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REVIEW ARTICLE
Year : 2017  |  Volume : 17  |  Issue : 3  |  Page : 129-134

High-intensity interval training and cardiac autonomic modulation


Centre for Physiotherapy and Rehabilitation Sciences, Jamia Millia Islamia, New Delhi, India

Date of Web Publication4-Oct-2017

Correspondence Address:
Jamal Ali Moiz
Centre for Physiotherapy and Rehabilitation Sciences, Jamia Millia Islamia, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/sjsm.sjsm_2_17

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  Abstract 

Cardiac autonomic dysfunction is associated with various pathological conditions and is characterized by hyperactive sympathetic nervous system. Autonomic imbalance may lead to increased morbidity and mortality from various diseases and conditions, including cardiovascular disease. Exercise training is a cornerstone intervention for impaired autonomic function. However, the form of exercise which elicits maximum benefits in a time-efficient manner is a contentious issue. High-intensity interval training (HIIT) includes high-intensity bouts interspersed with low-intensity recovery. This is more acceptable form of exercise since the overload placed by high intensity bout leads to optimal adaptations and recovery provided by intermittent nature makes it more tolerable. This review article explains the effect of HIIT on cardiac autonomic function and the possible mechanisms underlying its positive effect.

Keywords: Heart rate variability, interval training, parasympathetic nervous system, sympathetic nervous system


How to cite this article:
Bhati P, Moiz JA. High-intensity interval training and cardiac autonomic modulation. Saudi J Sports Med 2017;17:129-34

How to cite this URL:
Bhati P, Moiz JA. High-intensity interval training and cardiac autonomic modulation. Saudi J Sports Med [serial online] 2017 [cited 2023 Sep 29];17:129-34. Available from: https://www.sjosm.org/text.asp?2017/17/3/129/215917




  Introduction Top


High-intensity interval training (HIIT) is a type of exercise training characterized by brief, intermittent bursts of vigorous activity, interspersed with periods of low intensity activity. It is considered as an effective alternate to conventional endurance training, because, it causes similar physiological changes in healthy as well as diseased individuals, in spite of considerable less time commitment and reduced exercise volume.[1] Moreover, recent evidence suggests that HIIT is perceived to be more enjoyable than moderate intensity continuous exercise.[2] These findings are important from the perspective of public health, considering that “lack of time” remains one of the most commonly cited barriers to regular exercise participation.[3],[4]

Cardiac autonomic function is the control of heart by sympathetic and parasympathetic branches of autonomic nervous system (ANS). Heart rate variability (HRV) is a noninvasive, practical and reproducible measure of ANS function. HRV is believed to correspond to the balance between the sympathetic and parasympathetic influences on the sinoatrial (SA) node's intrinsic rhythm.[5] The ability of the ANS and SA node to respond dynamically to environmental changes results in increased HRV and generally indicates a healthy heart. Reduction in HRV indicates decreased ability of SA node's responsiveness to change and indicates an unhealthy heart.[6]

Exercise can improve cardiac autonomic function and hence HRV. Many studies have shown that endurance training enhances HRV through vagal modulation. However, the monotonous and time-consuming nature of traditional endurance training is found to be associated with lower rates of compliance. Moreover, intermittent recovery bouts in HIIT make this form of exercise more tolerable and interesting.[1],[2] This review article explains the literature on the effect of HIIT on cardiac autonomic function through HRV as an assessment tool in normal healthy and clinical population.


  High-Intensity Interval Training Top


HIIT in a variety of forms is today one of the most effective means of improving cardio-respiratory and metabolic function. HIIT involves repeated short-to-long bouts of high-intensity exercise interspersed with recovery periods.[7] It can serve as an effective alternate to traditional endurance training because it induces similar physiological adaptation and requires lower time commitment.[1] Several studies have indicated that intermittent HIIT may increase fat oxidation when compared with continuous training.[8] Possible mechanisms underlying the HIIT-induced fat loss effect include increased exercise and post-exercise fat oxidation and decreased post exercise appetite.[9] A study [10] demonstrated that interval exercise induced more use of lipids and glycogen as compared to continuous exercise in untrained individuals. HIIT have a significantly greater impact on ANS.[11] and it is more effective for enhancing cardiac vagal control than a low-intensity exercise program.[12] Evidence suggests that exercise training which involves high intensity is more effective in improving aerobic capacity than exercise training of moderate intensities in healthy population.[13],[14],[15]


  What Is Cardiac Autonomic Function? Top


The impulse that causes the heart to contract rhythmically originates within the heart muscles, in the SA node located in the right atrium. Although the heart muscles possess auto rhythmicity, the nerve supply to the heart also plays an important role in regulating the activity of the heart. In fact, both nervous and chemical factors are involved in the regulation of heart during rest and exercise.[16] ANS exerts a fine degree of control over the cardiovascular system.[17] ANS which supplies the parasympathetic or vagus nerve and the sympathetic or accelerator nerves to the SA node plays a prime role in regulating the heart rate (HR).[16]

Parasympathetic and sympathetic influences on heart

Stimulation of the parasympathetic nervous system (PNS) produces bradycardia and the region of the medulla where the PNS originates is called cardioinhibitory center. Bradycardia is induced by the release of the acetylcholine from the vagal nerve ends. Parasympathetic activity provides a regulatory balance in physiological autonomic function. Through its origination from cardio-accelaratory center in brainstem, sympathetic stimulation leads to increased HR by increase in firing rate of pacemaker cells in the heart.[18] This mechanism of the tachycardia is mediated by nor-epinephrine released from the sympathetic nerve ends.[19]


  Heart Rate Variability Top


It is a noninvasive, practical, and reproducible measure of ANS function. It expresses the total amount of variation of both instantaneous HR and NN interval.[20] It is used to evaluate the sympathovagal balance at the level of SA node.[21]

Analysis of HRV includes a series of measurements of successive NN (R-R) interval variations of sinus origin which provide information about autonomic tone [22] [Figure 1]. In 1996, a task force of the European Society of Cardiology and the North American Society of Electrophysiology and Pacing defined and established standards of measurement, physiological interpretation, and clinical use of HRV. Linear and nonlinear methods are applied for HRV analysis. Time domain and frequency domain indices constitute the standard clinically used parameters under linear HRV analysis.[23]
Figure 1: Electrocardiography record showing R‑R intervals (marked by dots)

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  Linear Heart Rate Variability Analysis Top


Time domain analysis

It measures the changes in HR over time or the intervals between successive normal cycles. From the electrocardiography (ECG) recording, each QRS complex is detected and the normal NN intervals are determined. The N-N interval is defined as the time between two adjacent QRS complexes and is a result of sinus depolarization.[20]

The calculated time domain variables include the mean NN and root mean square of successive difference of NN intervals (RMSSD).[23] Mean NN is the mean of the difference between adjacent NN interval. It reflects both vagal and sympathetic modulation and is measured in milliseconds (ms). RMSSD is the square root of the mean of sum of squares of differences between adjacent NN interval. It reflects alterations in autonomic tone that are predominantly vagally mediated and is measured in ms.[21] Indices such as standard deviation of the RR intervals (SDNN) which reflects overall HRV and the standard deviation of the 5 min mean RR intervals (SDANN) which reflects sympathetic activity are derived from direct measurements of RR intervals. The percentage of interval differences of adjacent RR intervals greater 50 ms (pNN50) are derived from difference between consecutive RR intervals which indicates vagal activity [23] [Figure 2] and [Table 1].
Figure 2: Heart rate variability report generated from electrocardiography record showing various time (standard deviation of the RR intervals, root mean square successive difference of NN intervals, pNN50) and frequency domain indices (total power, low frequency power, high frequency power, low frequency/high frequency ratio) of heart rate variability

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Table 1: Normative values of heart rate variability indices (Mean±SD) for adult healthy population

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Frequency domain analysis

It describes the periodic oscillations of the HR signal decomposed at different frequencies and amplitudes, and provides information on the amount of their relative intensity termed as variance or power in the heart's sinus rhythm.[24] Power spectral analysis is performed by the fast fourier transformation (FFT) method, which is characterized by discrete peaks for the several frequency components.[16]

When using the FFT the individual NN intervals stored in the computer are transformed into bands with different spectral frequencies. The result obtained can be transformed in Hertz (Hz) by dividing by the mean NN interval length. The power spectrum consists of frequency bands ranging from 0 to 0.5 Hz and can be classified into four bands: The ultra-low frequency band (ULF), the very low frequency band (VLF), the low frequency band (LF), and high frequency band (HF). Short-term spectral recordings of 5–10 min are characterized by the VLF, HF and LF components, whereas long-term recordings include a ULF component in addition to the three others. The most frequently used frequency domain parameters include LF, HF, LF/HF ratio. LF is the power in the LF range (0.04–0.15 Hz) and reflects a combination of sympathetic and parasympathetic input.[21] HF is the power in HF range (0.15–0.40 Hz) and reflects vagal function. The LF/HF ratio is the ratio of LF to HF and it reflects the global sympathovagal balance. In a normal adult in resting conditions, the ratio is generally between 1 and 2. Smaller ratios may represent parasympathetic dominance and larger ratios may represent sympathetic dominance [21] [Figure 2] and [Table 1].


  Nonlinear Heart Rate Variability Analysis Top


Nonlinear measuring methods try to quantify the structure and complexity of RR interval time series. The HRV signals are nonstationary and nonlinear in nature.[25] Nonlinear analysis is based on the observations suggesting that the mechanisms involved in cardiovascular regulation likely interact with each other in a nonlinear manner. The most important indexes which describes nonlinear HR dynamics are short-term fractal scaling exponent measured by detrended fluctuation analysis (DFA), the approximate entropy, which describes the complexity of R-R interval behavior and Poincare plots.[26] The DFA [27] is a technique for detecting correlations in time series. The scaling exponents characterize short or long-term fluctuations. The Poincare plot analysis is a graphical nonlinear method to assess the dynamics of HRV. This method provides summary information as well as detailed beat-to-beat information on the behavior of the heart. The Poincare plot parameters usually used are SD1, SD2, and SD1/SD2 ratio. SD1 is the standard deviation of projection of the Poincare plot on the line perpendicular to the line of identity. While the SD2 is defined as the standard deviation of the projection of the Poincare plot on the line of identity (y = x). The parameter SD1 has been correlated with HF power, whereas SD2 has been correlated with both low and HF powers. The ratio SD1/SD2 is associated with the randomness of the HRV signal. Thus, this ratio is a measure of the randomness in HRV time series. It has been suggested that the ratio SD1/SD2 has the strongest association with mortality in adults.[28]


  Clinical Importance of Heart Rate Variability Top


Reduced HRV may enclose indicators of current disease, or warnings about impending cardiac diseases. HRV indices have been proved to be critical in diagnosing and treating not just cardiovascular system diseases, but unrelated pathologies such as epilepsy, chronic migraines, and obstructive sleep apnea. All biological systems, even the healthy ones may show haphazard dynamics while systems suffering from disease show reduced levels of dynamics. Since all organs are dependent on the flow of blood from the heart, any cardiovascular abnormalities will affect all other organs and will affect the HR activity. Autonomic dysfunction is a key characteristic of heart and diseases.[22] Other conditions that show high HRV indices include congestive heart block, left branch bundle block, sick sinus syndrome and premature ventricular contraction, type 2 diabetes mellitus, fibromyalgia. Research findings suggest that decreased HRV is a prognostic indicator in individuals with a variety of clinical conditions. Research findings also suggest that depressed vagal cardiac modulation may contribute to adverse outcomes. HRV analysis using ECG recording could be effective in automatically detecting these pathological conditions.[29],[30]


  Effect of Hiit on Cardiac Autonomic Function Top


In a study carried out by Bond et al.,[31] 2 weeks of HIIT in adolescents improved HRV and flow-mediated dilation but not traditional cardiovascular risk factors (triglycerides, cholesterol, glucose, insulin, and blood pressure) in fasting and postprandial states. In this study, each training session consisted of eight to ten 1-min repetitions of cycling at 90% peak power interspersed with 75 s of unloaded cycling. These favorable changes were lost after 3 days of training suggesting that regularly performing high-intensity exercise is needed to maintain these benefits. On the contrary, literature [32] has demonstrated that 7 weeks of HIIT was not sufficient enough to underline a positive effect on the HRV though it induced positive changes on aerobic fitness. These nonsignificant changes in HRV were explained by the accumulation of fatigue after high-intensity exercise. Kiviniemi et al.,[33] have proved recently that HIIT is superior to traditional endurance training for improving cardiac autonomic function and suggested that improvements in autonomic function post-HIIT are related to an increased vagal or baroreflex-mediated modulation of the SA node. Koufaki et al.[34] examined the effect of HIIT and continuous moderate intensity exercise training on HRV, aerobic capacity, functional capacity and health-related quality of life in chronic heart failure patients and concluded that none of the training interventions induced changes in cardiac autonomic functioning. The authors explained these findings by stating that many patients experienced various health challenges that resulted in many pauses in the exercise training. It is also possible that the overall volume of work was not sufficient to provoke changes to or override the medication effects on, these indices of cardiac autonomic regulation. Another study [35] which compared moderate and heavy metabolic interval training showed that enhanced vagal activity and preferable cardiac autonomic modulations are achieved by moderate interval exercise training. Improved baroreflex sensitivity and vagal control were found to be the mechanisms involved in improving cardiac autonomic modulation post-HIIT [36] [Table 2].
Table 2: Studies on the effect of HIIT on cardiac autonomic function

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There are various potential adaptations which explain HIIT-induced positive changes in the autonomic functioning of heart. One of the potential mechanism underlying HIIT induced cardiac vagal tone may be Angiotensin II. Angiotensin II inhibits cardiac vagal activity.[37] Sedentary or physically inactive individuals have higher plasma rennin activity than athletes.[38] Therefore, sedentary individuals have higher Angiotensin II. Exercise causes suppression of Angiotensin II which may, to some extent, mediate enhancement of cardiac vagal tone.[39] Research have also suggested that exercise-induced nitric oxide bioavailability mediate changes in cardiac vagal tone and inhibit sympathetic influences.[40] Furthermore, HIIT induced increased baroreflex sensitivity and reduction in arterial stiffness may also be considered adaptation enhances cardiac vagal tone.[36]


  Conclusion Top


Impaired cardiac autonomic function is a sign of disturbed heart function and is found to be associated with many pathological conditions. Physical activity in the form of exercise training is an important lifestyle intervention which improves autonomic function of the heart. HRV is an indirect noninvasive technique to measure cardiac autonomic function. Since lack of time is cited as a major barrier to exercise in normal healthy and clinical population, HIIT emerges as an intervention of choice which is a time-saving strategy to enhance vagal modulation. After reviewing the literature of HIIT and HRV, it may be suggested that HIIT is a safe intervention for young, old and diseased population since none of the studies in this review reported any adverse events. However, since, vigorous exercise has been associated with increased risk of acute cardiovascular and musculoskeletal events,[41] concern should be taken regarding the safety of implementing HIIT in any clinical population. HIIT-induced adaptations lead to enhanced cardiac autonomic control which can serve as, protection of the heart from cardiovascular illnesses in healthy subjects and can improve the prognosis and outcomes to exercise training in clinical population with impaired cardiac autonomic function.

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Conflicts of interest

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    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2]


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