (from 34 to 23 mmHg), whereas in previous investigations during exercise (using 12% O2) we have repeatedly seen closer to a ∼1 mmHg reduction (from 3 to 2 mmHg) (Richardson et al.1995b, 1999b, 2002).

This phenomenon may occur as a result of the mitochondrial transition from a somewhat quiescent state during rest to an active more governing role, in terms of determining PiO2, during exercise. Therefore, these data support the theory that during a hypoxic challenge resting PiO2 is most likely the simple consequence of ambient hypoxia upon passive diffusion, while during exercise the large increase in metabolic rate and subsequent O2consumption reduce PiO2 and facilitate O2 transport to a greater extent, somewhat staving off the effect of ambient hypoxia.

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Inspiratory muscle training reduces blood lactate concentration during volitional hyperpnoea

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Med pustetrening blir melkesyrekonsentrasjonen lavere under trening. 2 studier her, første fra 2008 og den andre fra 2012.

Den første nevner at melkesyre synker med opptil 59% (25+34%)

http://www.ncbi.nlm.nih.gov/pubmed/18560878

Although reduced blood lactate concentrations ([lac(-)](B)) have been observed during whole-body exercise following inspiratory muscle training (IMT), it remains unknown whether the inspiratory muscles are the source of at least part of this reduction.

After 6 weeks, increases in [lac(-)](B) during volitional hyperpnoea were unchanged in the control group. Conversely, following IMT the increase in [lac(-)](B) during volitional hyperpnoea was reduced by 17 +/- 37% and 25 +/- 34% following 8 and 10 min, respectively (P < 0.05).

These findings suggest that the inspiratory muscles were the source of at least part of this reduction, and provide a possible explanation for some of the IMT-mediated reductions in [lac(-)](B), often observed during whole-body exercise.

Inspiratory muscle training abolishes the blood lactate increase associated with volitional hyperpnoea superimposed on exercise and accelerates lactate and oxygen uptake kinetics at the onset of exercise.

Den andre viser til en 15% laver melkesyrekonsentrasjon og at årsaken er pustemusklenes evne til å fjerne det.

http://www.ncbi.nlm.nih.gov/pubmed/21964908

Following the intervention, maximal inspiratory mouth pressure increased 19% in the IMT group only (P < 0.01). Following IMT only, the increase in [lac(-)](B) during volitional hyperpnoea was abolished (P < 0.05). In addition, the blood lactate (-28%) and phase II oxygen uptake (-31%) kinetics time constants at the onset of exercise and the MLSS [lac(-)](B) (-15%) were reduced (P < 0.05). We attribute these changes to an IMT-mediated increase in the oxidative and/or lactate transport capacity of the inspiratory muscles.

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Inspiratory muscle training lowers the oxygen cost of voluntary hyperpnea

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Nevner at innpustmuskel trening gir mindre oksygenbehov under trening og dermed mer utholdenhet. Innpustmuskler bruker opp mye av oksygenet kroppen trenger under trening så med svak pustefunksjon blir man fort sliten. Under maksimal trening krever pustemusklene 15% av oksygenet, men med pustetrening synker det til 8%. Den nevner at diafragma og pustemuskler blir sterkere og større. Den henviser også til studier som nevner at det gir mindre melkesyre. Noe av effekten kommer også av at man får en større reserve i lungene ved å øke inn- og utpust styrken.

http://jap.physiology.org/content/112/1/127.full

IMT significantly reduced the O2 cost of voluntary hyperpnea, which suggests that a reduction in the O2 requirement of the respiratory muscles following a period of IMT may facilitate increased O2 availability to the active muscles during exercise. These data suggest that IMT may reduce the O2cost of ventilation during exercise, providing an insight into mechanism(s) underpinning the reported improvements in whole body endurance performance; however, this awaits further investigation.

THE OXYGEN COST of breathing or energy requirement of the respiratory muscles are shown to increase relative to the level of ventilation (V̇E) and the work of breathing (Wb) (1, 8). During moderate-intensity exercise the respiratory musculature requires ∼3–6% of total oxygen consumption (V̇O2T), increasing to ∼10–15% at maximal exercise (1, 3).

Inspiratory muscle training (IMT) is an intervention that has been associated with improvements in whole body exercise performance (24, 31, 34), enhanced pulmonary oxygen uptake kinetics (5), reduced blood lactate concentrations (6, 24), diaphragmatic fatigue, and cardiovascular responsiveness (37).


The oxygen cost of voluntary hyperpnea (V̇O2RM) and V̇O2RM expressed as a percentage of total oxygen consumption (V̇O2T) graphed against V̇E at low (50% V̇O2 max), moderate (75% V̇O2 max), and high (100% V̇O2 max) exercise intensities for both IMT (A) and CON (B) groups, pre- and post-training (means ± SE).
•, Pre-IMT;
○, post-IMT;
▴, pre-CON;
Δ, post-CON.

To our knowledge this study is the first to investigate the influence of IMT on the oxygen cost of voluntary hyperpnea. The main findings of the present study are that the relationship between increasing ventilatory workloads and the O2 cost of voluntary hyperpnea is curvilinear in trained cyclists and that 6 wk of pressure threshold IMT significantly reduced the O2 cost of V̇E at high ventilatory workloads. Importantly, the finding that V̇O2RM is reduced at a V̇E above 50% V̇O2 max suggests that IMT may reduce the energy requirements of the respiratory musculature in maintaining a given V̇E.

The increase in energy expenditure as V̇E increases can be attributed to a variety of sources of respiratory muscle work, including the elastic recoil of the chest and lung wall, airway resistance (4,15), increased EELV (9), and high muscle shortening velocities (19, 23). It has been suggested that as tidal breathing approaches the maximal limits for inspiratory muscle pressure development and expiratory flow rates, energy expenditure may increase to overcome the additional respiratory muscle work (3). Conversely, if one or more of the additional sources of respiratory muscle work are reduced as a result of IMT, it is reasonable to suggest that the increase in the O2 cost maybe attenuated.

In the present study, following 6 wk of IMT, V̇O2RM was significantly reduced from pretraining values at submaximal and maximal levels of ventilation. The O2 cost of voluntary hyperpnea expressed as a percentage of V̇O2T was reduced by 1.5% at a V̇Ecorresponding to 75% V̇O2max following IMT. The greatest reduction in the O2 cost of voluntary hyperpnea was observed at V̇O2 max, where V̇O2RM was significantly reduced from 11% of V̇O2T to 8% V̇O2T following IMT.

Increased ventilatory demand was previously shown to elicit a sympathetically mediated metaboreflex (33), which increases heart rate and mean arterial pressure (MAP), reducing blood flow to the limb locomotor muscles during exercise (16) and potentially reducing whole body endurance performance (18). Furthermore, Witt et al. (37) showed that IMT attenuates this increase in HR and MAP, presumably by reducing or delaying the sympathetically mediated reflex.

The 22% increase in respiratory muscle strength shown in the present study is similar in magnitude to those previously reported using pressure-threshold IMT (11, 22, 30, 32, 37). Respiratory muscle structure has also been shown to change following IMT, with an increase in diaphragm thickness (11, 12) and hypertrophy of type II muscle fibers of the external intercostal muscles (27) being reported.

Aaron et al. (3) demonstrated that individuals who reached their reserve for expiratory flow and inspiratory muscle pressure development required 13–15% of V̇O2T compared with ∼10% of V̇O2T for non-flow-limited individuals. Thus, an increase in maximal expiratory flow rates or inspiratory pressure development would increase the ventilatory reserve, thereby increasing the maximal limits for ventilation.

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Energy cost of breathing at depth: effect of respiratory muscle training

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Om at å trene innpustmuskler gjør det lettere å puste normale og uanstrengt etterpå.

http://www.ncbi.nlm.nih.gov/pubmed/22908839

RRMT significantly reduced the energy cost of ventilation, measured as delta VO2/delta V(E) during ISEV, at a depth of 55 fsw. Whether this change was due to reduced work of breathing and/or increased efficiency of the respiratory muscles remains to be determined.

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Effects of Respiratory-Muscle Exercise on Spinal Curvature

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Nevner hvor mye diafragma og pustemuskler har å si for kontroll og stabilitet i bevegelse. Bla. kjernemuskulatur og intraabdominalt trykk.

http://posturalrestoration.com/media/pdfs/Effects_of_Respiratory-Muscle_Exercise_on_Spinal_Curvature.pdf

Respiratory-muscle exercises are used not only in the rehabilitation of patients with respiratory disease but also in endurance training for ath- letes. Respiration involves the back and abdominal muscles. These muscles are 1 of the elements responsible for posture control, which is integral to injury prevention and physical performance.

The results suggest that respiratory-muscle exercise straightened the spine, leading to good posture control, pos- sibly because of contraction of abdominal muscles.

In competitive sports, the spine of young athletes can have excess thoracic kyphosis and lumbar lordosis because it is the conduit for transferring mechanical power between the upper and lower extremities during rapid and forceful movements.1

Under the influence of these forces, athletes have much degeneration of the intervertebral disks,2 and the loss of disk height with denaturation is associated with increased spine curva- ture.1 Thoracic kyphosis and lumbar lordosis contribute to back pain.3

The loss or increase of lumbar lordosis correlates well with the incidence of chronic low back pain.4,5 In addition, thoracic kyphosis leads to shoulder pain.3

Spinal-alignment control is essential for preventing various injuries. Align- ment depends on muscle strength and balance, muscle tightness, and skeletal structure.9

The trunk muscles are grouped into 2 categories: global and local stabilizers.10 The global stabilizers com- prise superficial muscles such as the rectus abdominis and longissimus muscles, and the local stabilizers are deep muscles, for example, the transverse abdominal and multifidus muscles.10 Cholewicki et al11 reported that thecontraction of local stabilizers is indispensable to trunk stability; that is, the trunk becomes unstable in the case of contraction of global stabilizers alone. The unstable trunk increases stress to the ligament and bone that control the end of motion and cause pain such as back pain.12

Respiratory-muscle exercises are used in the reha- bilitation of chronic obstructive pulmonary disease18 and endurance exercise for athletes.19 The muscles comprise the diaphragm, intercostal muscles, and the accessory muscles of respiration.20 The accessory muscles of res- piration consist of several of the trunk muscles, includ- ing local stabilizers. Therefore, this study focused on exercises for the respiratory muscles, which have the advantage that the load can be accurately set by regulating frequency and depth of breathing.

Increased spine curvature is responsible for low back pain4,5 and swim- mer’s shoulder,6 so respiratory-muscle exercise may prevent these dysfunctions.

Because muscle strength for trunk flexion was noted to increase only in the exercise group, we conclude that the exercises strongly affected the abdominal muscles. Abe et al32 reported that the transverse abdominal muscle is the most powerful in the abdominal muscle group with respect to respiration. The transverse abdominal muscle may have been specifically targeted in this exercise. This important muscle is a key local stabilizer.

Contraction of the transverse abdominis increases intra-abdominal pressure, which leads to lumbar
straightening.33 In addition, a rise in intra-abdominal pres- sure presses the rib cage upward and effectively allows the extension of the thoracic vertebrae.34

In addition, we attribute the decrease of thoracic curvatures to a stretching effect on the thorax. In a previous study, Izumizaki et al35 reported that thoracic capacity and rib-cage movement were changed by thixotropy, which is the exercise of maxi- mal expiration from maximum inspiration. The stiffness of the rib cage leads to thoracic kyphosis.3 In this study, repetitive deep breathing resolved the stiffness of the rib cage and straightened thoracic kyphosis. This process may be responsible for altering the spinal curvature.

These training methods require a long period of 12 weeks for improvement. By contrast, our intervention period was 4 weeks, so spinal alignment may be improved in a much shorter period.

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Diaphragm Postural Function Analysis Using Magnetic Resonance Imaging

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Studie som bekrefter alt om diafragma og dens bevegelse. Bl.a. at den har mye mev holdning og bevegelse å gjøre, og at baksiden beveger seg mest. Nevner også hva som er optimal bevegelse av diafragma for best fungere som stabilisator av ryggraden i bevegelse.

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0056724

When a load was applied to the lower limbs, the pathological subjects were mostly not able to maintain the respiratory diaphragm function, which was lowered significantly. Subjects from the control group showed more stable parameters of both respiratory and postural function. Our findings consistently affirmed worse muscle cooperation in the low back pain population subgroup

The diaphragm and deep stabilization muscles of the body have been described as an important functional unit for dynamic spinal stabilization [1], [2]. The diaphragm precedes any movement of the body by lowering and subsequently establishing abdominal pressure which helps to stabilize the lumbar part of the spine. Proper activation of the diaphragm within the stabilization mechanism requires the lower ribs to be in an expiratory (low) position. During the breathing cycle, the lower ribs have to stay in the expiratory position and only expand to the sides. This is an important assumption for the straight and stabilized spine. Under these conditions, the motion of the diaphragm during respiration is smooth, and properly helps to maintain abdominal pressure.

Dysfunction of the cooperation among diaphragm, abdominal muscles, pelvic floor muscles and the deep back muscles is the main cause of vertebrogenic diseases and structural spine findings such as hernia, spondylosis and spondylarthrosis [3], [4].

Noen studier å se nærmere på her:
Studies focused on diaphragm activation with the aim of posture stabilization include Hodges[11]–[14], who concluded phase modulation corresponding to the movement of the upper limbs in diaphragm electromyography records. Some works deal with various modes of diaphragm functions in various respiration types [15], [16] or in situations not directly related to respiration, e.g. activation during breath holding [17]. These studies have always concentrated on healthy subjects who did not exhibit symptoms of respiratory disease or vertebrogenic problems.

Og enda fler å se nærmere på her, spesielt relatert til scoliose:
Gierada [20] also used MRI for observing the anteroposterior size of the thorax, the height of the diaphragm during inspiration and expiration, and also the ventral and dorsal costophrenic angle during maximal breathe in and out. Kotani[21] and Chu [22] assessed chest and diaphragm movements for scoliosis patients. Suga [23]compared healthy subjects and subjects with chronic obstructive pulmonary disease (COPD), measuring the height, excursions and antero-posterior (AP) size of the diaphragm with the zone of apposition. Paradox diaphragm movements for subjects with COPD were investigated by Iwasawa [10]. Iwasawa used deep breath sequences while comparing diaphragm height and costophrenic angles. The study consisted of healthy subjects and subjects with scoliosis. Kotani [21] concluded that there was ordinary diaphragm motion with limited rib cage motion in the scoliosis group. The position of the diaphragm was measured relative to the apex of the lungs to the highest point of the diaphragm. Chu [22] compared healthy subjects against subjects with scoliosis, finding the same amount of diaphragm movement for both groups. The scoliosis group had the diaphragm significantly lower in the trunk and relatively smaller lung volumes. The distance between the apex of the lungs and the diaphragm ligaments was measured by Kondo [24], comparing young and old subjects. The effect of intraabdominal pressure on the lumbar part of the spine was observed by MRI and pressure measurement by Daggfeldt and Thorstensson [25]. Differences in diaphragm movement while performing thoracic or pulmonary breathing with the same spirometric parameters were tested by Plathow[26]. Plathow also examined the vital capacity of the lungs compared with 2D and 3D views in[27]. He concluded that there was a better correlation between the lung capacity and the 3D scans. In another study, Plathow focused on dynamic MRI. He proved significant correlations among diaphragm length and spirometric values vital capacity (VC), forced expiratory volume (FEV1) and other lung parameters [28].

Nevner også hvordan MRI-funn i ryggraden ikke har noe med smerte å gjøre:
Jensen found no direct connection between certain types of structural changes and LBP. The only structural change related to pain was disk protrusion. Carragee [31] studied MRI findings of 200 subjects after a period of low LBP, and found no direct significant MRI finding related to low back pain.

Nevner at problemer med pustefunksjon kan være en større indikator på ryggsmerter enn forandringer i ryggsøylen:
The way in which the diaphragm is used for non-breathing purposes is affected by it’s recruitment for respiration [32]. There is evidence that the presence of respiratory disease is a stronger predictor for low back pain than other established factors [33]. However, the relationship between the respiratory function and the postural function is widely disregarded[34]. Body muscles coordination for posture stabilization is a complex issue, and the role of the diaphragm in this cooperation has not been intensively studied [35].

Målet med studien:
he main goal is to separate respiratory diaphragm movements from non-respiratory diaphragm movements, and then to evaluate their role in body stabilization.
We investigated diaphragm reactability and movement during tidal breathing and breathing while a load was applied to the lower limbs.

Eksempel på diafragmas bevegelse:

Viser normal(C2) reaksjon på aktivitet(S2) og forskjellen i unormal(C1) reaksjon ved rygglager:

Figure 4. Dif-curves (solid line) and extracted res-curves (red dashed line) and pos-curves (green dotted line).

Example of harmonic breathing (A), breath with a strong postural part after the load occurred (B), harmonic breath which became partly non-harmonic after the load occurred (C, D), and breath which almost lost its ability of respiration movement ability after the load occurred (E, F).

Om hvor mye diafragma beveger seg:

As in the case of respiratory frequency, there was no change in respiratory curve amplitude in the control group when a load was applied to the lower limbs (1823 journal.pone.0056724.e253&representation=PNG journal.pone.0056724.e254&representation=PNG, 1928 journal.pone.0056724.e255&representation=PNG journal.pone.0056724.e256&representation=PNG). By contrast, the pathological group showed lowered excursions when load was applied (870 journal.pone.0056724.e257&representation=PNG journal.pone.0056724.e258&representation=PNG, 540 journal.pone.0056724.e259&representation=PNG journal.pone.0056724.e260&representation=PNG). The inter-situational difference was significantly different amongst the groups with journal.pone.0056724.e261&representation=PNG. In comparison with the pathological group, the control group had 3 times bigger excursions in situation journal.pone.0056724.e262&representation=PNG, and 6.5 times bigger excursions in the situation journal.pone.0056724.e263&representation=PNG.

In addition, the measurements showed great motion of the posterior diaphragm part than of the anterior part. Injournal.pone.0056724.e266&representation=PNG, the antero-posterior ratio was journal.pone.0056724.e267&representation=PNG within the control group and journal.pone.0056724.e268&representation=PNG within the pathological group. In journal.pone.0056724.e269&representation=PNG, the control group raised the range of the posterior part to journal.pone.0056724.e270&representation=PNG mm, resulting in an antero-posterior ratio of journal.pone.0056724.e271&representation=PNG. The pathological group, by contrast, raised the range in the anterior area and reduced the range in posterior area, resulting in an antero-posterior ratio of journal.pone.0056724.e272&representation=PNG.

Om hvordan pusten reagererer annerledes ved ryggsmerter:

We concluded that there was slower and deeper respiratory motion (parameters journal.pone.0056724.e362&representation=PNG) for both observed situations. In addition, after the postural demands rose in situation journal.pone.0056724.e363&representation=PNG, the breathing speed increased significantly (journal.pone.0056724.e364&representation=PNG) in the pathological group. In the same manner the breath depth (journal.pone.0056724.e365&representation=PNG) lessened significantly (journal.pone.0056724.e366&representation=PNG) in the pathological group. There were bigger postural moves in the control group, and they remained bigger in both situations, rising equally for each group.

Ved ryggsmerter er diafragma høyere opp i kroppen og lungene blir mindre:

The inclination of the diaphragm was greater (i.e. it was more verticalized) in the control group. The pathological group had the diaphragm placed significantly higher in the trunk, as indicated by the journal.pone.0056724.e372&representation=PNG parameter.

Om forholdet mellom diafragma og smerte, hd er høyden på diafragma, jo høyere jo mer smerte:

Diaphragm height were the only diaphragm parameter which was statistically significantly correlated (p = 0.0035) with the subjects’ low back pain indicated during the month before imaging. Pearson correlation coefficient was 0.67.

Om hvor mye diafragma beveger seg:
In the results section, we concluded that there is a statistically significant difference in the range of motion (ROM) of the diaphragm. A two and three times greater ROM was noted in the control group, than in the pathological group in situations journal.pone.0056724.e379&representation=PNG and journal.pone.0056724.e380&representation=PNG. In addition, the average diaphragm excursions journal.pone.0056724.e381&representation=PNG (central part) in situation journal.pone.0056724.e382&representation=PNG were journal.pone.0056724.e383&representation=PNG mm in the control group and journal.pone.0056724.e384&representation=PNGmm in the pathological group. In situation journal.pone.0056724.e385&representation=PNG, journal.pone.0056724.e386&representation=PNG was journal.pone.0056724.e387&representation=PNG mm in the control group and journal.pone.0056724.e388&representation=PNG mm in the pathological group.

We observed that the diaphragm was significantly higher for the pathological group. This may be a mechanism by which the pathological group was able to keep the diaphragm excursions more evenly spread after the postural demands increased.

Diafragma beveger seg normalt mer på baksiden:
We also observed that the diaphragm was more contracted in the posterior part for the control group. Diaphragm inclination measurements showed significant lowering of the posterior part of the diaphragm relative to the anterior part of the diaphragm for the control group. The pathological group kept the diaphragm in a more horizontal position.

Suwatanapongched [43]concluded that there was flattening of the diaphragm in the older population in his study. Our results did not show any significant age-related correlation of diaphragm flatness. Instead, the only significant correlation that we observed was between diaphragm height and the LBP intensity of the pathological group during the month before the measurements were made.

Jo høyere opp diafragma er, jo vanskeligerere blir den å bevege:
We assume that this diaphragm bulging is due to worse ability to contract the diaphragm properly. To the best of our knowledge, there are no results in the literature for measurements of diaphragm flatness in subjects suffering from LBP. Worse ability to contract the diaphragm in the pathological group is also supported by the significantly higher position in the trunk.

No correlation was concluded between measured parameters and pain intensity except for bulging (i.e. long term pain) of the diaphragm, as was discussed above. The results indicate that, as the pain is long term, the patients do not change their respiratory patterns according to fluctuations in the chronic LBP.

The significant differences in the harmonicity of the diaphragm motion observed in this study indicate changes in the central nervous system related to diaphragm function in subjects with pathological spinal findings suffering from various intensities of chronic low back pain. Low back pain is a wide-spread and widely studied phenomenon. Alternating respiratory patterns and anatomical changes in the diaphragm have been assessed in LBP subjects. Studies concluding increased susceptibility to pain and injury [1], [13], [49] identified differences in muscle recruitment in people suffering from LBP. Janssens [50] used fatigue of inspiratory muscles, and observed altered postural stabilizing strategy in healthy subjects. Jenssens also observed non-worsening stabilization with an already altered stabilizing strategy in subjects suffering from LBP. Grimstone [51] measured respiration-related body imbalance in subjects suffering from LBP, observing worse stability in subjects with LBP. Kolar [44] investigated differences in diaphragm contractions between healthy subjects and LBP subjects. He observed lesser contractions in the posterior part of the diaphragm while the postural demands on the lower limbs increased, and he suspected that intra-abdominal pressure lowering might be the underlying mechanism of LBP. Roussel [34] assessed the altered breathing patterns of LBP subjects during lumbopelvic motor control tests, concluding that some subjects used an altered breathing pattern to provide stronger support for spinal stability.
In our measurements, we did not observe the same diaphragm excursions in the posterior part of the diaphragm for healthy subjects and for subjects suffering from LBP as were observed by[44]. The excursions were reduced in the pathological group. In contrast with Kolar’s findings[44], we concluded that there was also lowering of the diaphragm inspiratory position in the pathological group in situation journal.pone.0056724.e399&representation=PNG. Our measurements support the hypothesis of less diaphragm contraction in the pathological group, with a significant correlation between diaphragm bulging and the intensity of the patient’s low back pain.

Om hvordan magemuskler er nødvendig for diafragma stabilitet:
In the pathological group, the abdominal muscles lack the ability to hold the ribs in lower position. For this reason, the insertion parts of the diaphragm are not fixed and the diaphragm muscle changes its activation. The diaphragm is disharmonic in its motion, which causes problems with providing respiration and at the same time retaining abdominal pressure. The muscle principle for spine stabilization is therefore violated, and is replaced by a substitute model, which tends more easily toward the emergence of low back pain, spine degeneration or disc hernia.

Reversed causation is always a possibility, i.e. it is possible that the diaphragm behavior is changed in order to stabilize the spine after the deep intrinsic spinal muscles fail. During these changes, breathing patterns may occur, e.g. breath holding and decreased diaphragm excursions.

Our study shows a way to compare the diaphragm motion within the group of controls without spinal findings and those who have a structural spinal finding, e.g. a hernia, etc., not caused by an injury. In this way, we confirm our experience of the influence of the diaphragm on spinal stability and respiration. The control group show a bigger range of diaphragm motion with lower breathing frequency. The diaphragm also performs better harmonicity (coordination) within its movement. The postural and breathing components are better balanced. This fact is very important for maintaining the intraabdominal pressure, which helps to support the spine from the front. For this reason, it plays a key role in treating back pain, hernias, etc. In the group of controls we also found a lower position of the diaphragm while it was in inspiration position in tidal breathing and also while being loaded. These facts also support the ability of the diaphragm to play a key role in maintaining the good stability of the trunk. It is also important that we are able to separate the phases of diaphragm movement. This supports both the postural function and the breathing function of this muscle due to MR imaging.

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Pain Sensitivity and Analgesic Effects of Mindful States in Zen Meditators: A Cross-Sectional Study

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Nevner hvordan smerteopplevelse blir mindre med meditasjon, men viser også til at det sannsynligvis er pustefrekvensen som gir den smertestillende effekten. Pluss den nevner hvordan frontallappen bidrar med smertestillende opioider.

http://www.psychosomaticmedicine.org/content/71/1/106.long

These results indicated that Zen meditators have lower pain sensitivity and experience analgesic effects during mindful states. Results may reflect cognitive/self-regulatory skills related to the concept of mindfulness and/or altered respiratory patterns.

Mindfulness can be described as an equanimous state of observation of one’s own immediate and ongoing experience.

Mindfulness has been described as “intentional self-regulation of attention from moment to moment … of a constantly changing field of objects … to include, ultimately, all physical and mental events….” (5). Furthermore, an attitude of acceptance toward any and all experience is stressed. Traditional accounts of mental and emotional transformation accompanying mindful practice (6,7) are supported by scientific findings of psychological and biological effects on practitioners (8–10) and patients (5,11–15).

Mindfulness-based therapies have reported success treating anxiety (11,15), obsessive compulsive disorder (13), and depression (12,14). Positive correlations between meditation experience of Buddhist monks and positive affect (10) have been reported. Increases in positive affect have also been observed in a longitudinal study in which naïve subjects were trained to meditate (8).

It is well known that cognitive manipulations, such as hypnosis, attention, expectancy or placebo, can influence the experience of pain and the associated neurophysiological activity (17–19). There is also mounting evidence that mindfulness may be effective in treating chronic pain.

Significant positive improvements were found on all measures immediately after the 10-week training program. However, follow-up evaluation showed stable improvements on most measures with the exception of present moment pain. The authors interpreted the results as the acquisition of an effective coping strategy for pain, where the pain itself did not change but the relation or stance taken toward the pain was positively altered.

Changes in pain were further examined in relationship to meditation training. The amount of meditation experience of individual practitioners predicted the degree of pain intensity modulation (i.e., versus baseline) with more hours of experience leading to greater reductions in pain intensity during the mindfulness condition [r(9) = −.82, p< .01].

Notably, pain modulation induced by mindfulness (relative to baseline-1) was correlated with the corresponding changes in respiratory rate across all subjects [intensity: r(23) = .37, p = .03; unpleasantness: r(23) = .42, p = .02]. Furthermore, the significant decrease in pain intensity reported above in the meditators during the mindfulness condition relative to baseline-1 (Figure 2) did not reach significance after including the changes in respiration as a covariate [F(1,11) = 3.02, p = .11]. In contrast, the significant increase in pain intensity reported by the control subjects in the concentration condition remained significant after accounting for changes in respiratory rates [F(1,11) = 20.94, p = .001]. These effects suggest that the changes in pain induced by mindfulness, but not concentration, may be at least partly accounted for by changes in respiration.

The main findings are the following:

  • 1) Meditators required hotter temperatures than controls to experience moderate pain.
  • 2) As hypothesized, meditators experienced less pain while attending mindfully, whereas control subjects did not show such modulation.
  • 3) Unexpectedly, analgesic effects of mindfulness were more clear on the sensory dimension of pain (i.e., perceived intensity) than the affective dimension of pain (i.e., pain unpleasantness), although effects were observed in the same direction.
  • 4) The magnitude of the analgesic effect of mindfulness was predicted by the number of hours of meditation practice in meditators.
  • 5) When attention was directed toward the stimulation, with no mention of attending mindfully, control subjects showed the expected increase in pain intensity and unpleasantness whereas meditators did not differ from baseline.
  • 6) Physiologically, meditators had slower breathing rates than controls, consistent with their self-assessed reduced reactivity. Importantly, changes in respiratory rate predicted the changes in felt pain and the analgesic effect of mindfulness states was no longer significant after accounting for changes in respiratory rates (covariance).
  • 7) On a mindfulness scale, meditators scored higher on the tendency to be observant and nonreactive. Higher scores on these dimensions of mindfulness were further associated with lower pain sensitivity and slower respiratory rates.

Zen meditation was associated with lower pain sensitivity as demonstrated by the higher temperatures required to produce moderate pain. The observed difference (49.9°C versus 48.2°C) should be considered large as it typically corresponds to an increase of about 50% on a ratio scale of pain perception or 20 to 25 points on a 0 to 100 numerical pain scale, based on similar psychophysical methods (28,33).

While attending mindfully, the Zen practitioners showed reductions of 18% pain intensity. Remarkably, individuals with more extensive training experienced greater reduction in pain. This finding is extremely important as it suggests that the observed pain reduction may not simply reflect a predisposition to meditation (individual differences) but may also involve experience-dependent changes associated with practice. This is in line with other studies linking meditation training with mindfulness, medical symptoms, and well-being (16); attention performance, anxiety, depression, anger, cortisol and immunoreactivity (34); an inverted U-shaped function of attention-related brain activity (35); electrophysiological markers of positive affect (10); positive affect and stronger immune responses (8); and cortical thickness and gray matter density (9,36,37).

The analgesic effects of mindful attention may relate to the physiological state induced as suggested by the respiration data. Overall, the meditators breathed at a slower rate than control subjects in all conditions and their mean respiratory pattern followed that of their pain ratings. In contrast, respiratory rate did not change noticeably across conditions in the control subjects. Slower breathing rates (typically meditators) were associated with less reactivity and with lower pain sensitivity. These relationships suggested that the meditators were in a more relaxed, nonreactive physiological state throughout the study, which culminated in the mindfulness condition and which influenced the degree to which they experienced pain.

The covariance analysis suggested that this analgesic effect could be mediated at least in part by the observed change in respiration.

A neuro-chemical model of meditation put forth by Newberg and Iversen (47) offers a possible explanation for our results. Meditation practice, involving volitional regulation of attention, seems to activate prefrontal cortex (35,48,49); this has been observed during Zen practice (50). Increases in prefrontal activation can stimulate the production of b-endorphin (e.g., in the arcuate nucleus of the hypothalamus) (47). B-endorphin is an opiate associated with both analgesia and a reduction in respiratory rate as well as decreases in fear and increases in joy and euphoria (47). Interestingly, the direction of attention toward breathing and the volitional control of breathing rates are part of many meditative techniques; however, causation can obviously not be inferred from those observations.

Another related possibility is that meditation leads to reductions in stress and stress-related chemicals, such as cortisol which interact with the opiate system. A reduction of cortisol can greatly enhance the binding potential/efficacy of endogenous opioids (27), possibly contributing to a downregulation of nociceptive responses. Studies have reported evidence of reduced cortisol responses in meditators (34,52,53).

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Vascular Fasciatherapy Danis Bois Method: a Study on Mechanism Concerning the Supporting Point Applied on Arteries

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Studie som nevner svært mye interessant om blodsirkulasjon, tensegritet og om bindevev. Den er rettet mot en spesifikk metode for spontan bevegelse, men har mye interessante teamer som gjelder andre bodyworkmetoder også.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3242644/

«Vascular research especially made a jump forward with the Nobel Prize awarded to Furchgott, Ignarro and Murad for having discovered the endogenous production of nitric oxide (NO). »

«Mesenchyme differentiates and generates every type of connective tissue and many organs in adults(3) including bone, muscle, and the middle layer of the skin, excepting nervous tissue and the digestive track(7).»

«In this study, one can notice that they are totally or partially at the origin of vascular endothelium and mesothelium (peritoneum, pleura, pericardium)(6). And this vascular endothelium is the origin of blood, which is also considered as specialized connective tissue(6).»

Forskjellen mellom arterier og kapillærer:
«Capillaries have the function of distributing blood in the body, bringing about an exchange between blood and tissues. Structurally, arteries carry and separate blood and tissues.»

«Fascia is a very sensitive tissue that detects any kind of stress — physical, emotional or psycho-social. It reacts by contracting and imprisoning the organs it covers, thus impairing their physiological functions. Furthermore, the tightening of their connective parts induces a perceptible disturbance in mobility and rhythm of these organs.»

«ECs respond to increased blood flow by causing relaxation of the surrounding VSMCs. VSMC relaxation in response to flow occurs over seconds to minutes and if high flow persists, remodeling of the artery wall enlarges the lumen over time in a period of weeks to months(36). Decreased flow induces vessel narrowing(37), and extreme low flow may lead to complete vessel regression, which involves apoptosis of the ECs(38).»

«The human body seems to be made of the only and same tissue which is functionally differentiated: there are only tissue connections, simply a histological continuum without any clear separation between the skin and hypodermis, the vessels, the aponeurosis, and the muscles(46). So connective tissue, its cells, MEC, and fibers are an obvious link in this construction.»

«The theory of tensegrity emerged from the interests of architects (from Richard Buckminster Fuller to Rene Motro) and biologists (Donald Ingber(47)), and their meeting point of connection with our discussion can be found in these definitions: “a type of prestressed structural network, composed of opposing tension and compression elements that self-stabilizes its shape through establishment of a mechanical force balance”, and “tensegrity is used to stabilize the shape of living cells, tissue and organs, as well as our whole bodies”(4). Hence, the use of this architectural system for structural organization provides a mechanism to physically integrate part and whole(4).»

«Arteries have a special relation with fascias. Connective tissue is present in the three tunics of the artery. Adventitia is a typical sheathing fascia, which becomes tense in reaction to stress. Media is an association of muscle and connective tissue reacting to local mechanical variations (i.e. blood pressure) or general influence (i.e. stress) by tensing and/or by contracting. Intima, whose endothelium can be assimilated to a very big autocrine/paracrine formation(48)reacting mainly to the influence of blood qualities (i.e. type of flow, components), lies on a connective layer underlining endothelium.»

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The Architecture of the Connective Tissu e in the Musculoskel etal System-An Often Overlooked Function al Parameter as to P roprioception in the Locomotor Apparatus

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Om bindevevets struktur, mye om mechanoreceptors i bindevevet (golgi, ruffini og pacini spesielt), pluss den nevner «dynamic ligaments» som en del av bindevevet inni og igjennom muskler.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091473/

«The discrimination between so-called joint receptors and muscle receptors is an artificial distinction when function is considered. Mechanoreceptors, also the so-called muscle receptors, are arranged in the context of force circumstances-that is, of the architecture of muscle and connective tissue rather than of the classical anatomic structures such as muscle, capsules, and ligaments. »

«The receptors for proprioception are concentrated in those areas where tensile stresses are conveyed over the elbow joint. Structures cannot be divided into either joint receptors or muscle receptors when muscular and collagenous connective tissue structures function in series to maintain joint integrity and stability. In vivo, those connective tissue structures are strained during movements of the skeletal parts, those movements in turn being induced and led by tension in muscular tissue. In principle, because of the architecture, receptors can also be stimulated by changes in muscle tension without skeletal movement, or by skeletal movement without change in muscle tension. »

«A mutual relationship exists between structure (and function) of the mechanoreceptors and the architecture of the muscular and regular dense connective tissue. Both are instrumental in the coding of proprioceptive information to the central nervous system.»

«Schleip mentions the fascia as «the dense irregular connective tissue that surrounds and connects every muscle, even the tiniest myofibril, and every single organ of the body forming continuity throughout the body.»(

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Destroy user interface control3) In this way, fascia is considered an important integrative element in human posture and movement organization (locomotor apparatus) and is often referred to as the «organ of form.»(

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«The primary connective tissue of the body is the embryonic mesoderm. The mesoderm represents the matrix and environment within which the organs and structures of the body have been differentiated and therefore are embedded.»

«The principal function of mesoderm as «inner tissue» is «mediating» in the sense of «connecting» (binding) and «disconnecting» (shaping space). »

«Regular dense connective tissue structures such as ligaments convey (transmit) those forces «passively.»»

«Connective tissue and fasciae are richly innervated. Fascial layers may thus play an important role in proprioception and nociception. Considerations such as «architecture versus anatomy (topography),»mutatis mutandis may also apply for the spatial organization of mechanoreceptors, the morphologic substrate for proprioception. »

«Mechanoreceptors are in fact free nerve endings (FNEs), whether or not equipped with specialized end organs. The main stimulus for such receptors is deformation. Variation exists as to the microarchitecture of the ending.»

«Mechanoreceptors associated with muscles, including the muscle auxiliary structures such as tendons, are usually classified(14–

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Destroy user interface control17) as follows:

  • FNEs (unencapsulated)
  • Muscle spindles (sensory endings with encapsulated intrafusal muscle fibers)
  • GTOs (type III endings, relatively large-100 -600 μm diameter-spray-like endings, with high threshold and very slow-adapting)

The mechanoreceptors typically associated with joints are these:

  • FNEs (unencapsulated)
  • LCs (type II ending with a two- to five-layered capsule, less than 100 μm in length, with low threshold and rapidly adapting). Here, this term is preferred to paciniform corpuscle.
  • RCs (type I ending, relatively small-up to 100 μm-spray-like ending with low threshold and slow-adapting)»

«Those nerve fibers are involved in the afferent pathway of proprioceptive information from the transitional areas between the connective tissue layers and the muscle fascicles organized in series with them [shown schematically in Fig. 7(a)]. This also seems to represent a more ligamentous or articular «pattern of innervation» compared with the related nerve fascicles running on the «outside» of the innervated structure. This is actually a typical capsular or articular pattern [see Fig. 7(a)]. »

«An in series unit of muscular tissue/RDCT layer/skeletal element equipped with mechanosensitive substrate at the transitional areas between the various tissue components constitutes the basic unit of the spatial organization of the substrate of proprioception. Such a unit may occur as a muscle fraction in series with a muscle compartment wall that is shared with the muscular tissue of an adjacent muscle. It may also appear as a muscle compartment wall with muscle fascicles inserting unilaterally and with afferent nerve fibers reaching the related mechanoreceptors from the outer side. This was introduced earlier as the typical «dynamic ligament» (dynament-see Fig. 10, pattern 4).»

«The conclusion is that, in vivo, the activity of a mechanoreceptor is defined not only by its functional properties, but also by its architectural environment. If Abrahams, Richmond, and Bakker(

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Destroy user interface control34) state that the topography of mechanoreceptors provides a «subtle comparative function in the process of sensory coding of muscle events,» they raise the important issue of the spatial distribution of receptors in the process of proprioception. To this should be added the notion that the architecture of the muscular and connective tissue and consequent receptor distribution plays a significant role in the coding of the proprioceptive information that is provided.»