Breathing

[Guest guest]

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.

[Guest guest]

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.

>

>

>

>

 

 

 

 

 

 

[Guest guest]

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.

[Guest guest]

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.

[Guest guest]

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.

[Guest guest]

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.

[Guest guest]

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/

[Guest guest]

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.