Con­tin­u­ing with the theme of a Week of Sci­ence spon­sored by Just Sci­ence, we will high­light some of the key points in: Appel­hans BM, Luecken LJ. Heart Rate Vari­abil­ity as an Index of Reg­u­lated Emo­tional Respond­ing. Review of Gen­eral Psy­chol­ogy. 2006;10:229–240.

Defin­ing Heart Rate Vari­abil­ity
Effec­tive emo­tional reg­u­la­tion depends on being able to flex­i­bly adjust your phys­i­o­log­i­cal response to a chang­ing environment.

“… heart rate vari­abil­ity (HRV) is a mea­sure of the con­tin­u­ous inter­play between sym­pa­thetic and parasym­pa­thetic influ­ences on heart rate that yields infor­ma­tion about auto­nomic flex­i­bil­ity and thereby rep­re­sents the capac­ity for reg­u­lated emo­tional responding.”

“HRV reflects the degree to which car­diac activ­ity can be mod­u­lated to meet chang­ing sit­u­a­tional demands.”

The sym­pa­thetic (SNS) and parasym­pa­thetic (PNS) branches of the auto­nomic ner­vous sys­tem (ANS) antag­o­nis­ti­cally influ­ence the lengths of time between con­sec­u­tive heart­beats. Faster heart rates, which can be due to increased SNS and/or lower PNS activ­ity, cor­re­spond to a shorter inter­beat inter­val while slower heart rates have a longer inter­beat inter­val, which can be attrib­uted to increased PNS and/or decreased SNS activity.

The frequency-based HRV analy­ses are based on the fact that the vari­a­tions in heart rate pro­duced by SNS and PNS activ­ity occur at dif­fer­ent speeds, or fre­quen­cies. SNS is slow act­ing and medi­ated by nor­ep­i­neph­rine while PNS influ­ence is fast act­ing and medi­ated by acetylcholine.

Phys­i­o­logic Under­pin­nings of HRV

Breath­ing air into the lungs tem­porar­ily gates off the influ­ence of the parasym­pa­thetic influ­ence on heart rate, pro­duc­ing a heart rate increase (see Berntson, Cacioppo, & Quigley, 1993). Breath­ing air out of the lungs rein­states parasym­pa­thetic influ­ence on heart rate, result­ing in a heart rate decrease. This rhyth­mic oscil­la­tion in heart rate pro­duced by res­pi­ra­tion is called res­pi­ra­tory sinus arrhyth­mia (Bernardi, Porta, Gabutti, Spicuzza, & Sleight, 2001; Berntson et al., 1993).

The cen­tral auto­nomic net­work (CAN) assists emo­tional reg­u­la­tion by adjust­ing phys­i­o­log­i­cal arousal to appro­pri­ately match the exter­nal and inter­nal envi­ron­ments. The CAN con­sists of cor­ti­cal, lim­bic, and brain­stem com­po­nents. Its out­put is trans­mit­ted to the sinoa­trial node of the heart, among other organs.

HRV reflects the moment-to-moment out­put of the CAN and, by proxy, an individual’s capac­ity to gen­er­ate reg­u­lated phys­i­o­log­i­cal responses in the con­text of emo­tional expres­sion (Thayer & Lane, 2000; Thayer & Siegle, 2002).

Psy­chophys­i­o­log­i­cal The­o­ries of HRV
Two major the­o­ries causally relate auto­nomic flex­i­bil­ity, rep­re­sented by HRV, and the capac­ity for reg­u­lated emo­tional responding:

1. Poly­va­gal The­ory: an evo­lu­tion­ary expla­na­tion that the ANS devel­oped in stages to deal with changes in the envi­ron­ment and respond effec­tively. The last com­po­nent devel­oped, the ven­tral vagus com­plex, phys­i­cally con­nects with the facial mus­cles, voice pro­duc­tion, and other socially impor­tant behav­iors, which cre­ates a phys­i­cal con­nec­tion between the heart and emo­tional expression.
2. Neu­ro­vis­ceral Inte­gra­tion The­ory: an inte­gra­tive expla­na­tion that evo­lu­tion­ary forces led to the devel­op­ment of a rapidly respond­ing vagus nerve to sup­port appro­pri­ate emo­tional expres­sion and reg­u­la­tion through con­nec­tions with the cor­tex, lim­bic sys­tem, and brain­stem. By inhibit­ing other poten­tial responses through synap­tic activ­ity in the brain and vagal activ­ity in the body, the CAN acts as a “neu­ro­phys­i­o­log­i­cal com­mand cen­ter gov­ern­ing cog­ni­tive, behav­ioral, and phys­i­o­log­i­cal ele­ments into reg­u­lated emo­tion states”.

Both the­o­ries pre­sented above are sim­i­lar in that they (a) spec­ify a crit­i­cal role for parasym­pa­thet­i­cally medi­ated inhi­bi­tion of auto­nomic arousal in emo­tional expres­sion and reg­u­la­tion and (b) main­tain that HRV mea­sures are infor­ma­tive about indi­vid­u­als’ capac­ity for this aspect of reg­u­lated emo­tional responding.

Empir­i­cal Research With HRV

• Low HRV is an inde­pen­dent risk fac­tor for sev­eral neg­a­tive car­dio­vas­cu­lar outcomes
• Low HRV is a proxy for under­ly­ing car­dio­vas­cu­lar dis­ease processes
• Higher lev­els of rest­ing HRV have been asso­ci­ated with effec­tive cop­ing strategies
• Atten­tion con­trol is asso­ci­ated with higher HRV
• Patients with gen­er­al­ized anx­i­ety dis­or­der show lower HRV than controls
• Low HRV has been asso­ci­ated with depression

Sum­mary, Future Direc­tions, and Con­clu­sions
“HRV is emerg­ing as an objec­tive mea­sure of indi­vid­ual dif­fer­ences in reg­u­lated emo­tional respond­ing, par­tic­u­larly as it relates to social processes and men­tal health.”

“Fur­ther inves­ti­ga­tion should attempt to elu­ci­date those con­texts in which the auto­nomic flex­i­bil­ity rep­re­sented by greater HRV is par­tic­u­larly adap­tive, as well as sit­u­a­tions in which greater HRV may be mal­adap­tive. Although the­o­rists and researchers have empha­sized the impor­tance of parasym­pa­thet­i­cally medi­ated HRV in reg­u­lated emo­tional respond­ing, the rel­a­tive con­tri­bu­tion of sym­pa­thetic reg­u­la­tion of the heart has not yet been clarified.”

“Poten­tial clin­i­cal appli­ca­tions of HRV also exist, as increas­ing an individual’s capac­ity for inhibitory emo­tion reg­u­la­tion through HRV biofeed­back (Lehrer et al., 2003) may have ther­a­peu­tic impli­ca­tions for mood, anx­i­ety, and impulse con­trol disorders.”

“Unlike other psy­chophys­i­o­log­i­cal vari­ables, HRV pro­vides infor­ma­tion regard­ing both PNS and SNS activ­ity, thereby per­mit­ting infer­ences about both inhibitory and exci­ta­tory processes in emo­tion regulation.”

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