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

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.

Inspiratory muscle training reduces blood lactate concentration during volitional hyperpnoea

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.

Inspiratory muscle training lowers the oxygen cost of voluntary hyperpnea

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.

Hypoxia-generated superoxide induces the development of the adhesion phenotype

Viktig studie om mekanismen bak hvordan hypoxi gir arrvev (adhesions) i kroppen. Relatert til hyperventilering vil lite CO2 gir hypoxi og sammen med trange blodkar vil de utsatte stedene i kroppen utvikle arrvev mellom muskler og nerver. Nevner hvordan antioksidanter er viktig for å unngå arrvev, spesielt etter operasjoner. Og motsatt, at oksidanter kan skape arrvev fra friskt vev. Nevner også hvordan nitratreaksjoner er med å skaper arrvev, så mulig at CO2 bidrar med å dempe nitratreaksjonene og dermed dempe dannelsen av arrvev. Den viser også at det kan være mulig å få arrvev celler om til å bli normale celler.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574925/

«Adhesion fibroblasts exhibit higher TGF-β1 and type I collagen expression as compared to normal peritoneal broblasts. Furthermore, exposure of normal peritoneal fibroblasts to hypoxia results in an irreversible increase in TGF-β1 and type I collagen. We postulated that the mechanism by which hypoxia induced the adhesion phenotype is through the production of superoxide either directly or through the formation of peroxynitrite. »

«Hypoxia treatment resulted in a time-dependent increase in TGF-β1 and type I collagen mRNA levels in both normal peritoneal and adhesion fibroblasts.»

«In contrast, treatment with SOD, to scavenge endogenous superoxide, resulted in a decrease in TGF-β1 and type I collagen expression in adhesion fibroblasts to levels seen in normal peritoneal fibroblasts; no effect on the expression of these molecules was seen in normal peritoneal fibroblasts. »

«In conclusion, hypoxia, through the production of superoxide, causes normal peritoneal fibroblasts to acquire the adhesion phenotype. Scavenging superoxide, even in the presence of hypoxia, prevented the development of the adhesion phenotype. These findings further support the central role of free radicals in the development of adhesions.»

«Postoperative adhesions are a significant source of impaired organ functioning, decreased fertility, bowel obstruction, difficult reoperation, and possibly pain (1,2)

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«The processes that result in either normal peritoneal tissue repair or the development of adhesions include the migration, proliferation, and/or differentiation of several cell types, among them inflammatory, immune, mesothelial, and fibroblast cells (3)

«Hypoxia, resulting from tissue injury, has been suggested to play an important role in wound healing, and may therefore be a critical factor in the development of postoperative adhesions (4,7)

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Destroy user interface contrHypoxia is known to trigger the expression of TGF-β1, which consequently increases the expression of extracellular matrix proteins, including type I collagen (4) 

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Destroy user interface contr«Type I collagen synthesis has been shown to be crucially dependent on the availability of molecular oxygen in tissue culture, animal, and human wound healing experiments (8,9)

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Destroy user interface controlMoreover, exposure of normal peritoneal fibroblasts to hypoxia irreversibly induces TGF-β1 and type I collagen to levels seen in adhesion fibroblasts (4,10)

«Additionally, hypoxia is known to acutely promote superoxide (O2.−) generation from disparate intracellular sources that include xanthine dehydrogenase oxidase (11), mitochondrial electron transport chain (12), and NAD[P]H oxidase (13).

In biological systems, superoxide dismutase (SOD) protects against the deleterious actions of this radical by catalyzing its dismutation to hydrogen peroxide plus oxygen, (14) Whereas SOD breaks down O2.−, xanthine oxidase synthesizes O2.−. Xanthine oxidase appears to be one of the major superoxide-producing enzymes (14)«

«Scavenging superoxide restores both TGF-β1 and type I collagen mRNA levels in adhesion fibroblasts to levels observed in normal peritoneal fibroblasts»
«Normal peritoneal and adhesion fibroblasts treated with super-oxide dismutase, a O2.− scavenging enzyme, exhibited a dose–response decrease (0, 5, 10, 15, and 20 units/ml) in TGF-β1 and type I collagen mRNA levels in adhesion fibroblasts while not effecting normal peritoneal fibroblasts (Figs. 3A and B).»

«Scavenging superoxide during hypoxia exposure protects against the development of the adhesion phenotype»

«Peroxynitrite treatment increased the adhesion phenotype markers, TGF-β1 and type I collagen»

«Adhesion fibroblasts are myofibroblasts, defined as transiently activated fibroblasts exhibiting features intermediate between those of smooth muscle cells and fibroblasts, including the expression of α-SM actin (29,21) and a depleted antioxidant system (22). In normal wound healing, as the wound resolves, the cellularity decreases and the myofibroblasts disappear by apoptosis (23). However, in several pathological cases, including fibrosis, myofibroblastic differentiation persists and causes excessive scarring (24,25)

«This is further supported by the fact that when O2.− was scavenged, there was in a significant decrease in TGF-β1 and type I collagen in adhesion fibroblasts to levels seen in normal peritoneal fibroblasts. »

«Reactive oxygen species (ROS) are involved in TGF-β-stimulated collagen production in murine embryo fibroblasts (NIH3T3), and the effect of glutathione depletion on TGF-β-stimulated collagen production may be mediated by facilitating ROS signaling (37)

«Reactive oxygen and nitrogen intermediates control the synthesis of cytokines and growth factors in several in vitro models (40). For instance, they modulate the expression and/or release of monocyte chemoattractant protein-1 (41,42), tumor necrosis factor-α, interleukin (IL)-1 (43,44), IL-8 (45,46), platelet-derived growth factor (47,48), and TGF-β1 (49). «

«Adhesion fibroblasts exhibited a significantly lower level of nitric oxide (NO) and higher protein nitration as compared to normal peritoneal fibroblasts, although there was no difference in the iNOS expression level between the two cell lines (17,50,51). This strongly indicates that adhesion fibroblasts use NO to form ONOO−, and consequently their basal ONOO− levels are higher than normal peritoneal fibroblasts. «

«Thus, treatment with SOD might affect the homeostasis of myofibroblasts by inducing cell death or the phenotypic reversion of myofibroblasts into normal fibroblasts. »

«Our results clearly indicate that hypoxia generated O2.− is a key player in the formation of the adhesion phenotype. This became evident when normal peritoneal fibroblasts were treated with SOD under hypoxic conditions and no change in adhesion markers was seen.»


«In this model, hypoxia-generated O2.− exerts its effect directly by enhancing the expression of TGF-β1, which consequently leads to elevated levels of type I collagen, a hallmark of the adhesion phenotype.»

Elevated lactate during psychogenic hyperventilation

Om CO2 relatert til melkesyre. Denne er ifh panikkangst, men gjelder også ifh trening og hva som helst av aktivitet eller sykdom hvor melkesyre er et element å ta hensyn til.

http://emj.bmj.com/content/28/4/269.long

«Whereas high lactates are usually associated with acidosis and an increased risk of poor outcome, in patients with psychogenic hyperventilation, high lactates are associated with hypocapnia and alkalosis.»

«However, provoked hyperventilation, a less life-threatening condition, has been shown to result in elevated lactate levels as well. Passive overbreathing under anaesthesia has been shown to induce hyperlactataemia in various studies.9 10 Furthermore, active voluntary overbreathing in individuals with panic disorders has been related to the development of a marked hyperlactataemia as well.11 12»

«As expected, median Pco2 (4.3 (2.0–5.5)) was below the lower reference value of 4.6 kPa, and median pH was slightly increased (7.47 (7.40–7.68)). Po2 and saturation were normal in all the patients without supplementary oxygen (table 1). Fourteen participants had a lactate level above the reference value of 1.5 mmol/l, of which 11 were still hyperventilating at the moment of drawing their blood, as reflected by the Pco2 values <4.6 kPa. The participants who were still actively hyperventilating had a higher median pH of 7.50 (7.42–7.68) versus 7.44 (7.40–7.49) (p<0.01) and a higher median lactate level of 1.4 (0.7–4.4) versus 0.9 (0.5–3.5) (p<0.01) compared with the participants diagnosed as having psychogenic hyperventilation who had ceased to actively hyperventilate at the moment of drawing their blood. In line with the higher pH in this group, bicarbonate and potassium concentrations were lower (table 1).»

«In univariate correlation analysis, there was a significant positive correlation of plasma lactate with both Po2 and pH, whereas significant inverse relations were found for potassium and bicarbonate (table 2). Most interestingly, a significant negative correlation was found between Pco2 and arterial lactate (r=−0.50, p<0.001; figure 2). This negative correlation was specifically present in patients with hypocapnia (ie, Pco2 <4.6 kPa): in these patients, there was a moderate significant negative correlation between Pco2 and plasma lactate levels (r=−0.53, p<0.003), whereas this correlation was not seen in normocapnic participants (r=−0.17, NS).»

«Scatter plot of the relation of Pco2 with lactate for patients diagnosed as having psychogenic hyperventilation (n=46). Depicted are the regression line in bold (r2=0.25, p<0.001), with estimated 95% CIs. The vertical dashed line denotes the lower reference value of arterial Pco2; and the horizontal line, the upper reference value of lactate.»

«In our study, we showed that lactate levels are elevated in 30% of the participants with psychogenic hyperventilation who present at the ED. Furthermore, we demonstrate that under these circumstances, Pco2 is the most important predictor of arterial lactate levels and that in this context, an elevated lactate level should not be regarded as an adverse sign.»

«The reported 0.5% incidence of hyperventilation in our study population seems to be low compared with that in previous studies, reporting incidences of 6%–11%.14» «We suppose that the relatively low incidence in our study population could be related to a substantial amount of patients with psychogenic hyperventilation who are not referred to the hospital at all by their general practitioner.»

«Our present study is the first to describe the presence of hyperventilation-related hyperlactataemia in an otherwise healthy patient population presenting in the ED in an observational setting.»

«Pco2 being the strongest lactate predictor of the two, as changes in pH during hyperventilation are modulated by changes in breathing rate (and thus Pco2). Our findings are in line with those of previous studies, which showed that intracellular hypocapnia and alkalosis contribute directly to both an increased lactate production and a reduced lactate clearance.18–21»

«However, it should be noted that in patients with critical illnesses, lactate is a risk marker not a risk mediator22: several studies have shown that the administration of exogenous lactate is safe or even beneficial.23 Lactate can be reused directly as a substrate to generate adenosine triphosphate by many organs, including the heart, the brain and the kidneys.24 25»

TABLE 1

Total Pco2≥4.6 Pco2<4.6
n 46 17 29
Sex (% male) 46 41 48
Age (years) 30 (18–77) 26 (18–66) 35 (18–77)
Respiratory rate at triage 25 (20–35) 24 (20–30) 25 (20–35)
Pco2 (kPa) 4.3 (2.0–5.5) 4.9 (4.7–5.5) 3.9 (92.0–4.5)
Lactate level (mmol/l) 1.2 (0.5–4.4) 0.9 (0.5–3.5) 1.4 (0.7–4.4)*
Lactate level >1.5 mmol/l (n) 14 3 11
Base excess 1.4 (−3.2–4.8) 2.1 (−2.7–4.3) 0.6 (−3.2–4.8)*
Potassium (mmol/l) 3.5 (2.8–4.2) 3.8 (3.3–4.0) 3.4 (2.8–4.2)*
HCO3 (mmol/l) 23 (17–27) 26 (21–27) 22 (17–25)
pH 7.47 (7.40–7.68) 7.44 (7.40–7.49) 7.50 (7.42–7.68)
Po2 (kPa) 13.3 (9.3–17.9) 12.9 (10.3–15.6) 13.8 (9.3–17.9)*
Saturation (%) 98 (97–99) 98 (97–99) 98 (97–99)
  • Clinical and biochemical characteristics of the 46 patients as indicated in figure 1 and after stratification for the presence of hypocapnia (Pco2 <4.6). The data are presented as median (range). Statistical comparisons between the normocapnic and hypocapnic subgroups were made by the χ2 test for dichotomous variables and for continuous variables by Mann–Whitney U test.

  • * p<0.05 compared with normocapnic participants.

  • † p<0.001 compared with normocapnic participants.

Basilar Artery Response to Hyperventilation in Panic Disorder

Nevner hvordan hyperventilering fjerner CO2 og gjør at blodkar trekker seg sammen. Nevner spesielt basilary artery inni hjernen.

http://ajp.psychiatryonline.org/data/journals/ajp/3682/1603.pdf

«Gibbs (2) reported that nine panic disorder patients in a neurology clinic experienced a significantly greater decrease in basilar artery blood flow during voluntary hyperventilation (mean decrease, 62%) than did nine normal comparison subjects (mean decrease, 36%). However, no respiratory measures were assessed dur- ing hyperventilation, and this omission is important, since changes in carbon dioxide levels are critical in regulating cerebral arterial flow (3).»

«For mean blood flow, the panic patients had a 55% reduction (mean change=–21.1 cm/sec, SD=7.1), which was sig- nificantly greater than the 42% reduction for the com- parison group (mean change=–15.8 cm/sec, SD=5.4)»

«The increases in the dizziness ratings were associated with the percent- ages of the decreases in both peak flow (r=–0.60, N=24, p<0.01) and mean flow (r=–0.57, N=24, p<0.01).»

«The pCO2 level of the panic disorder patients decreased 33% during hyperventilation (pCO2 level dur- ing hyperventilation: mean=24.80 mm Hg, SD=7.29), which did not differ significantly from the 37% decrease for the comparison subjects (pCO2 during hyperventila- tion: mean=24.55 mm Hg, SD=3.09) (t=–0.14, df=7, n.s.).»

«The ratio of blood flow changes to pCO2 changes is approximately 1.0 in normative studies (4), which is consistent with the values for our comparison group. The patients with panic disorder had a ratio of blood flow change to pCO2 change that was almost twice that of the normal subjects. This suggests that the sensitivity of the basilar artery in patients with anxiety disorders may not be due solely to changes in respiratory physiology.»

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

Nevner at CO2 ikke er årsak til hyperventillering under trening, men at det er melkesyre. Pusten øker for å fjerne CO2 så syreoverskuddet holdes i balanse.

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

«During incremental exercise, blood lactate is progressively increased above the VT. This is buffered by the bicarbonate system. This results in progressive reduction of blood bicarbonate ion (Beaver et al. 1986a) and metabolic acidosis. In order to improve this metabolic acidosis, ventilation is driven and becomes hyperventilation above the VT in incremental exercise. As a result, Vco2excess is progressively increased above the VT.»

«The following findings suggest that hyperventilation in exercise is induced by metabolic acidosis due to an increase in blood lactate detected by peripheral chemoreceptors. »

«Secondly, it was found that intravenous infusion of bicarbonate during incremental exercise attenuated the decrease in blood pH above the VT and consequently reduced hyperventilation by 15-30 % (Peronnet et al. 2007). However, if this hyperventilation accompanies a decrease in Paco2, it would stimulate central chemoreceptors and peripheral receptors via its effect on pH (Clement et al. 1992) and consequently can attenuate the hyperventilation. »

«Thus, hyperventilation during second recovery did not increase despite an increase in blood lactate probably due to lower Paco2 than that during first recovery. »

«During recovery, lactate is not produced in muscle. However, lactate is transported from the muscle to blood. The buffering system is primarily a non-bicarbonate system in muscle cells (Hultman and Shalin, 1980) but a bicarbonate system in blood (Yano 1987, Peronnet and Aguilaniu 2006).»

«After the end of heavy, very heavy and cycling sprint, Paco2 becomes lower than the resting level (Kowalchuk et al. 1988, . Stringer et al. 1992). »