Regular physical activity is believed to influence the autonomic nervous activity, reducing the sympathetic activity and increase the vagal tone (4,28,32). Flexibility training is an important element of fitness (1) and may also induce favorable changes in the autonomic balance (18,20). Cardiovascular responses to stretching are because of the activation of mechanoreceptors and to the static contraction of antagonist muscle groups, which activate the autonomic nervous system through sympathetic and parasympathetic pathways (10,26).
The analysis of heart rate variability (HRV) is acknowledged as a measure of autonomic regulation of the cardiac activity, especially the sympathetic-parasympathetic balance (32). It has been therefore used in many research and clinical sets, including the study of the autonomic control during physical activity (3,13,27). The HRV is a well-recognized tool for assessing the autonomic modulation of the heart during the recovery phase after exercise (13). The heart rate (HR) and HRV responses during the postexercise are known to be related to parasympathetic reactivation, particularly in the first minutes of recovery (12). Because a higher parasympathetic reactivation and faster HR recovery after exercise are commonly associated with lower risk for cardiovascular disease (11,14), information about the potential effect of different types of exercise on the postexercise HR and autonomic balance is useful to improve health oriented physical activity intervention.
Unfortunately, studies focusing on the HRV responses to flexibility training are scarce. We were able to find just one research showing that athletes with limited flexibility increased their HRV after a 28-day routine of 15-minute daily stretching (25). A few more studies investigated the HR and HRV acute responses to stretching, usually demonstrating that the HR increases, whereas the HRV decreases during the exercise performance (10). However, to the best of our knowledge, the effects of stretching sessions on the HRV during the postexercise recovery have not yet been investigated. It remains therefore unclear whether flexibility training contributes to a better autonomic balance profile.
Another limitation of the available research is that the experimental protocols have generally applied stretching exercises to a single muscle group, which is not usual in the actual training context. This is also true for the number of sets per exercise. Flexibility training is hardly single set designed. Such an issue is essential because the number of sets may influence the cardiovascular responses to exercises involving prolonged muscle contraction (29). It seems to be the case of the static training method, which consists of stretching a muscle group to its farthest point and then holding that position through static contractions for several seconds.
Furthermore, it is well accepted that 1 of the main limiting factors during stretching is muscular resistance secondary to reflex activity (21). It has been shown in such a context that the electromyographic activity while stretching can be significantly higher in subjects with low flexibility compared to those with high flexibility levels (22,33). That is, for a given joint angle, tight subjects probably display greater stiffness, and therefore, more tension will be applied to sustain the position. Because the cardiovascular responses to stretching are related to the intensity and duration of the static contraction, it is feasible to think that possible effects on the autonomic balance would be more likely to occur in subjects with low flexibility levels compared to those who are highly flexible. In a health promotion perspective, it would therefore be useful to investigate the HR and HRV responses to flexibility training sessions performed with multiple sets and different exercises, especially in untrained and tight subjects.
Because information on the effect of stretching on the HRV seems to be lacking, the purpose of this study was to examine the effect of a flexibility training session including 3 exercises for the trunk and hamstrings performed with 3 sets and using the static method, on the HR and HRV during and after the exercise in subjects with low flexibility levels. It has been hypothesized that the sympathetic modulation to the heart would increase acutely during the stretching exercises, whereas the parasympathetic modulation would increase in the postexercise period. Additionally the HR at the end of the recovery period was expected to be lower than at the pre-exercise resting condition.
Experimental Approach to the Problem
This study observed the HR response and HRV indexes after 3 sets of stretching exercises for the trunk and hamstrings in subjects with low flexibility levels. Subjects were asked not to practice physical exercise or drink coffee or tea for at least 12 hours before the experiment. Data assessment took place in the Spring, always in the morning in a temperature controlled room (23 ± 1°C, air humidity between 60 and 65%). Participants were instructed not to engage in any form of physical exercise in the previous 24 hours, to abstain from alcohol, soft drinks and caffeine in the 8 hours preceding the test and to fast for 2 hours. Before the stretching session, the weight, height, and hip-trunk flexibility (sit-and-reach test with a standard box in which the ‘zero’ point was set at 26 cm) were measured. The sit-and-reach was used only to confirm that the volunteers had indeed limited flexibility levels, as self-reported as inclusion criteria to participate in the study (see ‘Subjects’). After that, the participants laid quietly for 10 minutes before assessing the HRV at rest.
The stretching protocol was performed according the static method in the following exercises: (a) trunk flexion with the right knee extended and the left lower limb relaxed in semiflexion; (b) trunk flexion with the left knee extended and the right lower limb relaxed in semiflexion; (c) trunk flexion with the feet united, hips abducted, and knees flexed—‘butterfly position.’ The session consisted of 3 stretches for 30 seconds at the maximum range of motion with a 30-second rest between sets and 1-minute rest between exercises. Each training session lasted approximately 10 minutes, and the HR was recorded continuously.
All subjects performed the same exercises, and the HR was recorded during 30 minutes at rest in the supine position, along the whole stretching session and throughout 30-minutes postexercise recovery also in the supine position. To test whether stretching sessions produce acute effects on the autonomic heart control, the last 10 minutes of the pre-exercise, exercise, and postexercise periods were used as windows to determine and compare the HRV indexes in the time and frequency domains. The HR was also compared at the beginning (HRi) and at the end (HRf) of each observation window (1st and 10th minutes of the pre-exercise, exercise, and postexercise periods).
Ten healthy male volunteers enrolled in the study (age: 23 ± 2 years; weight: 82 ± 13 kg; height: 177 ± 5 cm). All subjects have been practicing strength training for at least 1 year, 2 hours a day, and 3-5 times a week. They declared to have ‘very limited flexibility’ and have not stretched regularly for at least 2 years. The sit-and-reach results confirmed that all subjects had indeed low flexibility (mean: 23 ± 4 cm, minimum: 19 cm, maximum: 28 cm), being classified within percentiles 10-40 according to the American College of Sports Medicine (1). The following additional exclusion criteria were adopted: (a) use of drugs that could affect the cardiovascular responses; (b) locomotor problems limiting the performance of the exercises. The experimental approach had institutional ethical board approval and appropriate consent has been obtained from all subjects before participation in the study.
Heart Rate Variability Assessment
The HR was continuously assessed by an R-R monitor (Polar S 810i, Polar Electro Oy™, Kempele, Finland) in 3 periods of 30 minutes: at rest (pre-exercise), during the stretching protocol (exercise), and during recovery (postexercise). The validity of the system used to assess HRV data was described elsewhere (9,36). Time series of RR intervals were used for time and frequency domain analysis using a customized routine written in MATLAB (Mathworks™, Natick, MA, USA). The overall variability of RR intervals was assessed in the time and frequency domains by means of time series variance and Fast Fourier Transformation, respectively. Spectral analysis was performed using the Welch periodogram, with a Hanning window and 50% overlap. The area under the curve of the spectral peaks within the range of 0.01-0.4 Hz was defined as the total power, the area underneath the spectral bands within the range of 0.04-0.15 Hz was defined as the low-frequency power (LF), and the area underneath the spectral band within the range of 0.15-0.40 Hz was defined as the high-frequency power (HF). The normalized high-frequency power (nHF) was used as marker of vagal modulation, the normalized low-frequency power (nLF) as marker of sympathetic and vagal modulation, and the low-/high-frequency power ratio (LF/HF) as marker of sympathovagal balance. The normalized frequency indexes obtained by the present protocol were highly reproducible. The test-retest reliability for LF and HF repeated after a 3-hour interval in a sample of 8 subjects aged 24 ± 4 years showed intraclass correlation coefficients (ICCs) that were considered adequate for the purposes of the study (ICC at rest: LF = 0.81, p < 0.001 and HF = 0.79, p < 0.001; ICC stretching: LF = 0.90, p = 0.01 and HF = 0.91, p = 0.02; ICC postexercise: LF = 0.77, p = 0.03 and HF = 0.79, p = 0.01).
In the time domain analysis, the following HRV markers were calculated: (a) root mean of the squared sum of successive differences (RMSSD); (b) SD of normal NN intervals (SDNN); (c) number of pairs of adjacent RR intervals differing by >50 milliseconds in the entire recording divided by the total of all RR intervals (pNN50). It is generally accepted that RMSSD and pNN50 are related to the HR vagal modulation, whereas SDNN is considered to reflect both sympathetic and the parasympathetic influence on HRV (32). The test-retest reliability for the frequency domain markers was also satisfactory (ICC at rest: RMSSD = 0.76, p = 0.01; SDNN = 0.79, p = 0.03; pNN50 = 0.79, p = 0.01; ICC stretching: RMSSD = 0.80, p < 0.001; SDNN = 0.81, p = 0.04; pNN50 = 0.79, p = 0.02; ICC postexercise: RMSSD = 0.75, p = 0.05; SDNN = 0.77, p = 0.02; pNN50 = 0.79, p = 0.01).
The hypotheses of normality and variance homogeneity were proven, respectively, using the Wilk-Shapiro and Levene Tests. Within-group comparison between the results of HRV indexes in both time (SDNN, RMSDD, PNN50) and frequency (LF, HF, LF/HF) domains in each period of observation (pre-exercise × exercise × postexercise) was performed by repeated-measures analysis of variance (ANOVA). The Tukey post hoc verification was applied whenever necessary. The same procedure was applied to compare the results of HR. However, 2 HR values were obtained for each observation period (HRi at the first minute and HRf at the tenth minute of each observation window). Therefore, the number of successive measures increased from 3 to 6 (2 for each 10-minute window). Significance level was fixed in p ≤ 0.05. The Statistica 6.0 software was used in all calculations (Statsoft™, Tulsa, OK, USA).
The GPower™ 3.1 version (Universitat Kiel, Kiel, Germany) was used to verify the statistical power. The computed achieved power for the within-group repeated-measures ANOVA with an effect size = 0.4; α error probability = 0.05, total sample size = 10, and number of measurements = 6 (HR values) produced a critical F = 2.42 and a statistical power (1 − β error probability) = 0.91. The same criteria applied to time and frequency domains of HRV (3 repeated measurements) produced a critical F = 3.55 and a statistical power = 0.74. The effect-sizes related to each mean comparison were calculated by Cohen's d, based on the respective means (M 1 and M 2) and SDs (σ1 and σ2) as follows:
Table 1 presents the mean values (±SD) for the HR and HRV indexes in each experimental situation. Both time and frequency domain indexes changed significantly, suggesting that the autonomic control within the sets and along postexercise recovery was influenced by the stretching session. The SDNN increased during the exercise period and decreased during the postexercise recovery, albeit remaining higher than in the pre-exercise condition. The RMSSD decreased significantly during the exercises and increased in the postexercise period, to levels also significantly higher than at rest. There was a significant decrease of PNN50 while stretching followed by a slight increase during recovery. However, contrarily to the RMSSD, at the end of the postexercise recovery its value was not significantly higher compared to pre-exercise (p = 0.42/effect size = 0.06). The comparison between the HR measured at the beginning (HRi) and at the end (HRf) of each period showed that the HR increased during the exercise session and decreased throughout recovery to values significantly lower than those obtained at the pre-exercise assessment.
Figure 1 shows that the LF increased and the HF decreased during the exercise session, but no difference was found between the pre-exercise and postexercise values (p = 0.09/effect size = 0.61 and p = 0.3. effect size = 0.59, respectively). The LF/HF ratio is presented in Figure 2. A significant increase was observed during the stretching session. During the postexercise, the LF/HF declined significantly, albeit remaining still higher than at rest.
The purpose of this study was to investigate whether multiple sets of flexibility exercises could determine changes in HRV indexes associated with the sympathetic and parasympathetic activity. The main results were (a) The overall HRV was influenced by the stretching session, both during exercise and postexercise recovery; (b) The sympathetic activity increased and the vagal activity decreased during the stretching session; (c) A 10-minute stretching session composed of 3 sets of 3 stretching exercises for the trunk and hamstrings was capable to increase the postexercise vagal activity.
The autonomic balance profile is considered as potential predictor of the risk for cardiovascular disease (3,19). In this context, the HRV has been treated as marker of parasympathetic modulation and previous studies have used this approach to evaluate the autonomic heart control in response to exercise practice. It is generally accepted that during exercise there is parasympathetic withdrawal and sympathetic excitation, resulting in acceleration of the HR. These effects are reversed during the postexercise recovery (2,13).
Previous researches have demonstrated that muscle stretching may produce alterations in the heart autonomic control, which is probably because of mechanoreflex influence on the differential regulation of parasympathetic and sympathetic efferent discharges (6,26). The cardiac vagal and sympathetic responses are controlled separately and differentially by such muscle mechanoreflex. When the muscle contracts or stretches myelinated group III afferent fibers are probably stimulated, whereas unmyelinated group IV fibers are more susceptible to the influence of metabolic subproducts (17). The stimulation of group III mechanosensitive afferents during stretching may contribute to the adjustment of cardiac function via reflex sympathetic autonomic activity (23). It has been also demonstrated that the cardiac vagal modulation decreases along passive stretch, whereas cardiac sympathetic activity increases irrespective of arterial baroreceptor input, which concurs with the present results (6,10,26). The increase of sympathetic nervous activity would be related to the initial transient of the HR at the beginning of muscle stretch (5,24), whereas the withdrawal of parasympathetic activity would help sustaining the tachycardia throughout the later period of the exercise (26). Thus the HR was expected to increase during the stretching sessions because of both sympathetic enhanced activity and parasympathetic withdrawal (see Table 1 and Figure 1).
It is interesting to note that the vagal activity decrease depends on the muscle length and tension, which has obvious practical implications to flexibility training. During passive stretch, the group IV fibers are most likely not significantly stimulated compared to group III fibers, because practically no changes occur in the muscle blood environment (blood gases, pH, temperature, etc.) (31). On the other hand, successive sustained isometric contractions typical to static flexibility training may stimulate these receptors (6,34). Stretching to maximal levels beyond the physiological range of the muscle length may activate not only mechano- and metaboreceptors but also nociceptors, which can also elicit vagal and sympathetic reflex responses (26,35).
The role of muscle mechanoreflex in regulating the baroreflex control of the HR remains unclear. However, it has been shown that passive calf muscle stretch may decrease the spontaneous baroreflex sensitivity because of mechanoreflex, metaboreflex, and central command drives (30). The decline of baroreceptor sensitivity would be enhanced by local circulatory occlusion after isometric contraction of several intensities, as a result of different levels of metabolite accumulation (6).
The HRV can be assessed in the immediate postexercise recovery period and correlates with the parasympathetic reactivation in either healthy subjects or cardiac patients (12). Studies using selective adrenergic and parasympathetic blockade demonstrated that time domain indexes would be more reliable than spectral analysis to evaluate the parasympathetic activity in a non-steady-state HR setting (12), especially during postexercise recovery (27,37). As aforementioned, the SDNN is considered to reflect both sympathetic and parasympathetic influence on HRV (32). Our findings showed that the SDNN at the end of the postexercise period was higher than at rest, suggesting that the combined parasympathetic and sympathetic modulation (total HRV) were enhanced by the stretching session.
The RMSSD reflects the mean changes in the interval between the systoles, being more directly associated with the vagal modulation. It is likely to presume that successive sets of stretching sustained for a time compatible with muscle fatigue would enhance the sympathetic responses, perhaps affecting the postexercise autonomic balance. The significant increase of the RMSSD throughout the recovery period concurs with such premise, albeit further research is warranted to ratify our results.
Finally, the PNN50 represents the successive percent differences of RR intervals >50 milliseconds, being also related to the vagal modulation. The decrease of RMSSD and PNN50 during the stretching exercises was expected, suggesting that a parasympathetic withdrawal occurred regardless of the increase of sympathetic activity (26). The vagal reactivation probably occurs early after the end of the exercise session, and influences the HR within the postexercise recovery (16). This premise was confirmed by the present results for RMSSD and HR, which values, respectively, increased and decreased to levels significantly higher and lower than at the pre-exercise period.
Although the time domain indexes as SDNN and RMSSD can be used to analyze short duration recordings, the frequency domain indexes are considered to be more easily interpretable in terms of physiological regulation (32). The LF seems to be predominantly influenced by the sympathetic activity (especially when expressed in normalized units), whereas the HF is considered to be primarily a marker of vagal activity (7) or at least affected by both sympathetic and parasympathetic activity (27). Generally, an increase of LF and decrease of HF are expected during physical exercise (2), and by all means the LF/HF ratio reflects the autonomic balance in a given situation (19).
In this study the LF increased and HF decreased during the exercise session in comparison with the pre-exercise values. At the end of the postexercise recovery, the LF remained somewhat stable, whereas the HF rapidly increased to a level similar to the pre-exercise values. The LF response during the stretching exercises ratified the results for the time domain of HRV, indicating that the sympathetic activation was not swiftly recovered (8). On the other hand, the HF decrease during the stretching session seemed to confirm that a parasympathetic withdrawal takes place in response to successive static muscle contractions (8,28).
The LF/HF significantly increased during the stretching exercises, which was expected because of the sympathetic activation (28). In the postexercise period there was a decrease of LF/HF, although it remained still higher compared to the pre-exercise condition. It has been previously determined that in the first seconds of postexercise recovery there is a rapid reactivation of the vagal activity, which contributes to a quick HR decrease (15). Consequently, it is possible that the LF/HF reduction during recovery was rather because of a reactivation of the parasympathetic activity than to a postexercise sympathetic withdrawal.
All these results suggest that stretching exercise routines may acutely influence the HRV and enhance the vagal activity. It would therefore be interesting to investigate whether possible chronic parasympathetic adaptation to flexibility training could rely on successive exposition to such acute responses. A sole previous study showed that a significant increase of RMSSD at rest and after exercise occurred in athletes, who participated in a 28-day flexibility training (25). Unfortunately, it has not been yet established if this chronic enhancement of the parasympathetic activity would be progressively provoked by regular acute stretching effects. In such a case, additional investigation would be important to determine the dose-response relationships between flexibility training and changes in the autonomic modulation.
In conclusion, a multiple-set flexibility training session enhanced the vagal modulation and sympathovagal balance in the acute postexercise recovery, at least in subjects with low flexibility levels. On the other hand, the sympathetic activity increased significantly during the flexibility exercises and remained higher compared to pre-exercise throughout the postexercise recovery period.
The present results suggest that stretching routines may contribute to a favorable autonomic activity change in untrained subjects. Because sedentary persons have higher potential risk for the later development of cardiovascular disease, they could therefore benefit from the cardiovascular protection effect of flexibility training on the parasympathetic activity. From an applied research perspective, these findings warrant future investigation about the relationship between the enhanced vagal reactivation following stretching exercises with possible long-term effects of flexibility training on the autonomic modulation.
The authors thank Luis Viveiros de Castro for the technical support. This study was partially supported by grants from the Carlos Chagas Filho Foundation for the Research Support in the Rio de Janeiro State (FAPERJ, proc E-26/150.751/2007) and from the Brazilian Council for the Research Development (CNPq, proc 305729/2006-3).
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Keywords:© 2011 National Strength and Conditioning Association
sympathetic nervous system; parasympathetic nervous system; autonomic balance; physical training; fitness; health