Heart rate recovery: autonomic determinants, methods of assessment and association with mortality and cardiovascular diseases
Summary Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise – known...
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| Published in | Clinical physiology and functional imaging Vol. 34; no. 5; pp. 327 - 339 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Blackwell Publishing Ltd
01.09.2014
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Summary
Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise – known as heart rate recovery (HRR) – is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR. |
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| AbstractList | Cardiovascular disease (
CVD
) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several
CVD
s and is also linked to the increased risk of mortality in
CVD
patients. The quantification of heart rate decrement after exercise – known as heart rate recovery (
HRR
) – is a simple tool for assessing cardiac autonomic activity in healthy and
CVD
patients. Furthermore, since The Cleveland Clinic studies,
HRR
has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate
HRR
and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about
HRR
, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that
HRR
can be modelled by an exponential curve, with a fast and a slow decay component.
HRR
may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of
HRR
may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in
CVD
, helping to explain the slower
HRR
in such patients and the increased rate of mortality in individuals who present a slower
HRR
. Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise - known as heart rate recovery (HRR) - is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR.Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise - known as heart rate recovery (HRR) - is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR. Summary Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise - known as heart rate recovery (HRR) - is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR. [PUBLICATION ABSTRACT] Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise - known as heart rate recovery (HRR) - is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR. Summary Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise – known as heart rate recovery (HRR) – is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR. |
| Author | Peçanha, Tiago Forjaz, Cláudia Lúcia de Moraes Silva-Júnior, Natan Daniel |
| Author_xml | – sequence: 1 givenname: Tiago surname: Peçanha fullname: Peçanha, Tiago email: Tiago Peçanha, Av. Prof. Melo Moraes, 65 - Butantã - São Paulo, SP - 05508-030, Brazil, tiagopecanha@usp.br organization: Exercise Hemodynamic Laboratory, School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil – sequence: 2 givenname: Natan Daniel surname: Silva-Júnior fullname: Silva-Júnior, Natan Daniel organization: Exercise Hemodynamic Laboratory, School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil – sequence: 3 givenname: Cláudia Lúcia de Moraes surname: Forjaz fullname: Forjaz, Cláudia Lúcia de Moraes organization: Exercise Hemodynamic Laboratory, School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24237859$$D View this record in MEDLINE/PubMed |
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| CODEN | CPFICA |
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| ContentType | Journal Article |
| Copyright | 2013 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd 2013 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd. Copyright © 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine |
| Copyright_xml | – notice: 2013 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd – notice: 2013 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd. – notice: Copyright © 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine |
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| Keywords | exercise heart rate autonomic nervous system parasympathetic nervous system sympathetic nervous system |
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Post-exercise heart rate recovery in healthy, obeses, and COPD subjects: relationshi 1991; 17 1991; 14 2010; 108 2010a; 138 2013; 127 1982; 53 1988; 78 2006; 291 2000; 132 1971; 285 2010b; 30 2007; 74 2007a; 293 2012; 99 1997; 7 2010; 22 2009; 98 2005; 100 2002; 86 2009; 94 2006; 21 2007; 292 2008; 29 2004; 37 2002; 87 2007b; 293 1991; 84 2012; 29 2002; 90 1994; 72 1992; 2 2003; 42 2009; 15 2010; 9 1995; 52 2010; 35 2005; 352 2006; 57 1989; 256 1989; 411 2001; 281 2005; 112 2003; 35 1999; 341 2006; 110 2003; 290 2013a 2009; 296 2001; 24 2012; 32 2011; 9 2004; 52 2011; 301 1990; 23 2009; 76 1978; 45 2007; 153 2005; 95 2003; 26 1988; 23 2000; 81 1995; 268 2000; 80 2001; 38 2008; 40 1991; 325 1989; 58 2005; 99 2009; 105 2001; 91 2004; 66 2013b; 15 1990; 15 2002; 53 2000; 46 2010a; 33 2006; 77 2002; 51 1993; 66 2013; 167 2008; 9 1999; 87 1994; 24 2011; 14 2011; 151 2011; 16 2011; 270 2001; 104 2007; 37 2013; 18 2003; 91 2003; 92 2003; 9 2001; 19 1988; 254 2000; 284 2011; 21 2003; 1 2008; 156 2006; 367 1970; 187 2005; 150 2000; 279 2010 2006; 11 2002; 32 2006; 151 2011; 32 1988; 57 2006; 19 2008; 10 2011; 34 2007; 115 2007; 112 2004; 110 2004; 96 2012; 3 2004; 93 2010b; 145 2011; 48 2009; 3 1989; 14 2008; 295 2010; 95 2007; 49 e_1_2_6_114_1 e_1_2_6_53_1 e_1_2_6_76_1 e_1_2_6_95_1 e_1_2_6_118_1 e_1_2_6_30_1 Journeay WS (e_1_2_6_58_1) 2006; 77 e_1_2_6_72_1 e_1_2_6_91_1 e_1_2_6_110_1 e_1_2_6_133_1 e_1_2_6_19_1 e_1_2_6_11_1 e_1_2_6_34_1 e_1_2_6_38_1 e_1_2_6_57_1 e_1_2_6_99_1 e_1_2_6_125_1 e_1_2_6_64_1 e_1_2_6_87_1 e_1_2_6_106_1 e_1_2_6_129_1 e_1_2_6_41_1 e_1_2_6_60_1 e_1_2_6_83_1 e_1_2_6_121_1 e_1_2_6_102_1 e_1_2_6_9_1 Barak OF (e_1_2_6_14_1) 2010; 9 e_1_2_6_5_1 Achugbue FS (e_1_2_6_2_1) 2009; 3 Darr KC (e_1_2_6_39_1) 1988; 254 e_1_2_6_49_1 e_1_2_6_22_1 e_1_2_6_45_1 e_1_2_6_26_1 e_1_2_6_68_1 e_1_2_6_73_1 e_1_2_6_54_1 e_1_2_6_96_1 e_1_2_6_117_1 e_1_2_6_31_1 e_1_2_6_50_1 e_1_2_6_92_1 e_1_2_6_132_1 e_1_2_6_113_1 Esco MR (e_1_2_6_46_1) 2010; 22 e_1_2_6_35_1 e_1_2_6_12_1 e_1_2_6_77_1 e_1_2_6_16_1 e_1_2_6_42_1 e_1_2_6_105_1 e_1_2_6_128_1 e_1_2_6_65_1 e_1_2_6_80_1 e_1_2_6_109_1 e_1_2_6_61_1 e_1_2_6_120_1 e_1_2_6_101_1 e_1_2_6_124_1 e_1_2_6_6_1 e_1_2_6_23_1 e_1_2_6_88_1 e_1_2_6_69_1 e_1_2_6_51_1 e_1_2_6_74_1 e_1_2_6_97_1 e_1_2_6_116_1 e_1_2_6_32_1 e_1_2_6_70_1 e_1_2_6_93_1 e_1_2_6_131_1 Nobrega AC (e_1_2_6_94_1) 1990; 23 e_1_2_6_112_1 e_1_2_6_135_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_59_1 Cahalin LP (e_1_2_6_27_1) 2013 e_1_2_6_17_1 e_1_2_6_55_1 e_1_2_6_78_1 e_1_2_6_62_1 e_1_2_6_85_1 e_1_2_6_104_1 e_1_2_6_43_1 e_1_2_6_127_1 e_1_2_6_81_1 e_1_2_6_20_1 e_1_2_6_108_1 e_1_2_6_100_1 e_1_2_6_123_1 e_1_2_6_24_1 e_1_2_6_3_1 Bonde‐Petersen F (e_1_2_6_15_1) 1978; 45 e_1_2_6_66_1 e_1_2_6_89_1 e_1_2_6_28_1 e_1_2_6_47_1 e_1_2_6_52_1 e_1_2_6_98_1 e_1_2_6_115_1 e_1_2_6_75_1 e_1_2_6_10_1 e_1_2_6_119_1 e_1_2_6_71_1 e_1_2_6_90_1 e_1_2_6_130_1 e_1_2_6_111_1 e_1_2_6_134_1 e_1_2_6_33_1 e_1_2_6_18_1 e_1_2_6_56_1 e_1_2_6_37_1 e_1_2_6_79_1 e_1_2_6_103_1 e_1_2_6_126_1 e_1_2_6_86_1 e_1_2_6_21_1 e_1_2_6_107_1 Arai Y (e_1_2_6_7_1) 1989; 256 e_1_2_6_40_1 e_1_2_6_82_1 e_1_2_6_122_1 e_1_2_6_8_1 e_1_2_6_4_1 e_1_2_6_25_1 e_1_2_6_48_1 Kinugawa T (e_1_2_6_63_1) 1995; 268 McArdle WD (e_1_2_6_84_1) 2010 e_1_2_6_29_1 e_1_2_6_44_1 e_1_2_6_67_1 |
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Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several... Cardiovascular disease ( CVD ) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVD s... Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and... Summary Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several... |
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| SubjectTerms | autonomic nervous system Autonomic Nervous System - physiopathology Cardiovascular Diseases - diagnosis Cardiovascular Diseases - mortality Cardiovascular Diseases - physiopathology Electrocardiography Exercise Exercise Test Health risk assessment Heart - innervation Heart Rate Humans Methods Models, Biological Mortality parasympathetic nervous system Predictive Value of Tests Prognosis Recovery of Function Risk Factors sympathetic nervous system Time Factors |
| Title | Heart rate recovery: autonomic determinants, methods of assessment and association with mortality and cardiovascular diseases |
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