Guest guest Posted July 5, 2006 Report Share Posted July 5, 2006 Thanks Marty - I have contacted the author of that study (David S. Shannahoff-Khalsa) and he has sent me the info I was interested in. I would reccomend this technique for all heart disease patients - this is an ancient concept that has been used for centuries in India. Breaking the pathological breathing patterns in any disease process has the potential to break the generalized holding or blocking patterns - this is a basic concept in Yoga and Chi Kung. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 6, 2006 Report Share Posted July 6, 2006 Vinod, Marty: The abstract didn't come through on my email but the technique sounds quite useful. Can I google his name and find the info? Thank you, Jack --- Vinod Kumar <vinod3x3 wrote: > Thanks Marty - I have contacted the author of that > study (David S. > Shannahoff-Khalsa) and he has sent me the info I was > interested in. I > would reccomend this technique for all heart disease > patients - this > is an ancient concept that has been used for > centuries in India. > Breaking the pathological breathing patterns in any > disease process > has the potential to break the generalized holding > or blocking > patterns - this is a basic concept in Yoga and Chi > Kung. > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 6, 2006 Report Share Posted July 6, 2006 Here is the file that David sent. THE JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE Volume 10, Number 5, 2004, pp. 757–766 © Mary Ann Liebert, Inc. Hemodynamic Observations on a Yogic Breathing Technique Claimed to Help Eliminate and Prevent Heart Attacks: A Pilot Study DAVID S. SHANNAHOFF-KHALSA,1,2 B. BO SRAMEK, Ph.D.,3,4 MATTHEW B. KENNEL, Ph.D.,1 and STUART W. JAMIESON, M.B., F.R.C.S.5 ABSTRACT Objective: This pilot study investigated the hemodynamics of a yogic breathing technique claimed " to help eliminate and prevent heart attacks due to abnormal electrical events to the heart, " and to generally " enhance performance of the central nervous system (CNS) and to help eliminate the effects of traumatic shock and stress to the CNS. " Design: Parameters for (4) subjects were recorded during a preexercise resting period, a 31-minute exercise period, and a postexercise resting period. Settings/location: Parameters for subjects were recorded in a laboratory at the University of California, San Diego. Subjects: Parameters for 3 males (ages 44, 45, 67) and 1 female (age 41) were recorded. One (1) subject (male age 45) had extensive training in this technique. Interventions: This yogic technique is a 1 breath per minute (BPM) respiratory exercise with slow inspiration for 20 seconds, breath retention for 20 seconds, and slow expiration for 20 seconds, for 31 consecutive minutes. Outcome Measures: Fourteen beat-to-beat parameters were measured noninvasively and calculated for body surface area to yield: stroke index (SI), heart rate (HR), cardiac index, end diastolic index, peak flow, ejection fraction, thoracic fluid index, index of contractility, ejection ratio, systolic time ratio, acceleration index, and systolic, diastolic, and mean arterial pressures (MAPs). Left stroke work index (LSWI) and stroke systemic vascular resistance index (SSVRI) were calculated. Results: We report on SI, HR, MAP, LSWI, and SSVRI and how they can help to describe hemodynamicstate changes. This technique induces dramatic shifts in all hemodynamic variables during the 1 BPM exercise and can produce unique changes in the postexercise resting period after long-term practice that appears to have a unique effect on the brain stem cardiorespiratory center regulating the Mayer wave (0.1–0.01 Hz) patterns of the cardiovascular system. Conclusions: Preclinical studies are warranted to examine the possible long-term effects of this technique that appear to reset a cardiorespiratory brain-stem pacemaker. We postulate that this effect may be the basis for the purported yogic health claim. 757 1The Research Group for Mind–Body Dynamics, Institute for Nonlinear Science University of California, San Diego, La Jolla, CA. 2The Khalsa Foundation for Medical Science, Del Mar, CA. 3Czech Technical University Prague, Department of Mechanical Engineering, Prague, Czech Republic. 4International Hemodynamic Society, Sedona, AZ. 5Department of Surgery, Division of Cardiothoracic Surgery, University of California, San Diego, San Diego, CA. INTRODUCTION The effects of respiration on the cardiovascular system were first reported 270 years ago in the scientific literature. In 1733, Hales (Hales, 1733) described the fluctuation of arterial pressure with respiration. And von Haller (1760) reported fluctuations of heart rate (HR) with respiration. Approximately 1 century later, Ludwig (1847) reported respiratory-related fluctuations in HR and arterial pressure and showed that HR increases with inspiration and decreases with expiration, with the opposite occurring for blood pressure (BP). However, numerous studies have shown that respiratory movements alone are not solely responsible for the rhythmic patterns of the cardiovascular system but that there is a complex interaction between respiration and circulation (Daly, 1986). The autonomic, cardiovascular, and respiratory systems appear to be interlocked. Koepchen, Klussendorf, and Sommer (1981) discussed the intracentral coupling of the cardiovascular and respiratory brain-stem control centers and their coupling to autonomic rhythms. They stated that " cardiovascular neuronal activity also can be rhythmic on its own in different ranges of frequencies and also with frequencies in the range of the respiratory rhythm. The interaction in that case is similar to the interaction between coupled oscillators, where in most cases the respiratory rhythm is the leading one. But also the reverse can be observed. " Clearly, cardiac and respiratory activities are the result of the mutual interaction of central oscillatory systems and not just the result of respiratory influences on cardiovascular tone. However, the option of controlling respiratory patterns as a means to influence cardiovascular activity is an attractive one. Hirsh and Bishop (1981) have characterized the effects of tidal volume and breathing frequency on respiratory sinus arrhythmia (RSA) and demonstrated that the relationship is the same independent of whether it is spontaneous or voluntarily controlled. They also showed that RSA amplitude- to-respiratory frequency and RSA amplitude-to-respiratory volume relationships appear to be independent. Novak, Novak, De Champlain, Le Blanc, Martin, and Nadeau (1993) showed that a systematic slowing of respiration can pace hemodynamic fluctuation. They used equal times for inspiration to expiration and studied the changes in the low–(0.015-0.15 Hz) to high–(0.15-0.3 Hz) frequency rhythms. Using beat-to-beat measures, these researchers demonstrated how lengthening the respiratory period from 2.17 seconds to 20 seconds over an 8.5-minute interval paced the respiratory fluctuations in HR intervals, systolic blood pressure (SBP), and diastolic blood pressure (DBP) over the entire range of respiratory periods. Shannahoff- Khalsa, Kennedy, and Ziegler (1993) have studied the effects of varying the inspiration to expiration ratio for 10- minute periods using beat-to-beat measures to explore hemodynamic changes. These researchers compared two patterns with baselines. The first pattern used an inspiration period of 5 seconds with an expiration period of 20 seconds and the second pattern was the reverse. The researchers found that the prolonged expiration-to-inspiration pattern had the larger effect on the hemodynamic state which led to a 12% decrease in SI and a 6.5% increase in mean arterial pressure (MAP) compared to a 2% decrease in SI and a 3.4% increase in MAP. Yogis believe that the pattern with longer expiration produces a more " relaxing " effect on the body and that the pattern with prolonged inspiration is more " energizing. " Lepicovska, Novak, Drozen, and Fabian (1992) studied the effects of a continuous pattern of 8 seconds of inspiration with 32 seconds of breath holding and 8 seconds of expiration for 25 minutes on BP and HR in healthy subjects. The researchers showed the entrainment of the slow 0.03- Hz oscillations by repetitive breath holding and the occurrence of 0.1 Hz and 0.2 Hz respiratory components in both HR and BP. Telles and Desiraju (1991) reported the effects of two different yogic respiratory patterns on oxygen consumption. Both patterns were used for 4 minutes and compared to baselines. The first pattern had an inspiration, to hold, to expiration pattern of " about 1:1(or less):1 " at about 3.2 breaths per minute (BPM). The second pattern " was about 1:4:2 " with about 2.2 BPM. The first pattern increased oxygen consumption by 52% compared to baseline and the second pattern reduced oxygen consumption by 19%. These results show that slightly different patterns can lead to very different oxygen consumption rates. Most recently, Miyamura, Nishimura, Ishida, Katayama, Shimaoka, and Hiruta (2002) demonstrate the effects of 1 BPM for an hour with a single highly trained subject. The researchers found oxygen consumption at 256 mL/minute and a HR mean of 75 compared to a resting respiratory rate of 6 breaths/minute, 230 mL/minute, and an HR mean of 69. They described the respiratory maneuver as a " thoracic type of breathing; abdominal muscles play a passive role . . . a very deep inspiration is taken slowly with the glottis partially closed and the head erect. When the lungs are full, the head is bent forward until the chin touches the jugular notch firmly. After slow and deep expiration a new cycle is begun without pause. " They also measured arterial blood CO2 and O2 partial pressure, oxygen saturation, and hydrogen ion concentration. They conclude that reduced hypercapnic chemosensitivity in the well-trained yogi may be related to an adaptation to low arterial pH and/or to high partial pressure CO2. One popular yogic breathing pattern uses the selective use of one nostril to differentially affect autonomic tone. Unilateral forced nostril breathing (UFNB) through the right nostril at either 6 BPM or 2–3 breaths per second (a yogic breathing pattern called " breath of fire " or kapalabhatti) increased HR compared to left UFNB, while left UFNB comparatively increased end diastolic volume (Shannahoff- Khalsa and Kennedy, 1993). These two techniques differ- 758 SHANNAHOFF-KHALSA ET AL. entially stimulate lateralized sympathetic tone and probably the sino–atrial or atrio–ventricular nodes, respectively, thus demonstrating other unique autonomic-related respiratory effects on cardiovascular function. The pilot data presented here is an effort to investigate the possible hemodynamic changes using another yogic respiratory exercise that requires a 1 BPM rate for prolonged periods. The pattern involves an inspiration period lasting 20 seconds, with breath retention for 20 seconds, followed by expiration over 20 seconds while sitting erect. This pattern (20:20:20 breath) when perfected supposedly both " helps eliminate and prevent heart attacks that can be triggered by abnormal electrical events " (personal communication, Yogi Bhajan, Master of Kundalini Yoga) and is also said to " help eliminate the effects of traumatic shock and stress to the central nervous system. " MATERIALS AND METHODS Subjects Three males, ages 44, 45, and 67, and one female age 41 volunteered and were paid 25 dollars to participate. All subjects had significant experience (1–20 years) with a variety of yogic breathing techniques. However, only subject 1 (a male, age 45) had practiced this particular technique more than once prior to the experiment. The other 3 subjects, while being highly accomplished in similar but different yogic breathing techniques, were able to complete this specific 1 BPM pattern successfully at their first attempt without difficulty prior to the experiment. This was required to assure themselves and the authors that they would be able to repeat this performance under laboratory conditions without duress. Equipment and calculations All subjects were studied with simultaneous beat-to-beat recordings from both the BoMed NCCOM3-R7 Cardiodynamic Monitor (CardioDynamics International Corp., San Diego, CA) and the Finapres Blood Pressure Monitor 2300 (Ohmeda, Louisville, CO). The BoMed NCCOM3-R7 monitor measures thoracic electrical bioimpedance noninvasively and can measure global blood flow and parameters of left ventricular performance with adequate clinical accuracy (Sramek, 1988a, 1988b, 1991). Beat-to-beat values were recorded for stroke index (SI) (SI _ stroke volume/body surface area [bSA]) (where SV [mL] _ VEPT _ VET _ IC, VEPT _ volume of electrically participating tissue, VET _ ventricular ejection time, IC _ index of contractility [s_1 _ (dZ/dt)max/ TFI, TFI _ thoracic fluid index]); HR (beats/minute); cardiac output, (CO) (liters/minute) _ HR _ SV; end-diastolic volume, EDV (mL) _ 100 _ SV/EF; peak flow, PF (mL/second _ VEPT _ IC _ constant; ejection fraction, EF (%) _ SV/EDV _ (0.84 _ [0.64 _ STR]) _ 100; thoracic fluid index, TFI (ohms) _ Zo _ total impedance of thorax; index of contractility, IC (sec_1) _ (dZ/dT)max/TFI; ejection ratio, ER (%) _ 100 _ VET/HRP, HRP _ 60/HR; systolic time ratio, STR (%) _ PEP/VET _ 100, PEP _ preejection period (second); and acceleration index, ACI (sec_2) _ (d2Z/dt2)max/TFI. In this study we used SI instead of SV to help compare values across subjects. The Finapres measures SBP, DBP, MAP, and HR at beat-to-beat intervals. Recording at beat-to-beat intervals made it possible to also calculate systemic vascular resistance index [sVRI _ 80 _ (MAP-3/CO)/CI {dyn _ sec _ cm_5 _ meter2}]; stroke systemic vascular resistance index [sSVRI _ MAP _ 3)/SI _ 80 {dyn _ sec _ cm_2}]; left cardiac work index [LCWI _ (MAP _ 6) _ CI _ 0.0144 {kg _ m}]; and left stroke work index [LSWI _ (MAP _ 6) _ SI _ 0.0144 {g _ m}] (Sramek, 1995, 2002). All data (except for that of subject 1, run 1) was collected in an " indexing " mode that is a calculation based on body-surface area to allow comparable measures between subjects. Also, run 1, subject 1, was the only recording with only the BoMed NCCOM3-R7 Cardiodynamic Monitor. The computer and software for the BoMed NCCOM3-R7 and Finapres recordings was developed by the Sleeptrace Corp. (Dallas, TX). Data analysis was performed using DaDisp 2002 Software, (DSP Development Corp., Cambridge, MA) and Spectre, Version 5.0, (Solana Beach, CA). Graphics were displayed using Slide Write Plus Version 6.1 (Advanced Graphics Software, Encinitas, CA) and Harvard ChartXL, version 2.0 (Harvard Graphics, Hudson, NH). Each subject was seated in a chair at a desk and had chest and neck electrodes applied (Littman 3M Snap diagnostic EKG electrodes, No. 2350). The Finapres cuff was applied to the third digit of the left hand between the first and second joint. After a minimum of 30 minutes of rest a baseline was recorded for 10–20 minutes followed by the 31-minute respiratory exercise (20:20:20 breath), followed by 10–20 minutes of final baseline. Subjects 2–4 with little laboratory recording experience had 20-minute pre- and postrecording periods to help ensure acclimatization and a resting state. However, only the last 10 minutes of the preexercise period and the first 10 minutes of postexercise rest periods were analyzed to match the 10-minute pre- and postexercise data sets of subject 1 who had long-term experience with this experimental set up. Each subject was trained to observe a digital timer to monitor the respective 20-second respiratory phases. The subjects were observed for compliance. Eyes were open during the experiment and it was conducted in an air-conditioned room at 23°C. RESULTS The time series of subject 1 for SI, HR, and MAP for the 10-minute preexercise, 31-minute 20:20:20 breath exercise, BEAT-TO-BEAT HEMODYNAMICS 759 and 10 minute postexercise periods, respectively, are presented in Figures 1, 2, and 3 for the third experimental run with this subject. The raw beat-to-beat data had been treated with a rolling average over 25 points to help elucidate the endogenous Mayer wave activity exhibited at approximately 0.1–0.01 Hz that clearly exhibits a wide variance under normal resting conditions. In Figure 2, note that, during the 20:20:20 breath exercise period, the three cardiovascular measures all show a unique entrainment with the respiratory cycle and a dramatic variance compared to resting states. However, while the 1-BPM exercise entrains each cardiovascular measure during the exercise period, the Mayer wave frequency pattern is not linked to the resting respiratory cycle during the preexercise period. The Mayer wave is always slower than, and independent of, the respiratory rate (Polosa, 1984). Figure 3 also shows there is a unique sinusoidal Mayer wave pattern that is most clear in the SI and HR data in the postexercise period. We consider this to be an important and perhaps informative result. This effect was only observed after long term practice by this subject. The results of the other three subjects do not exhibit this unique sinusoidal result in either the pre- or postexercise periods. Figure 4 shows the pre- and postexercise SI patterns for all 4 subjects that first include the three separate runs for subject 1 (in descending order based on the time intervals between practice) recorded at different periods during his 760 SHANNAHOFF-KHALSA ET AL. FIG. 1. Three graphs of simultaneous measurements from the BoMed NCCOM3-R7 Cardiodynamic Monitor (CardioDynamics International Corp., San Diego, CA) and the Finapres Blood Pressure Monitor (Ohmeda, Louisville, CO). Stroke index (SI) and heart rate (HR) were captured from the BoMed monitor and mean arterial pressure (MAP) was captured by the Finapres monitor. The beat-to-beat data from each instrument were then subjected to a rolling average over 25 data points to help exhibit the natural endogenous Mayer wave rhythmic activity (0.01 Hz–0.1 Hz). The top graph shows 10 minutes of resting SI data, the middle graph shows HR, and the bottom shows MAP. These data are for subject #1 for the 10 minutes of preexercise rest; it is the third experiment conducted after extensive practice of the 20:20:20 breath technique. FIG. 2. Three graphs of simultaneous measurements from the BoMed NCCOM3-R7 Cardiodynamic Monitor (CardioDynamics International Corp., San Diego, CA) and the Finapres Blood Pressure Monitor (Ohmeda, Louisville, CO). Stroke index (SI) and heart rate (HR) were captured from the BoMed monitor and mean arterial pressure (MAP) were captured by the Finapres monitor. The beat-to-beat data from each instrument were then subjected to a rolling average over 25 data points to help exhibit the natural endogenous Mayer wave rhythmic activity (0.01 Hz–0.1 Hz). The top graph shows the 31-minutes of the 20:20:20 breath SI data, the middle graph shows HR, and the bottom shows MAP. This data are for subject #1 for the 31 minutes of the exercise period; it was the third experiment conducted after extensive practice of the 20:20:20 breath technique. training followed by the male subject age 67, the female subject age 41, and the male age 44. It is apparent that only run three in subject 1 (age 45) demonstrates this sinusoidal effect and it occurs only in the postexercise phase. This unique sinusoidal-like result does not occur in the data of the other runs and there is a slow progression toward this sinusoidal effect that appears to emerge somewhat in run 2 compared to run 1 for subject 1, but clearly exhibits in run 3. The time between run 1 and run 2 is approximately 8 months, and the time between run 2 and 3 is 1 month. The practice schedule for subject 1 between runs 1 and 2 was sporadic with a frequency of about one time per week, the practice schedule between runs 2 and 3 was about once every 2–3 days. Color figure 5 (subject 1, runs 2 and 3 and subjects 2, 3, and 4) shows 3-dimensional plots of SI (x-axis) versus MAP (y-axis) versus HR (z-axis) for the three respective recording periods of the experiment. The data here for subject 1, run 1, was recorded with only the BoMed NCCOM3-R7 and not the Finapress measures, and thus is not profiled because BEAT-TO-BEAT HEMODYNAMICS 761 FIG. 3. Three graphs of simultaneous measurements from the BoMed NCCOM3-R7 Cardiodynamic Monitor (CardioDynamic International Corp., San Diego, CA) and the Finapres Blood Pressure Monitor (Ohmeda, Louisville, CO). Stroke index (SI) and heart rate (HR) were captured from the BoMed monitor and mean arterial pressure (MAP) was captured by the Finapres monitor. The beat-to-beat data from each instrument were then subjected to a rolling average over 25 data points to help exhibit the natural endogenous Mayer wave rhythmic activity (0.01 Hz–0.1 Hz). The top graph exhibits the 10 min of the postexercise resting SI data, the middle graph shows HR, and the bottom shows MAP. These data are for subject #1 for the 10 minutes of the postexercise period; it is the third experiment conducted after extensive practice of the 20:20:20 breath technique. Note the highly sinusoidal Mayer wave pattern in all three parameters. FIG. 4. Two columns and six rows of data. The left column is from the 10-minute preexercise resting data for stroke index (SI). The right column is from the 10-minute postexercise resting data for SI. The left and right graphs in the same row are from the same subject in one experiment, before and after the 20:20:20 breath exercise. The SI data are expressed here as the rolling average over 25 points of the raw data. The first row is subject 1 (experiment 1), run before significant or any regular practice of the 20:20:20 breath exercise. Row 2 (experiment 2) is subject 1 approximately 8 months after weekly practice, and row 3 (experiment 3) is 1 month after experiment 2 in which there was practice at a frequency of approximately once every 2–3 days. Row 4 is a male subject (age 67), row 5 is a female (age 41), and row 6 is a male subject (age 44). These three subjects were all well-trained in slow-breathing techniques at 1 BPM but after only one prior run with this specific breath exercise technique before the laboratory recording. The ticks on the x-axis are 2-minute markers. The data are displayed to help accentuate the Mayer wave patterns of activity. Note the occurrence of the unique sinusoidal pattern in row 3, column 2. 762 SHANNAHOFF-KHALSA ET AL. FIG. 5. Figure 5 shows five 3-dimensional color plots. There are 2 columns, in the left column there are 2 figures, the upper figure is of subject 1, experiment 2, and the bottom left figure is subject 1, experiment 3. The right column shows 3 subjects: top, male age 67; middle, male age 44; and bottom, female age 41. The x-axis is the stroke index (SI) data paired with the y-axis data of the mean arterial pressure (MAP) measure plotted against the z-axis of HR. Each point is an x-y-z plot of the simultaneous measures of SI, MAP, and HR. The red lines are from the 10-minute preexercise resting data. The green lines are from the 10 minutes of postexercise resting data, and the purple lines are from the 31 minutes of the 20:20:20 breath exercise data. Note the return maps for all 3 phases of the experiment each have their own respective loci of points and that the exercise phase has a much larger excursion of data points to define the hemodynamics during that phase of the study. Also, note that the postexercise phase of the recordings usually is more central to the 3-dimensional figure. This may indicate a more normalized hemodynamic state. Further studies are required to help determine a " normalized " 3-dimensional expression of the hemodynamic state. MAP is missing. The beat-to-beat data is plotted again using the smoothing average of 25 to help elucidate the basic patterns of cardiovascular activity. These plots help to define the hemodynamic state better during the three phases of the experiment and clearly show that the three variables interact differently in these three phases when using this 3- dimensional array. While one variable cannot describe a physiologic state, we present the data here in a way that can help define a hemodynamic state. The red lines represent the 10-minute preexercise resting state, the purple lines represent the 31-minute exercise state, and the green lines represent the final 10-minute postexercise resting state. In addition to the broad areas covered by the 20:20:20 exercise, note the relative differences in the pre- and postexercise periods. The postexercise (green lines) state is usually more central in the 3-dimensional plot. Hemodynamic analysis of the 20:20:20 exercise for subject 1, run 3 (Figure 6) In Figure 6, the starting point of the 20:20:20 breath exercise, marked as point 1 in the two dimensional plot (be- BEAT-TO-BEAT HEMODYNAMICS 763 FIG. 6. This is a hemodynamic management chart structured for beat- to-beat parameters (see Sramek 1988b, 2002). Subject 1's (run 3) hemodynamic state is presented while performing the 20:20:20 breath exercise in an erect sitting posture plotted in an orthogonal system with the x–y coordinates of mean arterial pressure (MAP) and stroke index (SI). The south-west to north-east diagonal lines are isolines of systemic vascular resistance index (SSVRI), documenting the effects of vasoactivity (afterload) on the hemodynamic state. The north-west to south-east diagonal lines are isolines of left stroke work index (LSWI), documenting the combined effects of volume _ inotropy on the hemodynamic state. The center of the hexagon represents the ideal normotension (ideal MAP) and the normodynamic state/beat (ideal SI) for a supine resting adult with normovasoactivity, normovolume, and normoinotropy. The return map here for Subject 1 performing the 20:20:20 breath exercise is shown as a series of intersecting circles and the arrows and numbers indicate the starting point (point 1) of the inspiration phase, the starting point of the breath retention phase (point 2), and the starting point for the expiration phase (point 3) for the 31 minutes of the exercise period breathing at one breath/minute. The return map calculation of subject 1, run 3, presented in Figure 6 was created as follows. The raw data for SI and MAP came at every heartbeat interval and were, thus, at uneven time points and, hence, were interpolated linearly into a fine, even-time grid with a resolution of 0.1 second. These fine resolution data were then averaged point-wise over the 31 1-minute exercise cycles, that is, at each moment in the 60 seconds of one 20:20:20 breath cycle, we found the arithmetic average over the 31 replicas to provide the average waveform over the breathing cycle. This was done independently for both SI and MAP and the multiple channels were plotted on different axes to yield a phase–space plot of the average synchronized-to-breathing dynamics. This procedure highlights any consistent behavior over the various phases of the breathing cycle and suppresses replica-to-replica fluctuations. However, using this procedure for cardiac patients may obscure important short-term changes, although it may also help elucidate any consistent abnormal variations. ginning at inspiration) is defined by the highest intra-thoracic pressure and characterized by the following hemodynamic coordinates: MAP _ 99 Torr @ SI _ 24 ml/m2. Hemodynamics during the 20-second inspiration phase (points " 1 " _ " 2 " ) The 20-second inspiration phase is characterized by a balance between changes in contractility (volume and inotropy) and vasoactivity. The first half of the inspiration phase is characterized by a near doubling of SI (from SI _ 24 to SI _ 45 mL/m2) at an almost constant value of MAP (MAP __ 99 Torr). This is caused initially by almost a linear increase in intravascular volume (the result of increasing venous return), followed by a gradually increasing inotropic state. The combined increase in contractility is approximately 85% (from LSWI _ 31.8 to LSWI _ 58.9 g.m/m2). This decrease in contractility is accompanied by a near linear 94% increase in vasodilatation (from SSVRI _ 316 to SSVRI _ 163 dyn.sec.cm_5.m2), which explains the almost constant MAP value during this phase. The second part of the 20-second inspiration phase is characterized by _21% decrease in SI (from 45 to 38 mL/m2) with a mild decrease (3%) in MAP (from 97 to 94 Torr). This is caused by both a small decrease in intravascular volume (a further inspiratory decrease in intrathoracic pressure does not produce a corresponding increase in venous return) and by a decrease in inotropy. A simultaneous vasoconstriction, however, still maintains MAP at almost the same level. Hemodynamics during the 20-second breath retention phase (points " 2 " _ " 3 " ) The majority of the breath retention phase is characterized by almost a constant level of vasoactivity (_232 dyn.sec.cm_5.m2) accompanied by profound changes in volume and inotropy. The intrathoracic pressure remains at its minimal level during this entire phase. Gradually decreasing intravascular volume, which already started at the end of preceding phase, is initially compensated by a small increase in vasoconstriction, producing a small increase in MAP (from 94 to 97 Torr) and a decrease in SI (from 38 to 32 mL/m2). However, from this point, both MAP and SI drop precipitously to their lowest levels during the entire cycle (to MAP _ 63 Torr; SI _ 23 mL/m2). The original cause of this process is a profound volume depletion at almost a constant level of vasoactivity. The remainder of the breath retention phase produces a gradual increase in MAP (from 63 to 75) at almost a constant level of SI (SI __ 24 mL/m2). This is attributable mostly to an increase in inotropic state. Hemodynamics during the 20-second expiration phase (points " 3 " _ " 1 " ) The increasing intrathoracic pressure in the first half of the expiratory phase is responsible for gradually decreasing venous return, which is accompanied by an increasing level of inotropic state; the vasoactivity, at the same time, stays at almost the constant level (_232 dyn.sec.cm_5.m2) it was during the breath retention phase. The second half of the expiratory phase is characterized by a still-decreasing venous return, compensated by a further increase in inotropy, so that the total level of the ejection phase contractility is almost constant (LSWI __ 41.5 g.m/m2); this hemodynamic modulator activity is accompanied by an increase in vasoconstriction (to SSVRI _ 316 dyn.sec.cm_5.m2). Summary of the hemodynamic changes of the 20:20:20 breath The " T-shape " return map of the hemodynamic point trajectory during the entire cycle of the 20:20:20 respiratory exercise shows a controlling effect of ejection phase contractility during one part of the 1-BPM cycle while vasoactivity is essentially unchanged. The other part of the cycle is then controlled by a variation in vasoactivity, while the contractility parameters (volume and inotropy) either complement each other or stay at almost constant level. The effects of contractility and the effects of vasoactivity are about 90° out of phase during the 1-BPM cycle. When this 1-BPM respiratory cycle is practiced over an extended period of time, it appears to produce a hemodynamic " flywheel-like " phenomenon, which tries to maintain the 1-minute hemodynamic modulator cycles in the subsequent postexercise resting period. This resetting of the pacemaker functions of the brain stem cardiorespiratory control center may be why this 20:20:20 respiratory exercise has the claimed beneficial effects. DISCUSSION It is now well-known that the autonomic nervous system plays a critical role in the genesis of sudden cardiac death, (Lown, 1979; Schwartz and Stone, 1982; Corr et al., 1986; Schwartz et al., 1992). And this is especially true when there is ischemic heart disease already present. Sudden cardiac death resulting from ventricular tachycardia can be induced by an imbalance in sympathetic versus parasympathetic activity. Specifically, sympathetic hyperactivity promotes the occurrence of ventricular tachycardia, (Schwartz and Priori, 1990) and augmented vagal tone exerts a protective and antifibrillatory effect (Vanoli et al., 1991). The unique and rare result we see in the one case here with the induced sinusoidal effect on the Mayer wave pattern that occurs in SI, HR, and MAP suggests that the brainstem cardiorespiratory control center has been altered here after the long-term practice of the 20:20:20 breath. The Mayer wave was first described in 1876 (Mayer, 1876) and is known to be centrally regulated (Preiss and Polosa, 1974) and is an expression of autonomic activity (Polosa, 1984) mediated through the sympathetic and parasympathetic ner- 764 SHANNAHOFF-KHALSA ET AL. vous systems (Polosa, 1984; Koizumi et al., 1984). To our knowledge, this effect on the brainstem control center may be the first example of an endogenous pacemaker of the body being reset using the breath. We believe that this latent effect here is attributable to a resetting of the brainstem control center. The yogic claim is that, in addition to " helping to eliminate and prevent heart attacks, " this breath technique also " enhances performance of the CNS and helps to eliminate the effects of traumatic shock and stress to the CNS " (personal communications, Yogi Bhajan). Because Mayer wave patterns have also been observed in the human EEG and are postulated to reflect spontaneous periodic changes of cortical excitability with control at the brainstem level (Novak et al., 1992), it may be that the cortical expression of the Mayer wave activity is also reset with the extensive use of this yogic technique. It may be that during high levels of prolonged stress or under acute severe stress, that breathing patterns become quite irregular, unstable, and potentially lethal under circumstances in which autonomic tone has already been compromised and, thus, this feedback on the brainstem cardiorespiratory control center can then lead to an abnormal electrical event or accident triggering ventricular tachycardias resulting in death. The 20:20:20 breath technique may be a useful tool to help reduce the occurrence of sudden cardiac death and the latent effects of stress on the central nervous system. Because this technique ultimately requires an ability to reduce respiration to one BPM to obtain the apparent observed benefits, cardiac patients would require substantial training and practice to make maximum use of this technique. However, it is expected that, if the ratio is held constant and equal for the inspiration to breath retention to expiration phases, it may also be a helpful tool for cardiac rehabilitation at rates of less than one BPM in the early phases of training. Preclinical trials are warranted to help further explore the effects of this technique in additional normal subjects along with the versatility and safety of this tool in cardiac patients. ACKNOWLEDGMENTS We thank Paul Shragg, B.A., M.S., from the University of California San Diego, La Jolla, CA, General Clinical Research Center (GCRC) for computer and graphics assistance as supported in part by a grant from the GCRC Program, MO1 RR00827, of the National Center for Research Resources, National Institute of Health. Partial financial support to DSK for writing this manuscript was provided by the Baumgartel–DeBeer Family Fund. REFERENCES Corr PB, Yamada KA, Witkowski FX. Mechanisms controlling cardiac autonomic function and their relation to arrhythmogenesis. In: Fozzard HA, Haber E, Jennings RB, Katz AM, Morgan HE, eds. The Heart and Cardiovascular System, vol. 2. New York: Raven Press, 1986;1343–1403. Daly MDB. Interactions between respiration and circulation. In: Handbook of Physiology: The Respiratory System III, vol II: Control of Breathing. Bethesda: American Physiological Society, 1986:529–594. Hales S. Statical Essays: Containing Haemastaticks, London: Manby, 1733. (Reprinted [1964] No. 22, History of Medicine Series, Library of New York Academy of Medicine, New York: Hafner Publishing). Hirsh JA, Bishop B. Respiratory sinus arrhythmia in humans: How breathing pattern modulates heart rate. Am J Physiol (Heart Circ Physiol) 1981;10:H620–H629. Koepchen HP, Klussendorf D, Sommer D. Neurophysiological background of central neural cardiovascular–respiratory coordination: Basic remarks and experimental approach. J Autonom Ner Sys 1981;3:335–368. Koizumi K, Terui N, and Kollai M. Relationships between vagal and sympathetic activities in rhythmic fluctuations. In: Miyakawa K, Koepchen HP, Polosa C, eds. Mechanisms of Blood Pressure Waves. Tokyo: Japan Scientific Societies Press, and Berlin, Heidelberg, New York & Tokyo: Springer Verlag, 1984:43–56. Lepicovska V, Novak P, Drozen D, Fabian Z. Positive pressure on neck reduces baroreflex response to apnoea. Clin Autonom Res 1992;2:21–27. Lown B. Sudden cardiac death: The major challenge confronting contemporary cardiology. Am J Cardiol 1979;43:313–328. Ludwig C. Beitrage zur Kenntniss des Einflusses der Respirationsbewegungen auf den Blutlauf im Aortensysteme. Arch Anat Physiol Leipzig 1847;242–302. Mayer S. Studien zur physiologie des herzens und der blutgefasse: V. Über spontane blut druckschwankungen. Saech Akad Wiss Sitz Liepsig Math Naturw 1876;74:281–307. Miyamura M, Nishimura K, Ishida K, Katayama K, Shimaoka M, Hiruta S. Is man able to breathe once a minute for an hour? The effects of yoga respiration on blood gases. Japn J Physiol 2002;52:313–316. Novak P, Lepicovska V, Dostalek C. Periodic amplitude modulation of EEG. Neurosci Lett 1992;136:213–215. Novak V, Novak P, De Champlain J, Le Blanc AR, Martin R, Nadeau R. Influence of respiration on heart rate and blood pressure fluctuations. J Appl Physiol 1993;74:617–626. Polosa C. Rhythms in the activity of the autonomic nervous system: Their role in the generation of systemic arterial pressure waves. In: Miyakawa K, Koepchen HP, Polosa C, eds. Mechanisms of Blood Pressure Waves. Tokyo: Japan Scientific Societies Press, and Berlin, Heidelberg, & New York, Tokyo: Springer Verlag, 1984:27–41. Preiss G, Polosa C. Patterns of sympathetic neuron activity associated with Mayer waves. Am J Physiol 1974;226:724–730. Schwartz PJ, Stone HL. The role of the autonomic nervous system in sudden cardiac death. Ann N Y Acad Sci 1982;382:162–180. Schwartz PJ, Priori SG. Sympathetic nervous system and cardiac arrhythmias. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside. Philadelphia: WB Saunders, 1990:330–343. Schwartz PJ, La Rovere MT, Vanoli E. Autonomic nervous system and sudden cardiac death: Experimental basis and clinical observations for post-myocardial infarction risk stratification. Circulation 1992;85(suppl 1):177–191. BEAT-TO-BEAT HEMODYNAMICS 765 Shannahoff-Khalsa DS, Kennedy B, Ziegler MG. A study of the hemodynamic effects of varying the duration of inhalation and exhalation periods (abstr). Int J Psychophysiol 1993;14:149. Shannahoff-Khalsa DS, Kennedy B. The effects of unilateral forced nostril breathing on the heart. Int J Neurosci 1993;73:47–60. Sramek BB. Status report on BoMed's electrical bioimpedance. IEEE Eng Med Biol Soc 1988a;1:51. Sramek BB. Hemodynamic and pump performance monitoring by electrical bioimpedance: New concepts. Problems in Respiratory Care 1988b;2:274–290. Sramek BB. Hemodynamics and its role in oxygen transport. In: Sramek BB, Valenta J, Klimes F, eds. Biomechanics of the Cardiovascular System, Prague: Czech Technical University Press, 1995:209–231. Sramek BB. Online document at: www.hemosapians.com/ mgmtref.html Accessed July 28, 2004. Telles S, Desiraju T. Oxygen consumption during pranayamic type of very slow-rate breathing. Indian J Med Res 1991;94:357–363. Vanoli E, De Ferrari G, Stramba-Badiale M, Hull SS Jr, Foreman RD, Schwartz PJ. Vagal stimulation and prevention of sudden death in conscious dogs with a healed myocardial infarction. Circ Res 1991;68:1471–1481. von Haller A. Elementa Physiologica. T. II. Lit VI, Lausanne, France, 1760:330. Address reprint requests to: David S. Shannahoff-Khalsa The Research Group for Mind–Body Dynamics Institute for Nonlinear Science (mailcode 0402) University of California, San Diego 9500 Gilman Drive La Jolla, CA 92093-0402 E-mail: dsk 766 SHANNAHOFF-KHALSA ET AL. 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Guest guest Posted July 8, 2006 Report Share Posted July 8, 2006 Since I reccomended the Yogic breathing technique I would like to expand on that sunject a little bit. One of the fastest and most effective techniques we can use to alter our Autonomic Nervous System (ANS) are breathing exercises. This is a huge subject but a few basics go like this - high oxygen levels are symbolic of energetic relaxation - low oxygen levels are synonymous with tension, anxiety, and fear (test this by holding your breath for a minute - the feeling of anxiety that develops is oxygen deffeciency - if one pays close attention to that feeling you will see this is a fimilar state of mind - most have felt this oxygen defeciency many times in life to some degree or other) - excess carbon dioxide ( a waste product)causes a feeling of dullness and possible confusion with difficulty focusing the mind or remaining centered - this is also a common symptom that most feel often - removing this excess CO2 will clear the mind. Many traditional breathing therapies have been developed to deal with the imbalances in the ANS caused by the imbalances in these gases - like Pranayama and Chi Kung. Exhaling throws out the CO2 - inhaling fills the lungs with oxygen - holding the breath on the inhale forces more oxygen into the blood - holding the breath on the exhale forces the lungs to surrender CO2. These facts can be used theraputically to alter the balance of the blood gases and have been for thousands of years. Increasing oxygen levels will relax and calm us and removing excess CO2 will clear our blood of inhibatory dulling toxicity - both are relaxing with the oxygen side being a type of relaxed calmness and the CO2 side giving a relaxed clarity. Breathing exercises that emphasize both inhalation and exhalation (with no retention)are safe for most people as there is less chance of overoxygenating. In the case of the exercise we have recently been discussing it is a exercise for resetting the ANS by forcing increased oxygen levels - slowing the breath and balancing Oxygen/CO2 - slowing the breath and balancing the gases are the primary theraputic modalities here. This exercise emphasises the oxygen side - it could work as well on CO2 if we also held the breath on the exhale. Raising the oxygen level and reducing the CO2 levels while reducing the length of the breath is what eventually resets the ANS. As far as the actual theraputic application we must keep in mind that the study subjects were experienced breath practioners - this is not actually a valid model for this type of study - nevertheless this type of technique has been used for centuries with success. Non experienced people will not be able to follow this one minute breath for 31 minutes without long training. It is not possible - it is a learning and training process that might take some time to achieve. Start slowly - say 10 seconds inhale - 10 seconds retention - 10 seconds exhalation - add 1 second to each phase of the breath each week until 20 seconds are achieved - if any complications or side effects occur move back one or two seconds until stability is achieved and then start slowly adding 1 second at a time - start with a 5 minute practice period adding one minute whenever it is comfortable to do so until the one minute breath is achieved for 31 minutes. This is a powerful technique and very effective to balance the ANS - this is very good for breaking many types of reactivity caused by past trauma - it is the reactivity from these past traumas which are an important part of the Sympathetic Nervous System overexcitement which is a major component of heart disease - especially electrical conductivity pathologies (like arrythmias and A-fib). A simple breath that can be practiced for all anxiety and tension states is one that emphasizes exhalation. Example a common state is high CO2 and mid to high oxygen - emhasizing the exhalation will correct this - greatly relaxing the SNS. If one is not sure what the balance of gases are in oneself then simply slightly increase both inhalation and exhalation - do this for ten minutes at different times during the day. If in a reactive state that makes one feel anxious then emphasize the inhalation - if the reactive state feels like the mind is dull or 'stupid' - unfocused and moving around everywhere without our ability to control then emphasize the exhalation. Actually I feel that one should practice breathing exercises under the guidance of an expert as there are potentials for side-effects. Breathing exercises can be done on ones own if one is very desciplined and makes very sure to move at ones own pace - meaning the practice should be comfortable and easy at all times - do not let the exercise become stressful are the theraputic effect will be lost. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 9, 2006 Report Share Posted July 9, 2006 Too much oxygen and too little CO2 also can cause anxiety and even panic attacks. (Respiratory alkalosis.) The holding of the breath prevents this. That's why people who are anxious because of too much oxygen and too little CO2 are advisted to hold their breath or breath into and out of a paper bag. These people feel like they don't have enough oxygen and breathe harder and faster, but this makes the problem worse as it drives the oxygen levels even higher and the CO2 levels even lower. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 9, 2006 Report Share Posted July 9, 2006 Chinese Traditional Medicine , " victoria_dragon " <victoria_dragon wrote: > > Too much oxygen and too little CO2 also can cause anxiety and even > panic attacks. (Respiratory alkalosis.) The holding of the breath > prevents this. That's why people who are anxious because of too much > oxygen and too little CO2 are advisted to hold their breath or breath > into and out of a paper bag. These people feel like they don't have > enough oxygen and breathe harder and faster, but this makes the > problem worse as it drives the oxygen levels even higher and the CO2 > levels even lower. > There are many mechanisms that can trigger panic attacks - in blood gas imbalances both oxygen and CO2 issues can set them off - panic attacks and other powerful reactivity states can be triggered by any excessive imbalance in the basic parameters of functioning - oxygen/Co2 balance - acid/alkaline balance - potassium/sodium balance - hormonal balance - all of these functions must always be in a dynamic balance with each other - if any part of this balance switches suddenly and or there is defeciency or excess - then one with SNS overeactivity can start a reactivity storm. This also has a model in brain chemistry since the tendancy toward panic attacks has a brain chemical imbalance as it's mirror image - none of these factors are primary causes they are co-factors. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 11, 2006 Report Share Posted July 11, 2006 I observe the same mechanism on people who, when they get anxious, pull out a cigarette, they are breathing an oxigen-reduced air. Marcos --- victoria_dragon <victoria_dragon escreveu: > Too much oxygen and too little CO2 also can cause anxiety and > even > panic attacks. (Respiratory alkalosis.) The holding of the > breath > prevents this. That's why people who are anxious because of > too much > oxygen and too little CO2 are advisted to hold their breath or > breath > into and out of a paper bag. These people feel like they don't > have > enough oxygen and breathe harder and faster, but this makes the > > problem worse as it drives the oxygen levels even higher and > the CO2 > levels even lower. > > > > > > _____ Abra sua conta no Mail: 1GB de espaço, alertas de e-mail no celular e anti-spam realmente eficaz. .br/ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 21, 2006 Report Share Posted December 21, 2006 Breathe in through your nose and draw your breath down into the area just below your navel, allowing your stomach to expand as you breathe (Baby Breath) and filling your lungs entirely with each breath before exhaling through your nose. Breathing is the most important part of meditation and Kundalini Awakening. From our birth until death we breathe more or less continually, yet for the most part we do it without any awareness of our breath and its effects on us, and believe it or not most people in the western world do it wrong! Take a moment right now and feel your breath. Pay attention to the air as it flows in through your nostrils and down into your lungs. Don’t think about anything or do anything other than just breathe. 1. Are you taking a relatively shallow breath and just filling the upper lobes of your lungs? 2. Does your stomach move out as you breathe? 3. Do you feel the bones of your ribcage expanding and opening with each breath? For most people the answer to 1 is YES and the answers to 2 and 3 are NO so lets expand this exercise a bit. Draw your breath down to a point about 2 inches below your navel (the body’s center of gravity). When you do this you’ll feel your stomach expand and push out in front of you. Most westerners usually keep their stomach pulled in and their chest out, so if you do this you’ll have to relax your abdomen. Just take a moment and be aware of your breath as it flows down into your center. Now as you inhale and draw your breath down, also let your ribcage expand. You’ll feel your floating ribs at the bottom of your ribcage spread and move, and you may get a few pops out of your spine also. Now just take a few moments and breathe this way. Don’t think or let your mind wander, just breathe. If you’ve never meditated before then congratulations, you just did! It’s exactly that simple. There are many benefits to proper breathing. The extra oxygen in your system means that your heart doesn’t have to beat as fast, which lowers your pulse and your blood pressure. Drawing the breath down into your center also helps to massage your internal organs, providing more oxygen to them as well as helping to release the accumulated stresses that build up there. The long term health benefits are immeasurable and have been repeatedly proven for thousands of years. Breathing is by far the most important part of the kundalini awakening exercises, although it sounds so simple. Paying attention to the breath is the beginning of opening up your awareness and it’s use in meditation is seen in every culture on the planet. Take some time to practice this, as it’s the foundation for everything that comes next. If you have to dedicate your meditation time to breathwork for awhile then that’s good, as we all proceed at our own pace. I recently read a translation of some of Jesus’ teachings from the original Aramaic (the language he actually spoke, although he apparently wasn’t literate) and it was very interesting to me that in Aramaic they used the same word for wind, breath and spirit. Those with a Chi Kung background might find it interesting to take another look at the New Testament and insert the word breath every time you see the word spirit. Quote Link to comment Share on other sites More sharing options...
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