Time-frequency analysis of heart rate variability during immediate recovery from low and high intensity exercise

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1 Eur J Appl Physiol (2008) 102: DOI /s ORIGINAL ARTICLE Time-frequency analysis of heart rate variability during immediate recovery from low and high intensity exercise Kaisu Martinmäki Heikki Rusko Accepted: 3 October 2007 / Published online: 18 October 2007 Springer-Verlag 2007 Abstract Previous studies have neglected the Wrst recovery minutes after exercise when studying post-exercise heart rate variability (HRV). The present aim was to evaluate autonomic HR control immediately after exercise using Short-time Fourier transform (STFT) and to compare the evects of low [LI, 29(6)% of maximal power] and high [HI, 61(6)% of maximal power] intensity bicycle exercise on the HRV recovery dynamics. Minute-by-minute values for low (LFP ln, Hz) and high (HFP ln, Hz) frequency power were computed from R-R interval data recorded from 26 healthy subjects during 10 min recovery period after LI and HI. The HRV at the end of exercise and recovery was assessed with Fast Fourier transform as well. The results showed that LFP ln and HFP ln during the recovery period were avected by exercise intensity, recovery time and their interaction (P < 0.001). HFP ln increased during the Wrst recovery minute after LI and through the second recovery minute after HI (P <0.001). HFP ln was higher for LI than HI at the end of the recovery period [6.35 (1.11) vs (1.01) ln (ms 2 ), P < 0.001]. LFP ln showed parallel results with HFP ln during the recovery period. In conclusion, the present results obtained by the STFT method, suggested that fast vagal reactivation occurs after the end of K. Martinmäki H. Rusko KIHU, Research Institute for Olympic Sports, Jyväskylä, Finland K. Martinmäki H. Rusko Department of Biology of Physical Activity, University of Jyväskylä, P.O. Box 35 (LL), Jyväskylä, Finland K. Martinmäki (&) Rautpohjankatu 8, Jyväskylä, Finland kaisu.martinmaki@sport.jyu.w exercise and restoration of autonomic HR control is slower after exercise with greater metabolic demand. Keywords Autonomic nervous system Short-time Fourier transform Heart rate variability Introduction During exercise and recovery, autonomic nervous system regulates cardiovascular function to satisfy the metabolic demands of working muscles (Rowell 1986). An increase in heart rate (HR) results from vagal withdrawal at low exercise intensities and from both vagal withdrawal and sympathetic excitation at moderate and high intensities (Orizio et al. 1998; Robinson et al. 1966). With a transition from dynamic exercise to inactive recovery, there is a loss of central command and activation of the arterial barorexex resulting in a decrease in HR toward its pre-exercise level (O Leary 1996). It is generally agreed that the vagal system plays a major role in reducing HR immediately after cessation of exercise and the further decrease in HR is mediated by both the vagal and sympathetic system (Imai et al. 1994; Perini et al. 1989). However, evects of preceding exercise intensity on time-course of these changes during immediate recovery have remained unclear. The above studies have evaluated autonomic cardiac control during recovery by selective autonomic blockades, measurements of plasma catecholamines and computing mathematical descriptions of HR kinetics (Imai et al. 1994; Perini et al. 1989; Pierpont et al. 2000, 2004; Savin et al. 1982). Although selective autonomic blockades provide the most direct measure of vagal and sympathetic control, a pharmacological manipulation may interfere with normal autonomic control of the heart. In contrast, spectral analysis

2 354 Eur J Appl Physiol (2008) 102: of heart rate variability (HRV) provides non-invasive and practical, although partly incomplete, measure of autonomic cardiac control during recovery (Task Force 1996). Two diverent frequency components are usually examined: high frequency power (HFP, Hz at rest and Hz during exercise) rexecting vagal evects on heart and low frequency power (LFP, Hz) rexecting combined vagal and sympathetic evects on the heart (Akselrod et al. 1985; Martinmäki et al. 2006a). Studies using conventional spectral analysis of HRV [Fast Fourier transform (FFT) or autoregressive modeling] have shown that LFP and HFP expressed in absolute values (i.e. in ms 2 ) decrease with exercise (Arai et al. 1989; Casadei et al. 1995; Pichon et al. 2004) whereas results for LFP and HFP normalized with total power have been inconsistent (Bernardi et al. 1990; Casadei et al. 1995; Perini et al. 1990; Warren et al. 1997). During recovery, results for absolute and normalized LFP and HFP power have been highly variable but, in general, reduced HRV returns gradually reaching pre-exercise level within several minutes or hours depending on the exercise intensity (Bernardi et al. 1990; Perini et al. 1990; Terziotti et al. 2001). Only few studies have reported HRV after constant-load exercise with two or more submaximal intensities (Kaikkonen et al. 2007a; Perini et al. 1990; Terziotti et al. 2001). Conventional spectral analysis can only be applied to settings of a steady-state HR (Task Force 1996) and therefore most of the previous studies have excluded the immediate recovery after exercise. It is postulated that the rapid decrease in HR after cessation of exercise is an important mechanism for avoiding excessive cardiac work after exercise (Imai et al. 1994) and the immediate HR recovery has prognostic signiwcance (Cole et al. 2000; Nishime et al. 2000). Since the autonomic nervous system, especially vagal system, is responsible for the fast HR decrease after exercise, it is important to study HRV also during the immediate recovery period, not only later in recovery. Recently developed time-frequency analysis method, Short-time Fourier transform (STFT), provides instantaneous and continuous assessment of HRV during stationary as well as transition phases of the R-R interval (RRI) signal (Mainardi et al. 2002; Martinmäki et al. 2006b). The STFT method has been previously applied to examine HRV during various physiological conditions, including exercise (Cottin et al. 2006; Pichon et al. 2004) and recovery (Kaikkonen et al. 2007a, b). The primary aim of this study was to evaluate autonomic HR control immediately after the cessation of dynamic constant load exercise by using the STFT derived HRV indices. The secondary aim was to compare the evects of low and high exercise intensity on immediate postexercise HRV dynamics. Methods Subjects Thirty-two healthy subjects participated in the study. The data of six subjects were excluded from results because two subjects did not complete all exercise conditions and four wanted to discontinue respiratory gas collection immediately after the cessation of exercise. The characteristics of the remaining 26 subjects (13 men and 13 women) are presented in Table 1. All subjects were non-smokers and free of known cardiac, respiratory or other diseases. All subjects above 40 years of age went through a standard medical examination with a resting electrocardiogram. The subjects gave a written informed consent to participate. They had the right to withdraw from the study at any time. The study was approved by the Ethics Committee of the Central Hospital of Central Finland. Study protocol The tests were carried out in a quiet laboratory room (22 C). The subjects were asked to refrain from physical exertion starting 2 days before each test day. They were also asked to refrain from consumption of alcohol and caveinated beverages during the test days. The subjects performed a standardized incremental maximal exercise test and two constant-load exercise sessions: a low intensity exercise [LI, 29(6)% of maximal power] and a high intensity exercise [HI, 61(6)% of maximal power]. The constant-load exercise sessions were carried out on two diverent testing days, separated by at least 2 days, at the same time of day. LI session was always carried out on the Wrst testing day and HI session on the second testing day. LI and HI sessions consisted of a 5 min sitting baseline, a 10 min exercise at constant load and a 10 min recovery in a sitting posture. Exercise was performed in the upright-seated position on a cycle ergometer (ERGOLINE, Bitz, Germany), with a pedaling frequency of 60 rev min 1 and an individually standardised seat and handlebar heights. Table 1 Anthropometric and physiological characteristics of subjects (n =26) Parameter Value Age (years) 37 9 Height (cm) Weight (kg) VO 2max (ml min 1 kg 1 ) P max (W) HR max (bpm) BLa max (mmol L 1 ) VO 2max, maximal oxygen uptake; P max, maximal power; HR max, maximal heart rate; BLa max, maximal blood lactate concentration Values are mean SD

3 Eur J Appl Physiol (2008) 102: RRIs were continuously recorded throughout the experiments with a POLAR RR-Recorder (Polar Electro Ltd, Kempele, Finland), with a sampling frequency of 1,000 Hz from the ECG signal, providing an accuracy of 1 ms for each RRI. Fractional gas concentrations of expired O 2 and CO 2, respiratory frequency (RF), and tidal volume (Vt) were continuously recorded breath-by-breath (V max 229, Sensormedics, California, Palo Alto, USA). Before each measurement, the gas analyzer was calibrated using ambient air (20.9% O 2 and 0.04% CO 2 ) and calibration gas (15.87 and 4.17%). The calibration of the Xow meter of the analyzer was performed with a 3-L syringe. Fingertip venous blood samples for dewning blood lactate concentration (BLa) (Eppendorf EBIO 6666, Eppendorf, Hamburg, Germany) were taken after the 5 min sitting baseline, at the end of the 10 min exercise and at the recovery minutes 2, 5 and 10. Measurements of aerobic capacity Maximal aerobic capacity for each subject was assessed by a standardized incremental cycle ergometer test where the load was increased by 20 W every second minute, starting from 50 W up to voluntary maximum. RRIs, expiratory gas and BLa were collected using techniques mentioned above. A plateau of oxygen consumption (VO 2 ), respiratory exchange ratio exceeding 1.10, and HR and BLa approximating the age-predicted maximum were employed as criteria for the attainment of maximal power and VO 2max (Taylor et al. 1955). All subjects met at least two of these criteria. The highest moving 30s average during the last exercise minute was considered as VO 2max. All subjects above 40 years of age performed the maximal exercise test under the control of a medical doctor. Raw RRI series processing Signal processing and HRV computations were performed using the MATLAB 7 program (The MathWorks, Inc., 2004). The RRI series were checked and edited for artifacts using a detecting algorithm and subsequently veriwed by visual inspection. All analyses were performed from a signal, free from ectopic beats and technical artifacts. The original RRI series were resampled at a rate of 5 Hz using linear interpolation to obtain equidistantly sampled time series. A polynomial Wlter was used to remove low frequency trends from the RRI time series. The data were further Wltered and detrended by a digital FIR band-pass Wlter to remove variances below 0.04 Hz and above 1.0 Hz. Fast Fourier transform (FFT) The FFT method with Hanning window was used to obtain power spectrum estimates of HRV during the stationary phases of the experiment in order to enable comparisons between the results of this and previous studies (Task Force 1996). Stationary 3 min periods at the end of the sitting baseline (BL) and exercise (EXE 7 10 ) were extracted for HRV calculations. HRV was also calculated for a data period between the recovery minutes 7 and 10 (REC 7 10 ), when HR and respiratory parameters had already settled down. Low frequency ( Hz) and high frequency ( Hz) were calculated as integrals under the respective power spectral density curve. The higher frequency limit of 1.0 Hz was chosen to include the respiratory frequency during exercise. Spectral powers were expressed in natural log transformed values 1 [LFP ln and HFP ln, in ln(ms 2 )] and normalized units, i.e. relative to the sum of LFP and HFP (LFP nu and HFP nu, in n.u.). LFP nu and HFP nu have been suggested to rexect sympathetic and vagal out- Xow, respectively (Pagani 1986). We calculated the normalized spectral powers with the knowledge of the criticism against their use as autonomic indices (see e.g. Eckberg 2000). Short-time Fourier transform (STFT) The STFT method, an extension of the FFT, was used to study the time-evolution of dynamic changes in HRV (Oppenheim and Schafer 1999). BrieXy, the method provides a time-frequency decomposition of the RRI time series by calculating consecutive power spectra of short sections of the signal. A section of 512 samples was multiplied by the Hanning window function and the fast Fourier transform of their product was taken. The window was then shifted one sample ahead and the same calculations were performed again. This process was repeated until the whole RRI time series, including the exercise and recovery, was covered. Integrals of the power spectral density curve within the following frequency boundaries were calculated as a function of time: low frequency power (LFP, Hz) and high frequency power (HFP, Hz). For statistical analysis spectral powers were averaged for each successive 60 s period during recovery and expressed in natural log transformed values [LFP ln and HFP ln, in ln(ms 2 )]. In addition, we computed 1 min average values for the instantaneous frequency of peak power on high frequency band (HFP if, in Hz). Statistical analysis All values are expressed as means (SD). A paired twotailed t-test or Wilcoxon signed rank test was used to compare evects of exercise intensity on dependent vari- 1 Constant 1 was added to the absolute power value (x) and a natural log transformation of their sum was then calculated, y = ln (1 + x).

4 356 Eur J Appl Physiol (2008) 102: ables measured during BL, EXE 7 10 or REC Two (Exercise Intensity) 11 (Recovery Time) repeated measures ANOVA was used to compare the evects of exercise intensity on the minute-by-minute recovery dynamics of dependent variables. DiVerences between the successive recovery minutes were determined separately for LI and HI by ANOVA for repeated measures with a repeated contrast. DiVerences between means were considered signiwcant when P < The association between the within-subject dynamics of HFP if and RF was evaluated by calculating the mean error (ME) and mean error as a percentage of the true value (ME%) from minute-by-minute data during recovery, separately for each individual. Results HR and HRV during the stationary phases Figure 1 shows HR and conventional HRV indices derived from the FFT method during the stationary phases of the experiment (i.e. BL, EXE 7 10 and REC 7 10 ). Baseline values did not diver signiwcantly between LI and HI. HR was lower for LI than HI during EXE 7 10 as well as during REC 7 10 (P < 0.001). The recovery period after LI induced a signiwcant decrease in HR from 107 (10) bpm during EXE 7 10 to 72 (10) bpm during REC 7 10 restoring the pre-exercise baseline value. After HI, HR decreased signiwcantly from 145 (11) bpm during EXE 7 10 to 84 (10) bpm during REC 7 10 remaining higher than the baseline value. The HRV components expressed in log-transformed values (i.e. LFP ln and HFP ln ) were higher for LI than HI during EXE 7 10 (P < 0.001) and REC 7 10 (P < ). LFP ln increased signiwcantly from 4.96 (0.99) ln(ms 2 ) during EXE 7 10 to 6.91 (1.13) ln(ms 2 ) during REC 7 10 after LI and from (0.70) ln(ms 2 ) during EXE 7 10 to 6.34 (1.03) ln(ms 2 ) during REC 7 10 after HI. HFP ln increased signiwcantly from 4.12 (1.19) ln(ms 2 ) during EXE 7 10 to 6.35 (1.11) ln(ms 2 ) during REC 7 10 after LI and from 1.98 (0.60) ln(ms 2 ) during EXE 7 10 to 5.12 (1.01) ln(ms 2 ) during REC 7 10 after HI. Neither after LI nor HI LFP ln and HFP ln returned to the pre-exercise values. Figure 1 also shows the normalized HRV values during the stationary phases of the experiment. LI did not induce any signiwcant changes in LFP nu or HFP nu. HI induced a lower LFP nu and correspondingly a higher HFP nu during EXE 7 10 when compared to LI (P < 0.001). After HI, LFP nu increased signiwcantly from 0.42 (0.22) during EXE 7 10 to 0.74 (0.17) during REC 7 10 and HFP nu decreased from 0.58 (0.22) during EXE 7 10 to 0.26 (0.17) during REC 7 10.

5 Eur J Appl Physiol (2008) 102: Fig. 1 Heart rate and the FFT derived heart rate variability indices during the stationary phases of the experiment, i.e. the sitting baseline (BL), during the exercise (EXE 7 10 ) and recovery (REC 7 10 ) minutes seven to ten. LI low intensity exercise, HI high intensity exercise, HR heart rate, LFP low frequency power, HFP high frequency power. Statistically signiwcant diverence compared to BL at **P < 0.01 and ***P < 0.001, compared to EXE P < 0.01 and 999P < HR and HRV recovery dynamics Figure 2 demonstrates an example of changes in RRI and HRV during LI and HI exercise session. The data of this subject clearly demonstrated that HRV were depressed during exercise and after the cessation of exercise, HRV increased rapidly during the Wrst recovery minutes. After HI, restoration of HRV was slower and less complete than after LI. HR dynamics during the recovery period is shown in the top panel of Fig. 3. Main evect for Exercise Intensity, Recovery Time and their interaction were all signiwcant (P < 0.001). The minute-by-minute HR values decreased signiwcantly during the Wrst two recovery minutes after LI and through the seventh recovery minute after HI and stabilized thereafter. Figure 3 also shows the recovery dynamics of HFP ln and LFP ln for all subjects. Main evect for Exercise Intensity, Recovery Time and their interaction were all signiwcant for both HFP ln and LFP ln (P < 0.001). A signiwcant increase in the successive LFP ln values was observed only for the Wrst recovery minute after LI and for the Wrst three recovery minutes after HI. After LI, HFP ln increased signiwcantly during the Wrst recovery minute, decreased slightly after the second and third recovery minutes and stabilized thereafter. After HI, a signiwcant increase in HFP ln was observed during the Wrst two recovery minutes. When HRV indices derived from the STFT method during the last recovery minute were compared to those derived from the FFT method during the REC 7 10, no signiwcant diverences were found. Respiratory parameters The data of one subject were excluded from all respiratory analysis because of the problems with the respiratory gas analyzer. None of the baseline respiratory parameters divered between LI and HI. All respiratory parameters during EXE 7 10 were lower for LI than HI [VO 2, (3.47) ml min 1 kg 1 vs (6.37) ml min 1 kg 1 ; RF, 0.34 (0.05) Hz vs (0.08) Hz; Vt, 1.41 (0.37) L vs (0.42) L, P < 0.001]. The minute-by-minute recovery dynamics of all respiratory parameters were signiwcantly avected by the exercise intensity, recovery time as well as by their interaction (P < 0.001). After LI, RF and VO 2 decreased through recovery minute four (P < ) and Vt through recovery minute Wve (P < 0.001). After HI, RF and VO 2 decreased through recovery minute seven (P < ) and Vt through recovery minute six (P < 0.001). All respiratory parameters reached the preexercise baseline values during the 10 min recovery period, except RF after HI. Fig. 2 The time-dependent spectrum from the STFT method, RR interval (RRI) and high frequency power (HFP) and low frequency power (LFP) during the sitting baseline (from 0 to 5 min), exercise (from 5 to 15 min) and recovery (from 15 to 25 min). An example from one subject during the low intensity (LI, on the left) and high intensity (HI, on the right) exercise session. PSD Power spectral density

6 358 Eur J Appl Physiol (2008) 102: from which BLa decreased to 2.73 (1.06) mmol L 1 during the 10 min recovery period (P < 0.001), remaining still above the pre-exercise baseline value (P < 0.001). BLa at the end of the exercise and at the end of the recovery period were lower for LI than HI (P < 0.001). Discussion Fig. 3 Heart rate and the STFT derived heart rate variability indices during the last exercise minute (EXE) and recovery. LI low intensity exercise, HI high intensity exercise, LFP low frequency power, HFP high frequency power. Statistically signiwcant diverence between successive recovery minutes, separately for LI and HI, at *P < 0.05, **P < 0.01 and ***P < A reference line represents the pre-exercise value Within-subjects, the HFP if derived from the STFT method followed measured RF during the recovery period. At the group level, ME between HFP if and RF calculated for minute-by-minute values during recovery was 0.03(0.04) Hz for LI and 0.03(0.03) Hz for HI, with corresponding ME% of 7(15)% for LI and 10(10)% for HI. Blood lactate concentration The baseline BLa did not diver signiwcantly between LI and HI. During LI session, BLa did not exceed the preexercise baseline either at the end of the exercise or during the recovery period. During HI session, BLa increased to 4.64 (1.41) mmol L 1 at the end of the exercise (P < 0.001) We presented the STFT derived HRV dynamics during the 10 min recovery period after two Wxed exercise intensities, approximately 30 and 60% of maximal power. The rationale for choosing the present intensities was that we wanted to induce two clearly diverent combinations of vagal withdrawal and sympathetic activation. According to the literature, at the lower intensity level cardiac adjustments to exercise were mainly due to parasympathetic withdrawal. At the higher intensity level, parasympathetic outxow was negligible and sympathetic activation was substantially increased, but blood lactate still does not cumulate (Rowell 1986). Our main Wnding was a rapid increase in HFP ln, along with the decrease in HR, during the Wrst recovery minute after LI and through the second recovery minute after HI. This Wnding suggests a rapid vagal reactivation immediately after the exercise conwrming previous data on HR recovery obtained with diverent approaches. Studies based on HR kinetics have suggested that during the Wrst recovery minute, the vagal system plays a major role in reducing HR, independent of exercise intensity (Imai et al. 1994; Perini et al. 1989). This suggestion is also supported by studies using robust HRV based measures of vagal activity (Goldberger 2006; HatWeld 1998). HatWeld et al. (1998) found an increase in RSA (vagal index based on respiratory sinus arrhythmia) over the Wrst 2 min after cessation of maximal dynamic exercise, but not from minute two to three. Goldberger et al. (2006) computed MSSD (the root mean square of successive diverence of the R R intervals) and a novel index, dewned RMS (the root mean square residual), for consecutive short-scale segments (i.e s) after maximal exercise. MSSD and RMS increased rapidly after exercise and correlated positively with the parasympathetic evect dewned by blockade. In the present study, LFP ln showed parallel increases with HFP ln during the immediate recovery. LFP ln increased during the Wrst recovery minute after LI, as did also the HFP ln. After HI, LFP ln increased through the third recovery minute, 1 min longer than HFP ln. The interpretation of LFP ln is more complicated than HFP ln due the sympathovagal origin of low frequency oscillations (Akselrod et al. 1985). Considering that the vagal activity avects the entire frequency range of HRV, the observed LFP ln increases are mainly explained by vagal reactivation. Additional explanation

7 Eur J Appl Physiol (2008) 102: for the LFP ln increase after exercise may arise from changes in barorexex sensitivity, which is greatly inhibited during high-intensity exercise and partially restored with the cessation of exercise (Casadei et al. 1995). In previous studies on HR kinetics after submaximal exercise, HR has decreased exponentially toward pre-exercise values. It has been suggested that the HR decrease is mediated by both the vagal and sympathetic system, the relative role of the two systems depending on exercise intensity (Imai et al. 1994; Perini et al. 1989). We observed that despite stabilization of HRV, HR kept decreasing through the second recovery minute after LI and through the seventh recovery minute after HI. A likely explanation for the continued HR recovery after HI is a slow gradual decrease in sympathetic activity. In light of the previous evidence, plasma noradrenaline concentration remains constant or peaks during the Wrst minute after exercise, and then gradually decreases to pre-exercise level, with the kinetics of circulating noradrenaline being determined by preceding exercise intensity (Perini et al. 1989). We did not measure the sympathetic activity but the present lactate data during and after exercise conwrmed that HI induced an activation of the sympathetic nervous system. The STFT method has not been used in recovery studies until recently (Kaikkonen et al. 2007a) and therefore we also assessed HRV by the FFT method during the stationary phases of the experiment. We observed that the STFT and FFT methods provided uniform information about the evects of exercise intensity on autonomic HR control at the end of the recovery when RRI signal was stationary. Our data suggested more complete recovery of vagal activity after LI than HI as illustrated by greater LFP ln and HFP ln during recovery for LI than HI. In agreement with the present data, Kaikkonen et al. (2007a) reported that the increased intensity of the exercise resulted in slower recovery of HFP ln as well as lower levels of HFP ln when compared to low intensity exercise. They studied a 5 min recovery period after exercise at 50, 63 and 74% of the velocity of maximal oxygen uptake. Also results by Terziotti et al. (2001) showed higher absolute HFP at 15 min after exercise at 50% of the anaerobic threshold when compared to exercise intensity. We further found that at the end of recovery period after LI, LFP nu and HFP nu were similar with respect to pre-exercise baseline and after HI, LFP nu was higher and concomitantly HFP nu lower with respect to the baseline. This Wnding agrees with previous the data by Perini et al. (1990), obtained after exercise at 21, 49 and 70% maximal oxygen uptake. They found no diverence in the relative power components in comparison to rest, during or after low intensity exercise. After medium and high intensity exercise, they found a tendency for LFP percent to be higher and HFP per cent to be lower with respect to pre-exercise and concluded these Wndings resulting from the slow recovery of sympathetic activity to resting values. While the present results clearly conwrmed that HRV rexected the changes in autonomic HR control during recovery,the picture during exercise was not clear. In agreement with previous studies (Arai et al. 1989; Casadei et al. 1995; Cottin et al. 2004), we observed higher LFP ln and HFP ln during exercise for LI than HI. At the present exercise intensities, decreases in LFP ln and HFP ln most probably rexected the reduction of vagal activity in response to the increase in metabolic demand. We further observed higher LFP nu and concomitantly lower HFP nu during exercise for LI than HI, despite lower sympathetic activity. The present Wndings support the previous data suggesting that LFP nu and HFP nu do not indicate sympathetic and vagal outxow during exercise (Casadei et al. 1995; Cottin et al. 2004; Perini et al. 2000). Consequently, when interpreting the normalized HRV values, it would be recommendable to compare recovery values to values at rest instead of values during exercise. Limitations We did not control respiration because it could have disturbed the real autonomic modulation during the recovery. It is well evidenced that increased respiratory activity may avect high frequency component during exercise, especially at intensity levels above ventilatory threshold (Bernardi et al.1990; Cottin et al. 2006). The present study focusing on HRV recovery demonstrated that HFP ln and RF recovery dynamics divered clearly from each other despite the fact that HFP if followed the changes in RF during the recovery period. The lack of beat-to-beat measurements of blood pressure could be seen as a limitation of the present study since the time frequency analysis of blood pressure variability would have added information of sympathetic control. The present subjects were older than the subjects who participated in most of the HRV studies. However, HRV data obtained on elderly males and females (mean age 74 years) at rest and during exercise have been consistent with data of younger subjects (Perini et al. 2000). Conclusions We demonstrated HRV dynamics immediately after cessation of LI and HI using the STFT method and found a major inxuence of exercise intensity. LFP ln and HFP ln increased rapidly during the Wrst recovery minute after LI and through several recovery minutes after HI. In addition, LFP ln and HFP ln were higher after LI than HI throughout the recovery period. These results suggest that fast vagal reactivation occurs after the end of exercise and that restoration of autonomic HR control is slower after exercise

8 360 Eur J Appl Physiol (2008) 102: with greater metabolic demand. On the basis of the present results, the novel HRV analysis method provides a tool for monitoring autonomic HR control immediately after exercise when HR changes rapidly restraining the use of the conventional spectral methods. Acknowledgments This study was funded by grants from the Ministry of Education, Finland, and from TEKES-National Technology Agency of Finland. The authors thank Ph.D. Sami Saalasti for his help in performing the heart rate variability analyses. This study was partly funded by a grant from Sunto Ltd, Finland and Firstbeat Technologies Ltd, Finland. Heikki Rusko is currently stockowner of Firstbeat Technologies Ltd, Finland. References Akselrod S, Gordon D, Madwed JB, Snidman NC, Shannon DC, Cohen RJ (1985) Hemodynamic regulation: investigation by spectral analysis. 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