Download Hopelessness Is Associated With Decreased Heart Rate

Hopelessness Is Associated With Decreased Heart Rate Variability During
Championship Chess Games
ALFONS M. SCHWARZ, MD, HARTMUT SCHÄCHINGER, MD, ROLF H. ADLER, MD,
AND
STEFAN M. GOETZ, MD
Objective: Clinical observations suggest that negative affects such as helplessness/hopelessness (HE/HO) may induce autonomic
duration; affects were assessed for every move after reconstruction of the games. In all games compiled, 18 situation of intense
confidence/optimism and 20 of intense helplessness/hopelessness were observed. Results: Intense affects of HE/HO were
associated with decreasing HF-HRV (Fisher exact test, p ⫽ .003), increasing “nervousness” (p ⫽ .0005), decreasing “optimism”
(p ⫽ .0005), and decreasing “calmness” (p ⫽ .0005). Conclusions: Investigation of championship chess game players with an ELO
strength ⱖ 2300 in a natural field setting revealed increasing HE/HO being associated with reduced HF-HRV suggestive of vagal
withdrawal. Thus, our data may help link negative mood states, autonomic nervous system disturbances, and cardiac events.
ECG ⫽ electrocardiogram; ELO ⫽ ranking system of the International Chess Federation for the rating of competitive players, developed by Arpad Elo, Hungarian mathematician; HE ⫽ helplessness;
HF ⫽ high frequency; HO ⫽ hopelessness; HR ⫽ heart rate; HRV
⫽ heart rate variability; IPFM ⫽ Integral Pulse Frequency Modulator; LF ⫽ low frequency; LPFES ⫽ low pass filtering of event
series; RF ⫽ respiratory frequency; SD ⫽ standard deviation.
T
here is a long history of attempting to link psychosocial
factors to heart disease. Mental stress (1) as well as negative emotional states such as anxiety (2– 4), anger (5), and
vital exhaustion (6) have been linked to coronary pathology.
The Type D personality (pessimistic, easily irritated, lacking
self-esteem/assertiveness, symptoms of depression, and anxiety) is associated with coronary risks (7, 8). High levels of
depressive symptoms (9) are associated with increased risks of
myocardial infarction and mortality. Furthermore, depressive
symptoms differentially predicted survival, with depressive
affect and hopelessness (HO) being particularly important
(10).
In a prospective study, Anda (41) assessed depression by
the D subscale of the General Well-Being Schedule, a fouritem scale with a single item for HO. HO was associated with
an increased risk of ischemic heart disease (moderate HO: RR
⫽ 1.6, 95% CI ⫽ 1.0 –2.5; severe HO: RR ⫽ 2.1, 95% CI ⫽
1.1–3). Recently, Stern (11) confirmed these findings and
showed that HO predicts mortality from coronary heart disease and may be even a better predictor than depression.
Depression may be linked to increased cardiac mortality
(12) by autonomic nervous system disturbances, indicated by
altered heart rate variability (HRV). The potential mechanisms
connecting the feeling of HO with cardiovascular disease are
not well understood. Whether emerging HO induces autonomic disturbances has never been tested.
Championship chess games offer a natural setting for the
study of hopelessness and certain physiologic parameters –
From the Department of Internal Medicine (A.M.S., R.H.A., S.M.G.),
Medical Division Lory, University of Berne Medical School, Berne, Switzerland; and the Laboratory of Psychophysiology (H.S.), Department of Medicine, University of Basle Medical School, Basle, Switzerland.
Address reprint requests to: Rolf H. Adler, MD, Leiserenweg 4, CH-3122
Kehrsatz, Switzerland. Email: [email protected]
Received for publication February 24, 2002; revision received October 29,
2002.
Part of this material was presented as a poster at the annual meeting of the
American Psychosomatic Society, March 2001, Monterey, California.
DOI: 10.1097/01.PSY.0000075975.90979.2A
658
0033-3174/03/6504-0658
Copyright © 2003 by the American Psychosomatic Society
and possibly induce more intense mood states than other
inductive paradigms. The players are deeply committed, experience intense emotions, and their participation in a study
poses no ethical problems. Their heart rate variability can be
easily registered telemetrically and their behavior during the
games, which may last 7 hours, can be closely observed.
The aim of our study was to examine the association of
positive and negative affects, primarily helplessness (HE),
HO, and HRV, during chess games of players with an ELO
average score ⱖ 2300, ie, the strength of an international
master.
METHODS
Subjects
Nine male players were studied, ages 17 to 33 years. Inclusion criteria
were active chess players, ELO score ⱖ 2300, and willingness to participate
voluntarily. Exclusion criteria were concomitant disease and medication affecting autonomic nervous system control. The youngest participant was a
student; one participant was an unemployed repro-photographer; the others
were university students or in academic professions. All were in good health.
There was no anamnestic evidence of illicit drug abuse. All were studied
during championship games. They were asked to participate in the study by
personal contact and received a small compensation.
Procedure
The necessary installation was completed at least 10 minutes before the
start of the game. The experimenter sat beside the player. The experimenter
noted the length of elapsed time (on a laptop) for each of the player’s and
opponent’s moves. The players noted each move on the score sheets. After the
game, the player and the experimenter went through the score sheet several
times, the player marking several affects after each of his and his opponent’s
moves on numerical rating scales encompassing numbers from ⫹5 to -5.
Based on suggestions of master players concerning the affects experienced in
past games, the following pairs of affects were assessed: “general mood
between negative—positive,” “calm—nervous,” “energetic—tired,” “certain— uncertain,” “pleasantly surprised—frightened,” “proud—ashamed,”
“motivated— disinterested,” “happy— disappointed,” “euphoric—anxious,”
“determined— undetermined.” Special focus was given to the affect pair
“optimistic/in control— hopeless/helpless.”
We do not know how the players would have scored their affect levels
immediately after a move or days after the game. Our experience during team
sessions several days after the game led us to assume that the players relive
their games vividly.
Data Acquisition and HRV Analysis
The electrocardiogram (ECG) was telemetrically registered (HewlettPackard telemetry system) using three stick-pad electrodes placed on the left
thorax. It was transmitted from an emitter fixed on the subject’s body to a
receiver connected to a laptop. The ECG was recorded and visualized on the
screen during the entire game. Analog to digital conversion was performed at
1000 Hz. Data were stored on the personal computer in different files for each
move. Only files representing a minimum of 80 seconds duration were subject
Psychosomatic Medicine 65:658 – 661 (2003)
HEART RATE VARIABILITY AND AFFECT IN CHESS PLAYERS
to further analysis of HRV. Offline analysis (13, 14) revealed the beat-to-beat
heart rate (HR) from the electrocardiogram. HRV was assessed according to
published standards (15, 16). In brief, HRV was determined by low pass
filtering of event series (LPFES) method as suggested by Rompelman and
colleagues (17). This method is in accordance with the Integral Pulse Frequency Modulator (IPFM) concept, which represents a rational model for the
modulation of heart beat generation by autonomic nervous system influences
(18). Power of HRV was analyzed over the entire spectrum of 0.01 to 0.50 Hz
with a frequency resolution of 0.01 Hz. Low frequency (LF) power of HRV
was determined by integrating spectral power in the low frequency range
between 0.07 and 0.14 Hz. High frequency (HF) power of HRV was determined by integrating spectral power in the low frequency range between 0.15
and 0.4 Hz. Log transformation of power measures was performed to yield
normally distributed values. Respiratory frequency impacts HRV (19, 20).
Two independent procedures were employed to estimate dominant respiratory
frequency (RF) for each subject and period. RF was depicted from the peak
HF component of the HRV power spectrum. RF was further determined by
graphical display and subsequent analysis of the R-spike amplitude time
series. The R-spike amplitude varies little but consistently within the respiratory cycle. RF was calculated as the average of both methods only if the two
procedures revealed similar results (within 0.03 Hz). Previous data from our
laboratory (internal report) indicated a high correlation (Pearson r ⬎ 0.86)
between both methods and RF assessed by standard respiratory belt system.
Statistics
Values of recognized affects – LF-HRV, HF-HRV, and RF – were
assessed for each person and step in the chess game. These data were log
transformed and z-scored to derive standardized individual data. Changes of
at least 1 (from one step to the other), representing the standard deviation (SD)
of the entire game, were depicted as transitions. Fisher exact test was used to
test whether transitions of affects were associated with transitions of HRV and
RF. Z scores were used because individuals differed considerably in mean RT,
HRV, and reported affective states. Because of the irregular time-spaced
nature of the response data in chess games (ie, moves vary considerably in
length, the number of moves varies from game to game) a repeated-measures
ANOVA did not appear appropriate. Thus, the most simple alternative,
nonparametric direct comparisons, was preferred during the planning and
setup of the study. Furthermore, nonparametric tests are more robust – an
advantage if an unbalanced sample size is expected.
RESULTS
In the nine games, 18 situations with a transition toward
“optimism/in control” and 20 transitions toward “helplessness/hopelessness” (affect-intensity ⱖ SD above/below the
average affect-level during the entire game) were observed. At
least one change was detectable in each subject, therefore the
entire database of all games could be used. The average period
of transition to hopelessness was 146 ⫾ 55 seconds (previous
move: 273 ⫾ 62 seconds, following move: 245 ⫾ 68 seconds); the transition to hope and control was longer – 265 ⫾
77 seconds (previous move: 347 ⫾ 118 seconds, following
move: 293 ⫾ 89 seconds). As shown in Table 1, affecttransitions toward increasing “optimism/in control” were sigTABLE 1.
nificantly associated (p ⫽ .003) to HF-HRV. Affect-transitions toward increasing “helplessness/hopelessness” were
associated with decreasing HF-HRV. LF-HRV showed no
consistent change during transition of these affects. In transitions toward “optimism/in control,” heart rate increased in 10,
decreased in 8, and remained constant in 0 situations. RF
increased in 5, decreased in 7, and did not change in 6
situations. In transitions toward “helplessness/hopelessness”
heart rate increased in 10, decreased in 9, and remained
constant in 1 situation. RF increased in 5, decreased in 7, and
remained constant in 8 situations.
All other affects changed congruently, with an increase in
positive affects with “hope— control” and an increase of negative affects with “helplessness— hopelessness,” or showed
no change. The affect pair “calm—nervous” is mentioned in
detail because it helps to interpret our findings with respect to
“helplessness— hopelessness” (Table 2): calmness correlates
with “optimism— control” and “helplessness— hopelessness”
with “nervousness” (Fisher exact test, p ⫽ .0005). Similar
correlation was observed with respect to “pleasantly
surprised—frightened”.
DISCUSSION
Chess games important to players with ELO scores ⱖ 2300
represent a quasi-natural situation for the study of the correlation between affects of “optimism— control” and “helplessness— hopelessness” on the one hand and autonomic nervous
system influences on the heart on the other. The study situation may be closer to real life with respect to the intensity of
the evocation of “helplessness— hopelessness” than affect induction in the laboratory because the players are intensely
involved and cannot escape and withdraw as would be possible in a laboratory setting. Furthermore, such players are
capable of memorizing games and their affective experience
in important games for years. In our study, their affects were
assessed in retrospect to avoid disturbing the player with
questions during the game, a disadvantage which seemed
unavoidable in our chess paradigm. The main finding of the
current research is that transitions of HE/HO are associated
with HF-HRV, suggesting that increased HE/HO induces vagal withdrawal. Thus, analogous to what is known about
depression and coronary heart disease (12), our data may help
establish a model that links HE/HO to coronary pathology.
TABLE 2.
Situations of Helplessness-Hopelessness and Their
Correlation With Calmness-Nervousness
Increased
High Frequency Heart Rate Variability (HF-HRV)
Optimism/hope
Helplessness/
hopelessness
Increased
Decreased
Unchanged
N
8
3
2
13
8
4
18
20
() Optimism/helplessness, hopelessness ⬎ 1 SD).
Fisher exact test, p ⫽ .003.
Psychosomatic Medicine 65:658 – 661 (2003)
Helplessnesshopelessness
(ⱖ1 SD)
Optimismcontrol
(ⱖ1 SD)
Unchanged
N
15
4
20
0
4
18
Calmness
Nervousness
1
14
Fisher exact test, p ⫽ .0005.
659
A. M. SCHWARZ et al.
HE and HO are mood states linked, but not identical, with
depression.
The hopelessness which we assessed is a transitional affective state and is not identical with the hopelessness studied
epidemiologically (21) or the hopelessness in states of depression assessed in depression and survival of patients with
coronary artery disease (10). The term depression encompasses several clinical entities. Although diagnostic manuals
(ie, DSM-IV and ICD-10) and standardized diagnosis and
validated screening questionnaires (ie, BDI and HADS) are
available, the diversity of depression symptoms is reflected by
the use of various items. Indeed, past research (22) compared
16 depression scales and found that, of 54 symptoms appearing in at least two scales, only one – self-devaluation – was
present in all scales.
Negative emotions and depression are related to autonomic
nervous system disturbances. Increased sympathicotonia (23)
was observed in subjects with Type A personality who were
confronted with anger. Lowered HRV was found in very
anxious persons (24, 25). High frequency (HF)-HRV (heart
rate variability) decreases under mental stress (26, 27). By
inducing positive and negative affects with the “freeze-frame”
method under laboratory conditions (28), an increase in HRV
under positive and negative affects was found; with negative
affects, the low frequency (LF) component increased; positive
affects led to increases in LF and HF components. A drop in
heart rate accompanied by increasing HRV was found in
young healthy subjects listening to classical music, inducing
positive emotions (29, 30). Further research indicated (31–33)
that depression is linked to reduced HRV.
Reduced HRV may indicate autonomic nervous system
abnormalities of potential importance to coronary heart disease. A temporary decrease in parasympathetic tone after
acute myocardial infarction was found (34). Decreased HRV
has been associated with increased mortality after myocardial
infarction (35, 36), coronary angiography (37), and cardiac
failure (38).
Engagement and cognitive effort can lower heart rate variability. This might have confused our findings of lowered
HRV in the study. In a phase of hopelessness, lower task
engagement and less cognitive effort could be expected in the
chess players, which should increase HRV. However, we
observed the opposite, which makes the confusion less likely.
In the present study we observed that loss of “optimism—
control” and intensified “helplessness— hopelessness” correlated with a decrease of HF-HRV, suggestive of decreasing
vagal tone. The other affects studied changed in the same
direction, eg, nervousness, uncertainty, indecisiveness, and
fright increased in periods of intense “helplessness— hopelessness”. Our findings suggest a decrease of vagal tone and
not bradycardia in situations of increasing HE/HO. However,
HO has been observed (in experiments involving animals) to
be associated with parasympathetic activation and bradycardia
(Compare Richter (39) in rats in swimming experiments and
Corley et al. (40) in yoked-control monkeys). Our observations and findings in humans show that intense affects leading
660
to ventricular fibrillation and rarely to bradycardia need not be
disparate events. With increasing intensity of HE/HO mixed
with nervousness, sympathetic tone augments. On a clinical
level, this situation reflects the fight-flight condition. If the
sympathetic tone is intense enough and the heart electrically
unstable, ventricular fibrillation might ensue. If the intensity
of helplessness— hopelessness increases further, the fightflight pattern might be followed by increasing parasympathetic tone, conservation withdrawal on the phenomenological
level, and, with respect to the heart, increasing bradycardia
and finally asystole.
REFERENCES
1. Frasure-Smith N. In-hospital symptoms of psychological stress as predictors of long-term outcome after acute myocardial infarction in men.
Am J Cardiol 1991;67:121–7.
2. Haines AP, Imeson JD, Meade TW. Phobic anxiety and ischemic heart
disease. BMJ 1987;295:297–9.
3. Kawachi I, Colditz GA, Ascherio A, Rimm EB, Giovannucci E, Stampfer
MJ, Willett WC. Prospective study of phobic anxiety and ischemic heart
disease. Circulation 1994;89:1992–7.
4. Fleet R, Lavoie K, Beitman BD. Is panic disorder associated with
coronary artery disease? A critical review of the literature. J Psychosom
Res 2000;48:347–56.
5. Ironson G, Taylor CB, Boltwood M, Bartzokis T, Dennis C, Chesney M,
Spitzer S, Segall GM. Effects of anger on left ventricular ejection fraction
in coronary artery disease. Am J Cardiol 1992;70:281–5.
6. Kop WJ, Appels A, Leon CFMd, de_Swart HB, Bar FW. Vital exhaustion predicts new cardiac events after successful coronary angioplasty.
Psychosom Med 1994;56:281–7.
7. Denollet J, Brutsaert DL. Personality, disease severity, and the risk of
long-term cardiac events in patients with a decreased ejection fraction
after myocardial infarction. Circulation 1998;97:167–73.
8. Denollet J, Vaes J, Brutsaert DL. Inadequate response to treatment in
coronary heart disease: adverse effects of Type D personality and
younger age on 5-year prognosis and quality of life. Circulation 2000;
102:630 –5.
9. Barefoot JC, Schroll M. Symptoms of depression, acute myocardial
infarction, and total mortality in a community sample. Circulation 1996;
93:1976 – 80.
10. Barefoot JC, Brummett BH, Helms MJ, Mark DB, Siegler IC, Williams
RB. Depressive symptoms and survival of patients with coronary artery
disease. Psychosom Med 2000;62:790 –5.
11. Stern SL, Dhanda R, Hazuda HP. Hopelessness predicts mortality in
older Mexican and European Americans. Psychosom Med 2001;63:
344 –51.
12. Carney RM, Blumenthal JA, Stein PK, Watkins L, Catellier D, Berkman
LF, Czajkowski SM, O’Connor C, Stone PH, Freeland KE. Depression,
heart rate variability, and acute myocardial infarction. Circulation 2001;
104:2024 – 8.
13. Schachinger H, Weinbacher M, Kiss A, Ritz R, Langewitz W. Cardiovascular indices of peripheral and central sympathetic activation. Psychosom Med 2001;63:788 –96.
14. Haberthur C, Schachinger H, Langewitz W, Ritz R. Effect of beta
blockade with and without sympathomimetic activity (ISA) on sympathovagal balance and baroreflex sensitivity. Clin Physiol 1999;19:
143–52.
15. Mulder G, Mulder LJ. Information processing and cardiovascular control.
Psychophysiology 1981;18:392– 402.
16. Langewitz W, Ruddel H, Schachinger H. Reduced parasympathetic cardiac control in patients with hypertension at rest and under mental stress.
Am Heart J 1994;127:122– 8.
17. Rompelman O, Snijders JB, van Spronsen CJ. The measurement of heart
rate variability spectra with the help of a personal computer. IEEE Trans
Biomed Eng 1982;29:503–10.
18. Bayly EJ. Spectral analysis of pulse frequency modulation in the nervous
systems. IEEE Trans Biomed Eng 1968;15:257– 65.
19. Berntson GG, Cacioppo JT, Quigley KS. Respiratory sinus arrhythmia:
autonomic origins, physiological mechanisms, and psychophysiological
implications. Psychophysiology 1993;30:183–96.
Psychosomatic Medicine 65:658 – 661 (2003)
HEART RATE VARIABILITY AND AFFECT IN CHESS PLAYERS
20. Schachinger H, Oelke M, Curio I, Langewitz W, Ruddel H, Schulte W.
Impact of respiratory frequency on short-term blood pressure and heart
rate variability. J Hypertens Suppl 1991;9:S330 –1.
21. Everson SA, Kaplan GA, Golding DE, Salonen R, Salonen JT. Hopelessness and 4-year progression of carotid atherosclerosis. The Kuopio
Ischemic Heart Disease Risk Factor Study. Arterioscler Thromb Vasc
Biol 1997;17:1490 –5.
22. Levitt EE, Lubin B. Depression, concepts, controversies, and some new
facts. New York: Springer; 1975.
23. Williams RB, Lane JD, Kuhn CM, Melosh W, White AD, Schanberg SM.
Type A behavior and elevated physiological and neuroendocrine responses to cognitive tasks. Science 1982;218:483–5.
24. Offerhaus RE. Heart rate variability in psychiatry. In: Kitney RJ,
Rompelmann, editors. The study of heart rate variability. Oxford: Oxford
University Press; 1980. p. 225–38.
25. Kawachi I, Sparrow D, Vokonas PS, Weiss ST. Decreased heart rate
variability in men with phobic anxiety. Am J Cardiol 1995;75:882–5.
26. Sloan RP. Effects of mental stress throughout the day on cardiac autonomic control. Biol Psychol 1994;37:89 –99.
27. Dishman RK, Nakamura Y, Garcia ME, Thompson RW, Dunn AL, Blair
SN. Heart rate variability, trait anxiety, and perceived stress among
physically fit men and women. Int J Psychophysiol 2000;37:121–33.
28. McCraty R, Atkinson M, Tiller WA, Rein G, Watkins AD. The effects of
emotions on short-term power spectrum analysis of heart rate variability.
Am J Cardiol 1995;76:1089 –93.
29. Escher J, Evéquoz D. Musik und Herzfrequenzvariabilität. Untersuchung
des Effektes von Musik auf die Herzfrequenzvariabilität bei gesunden
Jugendlichen. Schweiz Rundsch Med Prax 1999;88:951–2.
30. McCraty R, Atkinson M, Rein G, Watkins AD. Music enhances the effect
of positive emotional states on salivary IgA. Stress Med 1996;12:167–75.
31. Yeragani VK, Pohl R, Balon R, Ramesh C, Glitz D, Jung I, Sherwood P.
Psychosomatic Medicine 65:658 – 661 (2003)
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
Heart rate variability in patients with major depression. Psychiatry Res
1991;37:35– 46.
Lehofer M, Moser M, Hoehn-Saric R, McLeod D, Liebmann P, Drnovsek
B, Egner S, Hildebrandt G, Zapotoczky HG. Major depression and
cardiac autonomic control. Biol Psychiatry 1997;42:914 –9.
Rechlin T, Weis M, Spitzer A, Kaschka WP. Are affective disorders
associated with alterations of heart rate variability? J Affect Disord
1994;32:271–5.
Rothschild M, Rothschild A, Pfeifer M. Temporary decrease in cardiac
parasympathetic tone after acute myocardial infarction. Am J Cardiol
1988;62:637–9.
La Rovere MT, Bigger JT, Jr, Marcus FI, Mortara A, Schwartz PJ.
Baroreflex sensitivity and heart-rate variability in prediction of total
cardiac mortality after myocardial infarction. ATRAMI (Autonomic
Tone and Reflexes After Myocardial Infarction) Investigators. Lancet
1998;351:478 – 84.
Kleiger RE, Miller JP, Bigger JT, Moss AJ. Decreased heart rate variability and its association with increased mortality after acute myocardial
infarction. Am J Cardiol 1987;59:256 – 62.
Rich MW, Saini JS, Kleiger RE, Carney RM, te_Velde A, Freedland KE.
Correlation of heart rate variability with clinical and angiographic variables
and late mortality after coronary angiography. Am J Cardiol 1988;62:714–7.
Saul JP, Aral Y, Berger RD, Lilly LS, Colucci WS, Cohen RJ. Assessment of autonomic regulation in congestive heart failure by heart rate
spectral analysis. Am J Cardiol 1988;61:1292–9.
Richter CP. On the phenomenon of sudden death in animals and man.
Psychosom Med 1957;19:92– 8.
Corley KC, Mauck HP, Shiel F. Cardiac responses associated with
“yoked-chair” shock avoidance in squirrel monkeys. Psychophysiology
1975;12:439 – 44.
Anda R. Depressed affect, hopelessness and the risk of ischemic heart
disease in a cohort of U.S. adults. Epidemiology 1993;4:285–94.
661