Postural function of the diaphragm in persons with and without chronic low back pain.

Denen Studien beskriver på en svært god måte hvordan diafragmas posisjon og bevegelse kan relateres til ryggplager. Når diafragm får lite bevegelse, spesielt i de fremre og mitre delene, blir vinkelen diafragma står i kroppen brattere. Dette kobles til ryggsmerter. Jo brattere vinkelen er, jo større sjangse for ryggsmerter. Bildene viser hvordan diafragma beveger seg mindre og står høyere opp i kroppen hos det med kroniske ryggsmerter. Den viser også hvordan største delen av bevegelsen i diafragma skjer på bakre del, ikke fremre eller midtre, men ved korsryggplager blir det minst bevegelse i fremre og midtre del, mens bakre del har lige god bevegelse. Spesielt interessant å legge merke til er at den viser ingen forskjell mellom Control og Patients diafragma bevegelse under Tidal Breathing (abdominal pust). Dette viser at for å øke styrke og bevegelse i diafragma må man ta i mer. Abdominal pust er ikke diafragma trening.

http://www.ncbi.nlm.nih.gov/pubmed/22236541/

Hele her: http://www.rehabps.cz/data/JOSPT.pdf

Abstract

STUDY DESIGN:

A case-control study.

OBJECTIVES:

To examine the function of the diaphragm during postural limb activities in patients with chronic low back pain and healthy controls.

BACKGROUND:

Abnormal stabilizing function of the diaphragm may be an etiological factor in spinal disorders. However, a study designed specifically to test the dynamics of the diaphragm in chronic spinal disorders is lacking.

METHODS:

Eighteen patients with chronic low back pain due to chronic overloading, as ascertained via clinical assessment and magnetic resonance imaging, and 29 healthy subjects were examined. Both groups presented with normal pulmonary function test results. A dynamic magnetic resonance imaging system and specialized spirometric readings were used with subjects in the supine position. Measurements during tidal breathing (TB) and isometric flexion of the upper and lower extremities against external resistance with TB were performed. Standard pulmonary function tests, including respiratory muscle drive (PI(max) and PE(max)), were also assessed.

RESULTS:

Using multivariate analysis of covariance, smaller diaphragm excursions and higher diaphragm position were found in the patient group (P<.05) during the upper extremity TB and lower extremity TB conditions. Maximum changes were found in costal and middle points of the diaphragm. A 1-way analysis of covariance showed a steeper slope in the middle-posterior diaphragm in the patient group both in the upper extremity TB and lower extremity TB conditions (P<.05).

CONCLUSION:

Patients with chronic low back pain appear to have both abnormal position and a steeper slope of the diaphragm, which may contribute to the etiology of the disorder.

 

Perhaps the most clinically important finding of this study concerns the ab- normal coordination of the diaphragm in the patient group during inspiration with postural tasks. This impairment was demonstrated by reduced move- ment of the diaphragm in the anterior and middle portion, while the posterior (crural) part moved in the same manner as in the control group. This pattern of diaphragmatic recruitment resulted in a steeper angle in the middle-posterior part of the diaphragm (FIGURE 4), which may exacerbate the symptomology of chronic low back pain by increasing the anterior shear forces on the ventral region of the spinal column.

Poor coordination of particular di- aphragmatic parts in the patients (points B and C) resulted in an asymmetric dia- phragmatic activation during inspiration, as demonstrated by a steeper slope of the crural part of the diaphragm. Evidently, limited motion of the costal part may result in a more domed inspiratory diaphragmatic position.

In healthy subjects, the diaphragm is able to perform the dual task (trunk stability and respiration) when trunk stability is challenged.19 Generally, dur- ing any body movement, with activation of the extremities during weight-bearing or weight-lifting activities and transi- tional movements, there is simultaneous spinal bracing and transdiaphragmatic pressure elevation.11,22 Intra-abdominal pressure increases, with a simultaneous decrease of intrapleural pressure, during a contraction of both the posterior (cru- ral) and anterior (costal) portions of the diaphragm.7 This coordination may be compromised in patients with chronic low back pain.

CONCLUSION

We found reduced diaphragm movement when isometric flexion against resistance of the up- per or lower extremities was applied. The combined, more cranial position in the anterior and middle portions of the diaphragm and, particularly, the steeper slope between the middle and crural por- tions of the diaphragm in patients with chronic low back pain may contribute to low back pain symptoms. However, given that the results are based on cross- sectional analysis, we cannot exclude the possibility of reverse causation. Still, the results support the theory that patients with low back pain complaints present with compromised diaphragm function, which may play an important role in pos- tural stability.

KEY POINTS

FINDINGS: We found reduced diaphragm movement in patients with chronic low back pain compared to healthy controls when isometric flexion against resis- tance of the upper or lower extremity was applied, mainly in the anterior

and middle portions. This pattern of diaphragmatic recruitment resulted in
a steeper angle in the middle-posterior part of the diaphragm and likely a great- er strain during activity on the ventral region of the spinal column. IMPLICATIONS: Abnormal postural activa- tion of the diaphragm during the pos- tural task of isometric resistance to the extremities may serve as 1 underlying mechanism of chronic low back pain. CAUTION: Only an isolated analysis of the diaphragm excursion was performed, due to the limited field of view. In ad- dition, the diaphragm excursion alone may not be sufficient to understand all mechanical actions of the rib cage and related musculature. We used a con- venience sample in which the patient and control groups differed in size and certain demographic characteristics. Because our study was cross-sectional in nature, we cannot exclude the possibil- ity that low back pain symptoms may be indicative of an initial pathogenic insult resulting in secondary quantitative as well as qualitative adaptive changes in diaphragmatic function.

To studier på hvordan Intercostal Stretch gir bedre pust

Nevner hvordan stretch øvelser av brystkassen sammen med innpust gir en lettere og roligere pust etterpå, og større bevegelse av diafragma. Dette prinsippet brukes i øvelsene i vårt Breathing System Diafragma trening.

Does Intercostal Stretch Alter Breathing Pattern and Respiratory Muscle Activity in Conscious Adults?

http://www.sciencedirect.com/science/article/pii/S0031940605609327

Summary

The effects of intercostal (IC) stretch on breathing patterns and respiratory muscle activity were monitored in nine healthy subjects. Tidal volume (Vt), breathing frequency (Fb), and inspiratory (Ti) and expiratory (Te) durations were determined from a pneumotachometer. Peak amplitudes and burst durations of activity in the diaphragm, parasternal ICs and external abdominal oblique muscles were determined from surface EMGs.

The third and eighth IC spaces were stretched in phase with inspiration or expiration when supine and 60° semi recumbent. Vt increased and Ti and Te were prolonged, resulting in a decreased Fb, independent of site of stretch, phase of breathing, or body position, during IC stretch compared to controls.

Peak amplitudes and burst durations of diaphragmatic EMG and burst durations of parasternal ICs were greater when the third and eighth IC spaces were stretched during inspiration compared to controls. Peak amplitudes of parasternal ICs increased only when the third IC space was stretched during inspiration. When applied during expiration, IC stretch increased only parasternal activity in the supine position. Intercostal stretch applied in phase with inspiration resulted in a slower, deeper breathing pattern with increased activity of the diaphragm and parasternal IC muscles. IC stretch may alter breathing sufficiently to improve gas exchange in some patients with pulmonary disorders.

 

EFFECT OF INTERCOSTAL STRETCH ON PULMONARY FUNCTION PARAMETERS AMONG HEALTHY MALES

Click to access Mohan_15062012_proof.pdf

The use of manual stretching procedures has become more prevalent in cardiorespiratory physiotherapy to improve pulmonary functions. However, limited evidence exists regarding evaluation of their effectiveness. The study aimed to determine the impact of Intercostal (IC) stretch in improving the dynamic pulmonary function parameters (Forced Expiratory Volume in the first second (FEV1), Forced Vital Capacity (FVC) and FEV1/FVC % and respiratory rate among healthy adults. Thirty healthy male subjects were recruited based on inclusion and exclusion criteria. Subjects were assigned to the experimental group and the control group through random sampling method. In the experimental group, subjects underwent IC stretch for ten breaths on the inspiratory phase of the respiratory cycle with breathing control exercises in semi recumbent position, while in the control group, breathing control exercises alone were performed in the semi recumbent position. The results of the study showed, FEV1/FVC % in the experimental group significantly improved with P=0.017 (p<0.05) than the control group, which means IC stretch increased lung volume and lead to improved lung function. This study suggested the IC stretching with breathing control may be more effective in improving dynamic lung parameters especially FEV1/FVC % than breathing control alone.

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

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

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

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

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

CONCLUSION:

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

Evolution of Air Breathing: Oxygen Homeostasis and the Transitions from Water to Land and Sky

Omfattende studie som beskriver hvordan vi har tilpasset oss høyere nivåer av oksygen. Bekrefter alle innspill jeg har hatt om oksygen sin destruktive effekt og at beskyttelsen mot oksygenets skadevirkninger er viktigere enn å få mer oksygen inn i kroppen. Lunger, sirkulasjonssystem, hemoglobin, antioksidantsystem og det at mitokondriene er godt gjemt inni en annen celle som er godt beskyttet av en tett cellevegg er forsvars- og reguleringsmekanismer mot det livsfarlige men også livsnødvendige oksygenet.

Nevner at den opprinnelige atmosfæren bestod av veldig lite O2(1-2% eller 2,4 mmHg) og mer enn dobbelt så mye CO2. Dette er miljøet mitokondriene ble utviklet i for 2,7 billioner år siden, og som de fortsatt lever i inni cellene våre. Om oksygennivået økes tilmer enn dette blir mitokondriene dårligere og mister sin funksjon.

Nevner også at forsvarsmekanismene mot oksygen var tilstede helt fra starten. Og hemoglobin (blodcelle i dyr) og klorofyll (i planter) tilfredstiller alle de nødvendige beskyttende egenskapene vi trenger mot oksygen.

Nevner at CO2 var den første antioksidanten i evolusjonen.

Beskriver også det som skjer i mitokondria, at hypoxi (lavere O2 tilgjengelighet) gir mindre ROS og økt mitochondrial uncoupling (produksjon av varme istedet for ATP). Vi kan se dette som om mitokondriene går på tomgang med lavt turtall, mens ATP produksjon er høyt turtall og dermed også mer slitasje.

Nevner også evolusjonen av diafragma som den primære pustemuskelen.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926130/

Abstract
Life originated in anoxia, but many organisms came to depend upon oxygen for survival, independently evolving diverse respiratory systems for acquiring oxygen from the environment. Ambient oxygen tension (PO2) fluctuated through the ages in correlation with biodiversity and body size, enabling organisms to migrate from water to land and air and sometimes in the opposite direction. Habitat expansion compels the use of different gas exchangers, for example, skin, gills, tracheae, lungs, and their intermediate stages, that may coexist within the same species; coexistence may be temporally disjunct (e.g., larval gills vs. adult lungs) or simultaneous (e.g., skin, gills, and lungs in some salamanders). Disparate systems exhibit similar directions of adaptation: toward larger diffusion interfaces, thinner barriers, finer dynamic regulation, and reduced cost of breathing. Efficient respiratory gas exchange, coupled to downstream convective and diffusive resistances, comprise the “oxygen cascade”—step-down of PO2 that balances supply against toxicity. Here, we review the origin of oxygen homeostasis, a primal selection factor for all respiratory systems, which in turn function as gatekeepers of the cascade. Within an organism’s lifespan, the respiratory apparatus adapts in various ways to upregulate oxygen uptake in hypoxia and restrict uptake in hyperoxia. In an evolutionary context, certain species also become adapted to environmental conditions or habitual organismic demands. We, therefore, survey the comparative anatomy and physiology of respiratory systems from invertebrates to vertebrates, water to air breathers, and terrestrial to aerial inhabitants. Through the evolutionary directions and variety of gas exchangers, their shared features and individual compromises may be appreciated.

Introduction

Oxygen, a vital gas and a lethal toxin, represents a trade-off with which all organisms have had a conflicted relationship. While aerobic respiration is essential for efficient metabolic energy production, a prerequisite for complex organisms, cumulative cellular oxygen stress has also made senescence and death inevitable. Harnessing the energy from oxidative phosphorylation while minimizing cellular stress and damage is an eternal struggle transcending specific organ systems or species, a conflict that shaped an assortment of gas-exchange systems.

The respiratory organ is the “gatekeeper” that determines the amount of oxygen available for distribution. Gas exchangers arose as simple air-blood diffusion interfaces that in active animals progressively gained in complexity in coordination with the cardiovascular system, leading to serial “step-downs” of oxygen tension to maintain homeostasis between uptake distribution and cellular protection.

While a comprehensive treatment of the evolutionary physiology of respiration is beyond the scope of any one article, here we focuses on the first step of the oxygen cascade—convection and diffusion in the gas-exchange organ—to provide an overview of the diversity of nature’s “solutions” to the dilemma of acquiring enough but not too much oxygen from the environment.

Ubiquity of Reactive Oxygen Species

As reviewed by Lane (407) and Maina (466), the primary atmosphere contained mainly nitrogen, carbon dioxide, and water vapor. Much of these were swept away by meteorite bombardment and replaced with a secondary atmosphere (416-418, 579, 590) consisting of hydrogen sulfide, cyanide, carbon monoxide, carbon doxide, methane, and more water vapor from volcanic eruptions. Only trace oxygen (<0.01% present atmospheric level) existed (418), originated from inorganic (photolysis and peroxy hydrolysis) (622) and organic (photosynthesis) sources.

Oxidative respiration is the reverse process as O2 accepts four electrons successively to form water. Many of these steps are catalyzed by transitional metal ions (e.g., iron, copper, and magnesium). Therefore, aerobic respiration, oxygen toxicity and radiation poisoning represent equivalent forms of oxidative stress (407).

Origin of Oxygen Sensing and Antioxidation—Metalloproteins

If oxidative stress was present from the beginning, early anaerobic organisms must have possessed effective antioxidant defenses, including mechanism(s) for controlled O2 sensing, storage, transport, and release as well as pathways for neutralizing ROS. The general class of compounds that fulfill these requirements is the metalloproteins that transfer electrons via transitional metals (766, 767), for example, heme proteins and chlorophyll (Fig. 2).

Hydrogen may have been the first electron donor and CO2 the first electron acceptor for synthesizing ATP by chemiosmosis (408).

Because of a high redox potential of O2 as the terminal electron acceptor in electron transport, aerobic respiration is far more efficient in energy production (36 moles of ATP per mole of glucose) than anaerobic respiration (~5 moles). Aerobic multicellular organisms arose approximately 1 Ga and more complex organisms such as marine molluscs thrived approximately 550 to 500 million years ago (Ma). Exposed to a still low O2 tension in the deep sea, these organisms uniformly possessed metalloprotein respiratory pigments with a characteristically high O2 affinity for efficient O2 storage and slow O2 release thereby avoiding flooding the cell with excessive ROS (783). Contemporary myoglobin continues to perform this regulatory function in muscle.

It is well recognized that embryos and undifferentiated cells grow better in a hypoxia (129, 153). A low O2 tension (1%-5%) is an important component of the embryonic and mesenchymal stem cell “niche” that maintains stem cell properties, minimizes oxidative stress, prevents chromosomal abnormalities, improves clonal survival, and perpetuates the undifferentiated characteristics (457). In addition, hypoxia stimulates endothelial cell proliferation, migration, tubulogenesis, and stress resistance (752, 850) as well as preferential growth and vascularization of many malignant tumor cells; the latter observation constitutes the basis for the use of adjuvant hyperoxia to enhance tumor killing during irradiation and chemotherapy (277,738). Collectively, these responses to O2 tension suggest that the pulmonary gas-exchange organs adapted in a direction toward controlled restriction of cellular exposure to O2.

Origin of the Oxygen Cascade

The oxygen cascade (Fig. 6) describes serial step-downs of O2 tension from ambient air through successive resistances across the pulmonary, cardiac, macrovascular and microvascular systems into the cell and mitochondria. These resistances adapt in a coordinated fashion in response to changes in ambient O2 availability or utilization (333). Traditional paradigm holds that the primary selection pressure in the evolution of O2 transport systems is the efficiency of O2 delivery to meet cellular metabolic demands. If this is the sole function of the cascade, why are there so many resistances? Once we accept the anaerobic origin of eukaryotes and their persistent preference for hypoxia, an alternative paradigm becomes plausible, namely, the entire oxygen cascade could be viewed as an elaborate gate-keeping mechanism the major function of which is to balance cellular O2 delivery against oxidative damage.

Mitochondria consume the majority of cellular O2, directly control intracellular O2 tension, and generate most of the cellular ROS (136). Intracellular O2 tension in turn regulates mitochondrial oxidative phosphorylation, ROS production, cell signaling, and gene expression. Via O2-dependent oxidative phosphorylation the mitochondria act as cellular O2 sensors in the regulation of diverse responses from local blood flow to electric activity (830). Earlier studies reported that hypoxia increases mitochondrial ROS generation (126, 782, 823) via several mechanisms: (i) O2 limitation at the terminal complex IV (cytochrome c oxidase) in the mitochondrial electron transport chain causes electrons to back up the chain with increased electron leak to form superoxide (•O2−). (ii) Hypoxia induces conformational changes in complex III (ubiquinol cytochrome c oxidoreductase) to enhance superoxide formation (88, 287). (iii) Oxidized cytochrome c scavenges superoxide (722). Hypoxia-induced O2 limitation at complex IV leads to cytochrome c reduction, limiting its ability to scavenge superoxide and enhancing mitochondrial ROS leakage. However, recent studies of isolated mitochondria show that hypoxia actually reduces mitochondrial ROS generation and causes mitochondrial uncoupling, suggesting extramitochondrial sources of ROS generation in hypoxia (330). These conflicting reports remain to be resolved. Nonetheless, moderate hypoxia rapidly and reversibly downregulates mitochondrial enzyme transcripts, in parallel with reductions in mitochondrial respiratory activity and O2 consumption (631).

As paleo-atmospheric O2 concentration increased and multicellular aerobic organisms arose, the endosymbiotic mitochondria-host relationship faced the challenge of balancing conflicting needs of aerobic energy generation for the host cell and anaerobic protection for its internal power generator. The host cell must finely control a constant supply of O2 to the mitochondria for oxidative phosphorylation while simultaneously protecting mitochondria against oxidative damage by maintaining a near-anoxic level of local O2 concentration. This trade-off may have led to the evolution of ever more elaborate physicochemical barriers that created and maintained successive O2 partial pressure gradients, by convection and diffusion in the lung, chemical binding to hemoglobin, distribution and release via cardiovascular delivery, dissociation from hemoglobin, and diffusion into peripheral cells with or without myoglobin facilitated transport. As a result, the primordial anoxic conditions of the Earth necessary for survival and optimal function of this proteobacterial remnant are preserved inside the host cell. In working human leg muscle O2 tension at the sarcoplasmic and mitochondrial boundaries has been estimated at approximately 2.4 mmHg (0.32 kPa) (835) and muscle mitochondrial O2 concentration at half-maximal metabolic rate 0.02 to 0.2 mmHg (834), that is, in the range of the ancient atmospheric level approximately 2 Ga. Raising O2 tension above these levels impairs mitochondrial activity (672). In this context, protection of mitochondria from O2 exposure likely constitutes a major selection factor in the evolution of complex aerobic life while the various forms of systemic O2 delivery systems are necessary but secondary functions that sustain the “gate-keeping” barrier apparatus to maintain adequate partial pressure gradients along the O2 transport cascade and preserve the near-anoxic intracellular conditions for the mitochondria. In parallel with physical barriers, cells also developed various biochemical scavenging and antioxidant pathways to counteract the toxic effects of ROS as ambient oxygenation increased.

Defense against the Dark Arts of Oxidation

To summarize, the evolution of life on Earth has adapted to a wide range of ambient O2 levels from 0% to 35%. Periods of relative hyperoxia promote biodiversity and gigantism but incur excess oxidative stress and mandating the upregulation of antioxidant defenses. Periods of relative hypoxia promote coordinated conservation of resources and downregulation of metabolic capacities to improve energy efficiency and channel some savings into compensatory growth of gas-exchange organs. The trajectory of early evolution is at least partly coupled to O2 content of the atmosphere and the deep ocean, and there is a plausible explanation for the coupling, namely, defense against the dark arts of oxidation. Oxygen is capable of giving and taking life. The anaerobic proteobacteria escaped the fate of annihilation by taking refuge inside another cell and in a brilliant evolutionary move coopted its own oxygen-detoxifying machinery to provide essential sustenance for the host cell in return for nourishment and physical protection from oxidation. As the threat of oxidation increased with rising environmental O2 concentration, selection pressure escalated for ever more sophisticated defense mechanisms against oxidative injury and in direct conflict with simultaneously escalating selection pressures to harness the energetic advantage of oxidative phosphorylation.

Trading off the above opposing demands shaped all known respiratory organs, from simple O2 diffusion across cell membranes to facilitated transport via O2 binding proteins to gas-exchange systems of varying complexity (skin, gills, tracheae, book lung, alveolar lung, and avian lung) (Sections 2-5). Concurrently evolving with a convective transport system, these increasingly elaborate respiratory organs not only increase O2 uptake but also maintain air-to-mitochondria O2 tension gradients and intracellular O2 fluxes at a hospitable ancestral level. This epic struggle began at the dawn of life and persisted to the present on a universal scale. The evolutionary trajectory of air breathing has continued contemporary significance to the understanding of oxygen-dependent metabolic homeostasis, especially in relation to maturation, senescence, and aging-related organ degeneration and disease.

High reliability of measure of diaphragmatic mobility by radiographic method in healthy individuals.

Nevner bevegelsen i diafragma under en spirometri test (innpust og utpust) og at noen har observert 9cm bevegelighet.

http://www.ncbi.nlm.nih.gov/pubmed/23778774

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-35552013000200128&lng=en&nrm=iso&tlng=en

There were large ranges of variation (in mm) in the obtained minimum and maximum values, and such variations were also reported in other studies8,6,24. Simon et al.13 observed a diaphragmatic value range from 0 to 85 mm, Houston et al.25 observed a range from 23 to 97 mm, Kantarci et al.27 observed a range from 25 to 84 mm and Boussuges et al.8 observed a range from 36 to 92 mm.

 

Måle Vitalkapasitet (lungevolum) med ballong

Denne videoen beskriver hvordan vital kapasitet måles enkelt med en ballong. En greit teknikk å bruke for å sjekke din fremgang med diafragma øvelsene i Verkstedet Breathing System.

Den nevner også hvordan man regner ut kroppens overflateareal, Body Surface Area: BSA = roten av ( (høyde (cm)*vekt (kg)) / 3600)

For så å kunne beregnes hva en vital kapsitet burde være (svaret vises i kubikkcentimeter, cm3):

Menn: BSA * 2500

Kvinner: BSA *  2000

Den virkelige vitalkapsiteten måles ved å blåse i en ballong (som er strekt ut først for å gjøre den mest mulig rund) 3 ganger, og så forholde seg til det største volumet.

Ballong diameteren viser lungevolum i denne grafen:

lungevolum ballong test

Man regner med at alt over 80% av forventet vitalkapsitet er normalt.

THE VALUE OF BLOWING UP A BALLOON

Dette er en veldig viktig artikkel for å forstå diafragmas rolle i både pust og bevegelse, og ifh smertetilstander i ryggraden. Nevner en lovende teknikk for å styrke diafragma og støttemuskulatur hvor man blåser opp en ballong og strammer kjernemuskulaturen. Nevner Zone of Apposition (ZOA) som beskriver diafragmas bevegelsesmuligheter. Ved lav ZOA har diafrgma lite bevegelse. Vi ønsker å øke ZOA. Denne øvelsen er konstruert basert på fysioterapeutisk prinsipper, men i Verkstedet Breathing System har vi øvelser som er gir samme resultater på diafragma, men bygget på lang og erfaringsbasert tradisjon fra tibetansk buddhisme.

Nevner også hvordan mage-pust minker bevegelsen i diafragma.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2971640/

Suboptimal breathing patterns and impairments of posture and trunk stability are often associated with musculoskeletal complaints such as low back pain. A therapeutic exercise that promotes optimal posture (diaphragm and lumbar spine position), and neuromuscular control of the deep abdominals, diaphragm, and pelvic floor (lumbar-pelvic stabilization) is desirable for utilization with patients who demonstrate suboptimal respiration and posture. This clinical suggestion presents a therapeutic exercise called the 90/90 bridge with ball and balloon. This exercise was designed to optimize breathing and enhance both posture and stability in order to improve function and/or decrease pain. Research and theory related to the technique are also discussed.

Many muscles used for postural control/stabilization and for respiration are the same, for example: the diaphragm, transversus abdominis, and muscles comprising the pelvic floor.16 Maintaining optimal posture/stability and respiration is important and is even more challenging during exercise. Exercise increases respiratory demand (e.g. running) and limb movements (e.g. arms moving while standing still) increase postural demands for stabilization.3,7

Many factors are potentially involved with suboptimal respiration and suboptimal (faulty) posture and may be associated with musculoskeletal complaints such as low back pain, and/or sacroiliac joint pain.8 (Table 1)

Suboptimal Respiration and Posture
Decreased/suboptimal Zone of Apposition of diaphragm
Decreased exercise tolerance
Decreased intra-abdominal pressure
Shortness of Breath/Dyspnea
Decreased respiratory efficiency
Decreased expansion of lower rib cage/chest
Decreased appositional diaphragm force
Decreased length of diaphragm (short)
Decreased transdiaphragm pressure
Increased use of accessory muscles of respiration
Poor neuromuscular control of core muscles
Increased lumbar lordosis
Increased anterior pelvic tilt
Increased hamstring length
Increased abdominal length
Rib elevation/external rotation
Sternum elevation
Increased activity of paraspinals
Increased lumbar-pelvic instability
Low back pain
Sacroiliac Joint pain
Thoracic Outlet Syndrome
Headaches
Asthma

One of the most critical factors, often overlooked by physical therapists, is maintaining an optimal zone of apposition of the diaphragm.3,911 The zone of apposition (ZOA) is the area of the diaphragm encompassing the cylindrical portion (the part of the muscle shaped like a dome/umbrella) which corresponds to the portion directly apposed to the inner aspect of the lower rib cage.12 The ZOA is important because it is controlled by the abdominal muscles and directs diaphragmatic tension. When the ZOA is decreased or suboptimal, there are several potential negative consequences. (Table 1) Two examples include:

  1. Inefficient respiration (less air in and out) because the transdiaphragmatic pressure is reduced.11 The smaller the ZOA, there will be less inspiratory action of the diaphragm on the rib cage.11
  2. Diminished activation of the transversus abdominis which is important for both respiration and lumbar stabilization.11,13

The incidence of LBP has been documented to be as high as 30% in the athletic population, and in many cases pain may persist for years.15 Low back pain is frequently correlated with faulty posture such as an excessive lumbar lordosis.1618 Excessive lumbar lordosis may be associated with over lengthened and weak abdominal musculature.1820 Poor neuromuscular control of core muscles (transversus abdominis, internal oblique, pelvic floor and diaphragm) has been described in individuals with SIJ pain21 and in individuals with lumbar segmental instability, potentially adversely affecting respiration.22

Richardson et al.27 describe coordination of the Transversus abdominis and the diaphragm in respiration during tasks in which stability is maintained by tonic activity of these muscles. During inspiration, the diaphragm contracts concentrically, whereas the transversus abdominis contracts eccentrically. The muscles function in reverse during exhalation with the diaphragm contracting eccentrically while the transversus abdominis contracts concentrically. Hodges et al. noted that during respiratory disease the coordinating function between the transversus abdominis and diaphragm was reduced.6 Thus, it is also possible that faulty posture such as over lengthened abdominals and excessive lordosis could reduce the coordination of the diaphragm and transversus abdominis during respiration and stabilization activities.

O’sullivan et al.21 studied subjects with LBP attributed to the sacroiliac joints and compared them to control subjects without pain. O’sullivan et al. compared respiratory rate and diaphragm and pelvic floor movement using real time ultrasound during a task that required load transfer through the lumbo-pelvic region (the active straight leg raise test). Subjects with pain had an increase in respiratory rate, descent of their pelvic floor and a decrease in diaphragm excursion as compared to the control subjects, who had normal respiratory rates, less pelvic floor descent, and optimal diaphragm excursion. While O’sullivan et al. concluded that an intervention program focused on integrating control of deep abdominal muscles with normal pelvic floor and diaphragm function may be effective in managing patients with LBP,21 they did not describe strategies or exercises to achieve this goal.21

While the role of the Transversus abdominis in lumbar stability is well documented, less well known is the role of the diaphragm in lumbar stability. While the primary function of the diaphragm is respiration, it also plays a role in spinal stability.3,28

The right hemidiaphragm attaches distally to the anterior portions of the first through third lumbar vertebrae (L1-3) and the left hemidiaphragm attaches distally on the first and second lumbar vertebrae (L1-2).29 This section of the diaphragm is referred to as the crura. Of interest is the asymmetrical attachment of the diaphragm with the left hemidiaphragm attaching to L1-2 and the right portion attaching to L1-3.

During the inhalation phase of ventilation, the dome of the diaphragm moves caudally like a piston creating a negative pressure in the thorax that forces air into the lungs. This action is normally accompanied by a rotation of the ribs outward (external rotation) largely in part due to the ZOA.12 (Figure 1) Apposition is a term that means multiple layers adjacent to each other.33 The normal force of pull on the sternal and costal portions of the diaphragm would produce an internal rotation of the ribs. The ZOA creates an external rotation of these ribs primarily because the pressure in the thoracic cavity prevents an inward motion. The crural portion of the diaphragm assists the caudal motion of the dome. It also pulls the anterior lumbar spine upward (cephalad and anterior). Additionally, the abdominal muscles and pelvic floor musculature are less active to allow visceral displacement due to the dome of the diaphragm dropping. With exhalation, this process is reversed. Abdominal muscle activity compresses the viscera in the abdominal cavity, the diaphragm is forced cephalad and the ribs internally rotate. As exhalation becomes forced as during exercise, abdominal activity (rectus abdominus, internal obliques, external obliques, and transversus abdominis) will be increased.3436

When the ZOA is optimized, the respiratory and postural roles of the diaphragm have maximal efficiency.37 In suboptimal positions (i.e. decreased ZOA), the diaphragm has a decreased ability to draw air into the thorax because of less caudal movement upon contraction and less effective tangential tension of the diaphragm on the ribs and therefore lower transdiaphragmatic pressure.38 This decreased ZOA is accompanied by decreased expansion of the rib cage, postural alterations, and a compensatory increase in abdominal expansion.12 (Figure 2)

One such adaptive breathing strategy would be to relax the abdominal musculature more than necessary on inspiration to allow for thoraco-abdominal expansion. This situation leads to decreased abdominal responsibility while breathing and can contribute to instability. This would reflect more upper chest breathing and less efficient diaphragm activity. If the body maintains this position and breathing strategy for an extended period of time, the diaphragm may adaptively shorten and the lungs may become hyperinflated.37,39,40 Hyperinflation may also contribute to over use of accessory muscles of respiration such as scalenes, sternocleidomastoid (SCM), pectorals, upper trapezius and paraspinals in an attempt to expand the upper rib cage.4144 Again, without an optimal dome shape/position of the diaphragm or an optimal ZOA the body compensates to get air in with accessory muscles since the more linear/flat/short diaphragm is less efficient for breathing.32

Instructions for Performance of the 90/90 Bridge with Ball and Balloon: 1. Lie on your back with your feet flat on a wall and knees and hips bent at a 90-degree angle. 2. Place a 4-6 inch ball between your knees. 3. Place your right arm above your head and a balloon in your left hand. 4. Inhale through your nose and as you exhale through your mouth, perform a pelvic tilt so that your tailbone is raised slightly off the mat. Keep low back flat on the mat. Do not press your feet into the wall, instead pull down with your heels. 5. You should feel the back of your thighs and inner thighs engage, keeping pressure on the ball. Maintain this position for the remainder of the exercise. 6. Now inhale through your nose and slowly blow out into the balloon. 7. Pause three seconds with your tongue positioned on the roof of your mouth to prevent airflow out of the balloon. 8. Without pinching the neck of the balloon and keeping your tongue on the roof of your mouth, inhale again through your nose. 9. Slowly blow out as you stabilize the balloon with your left hand. 10. Do not strain your neck or cheeks as you blow. 11. After the fourth breath in, pinch the balloon neck and remove it from your mouth. Let the air out of the balloon.12. Relax and repeat the sequence 4 more times. Copyright © Postural Restoration Institute™ 2009, used with permission

The patient/athlete is asked to hold the balloon with one hand and inhale through his/her nose with the tongue on the roof of the mouth (normal rest position) and then exhale through his/her mouth into the balloon. The inhalation, to about 75% of maximum, is typically 3-4 seconds in duration, and the complete exhalation is usually 5-8 seconds long followed by a 2-3 second pause. This slowed breathing is thought to further relax the neuromuscular system/parasympathetic nervous system and generally decrease resting muscle tone. Ideally the patient/athlete will be able to inhale again without pinching off the balloon with their teeth, lips, or fingertips. This requires maintenance of intra-abdominal pressure to allow inhalation through the nose without the air coming back out of the balloon and into the mouth.

When the exercise is performed by the patient/athlete with hamstring and gluteus maximus (glut max) activation (hip extensors) the pelvis moves into a relative posterior pelvic tilt and the ribs into relative depression and internal rotation. This pelvic and rib position helps to optimize abdominal length (decreases) and diaphragm length/ZOA (increases).

Clinical experience with the BBE includes utilization of the exercise for both female and male patients (more females than males), ages 5-89 with a wide variety of diagnoses including: low back pain, trochanteric bursitis, SIJ pain, asthma, COPD, acetabular labral tear, anterior knee pain, thoracic outlet syndrome (TOS) and sciatica.

Melatonin induces γ- glutamylcysteine syn thetase mediated by activator protein-1 in human vascular en dothelial cells

Det første bildet viser hvordan melatonin dobler glutathion konsentrasjon. Dette er interessant med tanke på at diafragmiske pust øker melatonin. Melatonin hemmer enzymet som bryter ned glutathion, derfor økes konsentrasjonen.

http://www.sciencedirect.com/science/article/pii/S0891584999001318

In the present study, we show that melatonin induces the expression of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting enzyme of glutathione (GSH) synthesis, in ECV304 human vascular endothelial cells.

As conclusion, induction of GSH synthesis by melatonin protects cells against oxidative stress and regulates cell proliferation.