Post Number: 8
|Posted on Sunday, November 28, 2010 - 01:22 am: |
I just received my kiko the other day and have starting to track some numbers upon waking daily.
Below are some numbers from one of the mornings.
I haven't been using my asthma medication very much at all as I have been able to control things even during racing over the past year.
however I found it interesting that my Peak number is fairly low and it feels hard for me to blow out hard and a little wheezy as well.
before test no asthma medication:: avgs of 3 attempts for all data
Then took medication and waited 10 minutes and::
Is there a type of training that may help this with spiro?
Might powerlung help this situation?
Is 20% difference enough to worry about here and look towards improving?
If I can improve through training I would like to rather than take the medication.
Post Number: 2
|Posted on Friday, January 14, 2011 - 08:31 am: |
Spirotiger for improving breathing with athsmatics- have you noticed any improvments??
I had a well known pysiologist tell me that it would not help with asthma since asthma is a problem with inhalation not exhilation but I beleive that you can train the diaphragm to work better therefore increasing your inhalation.
any feed back on this?
Post Number: 452
|Posted on Friday, January 14, 2011 - 09:05 am: |
Some of the first publishes studies on resp training were done on asthmatics, and showed clear improvements in hospital admission rates and symptom control. Your friend needs to do some reading.
Have a look at the Idiag site for journal publications, or do a lit search for resp training and asthma.
Post Number: 3025
|Posted on Friday, January 14, 2011 - 12:29 pm: |
Thanks for the infos here.
Z A short add on.
1. Great that the "spec" thinks that asthma is an inhalation problem.
To inhale you need some muscles : to exhale you need, at least at rest, no muscles.
So if we would improve respiration we would work first on inhalation.
Check out the different reasons of asthma.
Some would place it as a obstructive respiratory problem.
Meaning , that the airflow is "obstructed" well that could be in both directions ???
To avoid a conflict of interests to Spiro Tiger here a summary independent from studies with Spiro Tiger. The same groups where studied with Spiro tiger and some nice results as well and as you can imagine, training an endurance muscle with and endurance type of training may have at least the same or better results.
Here to read : " Studying the Effects of Inspiratory Muscle Training in Patients with Obstructive Lung Diseases
Share with others Shane Keene MBA, RRT-NPS, CPFT, RPSGT
College of Public and Allied Health
East Tennessee State University
Citation: S. Keene : Studying the Effects of Inspiratory Muscle Training in Patients with Obstructive Lung Diseases . The Internet Journal of Pulmonary Medicine. 2007 Volume 7 Number 2
Review Of Literature
Inspiratory Muscle Training (IMT) has been studied significantly as being used for pulmonary rehabilitation for patients with obstructive lung disease. By measuring the various test subjects' on the following parameters, researchers can develop a basis to determine whether the training is successful in helping the patients improve their inspiratory muscle function: level of dyspnea based on the Borg score, maximum inspiratory pressure, number of hospitalizations due to exacerbations of their disease, inspiratory muscle strength and endurance, 6 minute walking distance, exercise tolerance, and health related quality of life (HRQL). By assessing these critical values, researchers have determined that IMT does provide a significant form of exercise for the inspiratory muscles that can improve their function and offer many other health benefits.
Inspiratory Muscle Training (IMT) is theorized to offer a basis for pulmonary rehabilitation to patients with obstructive lung diseases. It works by providing a threshold of Inspiratory resistance that the patients inhale against to strengthen their Inspiratory muscles. The threshold device is used repeatedly during a training session and offers patients a constant level of resistance to work against. Through routine daily exercise sessions patients should be able to increase their Inspiratory muscle strength. With the strengthening of these muscles, the patients' levels of dypnea should decrease as the work of breathing becomes easier. Also with the decreased work of breathing, it should follow that patients should be able to perform physical activities more easily and improver their overall Health Related Quality of Life (HRQL).
Are there theoretical reasons for expecting any benefit from improved function of the inspiratory muscles?
Review Of Literature
Inspiratory muscle training (IMT) is a form of respiratory rehabilitation that is recognized as a key therapeutic tool in all clinical guidelines in managing COPD. According to Mota-Casals (2005), when assessing the IMT as a rehabilitation technique, the following questions should be addressed: 1. Are there theoretical reasons for expecting any benefit from improved function of the inspiratory muscles? 2. Can training improve muscle function of the inspiratory muscles in patients with COPD? 3. Does improved inspiratory muscle function produce a clinical benefit for these patients?
In a meta-analysis of 12 trials, it was found that when using a valve to create a resistance load, where the breathing pattern and pressure were not affected, allowed patients to develop a more regular breathing pattern. Further discoveries in this study showed that specific inspiratory training protocol with specified duration and work loads (>20% PImax) lead to improvement in strength and stamina of the inspiratory muscles. This increase in strength and stamina improve structural changes to the external intercostals, therefore producing functional changes with a structural basis when trained appropriately. A further sub analysis was performed and it was found that general training combined with specific training of the inspiratory muscles was significantly better at improving the strength and stamina of the inspiratory muscles. In this case, those subjects whose PImax was less than 60 cmH2O, there was an increase in the distance achieved during the 6 minute walk test.
Throughout the testing, one key point noted was that the control group, which trained at the minimal load allowed by the threshold device showed comparable improvement in all variables studied. This illustrates that low pressure administered at regular intervals provided a sufficient stimulus to induce training-related changes. These findings show that aggressive therapy is not necessarily the most beneficial to patients and more passive levels of training can be used in patients with severe cases of COPD.
In conclusion, all three of the previously proposed questions can be answered affirmatively with the following statement: There is a theoretical justification for using Inspiratory Muscle Training in the reduction of dyspnea, one of the main goals in managing COPD.
According to Weiner (2004), it is hypothesized that increasing the respiratory muscle strength and endurance with Specific Inspiratory Muscle Training (SIMT) will produce a reduction of symptoms in patients with asthma.
The study's design compared SIMT of 15 blinded patients with a “sham training” of 15 blinded patients who received no actual resistance training. The entire experiment was conducted over the course of a 6 month training session. Comparisons between the two groups were made in all of the following fields: inspiratory muscle strength, and endurance, hospitalization for asthma, asthma symptoms, absence from school or work, emergency department visits, and inhaled beta-2 agonists.
To develop a baseline for comparison, each of the 30 test subjects were asked to record in a daily journal the severity of their asthma symptoms based on the following three parameters: nighttime asthma, daytime asthma, and cough severity. The journaling began 3 months prior to the beginning of their training sessions and was continued through the duration of the study.
The patients were also asked to perform the following quantitative tests to develop a basis for measuring their improvement with the training: spirometry, respiratory muscle strength, and respiratory muscle endurance. The actual training was conducted in 30 minute sessions 5 times per week over the course of 6 months. With the conclusion of the training sessions there were found to be significant increases in the 3 quantitative assessments for all members of the SIMT group, where there was little to no improvement for those in the control group.
One of the key discussions that arose from this study is focused on the increased FVC that was measured by the SIMT group. (It was found that the SIMT group's FVC rose from 76.8 [+ or - 3.1] to 86.6 [+ or – 2.5] percent of predicted normal values.) It is known that the resistance to airflow varies with lung volumes.
By increasing the FVC of a patient, their overall lung volume increases. This produces a direct decrease in their airway resistance and presumably a decrease in their levels of dyspnea. In conclusion, SIMT is a proven way to increase an asthma patient's FVC. This aids in reducing their levels of dyspnea and in turn can be used as an alternative physiologic form of therapy to reduce their intake of systemic corticosteroids and inhaled beta-2 agonists.
Effect of Inspiratory Muscle Training on Muscle Strength and Quality of Live in Patients with Chronic Airflow Limitation: A Randomized Controlled Trial, (2005) looks at inspiratory muscle training and assesses it as a technique for managing Chronic Airway Limitation (CAL). The overall aim of this study was to quantitatively determine the effectiveness of inspiratory muscle training on improved physiological and functional variables. In the study, 18 control patients and 17 experimental patients were subjected to experimental intervention over the course of 2 months. The experimental patients performed inspiratory muscle training using a device that administered a resistive load of 40% their maximal inspiratory mouth pressure (PImax). The parameters that were assessed included: inspiratory muscle strength, respiratory function, exercise tolerance, and quality of life.
The results of the study showed that there was a significant increase in the inspiratory muscle strength of the experimental training group. PImax was found to improve 8.9 cmH2o per month of training. Concurrently, the health-related quality of life scores were found to improve by 0.56 points. In conclusion, the IMT with use of threshold device was found to effectively strengthen inspiratory muscles when measured by the PImax. It was detected that the level of improvement would be significant enough to be considered as a respiratory rehabilitation program to improve HRQL for the patients.
The purpose of this study was to determine the appropriate level to set the training load for the inspiratory muscle trainer, IMT. Two groups were trained using two different levels of their PImax to assess which level would be most effective when offering pulmonary rehabilitation to patients with chronic airflow limitation (CAL) (Lisboa, 1994). The training was assessed by measuring the following variables: PImax, Inspiratory Muscle Power Output (IMPO), Sustainable Inspiratory Pressure (SIP), Maximal Inspiratory Flow Rate (VImax), pattern of breathing during loaded breathing, Mahler's dyspnea scores, and 6 minute walking distance. After 5 weeks, group 1 (their resistance load was set at 30% of their predetermined PImax) exhibited significant increases in all the parameters. Group 2 (resistance was set at 12% of PImax) showed no significant improvement in these measurements. Dyspnea was found to be decrease for group 1 and this group also showed an increase in tidal volume and reduction in inspiratory time.
According to an article found in Chest (2002), the use of Inspiratory Muscle Training can be used to aid in the weaning of mechanically ventilated patients who were previously unable to be weaned from their ventilator (Martin 2002). Through aggressive training with high levels of intensity and low repetitions, the patients were able to increase their duration of spontaneous breathing periods (SBP). Each of the 10 patients started out with an average of 2.1 [+ or – 3.4] consecutive hours of SBPs. They had been on mechanical ventilation for an average of 34 [+ or – 31] days. The daily training consisted of four sets of six breaths through a threshold inspiratory muscle trainer. The initial resistance load was 7 [+ or – 3] cmH20 and it was increased to 18 [+ or – 7] cmH2O when the patient was successfully weaned. After 44 [+ or – 43] days, 9 of 10 patients were successfully weaned from mechanical ventilation. The use of endurance respiratory muscle training has been successful in aiding patients when weaning them off of the ventilator. This test was different than those previously attempted because it used a pressure threshold rather than a restrictive flow device and the inspiratory muscles were trained in strength rather than endurance. Based upon this study it is predicted that a “high-intensity pressure-threshold IMST program coupled with progressively longer SBPs would increase inspiratory muscle strength and endurance, decrease the patients' perception of respiratory distress during spontaneous breathing, and facilitate weaning.”
Weiner, (2003) compares specific inspiratory muscle training against training of both the inspiratory and expiratory muscles when training for improvement in respiratory muscle strength and endurance. Inspiratory Muscle Training has been used to decreased the severity of breathlessness and improve exercise tolerance in patients with COPD. In this study, there were 4 groups in randomized individuals to assess different training variations: group 1 received specific expiratory muscle training (SEMT), group 2 received specific inspiratory muscle training (SIMT), group 3 received a combination of SIMT and SEMT training, group 4 was the control group and received training with a minimal load. The training sessions lasted ˝ hour six days a week for 3 months.
The results of the study showed that there was a significant increase in the 6 minute walking distance for groups 1, 2, and 3, however the results for the SEMT group were not nearly as high as those for the SIMT and SIMT + SEMT groups. There was a decrease in the mean Borg score during breathing against resistance for the SIMT group and the SEMT + SIMT group, where as the SEMT and control group exhibited no change. In conclusion, both the inspiratory and expiratory muscle groups can be trained to have improved muscle strength and endurance. However, there is no additional benefit gained when combining SIMT and SEMT when comparing to SIMT alone.
The effects of inspiratory muscle training were recorded in an 8 week study performed on patients with cystic fibrosis (Beckerman, 2005). The patients (n=29) were randomized into three study groups. One group received 80% maximal inspiratory muscle training (n=9), one group received 20% maximal inspiratory muscle training (n=10), and one group (n=10) did not participate in inspiratory muscle training. The study demonstrated the benefits of inspiratory muscle training based on inspiratory muscle function, lung volumes, and psychosocial factors. In the two clinical trial groups, the following were observed: increased maximal inspiratory pressure and increased sustained maximal inspiratory pressure, increased vital capacity and total lung capacity, and decreased anxiety and depression scores.
Patients with mild asthma with high consumption of beta-2 agonists were studied to evaluate the effects of inspiratory muscle training (Enright, 2004). The patients were randomized into two groups, an experimental group and a control group. The experimental group received training for 3 months; the control group received sham training. The study was measured by perception of dyspnea and frequency of beta-2 agonist consumption. Inspiratory muscle training was found to decrease the perception of dyspnea of patients based on the Borg score. Furthermore, inspiratory muscle training was associated with decreased frequency of consumption of beta-2 agonists.
The effects of long-term inspiratory muscle training were documented in a study performed on 42 patients with COPD (Oh, 2003). All patients involved in the study exhibited at least a moderate obstructive component, as represented by FEV1 < 50%. The study was conducted for 1 year. The subjects were randomized into two groups: one group received the inspiratory muscle training and one group received a greatly reduced training program. The study conclusively showed the benefits of inspiratory muscle training based on inspiratory muscle strength, perception of dyspnea, improved exercise capacity, and decrease in primary care usage and hospitalization. In comparison to the control, the patients demonstrated improvement in maximal inspiratory pressure, decreased perception of dyspnea as evidenced by a decrease in the mean Borg score, improvement in six-minute walking distance, and decreased use of primary care physician, and decreased frequency of hospitalizations.
The effects of inspiratory muscle training were observed in patients with COPD in Spain (Lotters, 2002). The patients were randomized into two groups, an experimental group (n=10) and a control group (n=10). The experimental group trained at home for 30 minutes a day, 6 days a week, for 6 months. The control group did not participate in any form of inspiratory muscle training. The outcomes were measured in sustained maximal inspiratory pressure, shuttle walking test, and health related quality of life questionnaires. The results showed improvement in the measured factors in the experimental group, whereas the control group demonstrated no statistically significant improvement. Therefore, the study exhibited the correlation of inspiratory muscle training and relief of dyspnea, increased exercise capacity, and improved health related quality of life.
In a study performed in South Korea, the effects of inspiratory muscle training were observed in a home-based pulmonary rehabilitation program (Riera, 2001). The patients (n=23) were randomized into two groups, in which the first group (n=15) received inspiratory muscle training and the second group (n=8) only received education. All of the patients involved with the study exhibited a moderate to severe obstructive component in the presentation of COPD. The outcome measures were FEV1, level of dyspnea based on the Borg score, and six-minute walking distance. The experimental group demonstrated decreased perception of dyspnea and improved exercise capacity.
The documented effects of inspiratory muscle training were examined in a meta-analysis. The meta-analysis involved a thorough, systematic literature research to provide a critical examination of the effects of inspiratory muscle training (Weiner, 2000). The literature used in the meta-analysis was limited to patients with COPD. The study conclusively determined the beneficial effects of inspiratory muscle training. The effects were improved inspiratory muscle strength and endurance, improved functional exercise capacity, and decreased dyspnea, during exercise and at rest. The meta-analysis strongly suggested that inspiratory muscle training is a very essential addition to pulmonary rehabilitation programs.
The layouts for developing the different studies for patients using the Inspiratory Muscle Training follow the same clinical standards. The project was first introduced to IRB for acceptance. The patients were then informed of the nature of the study and signed written consent to participate. The studies were performed within compliance of HIPPA guidelines. The subjects were all selected at random in a double blind approach. The patients' disorders consisted of COPD, asthma, cystic fibrosis, and those who were ventilator dependent. Their physical ability as assessed by questionnaire and they were divided into a control group and an experimental group. The control group did not receive any inspiratory muscle training where the experimental group received various levels of threshold resistance training. The training lasted for a predetermined amount of time daily and was continued over the course of a preset time frame. The data from the experiments was collected and the information of the experiment group was compared to that of the control group. The data collected ranged from the following parameters: 6 minute walking distance, FEV1, level of dyspnea based of the Borg scale, HRQL, PImax, exercise tolerance, frequency of hospitalizations and primary care usage.
Based on the reviewed studies, the Inspiratory Muscle Training provides a form of muscle exercise that builds the inspiratory muscles for patients with obstructive lung disease. The resistance training helps them improve muscle function which leads to decrease in their levels of dyspnea and an increase in their HRQL.
All of the studies conducted were performed on a limited number of subjects. There has yet to be any collaboration between large research groups to quantitatively analyze the results of IMT on a large scale. An option for future studies is to incorporate a much larger number of test subjects to be studied and possibly off a definitive number for a threshold resistance load that might offer the highest level of results for specific chronic lung conditions.
There also seems to be a lack of unified measurements assessing the success of the IMT. For future studies, there should be a set of universal parameters that is measured for a basis to determine the full effects of the training. After a number of large studies have been conducted with these universal measurements, they can be generalized into a basis for setting goals for future patients receiving IMT.
Based on the previously discussed studies IMT does show a positive correlation between an optimal threshold resistance level and increased Inspiratory muscle strength in patients with obstructive lung diseases. This increased muscle strength contributes significantly to the patients' decreased work of breathing and level of dyspnea as graded on the Borg score. These studies prove that IMT does provide a successful form of pulmonary rehabilitation for obstructive lung patients. This offers improved lung function in those who trained with it appropriately. At optimal resistance levels, Inspiratory Muscle Training can be viewed as a successful way to help improve obstructive lung patients' overall health related quality of life.
Beckerman, Marinella, Magadle, R. (2005, November). The Effects of 1 Year of Specific Inspiratory Muscle Training in Patients with COPD. Chest, 5, 3177-3183. (s)
Enright, S., Chatham, K., Lonescu, A. (2004, August). Inspiratory Muscle Training Improves Lung Function and Exercise Capacity in Adults with Cystic Fibrosis. Chest, 2, 405-412. (s)
Enright, S. J., Unnithan, Viswanath B., Heward, C., Withnall, L., Davies, David H. (2006, March). Effect of High-Intensity Inspiratory Muscle Training on Lung Volumes, Diaphragm Thickness, and Exercise Capacity in Subjects Who Are Healthy. Physical Therapy, 86. (s)
Lisboa, C., Munoz, V., Beroiza, T., Leiva, A., Cruz, E., (1994). Inspiratory Muscle Training in Chronic Airflow Limitation: A Comparision of Two Different Training Loads with a Threshold Device. European Respiratory Journal, 7, 1266-1274. (s)
Lotters, F., Kwakkel, G., Gosselink, R. (2002, September 1). Effects on Controlled Inspiratory Muscle Training in Patients with COPD: A Meta-analysis. European Respiratory Journal, 20, 570-577. (s)
Martin, Daniel. (2002). Use of Inspiratory Muscle Strength Training to Facilitate Ventilator Weaning. Chest, 122, 192-196. (s)
Oh, Eui-Geum. (2003, November). The Effects of Home-Based Pulmonary Rehabilitation in Patients with Chronic Lung Disease. International Journal of Nursing Studies, 40, 873-880. (s)
Riera, H., Robio, T., Ruiz, F., Ramos, P., Otero, D. (2001, September). Inspiratory Muscle Training in Patients with COPD. Chest, 120, 748. (s)
S Mota-Casals (2005). What is the Role of Inspiratory Muscle Training in the Treatment of Chronic Obstructive Pulmonary Disease? Archivos De Bronconeumologia, 41, 593-595. (s)
Seron, P., Riedemann, P., Munoz, S., Doussoulin, A., Villarroel, P., Cea, X., (2005, November). Effects of Inspiratory Muscle Training on Muscle Strength and Quality of Life in Patients with Chronic Airflow Limitation: A Randomized Trail. [On-line]. Archivos De Bronconeumol, 11, 601-606. (s)
Weiner, Paltiel. (1992). Inspiratory Muscle Training in Patients with Bronchial Asthma. Chest. (s)
Weiner, P., Berar-Yanay, N., Davidovich, A., Magadle, R. (2000, March). Specific Inspiratory Muscle Training in Patients with Mild Asthma with High Consumption of Inhaled B2 Agonists. Chest, 117, 722. (s)
Weiner, P., Magadle, R., Mecerman, M., Weiner, M., Berar-Yanay, N. (2003). Comparison in Specific Expiratory, Inspiratory, and Combined Muscle Training Programs in COPD. Chest, 124, 1357-1364. (s)
Post Number: 35
|Posted on Saturday, January 22, 2011 - 07:54 am: |
Re: Posted on Friday, January 14, 2011 - 03:31 pm
Quote: "I had a well known pysiologist tell me that it would not help with asthma since asthma is a problem with inhalation not exhilation"
I've been waiting for someone else to pick up this glove, partially so that is not always me playing the devil's advocate on this forum. This has not happened so here we go:
Technically, asthma is neither a problem of inhalation nor a problem of exhalation that can be fixed by increasing the "fitness" of either inspiratory or exspiratory muscles. Narrowing of small calibre bronchi caused by smooth muscle spasms is the culprit (together with bronchial inflamation). However, clinically speaking, the typical symptom of an asthmatic attack is exspiratory dyspnea, meaning that patient is able to breathe in but has difficulty or is unable to breathe out. This cannot be overcame by increased exspiratory muscles effort though. Increased intrathoracic pressure trasferred (via intraalveolar pressure) onto the external walls of small bronchi narrowed by spasm makes these virtually to collapse. Hence the inability of patient to exhale. Further increase of intraalveolar pressure can lead to lung tissue damage.
There seems to be some validity in suggestions that yoga breathing with typical 1:4:2:1 pattern or its easier/simplified variations may be beneficial. Problem of these studies is that they are usually perforemed by "believers" and even people with no intentions to lie are prone to "wishfull thinking effect". Nevertheless, focusing on prolonged, relaxed, as much as possible passive exspirium makes more sense as a technique to overcome an asthmatic attack than increasing one's respiratory muscles strength.
Post Number: 21
|Posted on Saturday, January 22, 2011 - 08:51 am: |
I have been very consistent for two months now spiro 5 days a week.
I can't really say if it has improved my asthma as I have neem controlling pretty well last few years.
I can say that my FEV is up from the above posted non ventolin number of 5.46 to 6.11 during this time.
Post Number: 460
|Posted on Saturday, January 22, 2011 - 09:20 am: |
While Karl makes some very good points, and as always has done a great job with his explanation of asthma, his comments fail to recognize that some of the improvements we see in Spiro users, are not a result of increased strength and improved ability to increase intrathoracic pressure, but rather the coordinated movement of the muscles of respiration.
There are a number of published studies showing the benefit of Spiro training in asthmatics, that show an increased time to fatigue, and an improved quality of life over a period of 8-12 weeks of training.
There is also suggestions that the improved respiratory training improves laminar flow of the air through the inflamed airways, which helps to minimize the irritation and decrease the stimulus for more inflammatory mediators to be released.
As always, the theory and the practical application are still a number of years apart. By that, I mean, the theory on why asthma is exacerabted by exercise is a number of years behind explaining why asthmatics make significant gains in exercise tolerance after a very short period of work with Spiro.
As Karl indicates, yoga breathing, seems to help. I suggest this is due to the relearning of appropriate diaphragmatic breathing patterns, which can be taught much more efficiently and effectively with the aid of a Spiro-Tiger.
Post Number: 3059
|Posted on Sunday, January 23, 2011 - 04:46 am: |
Thanks for all the great feedback.
Karl do not worry , we like " friendly devils "
The key in Asthma treatment besides the typical medication treatments we see here in North America is a possibly other way , where the patient himself is more integrated in the rehabilitation and or at least in the control of his problems.
As I pointed out and than in much better way be Karl, Asthma is not really a problem of the respiratory muscles, as much rather a problem of the respiratory air ways.
As mentioned, some would classify this as an "obstructive " respiratory problem.
Meaning , that due to the inflammation and the restriction in air flow the actual work of respiration is much harder, than without this restrictions.
This has the uncomfortable effect, that R. Dempsey's metaboreflex is kicking in much earlier than in people without asthma.
This as a sign , that the normally 16 +- % of O2 needed for a healthy person from the respiratory system can increase dramatically with Asthma.
So a good trained respiratory muscle system , who can work very efficient can have some advantage in this case. Similar to a person , who has a hip arthrosis and has lost lot's of muscle strength due to under use or "overuse" over the years. Now replacing the hip will solve the pain and friction problem, but he still can't use the leg properly . Now a controlled strength rehabilitation workout could help as well to get him more benefit from his new hip.
The other part is airflow and speed of airflow.
Due to the obstruction any explosive ( coughing or fast expiratory or inspiratory airflow creates a very inefficient way of moving air in one or the other direction.
So air can stay trapped in side or simply has as well some problem to move in.
So the key is often to create a smooth and efficient airflow pattern.
The problem is the often strong dis-balance between inspiration and expiration.
Unfortunately the classical way of assessing fast asthma is a peak flow meter.
But the flow is only tested in the expiration.
We use a specific model of a peak flow meter, where we asses peak flow inspiration and peak flow expiration.
This way we can assess easier what is harder to do for the person , inspiration and or expiration.
Now the reason why I like to add some more here for perhaps further discussion is the way Asthma is treated since over 100 years in europe and mainly in eastern europe.( started end of 1890 with Fr. Miescher Noble price winner in the DNA reseaerch from Basel/Davos Switzerland )Davos ( my birth place , was a classical Asthma treatment center in the beginning of the 1930 and up , where respiration and CO2 was used ( lack of medication at that time ) and many european countries like Netherland, Belgium, Great Britain , Germany had their private clinics in Davos for their Asthma patients to get sent to altitude.
By now we know , that O2 can have an inflammatory and negative effect to the lungs if applied to high .
The natural antagonist for O2 is CO2.
There is a long time believe backed up by many studies, that a controlled ( so called permissive CO2 ) can have a very positive effect on the inflammatory situation in the airways an possibly as well in other body areas.
So that's where a very different way of using the Spiro Tiger comes in.
Using Spiro Tiger with a controlled hypercapnic effect and a controlled slow but efficient respiration. Here one of the very basic studies in that direction. " U.S. National Library of Medicine
National Institutes of Health Search:
Crit Care Med. 2008 Oct;36(10):2823-7.
The effects of CO2 on cytokine concentrations in endotoxin-stimulated human whole blood.
Kimura D, Totapally BR, Raszynski A, Ramachandran C, Torbati D.
Division of Critical Care Medicine, Miami Children's Hospital, Miami, FL, USA.
OBJECTIVES: Hypercapnia is known to modulate inflammation in lungs. However, the effect of hypocapnia and hypercapnia on blood cytokine production during sepsis is not well understood. We hypothesized that CO2 modulates ex vivo inflammatory cytokine production during endotoxin stimulation. To test this hypothesis, we measured the production of pro- and anti-inflammatory cytokines in endotoxin-stimulated human whole blood cultures under hypercapnic, normocapnic, and hypocapnic conditions.
DESIGN: Prospective randomized study.
SETTING: Basic research laboratory.
SUBJECTS: Ten male and 10 female volunteers.
INTERVENTIONS: Venous blood samples, taken from volunteers were cultured at 37 degrees C, under hypocapnic (2% CO2), normocapnic (5% CO2), and hypercapnic (7% CO2) conditions, with and without endotoxin stimulation. After 24 hrs of incubation, each culture's supernatant was analyzed for tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interleukin-10, and interferon-gamma concentrations by enzyme-linked immunosorbent assay. Data were analyzed using nonparametric repeated measures of analysis of variance followed by Dunn's multiple comparisons test. Analysis of variance with Bonferroni correction was used to compare gender differences in cytokine concentrations. The Pearson test was used to estimate correlation between hydrogen ion and individual cytokine concentrations.
MEASUREMENTS AND MAIN RESULTS: Concentrations of the proinflammatory cytokines tumor necrosis factor-alpha, interleukin-1beta and of the anti-inflammatory cytokine interleukin-10 under hypercapnic condition were significantly decreased (p < 0.05, 0.01, and 0.001, respectively) for both genders when compared with either normocapnic or hypocapnic conditions. Concentrations of tumor necrosis factor-alpha and interleukin-1beta were significantly higher in men. In women, concentrations of interleukin-6 were significantly decreased under hypercapnic condition when compared with hypocapnic condition. An inverse relationship was found between hydrogen ion concentration and concentrations of tumor necrosis factor-alpha and interleukin-10.
CONCLUSIONS: Our results are consistent with the hypothesis that CO2 can affect the production of pro- and anti-inflammatory cytokines after ex vivo stimulation with endotoxin.
Post Number: 3060
|Posted on Sunday, January 23, 2011 - 05:02 am: |
I thought I may add this information, so everybody can make up his own mind on the above discussions.
First what we know from a very simple point of view.
Higher CO2 in the circulatory system ( lower pH and higher H+ will help to release O2 from Hb .On the other side the higher CO2 will as well increase blood flow due to vasodilatation ( risk with certain CO2 filter controlled altitude equipment if we not use a O2 sensor with it for some headache and brain problems ) On the other side the higher CO2 seems to have the opposite effect in the pulmonary circulation with a vasoconstriction in that area.
That's why under certain operations they add CO2 as a protection of the lungs but as well a controlled O2 and nitric O2 to help to avoid the vasoconstriction.
Now here some information based on some physiological back ground , which may explain the discussion and why respiration properly done may be in additional way of treating and working with people with Asthma.
" Pulmonary vascular resistance"
What is a normal value for pulmonary vascular resistance?
Normal value of pulmonary vascular resistance
Pulmonary vascular resistance (PVR) is about 1/8 to 1/10 of the systemic vascular resistance
Mean pulmonary blood pressure = 15
Left atrium blood pressure = 5
Pulmonary blood flow = 5~6
PVR = Pressure difference / blood flow
= (15-5)/5 or (15-5)/6
= about 1.7~2.0 mmHgL-1min
= about 100 dyne.sec.cm-5
PVR = (Mean pulmonary artery pressure - mean pulmonary capillary wedge pressure) x 80 / cardiac output
= (in dyne.sec.cm-5)
All 3 of these variables can be measured with a Swan-Ganz catheter
Physiological factors influencing pulmonary vascular resistance
Factors that influence vascular resistance, both pulmonary and systemic:
(inversely proportional to 4th power of) vessel radius
Factors unique to lung pulmonary blood flow
- distension and recruitment
& its effect on alveolar and extra-alveolar vessels
hypoxic pulmonary vasoconstriction
=> include drugs, hormonal, pH, CO2
1. Pulmonary blood flow
As pulmonary blood flow increases, PVR drops because of:
recruitment - some capillaries, which were closed or open but with no blood flow, begins to conduct blood
distension - capillaries change from near flattened to more circular
Both mechanisms contribute, but:
at low pulmonary arterial pressure, recruitment dominate at high pulmonary arterial pressure, distension dominate
2. Lung volume
At high lung volumes
Resistance is increased because:
stretching of alveolar walls
=> decreased caliber of alveolar capillary
=> increased resistance
At low lung volumes
Resistance is increased because:
reduction in radial traction by lung parenchyma
=> decreased caliber of extra-alveolar capillary
=> increased resistance
hypoxia-induced vasoconstriction in collapsed alveoli
Lowest PVR occurs at functional residual capacity.
3. Hypoxic pulmonary vasoconstriction (HPV)
Occurs with decreased alveolar PO2 (PAO2)
Locally mediated => smooth muscle contraction in arteriole
=> ? inhibition of K channel
=> ? increased cytoplasmic [Ca2+]
NB: Hypoxia in all other tissues cause vasodilation not vasoconstriction.
NB: HPV reduces V/Q scatter, and responsible for pulmonary vascular redistribution to upper zones in cardiac failure
Factors causing contraction of smooth muscles
(thus increasing PVR)
(major effect) low PAO2 (i.e. HPV)
acidosis (drop in pH)
(weak effect) sympathetic stimulation
thromboxane A2, endothelin-1 (ET-1)
Factors causing relaxation of smooth muscles
(thus decreasing PVR)
(via release of endothelium-derived relaxing factor, mostly nitric oxide NO)
Post Number: 3061
|Posted on Sunday, January 23, 2011 - 05:18 am: |
And here another short and simple summary : This will explain as well ,why we are for the moment interested in the reactions and live info on NIRS by altering respiration. :
Vasodilation and CO2
Among arterial dilators, natural vasodilation agent CO2 is probably the most powerful chemical. The vasodilation effect is present in healthy people due to normal arterial CO2 concentration. According to Dr. M. Kashiba, MD and his medical colleagues from the Department of Biochemistry and Integrative Medical Biology, School of Medicine, Keio University in Tokyo, CO2 is a "potent vasodilator" (Kashiba et al, 2002), while Dr. H. G. Djurberg and his team from the Department of Anaesthesia, Armed Forces Hospital, in Riyadh, Saudi Arabia suggested that "Carbon dioxide, a most potent cerebral vasodilator..." (Djurberg et al, 1998).
Effects of arterial hypocapnia caused by hyperventilation
Based on tens medical research studies, we established presence of the hyperventilation syndrome in the sick due to elevated minute ventilation values. However, reduced perfusion of vital organs is the norm for modern normal subjects due to Prevalence of Hyperventilation: Present in Over 90% of Normal People with 24 medical publications.
What are the effects of chronic hyperventilation of the human body? One of the central carbon dioxide effects is constriction of arteries and arterioles due to CO2 deficiency. Instead of vasodilation, arteries and arterioles get constricted.
Medical publications related to CO2-induced vasodilation
Dr. K. P. Buteyko and his colleagues found vasoconstrictive effects of hypocapnia (CO2 deficiency) on arteries and peripheral blood vessels (Buteyko et al, 1964a; Buteyko et al, 1964b; Buteyko et al, 1964c; Buteyko et al, 1965; Buteyko et al, 1967), while additional CO2 causes vasodilation, which is a normal state of arteries and arterioles.
As western physiological studies found, vasodilation requires normal arterial CO2 concentration, while hypocapnia (low CO2 concentration in the arterial blood) decreased perfusion of the following organs:
- brain (Fortune et al, 1995; Karlsson et al, 1994; Liem et al, 1995; Macey et al, 2007; Santiago & Edelman, 1986; Starling & Evans, 1968; Tsuda et al, 1987),
- heart (Coetzee et al, 1984; Foëx et al, 1979; Karlsson et al, 1994; Okazaki et al, 1991; Okazaki et al, 1992; Wexels et al, 1985),
- liver (Dutton et al, 1976; Fujita et al, 1989; Hughes et al, 1979; Okazaki, 1989),
- kidneys (Karlsson et al, 1994; Okazaki, 1989),
- spleen (Karlsson et al, 1994),
- colon (Gilmour et al, 1980).
Some abstracts from these studies are provided at the bottom of this page.
Vasodilation in simple terms
What is the physiological mechanism of the reduced blood flow to vital organs? Arteries and arterioles have their own tiny smooth muscles that can constrict or dilate (vasodilation) depending on CO2 concentrations. When the breathe more, CO2 level becomes smaller, blood vessels constrict and vital organs (like the brain, heart, kidneys, liver, stomach, spleen, colon, etc.) get less blood supply. Similarly, hypocapnia causes spasm of all other smooth muscles of the human body: airways or bronchi and bronchioles, diaphragm, colon, bile ducts, etc.
This effect explains why sick people have less blood going to their brains, heart, liver, and other vital organs. Normal breathing pattern provides people with normal perfusion and oxygen supply for all vital organs due to CO2 vasodilation. However, since modern people breathe more than the medical norm (hyperventilate), they have to suffer from CO2 deficiency effects.
Are there any related systemic effects? The state of these blood vessels (arteries and arterioles) define total resistance to the systemic blood flow in the human body. Hence, hypocapnia increases strain on the heart. Normal CO2 parameters make resistance to blood flow in the cardiovascular system small. Hence, breathing directly participates in regulation of the heart rate. The father of cardiorespiratory physiology, Yale University Professor Yandell Henderson (1873-1944), investigated this effect about a century ago.
Among his numerous physiological studies, he performed experiments with anaesthetized dogs on mechanical ventilation. The results were described in his publication "Acapnia and shock. - I. Carbon dioxide as a factor in the regulation of the heart rate". In this article, published in 1908 in the American Journal of Physiology, he wrote, "... we were enabled to regulate the heart to any desired rate from 40 or fewer up to 200 or more beats per minute. The method was very simple. It depended on the manipulation of the hand bellows with which artificial respiration was administered... As the pulmonary ventilation increased or diminished the heart rate was correspondingly accelerated or retarded" (p.127, Henderson, 1908).
Be observant. When you get a small bleeding cut or a wound, deliberately hyperventilate and see if that can help stop the bleeding. It should. As an alternative, perform comfortable breath holding and breathe less and accumulate CO2. What would happen with your bleeding? (It should increase due to vasodilation.) Now you know what to do after dental surgeries, brain traumas, and other accidents involving bleeding. It is natural for humans and other animals to breathe heavily in such conditions. Hence, hyperventilation can be life-saving in cases of severe bleeding.
As many health professionals found, blood flow to vital organs is directly proportional to blood CO2 concentrations. Consider this example of vasodilation. According to the Handbook of Physiology (Santiago & Edelman, 1986), cerebral blood flow decreases 2% for every mm Hg decrease in CO2 pressure. When people have 20 mmHg CO2 in their blood (half of the official norm), they have about 40% less blood supply to the brain in comparison with normal conditions. Only skeletal muscles can get more blood in conditions of hyperventilation.
"…cerebral blood flow decreases 2% for every mm Hg decrease in CO2" Professor Newton, University of Southern California Medical Center, Hyperventilation Syndrome, 2004 June 17, Topic 270, p. 1-7 (www.emedicine.com).
Personal experiment. Take 100 deep and fast breaths through the mouth and you can pass out due to ... lack of oxygen and poor blood supply for the brain. Why? Because CO2 is a vasodilator (dilator of blood vessels).
Note that there is another powerful chemical NO (nitric oxide) that is also able to produce vasodilation. Humans generate nitric oxide in sinuses and, hence, mouth breathing prevents us from inhaling our own nitric oxide (see web page: Nasal Nitric Oxide Effects). Meanwhile, as some medical studies claim, CO2 is a most powerful known vasodilator. "
Post Number: 3064
|Posted on Monday, January 24, 2011 - 04:04 am: |
Here some additional information how CO2 or controlled hypercapnia is used in europe.
. The key is, that if properly done we can control pCO2 in a slightly elevated level with the Spiro Tiger.
We just have now a new small BIO marker device we will test the comming weeks to see, how we can use it in the field and with different training ideas.
If it works we will have an additional cheap tool in our biomarker tool kit and I hope I can combine it with Spiro Tiger but as well with some other ideas we have going on as well as the possibility to add it to the Fit Mate as a much cheaper and faster way thna a CO2 sensor, which has to be replaced regular. Will keep you updated.
Here to enjoy : Normal level of CO2 in the lungs and arterial blood (40 mm Hg or about 5.3% at seal level) is imperative for normal health.
Hypocapnia (CO2 deficiency) is a normal finding for chronic diseases due to prevalence of chronic hyperventilation among the sick (see Hyperventilation Syndrome data with medical references). Furthermore, as we discovered before, over 90% of modern people ("normal subjects") are hyperventilators (see Hyperventilation Table with over 20 medical research studies). Hence, chronic hypocapnia is very common for modern man.
Main Carbon Dioxide Health Effects include (follow the links for dozens of research references):
- Vasodilation (expansion of arteries and arterioles). As physiological studies found, hypocapnia (low CO2 concentration in the arterial blood) constricts blood vessels and leads to decreased perfusion of all vital organs
- The Bohr effect was first described in 1904 by the Danish physiologist Christian Bohr (father of physicist Niels Bohr). This law can be found in modern medical textbooks on physiology. The Bohr effect states that arterial hypocapnia will cause reduced oxygen release in tissue capillaries.
- Cells Oxygen Levels are controlled by alveolar CO2 and breathing. Hyperventilation, regardless of the arterial CO2 changes, alveolar hypocapnia leads to cell hypoxia (low cells oxygen concentrations).
- Oxygen Transport, therefore, depends on breathing and these 2 effects (Vasoconstriction-Vasodilation and the Bohr effect) are part of 2 diagrams that summarizes influences of hypocapnia (low CO2 content in the blood and cells) on circulation and O2 delivery.
- Free Radicals Generation take place due to anaerobic cell respiration caused by cell hypoxia. Hence, antioxidant defenses of the human body are also regulated by CO2 and breathing, as these medical studies have found.
- Inflammatory Response are also, in a long run (chronic inflammation), controlled by breathing since hypoxia leads to or intensifies inflammation. Therefore, hyperventilation naturally promotes inflammatory health problems and CO2 is the key anti-inflammatory agent.
- Nerve Stabilization is due to calmative or sedative effects of carbon dioxide on nervous cells. Lack of CO2 in the brain leads to "spontaneous and asynchronous firing of neurons" (medical quote) "inviting" virtually all mental and psychological abnormalities ranging from panic attacks and seizures to sleeping problems, depression and schizophrenia.
- Muscle relaxation or relaxation of muscle cells is normal at high CO2, while hypocapnia causes muscular tension, poor posture and, sometimes, aggression and violence.
- Brochodilation - dilation of airways: bronchi and bronchioles by carbon dioxide, and their constriction due to hypocapnia.
- Blood pH regulation and regulation of other bodily fluids.
- CO2: Lung Damage Healer: Elevated carbon dioxide prevents injury and promotes healing of lung tissues.
- CO2: Skin and Tissue Healer.
- Synthesis of Glutamine in the Brain, CO2 fixation, and other chemical reactions: there are many other regulatory and facilitating effects related to uses of carbon dioxide.
- Regularity and Smoothness of Breathing is controlled by CO2. Lack of CO2 leads to "hypocapnic central apnea", which is a popular scientific term used by many doctors and scientists to describe the origins of sleep apnea.
Post Number: 36
|Posted on Saturday, January 29, 2011 - 02:35 am: |
Where I failed most was to make myself clear that I neither own nor have any personal experience with Spiro Tiger and the only target I meant to pick on was the "well known physiologist" who claimed that asthma was a "problem with inhalation".
Personally I suspect that effect of any respiratory training in asthmatics is to some extent, if not mostly, psychological (does not make it any less beneficial) "teaching" them how to deal with situations of hypercapnia and increased demand on respiratory muscle effort without panicking. Which is probably where I meet you on your "coordinated movement of the muscles of respiration".
Post Number: 472
|Posted on Saturday, January 29, 2011 - 05:29 am: |
I agree with you, the "well known physiologist" has some 'spainin' to do to justify his quote, though we should be careful criticizing his quote which was posted here second hand.
I think your assumption that the research using Spiro Training resulted in primarily "psychological" benefits, is not very well supported. That is, each study looked at objective and measurable performance variables, including peak flow, maximal inspiratory pressure, maximum sustainable pressure and exercise tolerance. There is also a few studies that demonstrated increased diaphragm thickness after 8 weeks of respiratory endurance training.
Take a few moments to read some of the literature, which will at least give you a bit more background on the structural and functional changes that occur with respiratory endurance training.
http://www.idiag.ch/fileadmin/documents/ spirotiger_sport/studien/2010-1220-ST-Sc ientific-Publications-SpiroTiger-Sport-E N.pdf
Post Number: 3080
|Posted on Saturday, January 29, 2011 - 05:59 am: |
As so often in "research " we have both sides claiming to know how it works.
To balance the discussion:
here a very in depth study done in South Africa by Shaw and Krasilshikow ( independent to Spiro Tiger studies ) which would argue against the psychological effect
Breathing Training,Diaphragmatic breathing
exercises could benefit an asthmatic’s
condition since they compress the abdominal contents which increase intra-abdominal pressure that causes lateral transmission of pressure to the lower ribs laterally, upward and outward motion of the lower ribs and anterior/posterior motion of the upper ribs. This then results in an increase in thoracic volume that decreases intrathoracic pressure which facilitates inspiration . Breathing retraining is essential to an asthmatic since, breathing in an asthmatic is of the thoracic type and since dyspnea can cause the asthmatic to increase inspiration further leading to further overextension of the already over-inflated lungs. This is then worsened by the
increased dead-space ventilation,metabolic requirements and a tendency to maintain a low arterial partial pressure of oxygen. Asthmatics can have a decreased chest expansion and chest deformity as a result of a shortened diaphragm,
intercostals and accessory muscles from prolonged spasm. With asthma, the
accessory respiratory muscles are fully
contracted and the diaphragm is maximally depressed. The accessory muscles are overactive during inspiration which causes stenosis of the major airways leading to an abnormal
respiratory pattern. During an asthma
attack, the diaphragm is maximally extended and either contracts spasmodically or not at all. This poor excursion of the diaphragm can negatively affect airway reserve, vital capacity (VC) and alveolar gas exchange .
The physiological effects of diaphragmatic breathing are varied and it is claimed that diaphragmatic breathing can correct abdominal chest wall motion,decrease the work of breathing and dyspnea and improve ventilation distribution . The purpose of breathing exercises is to empty the lungs by prolonging the expiratory phase,retrain normal breathing patterns,
increase expansile forces in hypoventilated areas, increase lung volume, dilate airways, force mucus into larger airways, re-educate the autonomic diaphragmatic movements, reduce the thoracic type breathing, relax spasmodic
muscle contractions, mobilise the ribs and chest wall and correct kyphosis
. These benefits are achieved
by shortening inspiration and lengthening expiration , by performing expiration
via the pulling in of the abdominal muscles
dorsally towards the spine while
relaxing the abdominal, intercostals and neck musculature . This is achieved by using special weights or belts to increase
intra-abdominal pressure, by applying compression to the lower ribs to facilitate
expiratory ascent of the diaphragm during
expiration which can increase the
movement of secretions from the small bronchi into the respiratory passages,by exhaling through a resistive breathing device or by breathing while creating a hissing noise in order to reduce bronchial constriction. These techniques have led to symptom-free and
medication-free asthma, an improved ability to halt an imminent attack,improved loosening and expulsion of mucus, enlargement of the diaphragm excursion, improved chest expansion at the epigastrium, improved maximum breathing capacity and VC [21, 18].
Patients with elevated respiratory rates, low tidal volumes and abnormal arterial
blood gases have been identified as those who will benefit the most from diaphragmatic breathing exercises .
Diaphragmatic breathing exercises have also been proven to reduce patients’ anxiety levels and to alter their attitude towards work  while breathing retraining has been shown to decrease
bronchodilator use and acute exacerbations and to improve quality of life . Ambrosino, Paggiaro, Macchi,
Filieri, Toma, Lombardi, Del Cesta,
Parlanti, Loi and Baschieri  in turn, have found that deep diaphragmatic breathing and pursed lip breathing can increase a lung patient’s maximal exercise tolerance. Diaphragmatic breathing can also lead to an increase in alveolar ventilation due to the changes in breathing pattern via decreases in breathing frequency and increases in tidal volume resulting in increases minute ventilation
. Additional benefits of breathing
exercises are to correct deviant posture, strengthen abdominal muscles, teach
diaphragmatic and lower costal breathing
and increase chest expansion . Fluge, Richter, Fabel, Zysno, Weller and Wagner
 demonstrated that breathing exercises have been found to increase FEV1, VC and to reduce RV significantly while Strunk et al.  also indicated that breathing exercises can decrease the work of breathing, improve ventilation,
decrease oxygen consumption and decrease psychological anxiety.
Yoga is a preferred method of training in older adults and the active or fitness-based yoga that emphasises cardiovascular fitness, resistance training, flexibility and relaxation is an effective treatment for asthmatics .
Nagarathna and Nagendra 
pointed out that yoga techniques can benefit asthmatics by reducing psychological overactivity and emotional instability and thereby reducing efferent
ISN Bulletin Volume 1, No. 2, 2008 5
vagal discharge while decreasing vagal
outflow to the lung which can cause
bronchodilation and a small decrease in bronchial reactivity. Yoga can also increase
endogenous corticosteroid release,
possibly decreasing bronchial reactivity . Breathing exercises have been found to decrease anxiety during an asthma attack and also prevent the onset of an attack . Breathing exercises have resulted in clinical improvements which translated into improved school attendance, exercise tolerance, asthma control and self-confidence .
Improvements have also been observed in breathing capacity, VC, but not FEV1 . However, Sly et al. , found that a combination of physical conditioning and breathing exercises can improve VC,
reduce the severity of asthma attacks and the need for symptomatic medication,but no change in psychological adjustment and subjectively was there a change in independence, outgoingness, getting along with others, feelings of
acceptance, enthusiasm and capability to be a follower . Up to eight month of breathing exercises have resulted in improved pulmonary function, decreased absenteeism and improved sociability,self-assertion and peer relationships. Subjectively, the subjects reported an improvement in their control of asthma, exercise tolerance and emotional stability
. Girodo, Ekstrand and Metivier  also found reductions in medication usage
and in the intensity of asthmatic
symptoms of 32 asthmatic patients
utilising breathing training making use of a physical corset.One of the problems with
prescribing breathing exercises is, that although eagerly accepted by asthma
patients, they are just as easily found boring and soon forgotten .
Therefore, the structure and setting of the exercises are important since it has been established that breathing exercises have resulted in thousands of asthma suffers
reducing their medication intake and
experiencing a sense of control even though this breathing technique does not alter the disease process . This is notable in that improvements in subjective attributes and perceptions in asthmatic patients may have major
effects on their quality of life and the
ability to cope with their disease.
Inspiratory Resistive Breathing Training
The purpose of inspiratory resistive
breathing training is to enhance
respiratory muscle function and in doing
so possibly reduce the severity of
breathlessness and improve exercise
tolerance. This may benefit the
asthmatic patients, especially those with severe asthma, since asthmatics
could suffer from respiratory muscle
dysfunction due to the loss in
respiratory muscle bulk and resultant
respiratory muscle strength. The use of inspiratory resistive breathing training
in asthmatic patients could possibly result
in improvements in inspiratory muscle
coordination, improvements in inspiratory muscle strength and endurance and the correction of
inappropriate respiratory muscle effort
[37, 38]. These improvements and corrections then possibly result in improvements in spirometry variables,a desensitisation to dyspnea, lessening of asthma symptoms, reduced
hospitalisations, less emergency room contacts, absences from school and work and/or the decreased use of medication
Now one of the major problems is, that equipment like the Spiro Tiger are not yet used in stduies in North America and therefor we clearly tend to go with north american research, which often still claims that respiration is never a limitation ( based on a strange idea of the MMV ( maximal minute volume ) as a "proof" that in a step test we never reach the MMV.
This ideas is very questionable to use as a "proof" that respiration is never a limitation, as a 400 m all out run is not used as a proof , that endurance is no limitation in a marathon run.In contrary we would use a 400 m run to proof , that speed is not a problem in a marathon runner but endurance.
Now here, why we tend to use Karls point more here in North america.
Inspiratory muscle training for asthma
Ram FSF, Wellington SR, Barnes NC
Inspiratory muscle training for asthma
In moderate to severe chronic obstructive pulmonary disease, there is good evidence of a generalised loss of muscle bulk (including the respiratory muscles). It is possible that similar loss of respiratory muscle strength could occur in asthma, particularly in more severe asthma requiring high doses of steroid therapy. Thus respiratory muscle training may be useful in asthma but there is insufficient research at present to support this theory.
, Wellington SR, Barnes NC. Inspiratory muscle training for asthma. Cochrane Database of Systematic Reviews 2003, Issue 4. Art. No.: CD003792. DOI: 10.1002/14651858.CD003792
This version first published online: October 20. 2003
In moderate to severe chronic obstructive pulmonary disease there is good evidence of a generalised loss of muscle bulk (including the respiratory muscles). It is possible that similar loss of respiratory muscle strength occur particularly in more severe asthma related in part to the effects of steroid therapy. Thus the respiratory muscle function may well be of relevance in asthma and if dysfunctional, may be a suitable target for training.
To evaluate the efficacy of inspiratory muscle training with an external resistive device in patients with asthma.
We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 1, 2002), MEDLINE (January 1966 to March 2002), EMBASE (January 1985 to March 2002), CINAHL (to March 2002) and the UK National Research Register of trials (January 1982 to March 2002) and reference lists of articles. We also searched on line respiratory journals and contacted manufacturers of training devices to obtain trials.
All randomised-controlled trials that involved the use of an external inspiratory muscle training device versus a control (sham or no inspiratory training device) were considered for inclusion.
Data collection and analysis
Two reviewers independently selected articles for inclusion, evaluated methodological quality of the studies and abstracted data.
Five studies were included in the review with four of the studies being produced by the same group. PImax (maximum inspiratory pressure) reported in three studies with 76 patients showed significant improvement with inspiratory muscle training when compared to the control group (WMD 23.07 cmH2O, 95%CI 15.65 to 30.50). Unfortunately, due to the paucity of included studies and data no other outcome was reported by more than one study. Therefore it is not possible to confirm whether this increase seen with PImax translates into any measurable clinical benefit.
Currently there is insufficient evidence to suggest that inspiratory muscle training provides any clinical benefit to patients with asthma. Due to the limited availability of studies in this area there is a need for further trials evaluating the efficacy of inspiratory muscle training devices in patients with asthma. These studies should investigate asthmatics with a range of severity. They should investigate clinically relevant outcomes such as lung function, symptoms, exacerbation rate and concomitant medications.
Post Number: 37
|Posted on Saturday, January 29, 2011 - 09:00 am: |
As I said, I have no personal experience with Spiro Tiger and never meant to comment on its usability in asthma patients. Also, I don't think I was too harsh with the "well known physiologist" considering no one knows whom we are talking about. Nevertheless, you are perfectly right about the information being second hand.
Talking about psychological effects I meant mainly yoga breathing and similar exercises. I apologize if I made an impression to have an opinion regarding Spiro Tiger. Again, there is nothing I could base such an opinion on.
Too bad your link does not work but thank you anyway.
Post Number: 38
|Posted on Saturday, January 29, 2011 - 10:44 am: |
Oops! The link did not work on my work computer but seems to be working fine on my home PC. Thanks for interesting reeding!
Post Number: 3084
|Posted on Sunday, January 30, 2011 - 04:35 am: |
Here is an add on to the very interestig discussion. http://www.ncbi.nlm.nih.gov/pmc/articles /PMC471750/?page=4
One of the question seems to evolve is the influence of pCO2 in the reactions of respiratory workouts.
The major difference between all existing respiratory devices out there, like the group similar to power lung to the Spiro Tiger is excatly on that level.
We mentioned many times before ,in a much simpler way, that the respiratory devices out there similar or like power lungs are basically "leg press equipments" for the respiratory muscles, compared to a treadmill which would be the Spiro Tiger.
In other words here now:
Due to the increased respiration with any of the current respiratory devices , we create in all of them earlier or later a hypocapnic situation. That's why all the recommendations are based on 20 to 30 breath maximum.
The reason is not that this will give a great respiratory endurance stimmulation but much rather is given by the nomral reaction of hypocapnic reaction caused by this breathing and people simply will have to stop and or will feel dizzy.
When the university of Zuerich ( Spengler, Boutellier ) developed the idea leading up to the Spiro Tiger , they had to do some ground work to find out what the amount of CO2 has to be , when breathing a certain VE with a certain respiratory frequency and a certain tidal volume.
Than they had to assess the reaction of the pCO2 levels on vasodilatation and vasoconstriction and than had to make a "saftey level" where the equipment simply will shut down, if you breath too much or not enough CO2.
The final result is a patent on a nice equipment, which will guide you through a save respiration workout, where you can move a VE which can be even higher than you may be able to breath during a step test or a race.
This is as well , where we can see , whether the respiration may in fact be a LIMITER.
Example: If we have a VE at LBP of 105 liter and or a VE at the end of a test of 135, than we can basically "load " the same VE and move that air without additional involvment of extremity muscles and or cardiac involvement ( minimal )
To move 135 VE many people will have to bike and or run with a HR of 150 and higher but with the Spiro Tiger HR may stay even far below 100.
So if we now make a Spiro Tiger workout with the goal to move 135 VE with the RF and TV we had in the VO2 test and the client barely can do that for 3 min we may have to assume, that in the step test , where he as well had a high CO and a high muscle activity, the VE of 135 was or is in fact his limitation in airflow.
When we than go to the 105 at LBP and do the same and let the person breath for 30 - 60 min and he can't really do that , we as well have to assume that respiration may be one of the reason why performance has to slow down. For all readers having a Fit Mate or any VO2 equipment and a Spiro Tiger they easy can do that testing.
The next step is to compare "quality " of respiration ( diaphragm respiration ) with the Spiro Tiger to the actual respiratory activity in the sport. For this, we show live the sinus wave on the Bioharness and than run or bike and see, whether the same quality is still existing. Just some thoughts.