Physical activity, by enhancing parasympathetic tone and activating the cholinergic anti-inflammatory pathway, is a therapeutic strategy to restrain chronic inflammation and prevent many chronic diseases.

Beskriver hvordan trening aktiverer vagus og demper betennelser.

http://www.ncbi.nlm.nih.gov/pubmed/23395411 

Chronic diseases are the leading cause of death in the world and chronic inflammation is a key contributor to many chronic diseases. Accordingly, interventions that reduce inflammation may be effective in treating multiple adverse chronic conditions. In this context, physical activity is documented to reduce systemic low-grade inflammation and is acknowledged as an anti-inflammatory intervention. Furthermore, physically active individuals are at a lower risk of developing chronic diseases. However the mechanisms mediating this anti-inflammatory phenotype and range of health benefits are unknown. We hypothesize that the «cholinergic anti-inflammatory pathway» (CAP) mediates the anti-inflammatory phenotype and range of health benefits associated with physical activity. The CAP is an endogenous, physiological mechanism by which acetylcholine from the vagus nerve, interacts with the innate immune system to modulate and restrain the inflammatory cascade. Importantly, higher levels of physical activity are associated with enhanced parasympathetic (vagal) tone and lower levels of C-reactive protein, a marker of low-grade inflammation. Accordingly, physical activity, by enhancing parasympathetic tone and activating the CAP, may be a therapeutic strategy to restrain chronic inflammation and prevent many chronic diseases.

Slow Breathing Increases Arterial Baroreflex Sensitivity in Patients With Chronic Heart Failure

Nevner at 6 pust i minuttet gir beste respons på HRV og vagusnerven. I tillegg til å dempe blodtrykk markant. Studien ga disse resultatene med en bare 4 minutters pustesession.

http://circ.ahajournals.org/content/105/2/143.full

Background It is well established that a depressed baroreflex sensitivity may adversely influence the prognosis in patients with chronic heart failure (CHF) and in those with previous myocardial infarction.

Methods and Results We tested whether a slow breathing rate (6 breaths/min) could modify the baroreflex sensitivity in 81 patients with stable (2 weeks) CHF (age, 58±1 years; NYHA classes I [6 patients], II [33], III [27], and IV [15]) and in 21 controls. Slow breathing induced highly significant increases in baroreflex sensitivity, both in controls (from 9.4±0.7 to 13.8±1.0 ms/mm Hg, P<0.0025) and in CHF patients (from 5.0±0.3 to 6.1±0.5 ms/mm Hg, P<0.0025), which correlated with the value obtained during spontaneous breathing (r=+0.202, P=0.047). In addition, systolic and diastolic blood pressure decreased in CHF patients (systolic, from 117±3 to 110±4 mm Hg, P=0.009; diastolic, from 62±1 to 59±1 mm Hg, P=0.02).

Conclusions These data suggest that in patients with CHF, slow breathing, in addition to improving oxygen saturation and exercise tolerance as has been previously shown, may be beneficial by increasing baroreflex sensitivity.

Breathing at 6 breaths/min, compared with spontaneous breathing, slightly increased overall spontaneous fluctuations in RR interval, reduced fluctuations in blood pressure, and significantly increased the baroreflex sensitivity in both CHF patients (from 5.0±0.3 to 6.1±0.5 ms/mm Hg, P<0.0025) and controls (from 9.4±0.7 to 13.8±1.0 ms/mm Hg, P<0.0025) (Figure 1).

The slow breathing rate in the CHF group also produced an increase in mean RR interval of 20 ms and a decrease in both systolic and diastolic blood pressure (systolic, from 117±3 to 110±4 mm Hg, P=0.009; diastolic, from 62±1 to 59±1 mm Hg, P=0.02) (Figure 2).

 

 

Effect of short-term practice of breathing exercises on autonomic functions in normal human volunteers

Nevner hvordan sakte pust bedrer tilstanden i det autonome nervesystem. De bruker 6 sek inn og 6 sek ut i denne studien, som stimulerer vagusnerven best.

http://www.icmr.nic.in/ijmr/2004/0807.pdf

Background & objectives: Practice of breathing exercises like pranayama is known to improve autonomic function by changing sympathetic or parasympathetic activity. Therefore, in the present study the effect of breathing exercises on autonomic functions was performed in young volunteers in the age group of 17-19 yr.

Methods: A total of 60 male undergraduate medical students were randomly divided into two groups: slow breathing group (that practiced slow breathing exercise) and the fast breathing group (that practiced fast breathing exercise). The breathing exercises were practiced for a period of three months. Autonomic function tests were performed before and after the practice of breathing exercises.

Results: The increased parasympathetic activity and decreased sympathetic activity were observed in slow breathing group, whereas no significant change in autonomic functions was observed in the fast breathing group.

Interpretation & conclusion: The findings of the present study show that regular practice of slow breathing exercise for three months improves autonomic functions, while practice of fast breathing exercise for the same duration does not affect the autonomic functions.

One molecule, many derivatives: a never-ending interaction of melatonin with reactive oxygen and nitrogen species?

Alt om hvordan melatonin virker som en antioksidant. Jo større ROS utfordring vi har, jo mer spiser det av melatoninlagrene våre. Når vi får mindre ROS, feks gjennom kostholdsendringer og stressreduksjon, så økes melatonin igjen.

http://www.ncbi.nlm.nih.gov/pubmed/17198536

Melatonin is a highly conserved molecule. Its presence can be traced back to ancient photosynthetic prokaryotes. A primitive and primary function of melatonin is that it acts as a receptor-independent free radical scavenger and a broad-spectrum antioxidant. The receptor-dependent functions of melatonin were subsequently acquired during evolution. In the current review, we focus on melatonin metabolism which includes the synthetic rate-limiting enzymes, synthetic sites, potential regulatory mechanisms, bioavailability in humans, mechanisms of breakdown and functions of its metabolites. Recent evidence indicates that the original melatonin metabolite may be N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) rather than its commonly measured urinary excretory product 6-hydroxymelatonin sulfate. Numerous pathways for AFMK formation have been identified both in vitro and in vivo. These include enzymatic and pseudo-enzymatic pathways, interactions with reactive oxygen species (ROS)/reactive nitrogen species (RNS) and with ultraviolet irradiation. AFMK is present in mammals including humans, and is the only detectable melatonin metabolite in unicellular organisms and metazoans. 6-hydroxymelatonin sulfate has not been observed in these low evolutionary-ranked organisms. This implies that AFMK evolved earlier in evolution than 6-hydroxymelatonin sulfate as a melatonin metabolite. Via the AFMK pathway, a single melatonin molecule is reported to scavenge up to 10 ROS/RNS. That the free radical scavenging capacity of melatonin extends to its secondary, tertiary and quaternary metabolites is now documented. It appears that melatonin’s interaction with ROS/RNS is a prolonged process that involves many of its derivatives. The process by which melatonin and its metabolites successively scavenge ROS/RNS is referred as the free radical scavenging cascade. This cascade reaction is a novel property of melatonin and explains how it differs from other conventional antioxidants. This cascade reaction makes melatonin highly effective, even at low concentrations, in protecting organisms from oxidative stress. In accordance with its protective function, substantial amounts of melatonin are found in tissues and organs which are frequently exposed to the hostile environmental insults such as the gut and skin or organs which have high oxygen consumption such as the brain. In addition, melatonin production may be upregulated by low intensity stressors such as dietary restriction in rats and exercise in humans.

Intensive oxidative stress results in a rapid drop of circulating melatonin levels. This melatonin decline is not related to its reduced synthesis but to its rapid consumption, i.e. circulating melatonin is rapidly metabolized by interaction with ROS/RNS induced by stress. Rapid melatonin consumption during elevated stress may serve as a protective mechanism of organisms in which melatonin is used as a first-line defensive molecule against oxidative damage. The oxidative status of organisms modifies melatonin metabolism. It has been reported that the higher the oxidative state, the more AFMK is produced. The ratio of AFMK and another melatonin metabolite, cyclic 3-hydroxymelatonin, may serve as an indicator of the level of oxidative stress in organisms.

Relationship between Hyperventilation and Excessive CO2 Output during Recovery from Repeated Cycling Sprints

Viktig studie som beskriver de fleste faktorer rundt hvordan hyperventilering under trening fjerner CO2 som igjen øker melkesyre. Viser et bilde av den direkte sammenhengen mellom CO2 og melkesyre.

http://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/51990/1/repeat-ex-PR.pdf

 

Ten Steps to Understanding Manual and Movement Therapies for Pain

Alt om smerte, kort fortalt, fra: http://www.somasimple.com/forums/showthread.php?t=4942
Nothing Simple – Ten Steps to Understanding Manual and Movement Therapies for Pain

1. Pain is a category of complex experiences, not a single sensation produced by a single stimulus.

2. Nociception (warning signals from body tissues) is neither necessary nor sufficient to produce pain. In other words, pain can occur in the absence of tissue damage.

3. A pain experience may be induced or amplified by both actual and potential threats.

4. A pain experience may involve a composite of sensory, motor, autonomic, endocrine, immune, cognitive, affective and behavioural components. Context and meaning are paramount in determining the eventual output response.

5. The brain maps peripheral and central neural processing into each of these components at multiple levels. Therapeutic input at a single level may be sufficient to resolve a threat response.

6. Manual and movement therapies may affect peripheral and central neural processes at various stages:
- transduction of nociception at peripheral sensory receptors
- transmission of nociception in the peripheral nervous system
- transmission of nociception in the central nervous system
- processing and modulation in the brain

7. Therapies that are most likely to be successful are those that address unhelpful cognitions and fear concerning the meaning of pain, introduce movement in a non-threatening internal and external context, and/or convince the brain that the threat has been resolved.

8. The corrective physiological mechanisms responsible for resolution are inherent. A therapist need only provide an appropriate environment for their expression.

9. Tissue length, form or symmetry are poor predictors of pain. The forces applied during common manual treatments for pain generally lack the necessary magnitude and specificity to achieve enduring changes in tissue length, form or symmetry. Where such mechanical effects are possible, the clinical relevance to pain is yet to be established. The predominant effects of manual therapy may be more plausibly regarded as the result of reflexive neurophysiological responses.

10. Conditioning for the purposes of fitness and function or to promote general circulation or exercise-induced analgesia can be performed concurrently but points 6 and 9 above should remain salient.

Bibliography

Books:
Pain: The Science of Suffering – Patrick Wall
The Challenge of Pain – Patrick Wall, Ronald Melzack
Explain Pain – David Butler, Lorimer Moseley
The Sensitive Nervous System – David Butler
Phantoms in the Brain – V. S. Ramachandran
Topical Issues in Pain Vol’s 1-5 – Louis Giffiord (ed)
The Feeling of What Happens – Antonio Damasio
Clinical Neurodynamics – Michael Shacklock
Eyal Lederman – The Science and Practice of Manual Therapy

Research articles:
Melzack R. Pain and the neuromatrix in the brain. J Dental Ed. 2001;65:1378-82.
Craig AD. Pain mechanisms: Labeled lines versus convergence in central processing. Ann Rev Neurosci. 2003;26:130.
Craig AD. How do you feel? Interoception: the sense of the physiological condition of the body. Nature Rev Neurosci. 2002;3:655-66.
Henderson LA, Gandevia SC, Macefield VG. Somatotopic organization of the processing of muscle and cutaneous pain in the left and right insula cortex: A single-trial fMRI study. Pain. 2007;128:20-30.
Olausson H, Lamarre Y, Backlund H, Morin C, Wallin BG, Starck G, Ekholm S, Strigo I, Worsley K, Vallbo AB, Bushnell MC. Unmyelinated tactile afferents signal touch and project to insular cortex. Nature Neurosci. 2002;5:900–904.
Moseley GL. A pain neuromatrix approach to patients with chronic pain. Manual Ther. 2003;8:130-40.
Moseley GL. Unravelling the barriers to reconceptualisation of the problem in chronic pain: The actual and perceived ability of patients and health professionals to understand the neurophysiology. J Pain. 2003;4:184-89.
Moseley GL, Arntz A. The context of a noxious stimulus affects the pain it evokes. Pain. 2007;133(1-3):64-71.
Moseley, GL, Nicholas, MK and Hodges, PW. A randomized controlled trial of intensive neurophysiology education in chronic low back pain. Clin J Pain. 2004;20:324-30.
Crombez G, Vlaeyen JWS, Heuts PH et al. Pain-related fear is more disabling than pain itself. Evidence on the role of pain-related fear in chronic back pain disability. Pain. 1999;80:329-40.
Zusman M. Forebrain-mediated sensitization of central pain pathways: ‘non-specific’ pain and a new image for manual therapy. Manual Ther. 2002;7:80-88.
Dorko B. The analgesia of movement: Ideomotor activity and manual care. J Osteopathic Med. 2003;6:93-95.
Threlkeld AJ. The effects of manual therapy on connective tissue. Phys Ther. 1992;72:893-902.
Lederman E. The myth of core stability. Retrieved at: http://www.ppaonline.co.uk/

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.

The nutriceutical bovine colostrum truncates the increase in gut permeability caused by heavy exercise in athletes

Studie som nevner at hard trening gir lekk tarm, og at Colostrum (hoppemelk) lukker tarmen. Dette kan forklare hvorfor så mange vektløftere og toppidrettsutøver har problemer med tarm og immunsystem. I studien brukte de 20g colostrum daglig, som er ganske mye.

http://ajpgi.physiology.org/content/300/3/G477

Heavy exercise causes gut symptoms and, in extreme cases, “heat stroke” partially due to increased intestinal permeability of luminal toxins. We examined bovine colostrum, a natural source of growth factors, as a potential moderator of such effects. Twelve volunteers completed a double-blind, placebo-controlled, crossover protocol (14 days colostrum/placebo) prior to standardized exercise. Gut permeability utilized 5 h urinary lactulose-to-rhamnose ratios. In vitro studies (T84, HT29, NCM460 human colon cell lines) examined colostrum effects on temperature-induced apoptosis (active caspase-3 and 9, Baxα, Bcl-2), heat shock protein 70 (HSP70) expression and epithelial electrical resistance. In both study arms, exercise increased blood lactate, heart rate, core temperature (mean 1.4°C rise) by similar amounts. Gut hormone profiles were similar in both arms although GLP-1 levels rose following exercise in the placebo but not the colostrum arm (P = 0.026). Intestinal permeability in the placebo arm increased 2.5-fold following exercise (0.38 ± 0.012 baseline, to 0.92 ± 0.014, P < 0.01), whereas colostrum truncated rise by 80% (0.38 ± 0.012 baseline to 0.49 ± 0.017) following exercise. In vitro apoptosis increased by 47–65% in response to increasing temperature by 2°C. This effect was truncated by 60% if colostrum was present (all P < 0.01). Similar results were obtained examining epithelial resistance (colostrum truncated temperature-induced fall in resistance by 64%, P < 0.01). Colostrum increased HSP70 expression at both 37 and 39°C (P < 0.001) and was truncated by addition of an EGF receptor-neutralizing antibody. Temperature-induced increase in Baxα and reduction in Bcl-2 was partially reversed by presence of colostrum. Colostrum may have value in enhancing athletic performance and preventing heat stroke.

SEVERAL STRESSES AFFECT the integrity of the intestinal barrier. These include prolonged strenuous exercise (10), heat stress (11), and drugs such as nonsteroidal anti-inflammatory agents. Loss of intestinal barrier integrity leading to increased intestinal permeability may result in passage of luminal endotoxins into the circulation. This, in turn, results in an inflammatory cascade, exacerbating the loss of barrier function and, in severe cases, resulting in severe systemic effects.

Gastrointestinal symptoms including cramps, diarrhea, nausea, and bleeding are commonly reported by long-distance runners (16). These symptoms are likely to be due to a combination of reduced splanchnic blood flow, hormonal changes, altered gut permeability, and increased body temperature.

Colostrum is the first milk produced after birth and is particularly rich in immunoglobulins, antimicrobial peptides (e.g., lactoferrin, lactoperoxidase), and other bioactive molecules including growth factors (20).

We have previously shown, using a combination of in vitro and in vivo studies, that a commercially available defatted bovine colostral preparation can reduce NSAID-induced upper intestinal gut injury in rats, mice, and humans (19, 21).

The total protein content of the colostrum was 80%. The concentrations of the various growth factors present in the colostrum preparation are incompletely defined but include IGF-I at 213 ng/g, TGF-β1 at 113 ng/g, and TGF-β2 at 441 ng/g.

In a double-blind crossover design, subjects received oral supplementation with 20 g/day bovine colostrum or the isoenergetic and isomacronutrient placebo.

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

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

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

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

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