The trouble began with industrialization. «Up until the past 100 or 150 years, our daily activities – farm chores, hunting animals, hard manual labor – required that we use our diaphragms as our main breathing muscle,» says Dr. Louis Libby, a pulmonary physician at the Oregon Clinic, in Portland. «In the past century we’ve become sedentary. We can go days without using our diaphragms. We’ve become lazy, sitting in front of computers and using the weaker intercostal breathing muscles in the rib cage for breaths that are incomplete but adequate for living.»
http://www.mensjournal.com/magazine/you-re-breathing-all-wrong-20130227

How does one justify the use of ultrasound when the biophysical (Baker et al 2001) and clinical (Robertson et al 2001) effects have been so thoroughly disproven? Why are we still taught that we are molders of connective tissue, when the forces required to create plastic deformation of connective tissue ranges between 50 and 250 pounds of force (Threlkeld 1992)? When are we going to accept the fact that our palpatory exams lack reliability (French et al 2000) (Lucas et al 2009) and validity (Najm et al 2003) (Landel et al 2008) (Preece et al 2008)? When will we stop telling students, colleagues, and patients that pain is related to their posture, muscle length, muscle strength, or biomechanics (Edmondston et al 2007) (Lewis et al 2005) (Nourbakhsh et al 2002)? When will we cease blaming pain on something found on an image (Reilly et al 2006) (Beattie et al 2005) (Borenstein et al 2001)? When will we stop thinking that we can change someone’s static posture with strengthening (Walker et al 1987) (Diveta et al 1990)?

http://blog.theravid.com/patient-care/redefining-evidence-ebp-in-experience-cut/

Denen Studien forteller mye om hvordan CO2 forholder seg i trening, og viser med bilder hvordan de med hjerteproblemer har en mye lavere CO2 i utgangspunktet og en dårligere toleranse for økningen, selv når CO2 nivået er langt under normalnivåer likevel.

Viser også hvordan økt CO2 gir en økt opptak av oksygen.

http://journal.publications.chestnet.org/article.aspx?articleid=1079553

It has been shown that P(a-ET)co2 goes from + 2.5 mm Hg at rest to − 4 mm Hg during heavy exercise in normal subjects.,6 The result of the present study, which shows that P(a-ET)co2 goes from+ 2.4 ± 2.3 mm Hg at rest to − 5.3 ± 3.3 mm Hg at peak exercise in control subjects, is comparable to previous studies.

Viser hvordan muskler utmattes med opphopning av K+ kationer i den ekstracellulære væske, mens når CO2 økes fra 4% til 25% holder musklene lenger før utmattelse. Så for musklene er virker det som at de tåler mer i et mer surt miljø enn et basisk. Dette kan spille inn i Metabolsk pust hvor CO2 holdes igjen så godt som mulig istedet for å pustes ut.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2217490/

Effects of elevated extracellular K+ and muscle acidification on steady tetanic force in split muscles from adult rats. The figure shows summarized results from experiments performed essentially like the experiments illustrated in Fig. 1 except that muscles were stimulated by field stimulation. When force at elevated [K+]o had reached a steady level at normal pH (•), muscles were acidified by increasing the percentage of CO2 in the gas from 5 to 24% (○). Data were fitted to a Boltzmann sigmoidal curve. Data show means ± SEM from four muscles with 100% corresponding to 0.60 ± 0.03 N.

Nevner hvordan økt CO2 korrelerer med økt pustefrekvens under kort, intens intervalltrening.

http://www.waset.org/journals/waset/v71/v71-198.pdf

Abstract—We investigated this hypothesis that arterial CO2 pressure (PaCO2) drives ventilation (VE) with a time delay during recovery from short impulse-like exercise (10 s) with work load of 200 watts. VE and end tidal CO2 pressure (PETCO2) were measured continuously during rest, warming up, exercise and recovery periods. PaCO2 was predicted (PaCO2 pre) from PETCO2 and tidal volume (VT). PETCO2 and PaCO2 pre peaked at 20 s of recovery. VE increased and peaked at the end of exercise and then decreased during recovery; however, it peaked again at 30 s of recovery, which was 10 s later than the peak of PaCO2 pre. The relationship between VE and PaCO2pre was not significant by using data of them obtained at the same time but was significant by using data of VE obtained 10 s later for data of PaCO2 pre. The results support our hypothesis that PaCO2 drives VE with a time delay.

VE started to increase and peaked once again at 30 s of recovery, which was 10 s later than the peaks of PETCO2 and PaCO2 pre (20 s of recovery).Thus, this further drive and the second peak of VE might be attributed to PaCO2. It is known that carotid bodies respond to hypercapnia [15], and central chemoreceptors would be stimulated more by hypercapnia than by acute metabolic acidosis of arterial blood because the blood-brain barrier is relatively impermeable to H+ but is permeable to CO2 [16].

Denen Studien nevner at laktat og CO2 var en bedre beskyttelse for utslitte muskler enn glukose. Kan virkelig en mild acidifisering av blodet være bedre restitusjon enn karbohydratpåfyll??

Det kan se ut som at det er opphopning av K+ utenfor muskelcellene som styrer utmattelse, og dermed vil en økning av CO2 som gir acifdifisering virke restituerende. Men dette må jeg undersøke nærmere.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278832/

1. During strenuous exercise lactic acid accumulates producing a reduction in muscle pH. In addition, exercise causes a loss of muscle K+ leading to an increased concentration of extracellular K+ ([K+]o). Individually, reduced pH and increased [K+]o have both been suggested to contribute to muscle fatigue.
2. To study the combined effect of these changes on muscle function, isolated rat soleus muscles were incubated at a [K+]o of 11 mm, which reduced tetanic force by 75 %. Subsequent addition of 20 mm lactic acid led, however, to an almost complete force recovery. A similar recovery was observed if pH was reduced by adding propionic acid or increasing the CO2 tension.
3. The recovery of force was associated with a recovery of muscle excitability as assessed from compound action potentials. In contrast, acidification had no effect on the membrane potential or the Ca2+ handling of the muscles.
4. It is concluded that acidification counteracts the depressing effects of elevated [K+]o on muscle excitability and force. Since intense exercise is associated with increased [K+]o, this indicates that, in contrast to the often suggested role for acidosis as a cause of muscle fatigue, acidosis may protect against fatigue. Moreover, it suggests that elevated [K+]o is of less importance for fatigue than indicated by previous studies on isolated muscles.

More importantly, this study also shows that in muscles where force and excitability are depressed by high [K+]o, lactic acid produces a pronounced recovery of force. A recovery of force could also be obtained by acidifying the muscle fibres using CO2 or propionic acid. In contrast, 20 mm glucose failed to induce a recovery of force. These findings indicate that the effect of lactic acid was related to the acidification of the muscles rather than to a possible metabolic effect (Van Hall, 2000). The pH of the muscles in the presence of 20 mm lactic acid was similar to the values for muscle pH observed after intensive exercise (Sjøgaard et al. 1985).

Denen Studien fra 2001 nevner at acidose fra CO2 ikke bidrar til utmattelse i musklene, slik vi har trodd under trening, f.eks. ved det som kalles melkesyreterskel. Det er andre faktorer som styrer treningsutmattelse.

http://www.ncbi.nlm.nih.gov/pubmed/9688723/

It is concluded that, at 28 degrees C, acidosis per se does not accelerate the development of fatigue during repeated tetanic stimulation of isolated mouse skeletal muscle fibers.