International Journal of Sports Physiology and Performance, 2015, 10, 388-395 http://dx.doi.org/10.1123/ijspp.2014-0225 © 2015 Human Kinetics, Inc.
www.IJSPP-Journal.com ORIGINAL INVESTIGATION
Effect of Whole-Body Vibration Therapy on Performance Recovery Nuttaset Manimmanakorn, Jenny J. Ross, Apiwan Manimmanakorn, Samuel J.E. Lucas, and Michael J. Hamlin Purpose: To compare whole-body vibration (WBV) with traditional recovery protocols after a high-intensity training bout. Methods: In a randomized crossover study, 16 athletes performed 6 × 30-s Wingate sprints before completing either an active recovery (10 min of cycling and stretching) or WBV for 10 min in a series of exercises on a vibration platform. Muscle hemodynamics (assessed via near-infrared spectroscopy) were measured before and during exercise and into the 10-min recovery period. Blood lactate concentration, vertical jump, quadriceps strength, flexibility, rating of perceived exertion (RPE), muscle soreness, and performance during a single 30-s Wingate test were assessed at baseline and 30 and 60 min postexercise. A subset of participants (n = 6) completed a 3rd identical trial (1 wk later) using a passive 10-min recovery period (sitting). Results: There were no clear effects between the recovery protocols for blood lactate concentration, quadriceps strength, jump height, flexibility, RPE, muscle soreness, or single Wingate performance across all measured recovery time points. However, the WBV recovery protocol substantially increased the tissue-oxygenation index compared with the active (11.2% ± 2.4% [mean ± 95% CI], effect size [ES] = 3.1, and –7.3% ± 4.1%, ES = –2.1 for the 10 min postexercise and postrecovery, respectively) and passive recovery conditions (4.1% ± 2.2%, ES = 1.3, 10 min postexercise only). Conclusion: Although WBV during recovery increased muscle oxygenation, it had little effect in improving subsequent performance compared with a normal active recovery. Keywords: lactate, muscle function, muscle soreness, muscle oxygenation Promoting recovery after exercise is essential for athletes to improve subsequent sport performance. Whole-body vibration (WBV), widely promoted in commercial gyms, uses oscillatory movement as an innovative technique for recovery. Vibration machines transfer vibration force from a moving platform to the human body, which has been suggested to increase tissue blood flow for promoting recovery after exercise.1–3 Previous research indicates that WBV may increase tissue blood flow1–4 via the vasodilatation process by increasing endotheliumderived vasodilators such as nitric oxide and prostaglandins2,3 or by reducing the release of the vasoconstrictor substance endothelin from smooth muscle.5 Such changes in vascular perfusion resulting from vibration alone or vibration during exercise may result in more effective removal of waste products and perhaps an increased delivery (and uptake) of oxygen resulting in enhanced phosphocreatine resynthesis after exercise.6,7 WBV may also help the recovery of muscle after exercise by improving flexibility and jumping performance and reducing muscle pain.8–10 However, Edge et al11 found no statistical difference in oxygen consumption, respiratory-exchange ratio, blood lactate concentration, creatine kinase, or performance levels (3-km time trial) after 24 hours recovery from high-intensity exercise training between WBV and control groups. Because of this uncertainty in the literature on the beneficial effects of vibration training as a recovery tool, further investigation is warranted. In particular, little is known N. Manimmanakorn is with the Dept of Rehabilitation Medicine, and A. Manimmanakorn, the Dept of Physiology, Khon Kaen University, Khon Kaen, Thailand. Ross and Hamlin are with the Dept of Social Science, Parks, Recreation, Tourism & Sport, Lincoln University, Christchurch, New Zealand. Lucas is with the School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham, Birmingham, UK. Address author correspondence to Nuttaset Manimmanakorn at [email protected]. 388
about muscle oxygenation during WBV exercise and subsequent performance after high-intensity repeated-sprint work, similar to what team athletes might endure during a match. The aim of this study was therefore to investigate the effect of a WBV recovery program (passive vibration and stretching on a vibration machine) on muscle hemodynamics, blood lactate, muscle power, strength and flexibility, rating of perceived exertion, muscle soreness, and Wingate performance compared with a traditional recovery program or no recovery program at all (ie, passive recovery).
Methods Participants in this randomized crossover study were 16 rugby union players from a local premier division 1 team (age 19.1 ± 1.4 y, body weight 86.8 ± 11.4 kg, height 182.8 ± 6.2 cm, and bodymass index 25.9 ± 2.9 kg/m2, mean ± SD). Participants with serious or uncontrolled health problems such as diabetes, hypertension, or back, hip, knee, and ankle pain, including those with previous back, hip, knee, or ankle surgery, were excluded from the study. All participants gave informed consent, and all procedures were approved by the local university human research ethics committee and conformed to the Declaration of Helsinki. The participants performed a series of highly intensive exercises to simulate in a controlled manner what might be expected of them during a typical training session or game. The exercises consisted of 6 × 30-second Wingate tests on a Velotron cycle ergometer (Velotron Wingate software, version 1.0, Racermate Inc, Seattle, WA, USA). Each bout was interspersed with 30 seconds of active recovery (cycling at comfortable load, ~40 W). Subjects’ body mass was entered into the software and a workload of 9.8% of body mass was used during the test. During the test the athletes were given verbal encouragement to keep cycling as fast as pos-
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sible. Before the Wingate test, participants completed a 5-minute warm-up comprising cycling and also stretching of the hamstring, calf, and quadriceps muscles. The athletes were familiarized with the equipment and all of the testing procedures 1 week before the first main trial. The athletes were randomized into 2 groups; group 1 completed the active recovery trial first while group 2 completed the WBV recovery trial first. After the high-intensity interval-training session, participants in the active recovery condition completed 5 minutes of cycling at 50% of maximum heart rate12 and 5 minutes of stretching exercises (quadriceps, hip flexors, hamstrings, calf, and adductors, 3 sets of 10 seconds for each muscle group). For the WBV condition participants completed their recovery program on a 3-dimensional PowerPlate vibration machine (PowerPlate Pro5, PowerPlate North America Inc, Northbrook, IL, USA). Since footwear has been found to alter the neuromuscular response to WBV we asked that all participants wear footwear during the study.13 The WBV recovery protocol followed the manufacturer’s instructions and consisted of a series of stretching exercises and resting positions on the platform. The WBV recovery included hamstring and quadriceps stretches
Figure 1 — Positions of whole-body-vibration training for recovery.
(30 Hz, low [1.2 mm], 1.6 g,14 and 30 s, for the vibration frequency, amplitude, peak acceleration, and duration, respectively), followed by 2 sets of lateral thigh muscles, hamstrings, quadriceps, and calf muscles vibration massage on the vibration platform (40 Hz, high [2.2 mm], 5.3 g,14 60 s), interspersed with 5 seconds rest for the changing from one position to another (Figure 1). The total recovery duration was 10 minutes for both groups. After a 1-week washout period the groups were crossed over and participants repeated the protocol in the other recovery condition. As shown in Figure 2 and detailed following, participants were evaluated before exercising (baseline), immediately after the series of Wingate tests, during and immediately after the recovery protocol, and then 30 minutes, 60 minutes, and 1, 2, and 3 days postexercise. The order in which the testing occurred at baseline and 30 and 60 minutes postexercise was the following: rating of perceived exertion and muscle soreness, followed by blood lactate test, 3-second maximum voluntary contraction (MVC), sit-and-reach, countermovement-jump test, and finally a single Wingate performance (with 2 min between tests). Muscle hemodynamics were monitored at rest before the exercise (baseline), during the exercise
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Figure 2 — Summary of testing schedule and measurements taken in this study. Abbreviations: RPE, rate of perceived exertion; MVC, maximum voluntary contraction; NIRS, near-infrared spectroscopy; WBV, whole-body vibration.
bout, and during the 10-minute recovery program and then again during a 1-minute rest after the recovery program (post; Figure 2). A drop of capillary blood was taken from the fingertip (using standard aseptic technique) at baseline, immediately after the bout of Wingate tests, and at 30 and 60 minutes postexercise. Samples were immediately analyzed using a portable lactate analyzer (Lactate Pro, Arkray Inc, Kyoto, Japan). The Wingate variables recorded for each test included anaerobic power (peak power divided by body weight) and fatigue index (peak power minus minimum power divided by testing duration). Explosive power was determined by the maximum-effort countermovement-jump test using standard procedures (Yardstick, Swift Performance Equipment, New South Wales, Australia). The best of 3 attempts was recorded. Quadriceps strength was evaluated by measuring the 3-second MVC of the knee-extensor muscles. In a sitting position (with the knee flexed at 80°), athletes were verbally encouraged to exert a maximal force lasting 3 seconds. A load cell (Tension/S-beam load cell, 10 Hz, AST 500, PT instruments, UK) attached to the ankle with a Velcro strap 3 cm above the medial malleolus was used to measure the force. Lower-back and hamstring flexibility was evaluated using the traditional sit-and-reach test, for which the best of 3 attempts was recorded. The reliabilities of performance tests (measured via the intraclass correlation coefficient) were .74 for anaerobic power, .79 for the fatigue index, .98 for the jump test, .93 for the 3-second MVC, and .98 for the sit-and-reach test. Participants’ ratings of perceived exertion were evaluated using the 15-point Borg scale (range 6–20: 6 = no exertion, 20 = maximal exertion).15 Muscle soreness was determined using a visual analog scale (range 0–10: 0 = no pain, 10 = the worst pain). The scale was previously validated as a reliable instrument for measuring pain intensity.16 Both scales were rated at baseline, immediately after the Wingate sprints, and at 30 and 60 minutes postexercise. Only the muscle-soreness score was rated during baseline and at 1, 2, and 3 days postexercise. Muscle hemodynamics were assessed by near-infrared spectroscopy (NIRS; NIRO-200, Hamamatsu Photonics KK, Hamamatsu, Japan). The NIRO-200 provides changes in oxygenated hemoglobin (O2Hb) and deoxygenated hemoglobin (HHb) and
derived changes in total hemoglobin (tHb = O2Hb + HHb), as previously described.17,18 Tissue oxygen saturation is also reported as the tissue-oxygenation index (TOI, percentage ratio of oxygenated to total hemoglobin), calculated by the NIRS system via spatially resolved spectroscopy from the light-attenuation slope along the distance from the emitting point as detected by 2 photodiodes in the detection probe. The probes, separated by 4.5 cm, were housed in an optically dense plastic holder and securely attached to the middle portion of the right vastus lateralis muscle at the midthigh level and parallel with the long axis of the muscle with tape to minimize extraneous light contamination. At the site, the skin was shaved and marked with a permanent marker, and the location measurements were recorded to ensure repeated testing at the same location for subsequent trials. The probes were attached before any exercise and remained attached throughout the exercise and the recovery period. The NIRS data were analyzed by averaging values over a 1-minute period at baseline, 1-minute post-Wingate tests, initial 5 minutes and last 5 minutes of the recovery program, and finally 1 minute after the recovery program. After 16 participants finished the WBV and active recovery, a subset of 6 participants repeated the testing, at least 1 week after their last trial, while doing a passive recovery program that involved sitting quietly in a chair for the 10 minutes of recovery to investigate differences in tissue hemodynamics without any recovery at all (ie, a control condition). A cycle ergometer rather than a treadmill was used in these athletes because of the ease with which to gather the NIRS data. A spreadsheet for the analysis of crossover trials was used to estimate worthwhile differences and chances that true effects were substantial.19 The spreadsheet for within-subject modeling used the unequal-variances statistic to assess for statistically worthwhile differences among repeated-measurement analysis.20 The smallest worthwhile change was set at 1% for performances and 0.20 standardized units (change in the mean divided by the between-subjects SD at baseline) for physiological variables.21 Uncertainties in the estimate of change are presented as the 95% confidence intervals and likelihoods that the true value of the effect was a substantial enhancement or impairment. P values were also taken from the spreadsheet for researchers who are not accustomed to magnitudebased inference statistics.
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Results Blood lactate concentration followed a similar pattern of change throughout the recovery period (Table 1); however, relative to the active recovery condition blood lactate concentration was
substantially higher 30 minutes postexercise among participants undertaking WBV. Anaerobic power followed a similar pattern of change throughout the series of Wingate tests and during the recovery period in both conditions (Table 1). Anaerobic performance and fatigue
Table 1 Baseline (Pretest), Prerecovery (Immediately After Exercise), and Postrecovery (30 min and 60 min) Changes in Measured Parameters in the WBV and Active-Recovery Groups and the Chances That True Differences Between Groups Were Substantial Chances That True Differences Are Substantialb
% Change Measure
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Lactate (mmol/L)
Rating of perceived exertion
Anaerobic power (W/kg)
Fatigue index (W/s)
MVC (kg)
Jump height (cm)
Sit-and-reach (cm)
Muscle soreness
Timea
WBV
Active
1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 5 6 7
2.1 15.0 8.3 8.2 6.4 18.3 9.6 8.2 9.5 7.3 9.3 9.6 11.7 12.7 11.6 11.3 67.6 — 61.4 63.2 43.9 — 42.3 43.1 24.9 — 24.8 25.8 0.9 7.9 3.6 2.6 1.4 0.8 0.6
2.4 15.6 7.2 8.2 6.7 18.2 10.6 8.8 9.3 7.8 9.4 9.5 11.8 13.3 11.5 11.7 68.5 — 62.1 64.0 44.8 — 43.1 42.8 24.9 — 25.4 26.4 0.8 8.1 3.7 2.9 1.8 1.0 0.4
WBV
Active
% difference ± 95%CI
%
Qualitative
P
614.3 –44.7 –1.2
550.0 –53.8 13.9
64.3 ± 227.8 9.1 ± 9.0 –15.1 ± 33.9
12 96 17
Unclear Very likely Unclear
.37 .05 .43
185.9 –47.5 –14.6
171.6 –41.8 –17.0
14.3 ± 32.9 –5.7 ± 5.8 2.4 ± 12.0
21 89 7
Unclear Trivial Unclear
.74 .10 .30
–23.2 27.4 3.2
–16.1 20.5 1.1
–7.1 ± 7.1 6.9 ± 8.9 2.1 ± 11.3
6 56 25
Unclear Unclear Unclear
.30 .43 .52
8.5 –8.7 –2.6
12.7 –13.5 1.7
–4.2 ± 18.9 4.8 ± 13.1 –4.3 ± 16.6
12 48 10
Unclear Unclear Unclear
.61 .48 .60
–9.2 2.9
–9.3 3.1
0.1 ± 8.8 –0.2 ± 14.2
35 15
Unclear Unclear
.70 .85
–3.6 1.9
–3.8 –0.7
0.2 ± 3.6 2.6 ± 2.7
3 22
Unclear Trivial
.91 .07
–0.4 4.0
2.0 3.9
–2.4 ± 8.0 0.1 ± 7.9
21 6
Trivial Unclear
.42 .89
777.8 –54.4 –27.8 –46.2 –42.9 –25.0
912.5 –54.3 –21.6 –37.9 –44.4 –60.0
–134.7 ± 76.1 –0.1 ± 10.4 –6.2 ± 20.9 –8.3 ± 40.9 1.5 ± 30.0 35 ± 15.0
53 15 59 39 18 61
Unclear Unclear Unclear Unclear Unclear Trivial
.57 .62 .41 .72 .84 .19
Abbreviations: WBV, whole-body-vibration group; active, active-recovery group; CI, confidence interval; MVC, 3-s maximal voluntary contraction. a 1 = baseline (or 1st Wingate), 2 = immediately postexercise (prerecovery or 6th Wingate), 3 = 30 min postrecovery, 4 = 60 min postrecovery, 5 = 1 d postrecovery, 6 = 2 d postrecovery, and 7 = 3 d postrecovery. b Based on the smallest substantial change set at 1% for performances ± 95% CI: add and subtract this number to the mean effect to obtain confidence intervals for the true difference.
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Muscle soreness increased substantially immediately after the series of Wingate tests (Table 1); however, there was little effect of WBV relative to active recovery on muscle-soreness recovery over the following 3 days. Changes in O2Hb, HHb, tHb, and TOI from the preexercise baseline across the 4 time points assessed during the first 12 minutes of recovery are illustrated in Figure 3. During WBV recovery, participants had a substantially greater increase in O2Hb from baseline levels at 10 minutes postexercise (197.7 ± 68.5 μM/cm,
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index were similar between the WBV and active recovery condition during recovery, with all differences being small and unclear. In addition, relative to the active recovery, WBV had little effect on recovery from 3-second MVC, vertical jump, or flexibility at 30 and 60 minutes postexercise. After strenuous exercise, rating of perceived exertion dramatically declined at 30 and 60 minutes postexercise for both conditions. Differences between recovery programs were trivial or unclear at 30 and 60 minutes postexercise (Table 1).
Figure 3 — Changes in oxygenated hemoglobin (O2Hb), deoxygenated hemoglobin (HHb), total hemoglobin (tHb), and tissue-oxygenation index (TOI) at the pretest (rest), start of the recovery program (0 min after the 6 Wingate test), 5 and 10 minutes during postrecovery program and post (after the 10-min recovery program) for the passive (triangles), active (closed circles), and whole-body-vibration (WBV) (open circles) groups, mean ± SD. aSubstantial difference between the WBV and passive groups. bSubstantial difference between the active and passive groups. cSubstantial difference between the WBV and active groups.
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Vibration and Performance Recovery 393
mean ± 95% CI) than with either a traditional active recovery protocol (138.2 ± 35.6 μM/cm) or passive recovery (119.4 ± 34.9 μM/cm). The WBV condition also had a substantially greater increase in O2Hb postrecovery (1 min after the 10-min recovery protocol; 227.1 ± 69.0 μM/cm) than with passive recovery (99.1 ± 36.6 μM/cm). For the active recovery condition there was a substantially greater increase in HHb levels 10 minutes postexercise and at postrecovery (106.5 ± 37.8 and 12.5 ± 11.3 μM/cm, respectively) than with both passive recovery (–1.6 ± 36.5 and –3.8 ± 36.5 μM/ cm) and the WBV condition (–64.3 ± 36.8 and –31.1 ± 37.7 μM/cm), while the changes from baseline for passive recovery HHb levels were substantially greater than WBV for the same time. The active recovery and WBV conditions had substantially greater increases in tHb levels 5 and 10 minutes postexercise and postrecovery (active recovery: 223.4 ± 42.8, 244.7 ± 32.0, 163.3 ± 32.9 μM/cm; WBV: 197.5 ± 55.7, 133.4 ± 78.3, 196.0 ± 80.6 μM/cm, respectively) than with passive recovery (182.5 ± 20.29, 117.9 ± 23.8, 95.3 ± 25.3 μM/cm, respectively) Active recovery substantially increased tHb levels from baseline more than with WBV at 10 minutes postexercise, while at postrecovery, tHb levels after WBV were substantially higher than with active recovery. Muscle oxygenation (TOI) during active recovery was substantially lower 10 minutes postexercise and postrecovery (63.7% ± 3.8%, 69.5% ± 1.8%) than with WBV (74.5% ± 1.4%, 72.2% ± 2.3%) and the passive recovery condition (72.9% ± 2.9%, 71.9% ± 2.4%). Furthermore, TOI at 10 minutes postexercise for the WBV condition was substantially higher than with passive recovery.
Discussion The novel finding of this study was that the WBV recovery program increased muscle oxygenation (TOI) compared with the active recovery program. However, even with increased oxygenation at the muscle level with WBV recovery, metabolic and performance variables changed little compared with the active recovery program over the first hour after an intense exercise session. We found that WBV during recovery was no better at decreasing blood lactate concentration after a high-intensity exercise session than a traditional active recovery. Moreover, at 30 minutes postexercise, WBV washed out lactate substantially less than the active program. However, the effect of WBV recovery on lactate clearance at 60 minutes postexercise was similar to the active program (ie, reduction from postexercise peak was the same). The mechanism for eliminating blood lactate with WBV exercise may be similar to that of the active recovery program, namely, by increasing blood perfusion for rapid distribution of lactate to be metabolized.22–24 Vibration increases vasodilatation effects through an increase in endothelium-derived vasodilators such as nitric oxide and prostaglandins2,3,25 or by reducing the release of the vasoconstrictor substance endothelin from vascular smooth muscle.5 However, this increased muscle blood flow did not seem to wash blood lactate out any faster in our participants. Our study demonstrated that WBV had effects similar to those of a traditional active protocol in terms of power and strength performance. Edge et al11 found that WBV training (12 Hz, 6-mm amplitude) had no substantial effect on lactate clearance and sport performance when undertaken on the following day compared with a control group. Those authors claimed that their WBV protocol at low frequency may not have been adequate to provide subsequent changes to enhance the recovery process. In contrast, Marin et al9 used high-frequency WBV (35–50 Hz, 1- to 2-mm amplitude, 30
min) combined with the traditional cooldown and found beneficial effects on improvement of vertical-jump height at 24 hours after vibration compared with the traditional cooldown. Our WBV protocol was comparable to the protocol of Marin et al, but we found no beneficial effect of WBV when compared with a conventional active program. However, our study only evaluated power and strength performance up to 60 minutes postexercise, which may be too short a period to detect significant beneficial effects of WBV. Similar to active recovery programs, it has been suggested that the elevated blood perfusion induced by WBV training enhances removal of blood lactate, H+, and other pain-causing substances, as well as reducing the inflammation process.22–24,26 We found that WBV and the active recovery program had similar effects on reported muscle soreness after strenuous exercise in athletes. Likewise, Marin et al9 found no significant difference in pain reduction between vibration and control cooldown recovery in soccer players.9 In contrast, Rhea et al10 showed that stretching and massage in conjunction with vibration significantly reduced perceived pain compared with stretching only in untrained volunteers. The differences between these 2 findings may be due to the fact that untrained subjects usually suffer more pain than trained athletes27 such as those in this study. As with the blood lactate and muscle-soreness results, we found no substantial difference in perceived exertion between the WBV and active recovery programs. Ratings of perceived exertion have been associated with levels of lactate, muscle soreness, and cardiopulmonary and psychological stress.28 The findings of our study indicated that WBV reduced overall perceived exertion in a fashion similar to that of the active recovery program. We also observed that WBV had a similar effect on flexibility compared with active recovery. Cronin et al29 found a greater improvement in flexibility at a higher vibration load (44 Hz, 5 mm for 30 s). In addition, Issurin et al8 found that vibration (44 Hz, 3 mm, total 7 min) during stretching exercise 3 times a week for 3 weeks significantly increased leg and trunk flexibility compared with conventional stretching (by 7.5% and 37.8%, respectively). We applied a vibration frequency and amplitude approximately similar to these previous studies; however, to increase flexibility, it seems likely that more than 1 session of WBV is required. The current study found that both WBV and active recovery programs increased muscle blood flow during recovery (ie, increased tHb indicating an increased muscle blood volume), which may signal increased oxygen availability to the muscle. Furthermore, the data obtained from the subset of participants who also performed a passive recovery protocol support this elevated perfusion relative to being inactive during recovery. However, at the end of the recovery protocol (at 10 min), the active recovery condition had a higher tHb than with the WBV. This apparent contrasting effect requires explanation. We observed similar performance measures during the Wingate tests before both recovery conditions, so muscle blood flow was presumably the same. However, after 10 minutes of the recovery program, muscle blood flow appeared more elevated in the active condition, which we suggest is probably due to the added metabolic demands of the active recovery protocol that may require more blood flow relative to the shearing stress-mediated response induced via the vibration.2,3,25 In addition, WBV increased muscle oxygenation (TOI) while the active program decreased it. The underlying mechanism is likely to be linked to the vasodilatation process linked with muscle metabolism (as reflected by increased O2Hb and decreased HHb). While the active recovery probably increases muscle workload, thereby increasing the need for oxygen supplied (increased flow) and increasing the amount of oxygen extracted (resulting in increased
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HHb concentration), the WBV recovery may cause vasodilatation without the need for an increase in oxygen uptake at the muscles. In contrast, previous research revealed that WBV training increases oxygen utilization and decreases muscle oxygenation levels similar to light or moderate exercise.30,31 However, Mileva et al30 used WBV during squatting or knee-extension exercises, while our study used stretching and vibration massage during WBV, which is likely to produce less muscle workload and perhaps a greater vasodilatation effect independent of metabolism. In terms of muscle-oxygenation levels, stretch or massage during WBV may be more suitable as a recovery program than static or dynamic exercise. Furthermore, we found that the vasodilatation effect of WBV persisted at 1 minute after the recovery protocol (as reflected in increased tHb and increased O2Hb) compared with the active recovery and passive recovery conditions. Likewise, previous studies have found a vasodilatation effect after WBV training.2,32 Reduction of vasoconstrictor substances and increasing vasodilators may be preserved after vibration.2,5 The vasodilatation after WBV may well enhance blood flow to the muscle for longer, perhaps benefiting subsequent performances. Future research is required to investigate the post-WBV vasodilatation effect on performance recovery, particularly aerobic performance since enhanced oxygenation of the muscle tissue should have its greatest effect on aerobic metabolism. We acknowledge that a limitation of this study is the relatively small number of participants in the passive recovery group, which was lower than in the other 2 recovery groups. Initially, this study aimed to compare the effect of WBV recovery with conventional exercise recovery, but it became obvious that little information existed for NIRS data on passive recovery, so we asked the subjects to return for further passive recovery testing. Unfortunately, a number of participants had prior engagements and were unable to attend this testing. Accordingly, the results of the passive recovery testing should be considered hypothetical until substantiated with further research on a larger subject pool. A further limitation is that the PowerPlate device used in this study did not directly calculate the amplitude and acceleration values. These values were calculated from the peak-to-peak displacement and acceleration using information from Pel et al.14 Similarly, we did not measure acceleration of WBV when only part of body was placed on the platform (as in some of the exercises used in this study) and suggest that future studies investigate changes in these parameters when only part of the body is placed on the vibrating platform.
Practical Applications WBV has an effect on short-term explosive-performance recovery similar to that of conventional recovery protocols. The increase in muscle oxygenation found after WBV may assist recovery of aerobic metabolism, but the added cost and logistics of using WBV may overcome any potential benefits.
Conclusion Monitoring of muscle oxygenation levels revealed that the WBV recovery program improved muscle oxygenation without the subsequent increase in energy demand required by active recovery. However, the WBV and the active recovery program had similar effects on lactate recovery, power, strength, flexibility, rating of perceived exertion, and muscle pain after intensive exercise in rugby players.
Acknowledgments Special thanks to the athletes for their contribution and participation and the PowerPlate Company for supporting the vibration machine. The results of the current study do not constitute endorsement of the product by the authors or the journal.
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16. Summers S. Evidence-based practice part 2: reliability and validity of selected acute pain instruments. J Perianesth Nurs. 2001;16(1):35–40. PubMed doi:10.1016/S1089-9472(01)19774-1 17. Al-Rawi PG, Smielewski P, Kirkpatrick PJ. Evaluation of a nearinfrared spectrometer (NIRO 300) for the detection of intracranial oxygenation changes in the adult head. Stroke. 2001;32(11):2492–2500. PubMed doi:10.1161/hs1101.098356 18. Lucas SJ, Ainslie PN, Murrell CJ, Thomas KN, Franz EA, Cotter JD. Effect of age on exercise-induced alterations in cognitive executive function: relationship to cerebral perfusion. Exp Gerontol. 2012;47(8):541–551. PubMed doi:10.1016/j.exger.2011.12.002 19. Hopkins WG. Spreadsheets for analysis of controlled trials, with adjustment for a subject characteristic. Sportscience. 2006;10:46–50. 20. Hopkins WG. Repeated measures models. Sportscience. 1997. http:// www.sportsci.org/. Accessed July 4, 2011. 21. Cohen J. Statistical Power Analysis for the Behavioral Sciences. 2nd ed. Hillsdale, NJ: Lawrence Erlbaum; 1988. 22. Ahmaidi S, Granier P, Taoutaou Z, Mercier J, Dubouchaud H, Prefaut C. Effects of active recovery on plasma lactate and anaerobic power following repeated intensive exercise. Med Sci Sports Exerc. 1996;28(4):450–456. PubMed doi:10.1097/00005768-19960400000009 23. Bogdanis GC, Nevill ME, Lakomy HK, Graham CM, Louis G. Effects of active recovery on power output during repeated maximal sprint cycling. Eur J Appl Physiol Occup Physiol. 1996;74(5):461–469. PubMed doi:10.1007/BF02337727 24. Corder KP, Potteiger JA, Nau KL, Figoni SE, Hershberger SL. Effects of active and passive recovery conditions on blood lactate, rating of
perceived exertion, and performance during resistance exercise. J Strength Cond Res. 2000;14(2):151–156. 25. Sackner MA, Gummels E, Adams JA. Nitric oxide is released into circulation with whole-body, periodic acceleration. Chest. 2005;127(1):30–39. PubMed doi:10.1378/chest.127.1.30 26. Zainuddin Z, Newton M, Sacco P, Nosaka K. Effects of massage on delayed-onset muscle soreness, swelling, and recovery of muscle function. J Athl Train. 2005;40(3):174–180. PubMed 27. Evans WJ, Meredith CN, Cannon JG, et al. Metabolic changes following eccentric exercise in trained and untrained men. J Appl Physiol. 1986;61(5):1864–1868. PubMed 28. O’Sullivan SB. Perceived exertion. a review. Phys Ther. 1984;64(3):343–346. PubMed 29. Cronin JB, Nash M, Whatman C. The effect of four different vibratory stimuli on dynamic range of motion of the hamstrings. Phys Ther Sport. 2007;8(1):30–36. doi:10.1016/j.ptsp.2006.11.003 30. Mileva KN, Naleem AA, Biswas SK, Marwood S, Bowtell JL. Acute effects of a vibration-like stimulus during knee extension exercise. Med Sci Sports Exerc. 2006;38(7):1317–1328. PubMed doi:10.1249/01. mss.0000227318.39094.b6 31. Yamada E, Kusaka T, Miyamoto K, et al. Vastus lateralis oxygenation and blood volume measured by near-infrared spectroscopy during whole body vibration. Clin Physiol Funct Imaging. 2005;25(4):203– 208. PubMed doi:10.1111/j.1475-097X.2005.00614.x 32. Zhang Q, Ericson K, Styf J. Blood flow in the tibialis anterior muscle by photoplethysmography during foot-transmitted vibration. Eur J Appl Physiol. 2003;90(5–6):464–469. PubMed doi:10.1007/s00421003-0904-5
www.IJSPP-Journal.com ORIGINAL INVESTIGATION
Effect of Whole-Body Vibration Therapy on Performance Recovery Nuttaset Manimmanakorn, Jenny J. Ross, Apiwan Manimmanakorn, Samuel J.E. Lucas, and Michael J. Hamlin Purpose: To compare whole-body vibration (WBV) with traditional recovery protocols after a high-intensity training bout. Methods: In a randomized crossover study, 16 athletes performed 6 × 30-s Wingate sprints before completing either an active recovery (10 min of cycling and stretching) or WBV for 10 min in a series of exercises on a vibration platform. Muscle hemodynamics (assessed via near-infrared spectroscopy) were measured before and during exercise and into the 10-min recovery period. Blood lactate concentration, vertical jump, quadriceps strength, flexibility, rating of perceived exertion (RPE), muscle soreness, and performance during a single 30-s Wingate test were assessed at baseline and 30 and 60 min postexercise. A subset of participants (n = 6) completed a 3rd identical trial (1 wk later) using a passive 10-min recovery period (sitting). Results: There were no clear effects between the recovery protocols for blood lactate concentration, quadriceps strength, jump height, flexibility, RPE, muscle soreness, or single Wingate performance across all measured recovery time points. However, the WBV recovery protocol substantially increased the tissue-oxygenation index compared with the active (11.2% ± 2.4% [mean ± 95% CI], effect size [ES] = 3.1, and –7.3% ± 4.1%, ES = –2.1 for the 10 min postexercise and postrecovery, respectively) and passive recovery conditions (4.1% ± 2.2%, ES = 1.3, 10 min postexercise only). Conclusion: Although WBV during recovery increased muscle oxygenation, it had little effect in improving subsequent performance compared with a normal active recovery. Keywords: lactate, muscle function, muscle soreness, muscle oxygenation Promoting recovery after exercise is essential for athletes to improve subsequent sport performance. Whole-body vibration (WBV), widely promoted in commercial gyms, uses oscillatory movement as an innovative technique for recovery. Vibration machines transfer vibration force from a moving platform to the human body, which has been suggested to increase tissue blood flow for promoting recovery after exercise.1–3 Previous research indicates that WBV may increase tissue blood flow1–4 via the vasodilatation process by increasing endotheliumderived vasodilators such as nitric oxide and prostaglandins2,3 or by reducing the release of the vasoconstrictor substance endothelin from smooth muscle.5 Such changes in vascular perfusion resulting from vibration alone or vibration during exercise may result in more effective removal of waste products and perhaps an increased delivery (and uptake) of oxygen resulting in enhanced phosphocreatine resynthesis after exercise.6,7 WBV may also help the recovery of muscle after exercise by improving flexibility and jumping performance and reducing muscle pain.8–10 However, Edge et al11 found no statistical difference in oxygen consumption, respiratory-exchange ratio, blood lactate concentration, creatine kinase, or performance levels (3-km time trial) after 24 hours recovery from high-intensity exercise training between WBV and control groups. Because of this uncertainty in the literature on the beneficial effects of vibration training as a recovery tool, further investigation is warranted. In particular, little is known N. Manimmanakorn is with the Dept of Rehabilitation Medicine, and A. Manimmanakorn, the Dept of Physiology, Khon Kaen University, Khon Kaen, Thailand. Ross and Hamlin are with the Dept of Social Science, Parks, Recreation, Tourism & Sport, Lincoln University, Christchurch, New Zealand. Lucas is with the School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham, Birmingham, UK. Address author correspondence to Nuttaset Manimmanakorn at [email protected]. 388
about muscle oxygenation during WBV exercise and subsequent performance after high-intensity repeated-sprint work, similar to what team athletes might endure during a match. The aim of this study was therefore to investigate the effect of a WBV recovery program (passive vibration and stretching on a vibration machine) on muscle hemodynamics, blood lactate, muscle power, strength and flexibility, rating of perceived exertion, muscle soreness, and Wingate performance compared with a traditional recovery program or no recovery program at all (ie, passive recovery).
Methods Participants in this randomized crossover study were 16 rugby union players from a local premier division 1 team (age 19.1 ± 1.4 y, body weight 86.8 ± 11.4 kg, height 182.8 ± 6.2 cm, and bodymass index 25.9 ± 2.9 kg/m2, mean ± SD). Participants with serious or uncontrolled health problems such as diabetes, hypertension, or back, hip, knee, and ankle pain, including those with previous back, hip, knee, or ankle surgery, were excluded from the study. All participants gave informed consent, and all procedures were approved by the local university human research ethics committee and conformed to the Declaration of Helsinki. The participants performed a series of highly intensive exercises to simulate in a controlled manner what might be expected of them during a typical training session or game. The exercises consisted of 6 × 30-second Wingate tests on a Velotron cycle ergometer (Velotron Wingate software, version 1.0, Racermate Inc, Seattle, WA, USA). Each bout was interspersed with 30 seconds of active recovery (cycling at comfortable load, ~40 W). Subjects’ body mass was entered into the software and a workload of 9.8% of body mass was used during the test. During the test the athletes were given verbal encouragement to keep cycling as fast as pos-
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sible. Before the Wingate test, participants completed a 5-minute warm-up comprising cycling and also stretching of the hamstring, calf, and quadriceps muscles. The athletes were familiarized with the equipment and all of the testing procedures 1 week before the first main trial. The athletes were randomized into 2 groups; group 1 completed the active recovery trial first while group 2 completed the WBV recovery trial first. After the high-intensity interval-training session, participants in the active recovery condition completed 5 minutes of cycling at 50% of maximum heart rate12 and 5 minutes of stretching exercises (quadriceps, hip flexors, hamstrings, calf, and adductors, 3 sets of 10 seconds for each muscle group). For the WBV condition participants completed their recovery program on a 3-dimensional PowerPlate vibration machine (PowerPlate Pro5, PowerPlate North America Inc, Northbrook, IL, USA). Since footwear has been found to alter the neuromuscular response to WBV we asked that all participants wear footwear during the study.13 The WBV recovery protocol followed the manufacturer’s instructions and consisted of a series of stretching exercises and resting positions on the platform. The WBV recovery included hamstring and quadriceps stretches
Figure 1 — Positions of whole-body-vibration training for recovery.
(30 Hz, low [1.2 mm], 1.6 g,14 and 30 s, for the vibration frequency, amplitude, peak acceleration, and duration, respectively), followed by 2 sets of lateral thigh muscles, hamstrings, quadriceps, and calf muscles vibration massage on the vibration platform (40 Hz, high [2.2 mm], 5.3 g,14 60 s), interspersed with 5 seconds rest for the changing from one position to another (Figure 1). The total recovery duration was 10 minutes for both groups. After a 1-week washout period the groups were crossed over and participants repeated the protocol in the other recovery condition. As shown in Figure 2 and detailed following, participants were evaluated before exercising (baseline), immediately after the series of Wingate tests, during and immediately after the recovery protocol, and then 30 minutes, 60 minutes, and 1, 2, and 3 days postexercise. The order in which the testing occurred at baseline and 30 and 60 minutes postexercise was the following: rating of perceived exertion and muscle soreness, followed by blood lactate test, 3-second maximum voluntary contraction (MVC), sit-and-reach, countermovement-jump test, and finally a single Wingate performance (with 2 min between tests). Muscle hemodynamics were monitored at rest before the exercise (baseline), during the exercise
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Figure 2 — Summary of testing schedule and measurements taken in this study. Abbreviations: RPE, rate of perceived exertion; MVC, maximum voluntary contraction; NIRS, near-infrared spectroscopy; WBV, whole-body vibration.
bout, and during the 10-minute recovery program and then again during a 1-minute rest after the recovery program (post; Figure 2). A drop of capillary blood was taken from the fingertip (using standard aseptic technique) at baseline, immediately after the bout of Wingate tests, and at 30 and 60 minutes postexercise. Samples were immediately analyzed using a portable lactate analyzer (Lactate Pro, Arkray Inc, Kyoto, Japan). The Wingate variables recorded for each test included anaerobic power (peak power divided by body weight) and fatigue index (peak power minus minimum power divided by testing duration). Explosive power was determined by the maximum-effort countermovement-jump test using standard procedures (Yardstick, Swift Performance Equipment, New South Wales, Australia). The best of 3 attempts was recorded. Quadriceps strength was evaluated by measuring the 3-second MVC of the knee-extensor muscles. In a sitting position (with the knee flexed at 80°), athletes were verbally encouraged to exert a maximal force lasting 3 seconds. A load cell (Tension/S-beam load cell, 10 Hz, AST 500, PT instruments, UK) attached to the ankle with a Velcro strap 3 cm above the medial malleolus was used to measure the force. Lower-back and hamstring flexibility was evaluated using the traditional sit-and-reach test, for which the best of 3 attempts was recorded. The reliabilities of performance tests (measured via the intraclass correlation coefficient) were .74 for anaerobic power, .79 for the fatigue index, .98 for the jump test, .93 for the 3-second MVC, and .98 for the sit-and-reach test. Participants’ ratings of perceived exertion were evaluated using the 15-point Borg scale (range 6–20: 6 = no exertion, 20 = maximal exertion).15 Muscle soreness was determined using a visual analog scale (range 0–10: 0 = no pain, 10 = the worst pain). The scale was previously validated as a reliable instrument for measuring pain intensity.16 Both scales were rated at baseline, immediately after the Wingate sprints, and at 30 and 60 minutes postexercise. Only the muscle-soreness score was rated during baseline and at 1, 2, and 3 days postexercise. Muscle hemodynamics were assessed by near-infrared spectroscopy (NIRS; NIRO-200, Hamamatsu Photonics KK, Hamamatsu, Japan). The NIRO-200 provides changes in oxygenated hemoglobin (O2Hb) and deoxygenated hemoglobin (HHb) and
derived changes in total hemoglobin (tHb = O2Hb + HHb), as previously described.17,18 Tissue oxygen saturation is also reported as the tissue-oxygenation index (TOI, percentage ratio of oxygenated to total hemoglobin), calculated by the NIRS system via spatially resolved spectroscopy from the light-attenuation slope along the distance from the emitting point as detected by 2 photodiodes in the detection probe. The probes, separated by 4.5 cm, were housed in an optically dense plastic holder and securely attached to the middle portion of the right vastus lateralis muscle at the midthigh level and parallel with the long axis of the muscle with tape to minimize extraneous light contamination. At the site, the skin was shaved and marked with a permanent marker, and the location measurements were recorded to ensure repeated testing at the same location for subsequent trials. The probes were attached before any exercise and remained attached throughout the exercise and the recovery period. The NIRS data were analyzed by averaging values over a 1-minute period at baseline, 1-minute post-Wingate tests, initial 5 minutes and last 5 minutes of the recovery program, and finally 1 minute after the recovery program. After 16 participants finished the WBV and active recovery, a subset of 6 participants repeated the testing, at least 1 week after their last trial, while doing a passive recovery program that involved sitting quietly in a chair for the 10 minutes of recovery to investigate differences in tissue hemodynamics without any recovery at all (ie, a control condition). A cycle ergometer rather than a treadmill was used in these athletes because of the ease with which to gather the NIRS data. A spreadsheet for the analysis of crossover trials was used to estimate worthwhile differences and chances that true effects were substantial.19 The spreadsheet for within-subject modeling used the unequal-variances statistic to assess for statistically worthwhile differences among repeated-measurement analysis.20 The smallest worthwhile change was set at 1% for performances and 0.20 standardized units (change in the mean divided by the between-subjects SD at baseline) for physiological variables.21 Uncertainties in the estimate of change are presented as the 95% confidence intervals and likelihoods that the true value of the effect was a substantial enhancement or impairment. P values were also taken from the spreadsheet for researchers who are not accustomed to magnitudebased inference statistics.
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Results Blood lactate concentration followed a similar pattern of change throughout the recovery period (Table 1); however, relative to the active recovery condition blood lactate concentration was
substantially higher 30 minutes postexercise among participants undertaking WBV. Anaerobic power followed a similar pattern of change throughout the series of Wingate tests and during the recovery period in both conditions (Table 1). Anaerobic performance and fatigue
Table 1 Baseline (Pretest), Prerecovery (Immediately After Exercise), and Postrecovery (30 min and 60 min) Changes in Measured Parameters in the WBV and Active-Recovery Groups and the Chances That True Differences Between Groups Were Substantial Chances That True Differences Are Substantialb
% Change Measure
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Lactate (mmol/L)
Rating of perceived exertion
Anaerobic power (W/kg)
Fatigue index (W/s)
MVC (kg)
Jump height (cm)
Sit-and-reach (cm)
Muscle soreness
Timea
WBV
Active
1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 5 6 7
2.1 15.0 8.3 8.2 6.4 18.3 9.6 8.2 9.5 7.3 9.3 9.6 11.7 12.7 11.6 11.3 67.6 — 61.4 63.2 43.9 — 42.3 43.1 24.9 — 24.8 25.8 0.9 7.9 3.6 2.6 1.4 0.8 0.6
2.4 15.6 7.2 8.2 6.7 18.2 10.6 8.8 9.3 7.8 9.4 9.5 11.8 13.3 11.5 11.7 68.5 — 62.1 64.0 44.8 — 43.1 42.8 24.9 — 25.4 26.4 0.8 8.1 3.7 2.9 1.8 1.0 0.4
WBV
Active
% difference ± 95%CI
%
Qualitative
P
614.3 –44.7 –1.2
550.0 –53.8 13.9
64.3 ± 227.8 9.1 ± 9.0 –15.1 ± 33.9
12 96 17
Unclear Very likely Unclear
.37 .05 .43
185.9 –47.5 –14.6
171.6 –41.8 –17.0
14.3 ± 32.9 –5.7 ± 5.8 2.4 ± 12.0
21 89 7
Unclear Trivial Unclear
.74 .10 .30
–23.2 27.4 3.2
–16.1 20.5 1.1
–7.1 ± 7.1 6.9 ± 8.9 2.1 ± 11.3
6 56 25
Unclear Unclear Unclear
.30 .43 .52
8.5 –8.7 –2.6
12.7 –13.5 1.7
–4.2 ± 18.9 4.8 ± 13.1 –4.3 ± 16.6
12 48 10
Unclear Unclear Unclear
.61 .48 .60
–9.2 2.9
–9.3 3.1
0.1 ± 8.8 –0.2 ± 14.2
35 15
Unclear Unclear
.70 .85
–3.6 1.9
–3.8 –0.7
0.2 ± 3.6 2.6 ± 2.7
3 22
Unclear Trivial
.91 .07
–0.4 4.0
2.0 3.9
–2.4 ± 8.0 0.1 ± 7.9
21 6
Trivial Unclear
.42 .89
777.8 –54.4 –27.8 –46.2 –42.9 –25.0
912.5 –54.3 –21.6 –37.9 –44.4 –60.0
–134.7 ± 76.1 –0.1 ± 10.4 –6.2 ± 20.9 –8.3 ± 40.9 1.5 ± 30.0 35 ± 15.0
53 15 59 39 18 61
Unclear Unclear Unclear Unclear Unclear Trivial
.57 .62 .41 .72 .84 .19
Abbreviations: WBV, whole-body-vibration group; active, active-recovery group; CI, confidence interval; MVC, 3-s maximal voluntary contraction. a 1 = baseline (or 1st Wingate), 2 = immediately postexercise (prerecovery or 6th Wingate), 3 = 30 min postrecovery, 4 = 60 min postrecovery, 5 = 1 d postrecovery, 6 = 2 d postrecovery, and 7 = 3 d postrecovery. b Based on the smallest substantial change set at 1% for performances ± 95% CI: add and subtract this number to the mean effect to obtain confidence intervals for the true difference.
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Muscle soreness increased substantially immediately after the series of Wingate tests (Table 1); however, there was little effect of WBV relative to active recovery on muscle-soreness recovery over the following 3 days. Changes in O2Hb, HHb, tHb, and TOI from the preexercise baseline across the 4 time points assessed during the first 12 minutes of recovery are illustrated in Figure 3. During WBV recovery, participants had a substantially greater increase in O2Hb from baseline levels at 10 minutes postexercise (197.7 ± 68.5 μM/cm,
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index were similar between the WBV and active recovery condition during recovery, with all differences being small and unclear. In addition, relative to the active recovery, WBV had little effect on recovery from 3-second MVC, vertical jump, or flexibility at 30 and 60 minutes postexercise. After strenuous exercise, rating of perceived exertion dramatically declined at 30 and 60 minutes postexercise for both conditions. Differences between recovery programs were trivial or unclear at 30 and 60 minutes postexercise (Table 1).
Figure 3 — Changes in oxygenated hemoglobin (O2Hb), deoxygenated hemoglobin (HHb), total hemoglobin (tHb), and tissue-oxygenation index (TOI) at the pretest (rest), start of the recovery program (0 min after the 6 Wingate test), 5 and 10 minutes during postrecovery program and post (after the 10-min recovery program) for the passive (triangles), active (closed circles), and whole-body-vibration (WBV) (open circles) groups, mean ± SD. aSubstantial difference between the WBV and passive groups. bSubstantial difference between the active and passive groups. cSubstantial difference between the WBV and active groups.
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Vibration and Performance Recovery 393
mean ± 95% CI) than with either a traditional active recovery protocol (138.2 ± 35.6 μM/cm) or passive recovery (119.4 ± 34.9 μM/cm). The WBV condition also had a substantially greater increase in O2Hb postrecovery (1 min after the 10-min recovery protocol; 227.1 ± 69.0 μM/cm) than with passive recovery (99.1 ± 36.6 μM/cm). For the active recovery condition there was a substantially greater increase in HHb levels 10 minutes postexercise and at postrecovery (106.5 ± 37.8 and 12.5 ± 11.3 μM/cm, respectively) than with both passive recovery (–1.6 ± 36.5 and –3.8 ± 36.5 μM/ cm) and the WBV condition (–64.3 ± 36.8 and –31.1 ± 37.7 μM/cm), while the changes from baseline for passive recovery HHb levels were substantially greater than WBV for the same time. The active recovery and WBV conditions had substantially greater increases in tHb levels 5 and 10 minutes postexercise and postrecovery (active recovery: 223.4 ± 42.8, 244.7 ± 32.0, 163.3 ± 32.9 μM/cm; WBV: 197.5 ± 55.7, 133.4 ± 78.3, 196.0 ± 80.6 μM/cm, respectively) than with passive recovery (182.5 ± 20.29, 117.9 ± 23.8, 95.3 ± 25.3 μM/cm, respectively) Active recovery substantially increased tHb levels from baseline more than with WBV at 10 minutes postexercise, while at postrecovery, tHb levels after WBV were substantially higher than with active recovery. Muscle oxygenation (TOI) during active recovery was substantially lower 10 minutes postexercise and postrecovery (63.7% ± 3.8%, 69.5% ± 1.8%) than with WBV (74.5% ± 1.4%, 72.2% ± 2.3%) and the passive recovery condition (72.9% ± 2.9%, 71.9% ± 2.4%). Furthermore, TOI at 10 minutes postexercise for the WBV condition was substantially higher than with passive recovery.
Discussion The novel finding of this study was that the WBV recovery program increased muscle oxygenation (TOI) compared with the active recovery program. However, even with increased oxygenation at the muscle level with WBV recovery, metabolic and performance variables changed little compared with the active recovery program over the first hour after an intense exercise session. We found that WBV during recovery was no better at decreasing blood lactate concentration after a high-intensity exercise session than a traditional active recovery. Moreover, at 30 minutes postexercise, WBV washed out lactate substantially less than the active program. However, the effect of WBV recovery on lactate clearance at 60 minutes postexercise was similar to the active program (ie, reduction from postexercise peak was the same). The mechanism for eliminating blood lactate with WBV exercise may be similar to that of the active recovery program, namely, by increasing blood perfusion for rapid distribution of lactate to be metabolized.22–24 Vibration increases vasodilatation effects through an increase in endothelium-derived vasodilators such as nitric oxide and prostaglandins2,3,25 or by reducing the release of the vasoconstrictor substance endothelin from vascular smooth muscle.5 However, this increased muscle blood flow did not seem to wash blood lactate out any faster in our participants. Our study demonstrated that WBV had effects similar to those of a traditional active protocol in terms of power and strength performance. Edge et al11 found that WBV training (12 Hz, 6-mm amplitude) had no substantial effect on lactate clearance and sport performance when undertaken on the following day compared with a control group. Those authors claimed that their WBV protocol at low frequency may not have been adequate to provide subsequent changes to enhance the recovery process. In contrast, Marin et al9 used high-frequency WBV (35–50 Hz, 1- to 2-mm amplitude, 30
min) combined with the traditional cooldown and found beneficial effects on improvement of vertical-jump height at 24 hours after vibration compared with the traditional cooldown. Our WBV protocol was comparable to the protocol of Marin et al, but we found no beneficial effect of WBV when compared with a conventional active program. However, our study only evaluated power and strength performance up to 60 minutes postexercise, which may be too short a period to detect significant beneficial effects of WBV. Similar to active recovery programs, it has been suggested that the elevated blood perfusion induced by WBV training enhances removal of blood lactate, H+, and other pain-causing substances, as well as reducing the inflammation process.22–24,26 We found that WBV and the active recovery program had similar effects on reported muscle soreness after strenuous exercise in athletes. Likewise, Marin et al9 found no significant difference in pain reduction between vibration and control cooldown recovery in soccer players.9 In contrast, Rhea et al10 showed that stretching and massage in conjunction with vibration significantly reduced perceived pain compared with stretching only in untrained volunteers. The differences between these 2 findings may be due to the fact that untrained subjects usually suffer more pain than trained athletes27 such as those in this study. As with the blood lactate and muscle-soreness results, we found no substantial difference in perceived exertion between the WBV and active recovery programs. Ratings of perceived exertion have been associated with levels of lactate, muscle soreness, and cardiopulmonary and psychological stress.28 The findings of our study indicated that WBV reduced overall perceived exertion in a fashion similar to that of the active recovery program. We also observed that WBV had a similar effect on flexibility compared with active recovery. Cronin et al29 found a greater improvement in flexibility at a higher vibration load (44 Hz, 5 mm for 30 s). In addition, Issurin et al8 found that vibration (44 Hz, 3 mm, total 7 min) during stretching exercise 3 times a week for 3 weeks significantly increased leg and trunk flexibility compared with conventional stretching (by 7.5% and 37.8%, respectively). We applied a vibration frequency and amplitude approximately similar to these previous studies; however, to increase flexibility, it seems likely that more than 1 session of WBV is required. The current study found that both WBV and active recovery programs increased muscle blood flow during recovery (ie, increased tHb indicating an increased muscle blood volume), which may signal increased oxygen availability to the muscle. Furthermore, the data obtained from the subset of participants who also performed a passive recovery protocol support this elevated perfusion relative to being inactive during recovery. However, at the end of the recovery protocol (at 10 min), the active recovery condition had a higher tHb than with the WBV. This apparent contrasting effect requires explanation. We observed similar performance measures during the Wingate tests before both recovery conditions, so muscle blood flow was presumably the same. However, after 10 minutes of the recovery program, muscle blood flow appeared more elevated in the active condition, which we suggest is probably due to the added metabolic demands of the active recovery protocol that may require more blood flow relative to the shearing stress-mediated response induced via the vibration.2,3,25 In addition, WBV increased muscle oxygenation (TOI) while the active program decreased it. The underlying mechanism is likely to be linked to the vasodilatation process linked with muscle metabolism (as reflected by increased O2Hb and decreased HHb). While the active recovery probably increases muscle workload, thereby increasing the need for oxygen supplied (increased flow) and increasing the amount of oxygen extracted (resulting in increased
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HHb concentration), the WBV recovery may cause vasodilatation without the need for an increase in oxygen uptake at the muscles. In contrast, previous research revealed that WBV training increases oxygen utilization and decreases muscle oxygenation levels similar to light or moderate exercise.30,31 However, Mileva et al30 used WBV during squatting or knee-extension exercises, while our study used stretching and vibration massage during WBV, which is likely to produce less muscle workload and perhaps a greater vasodilatation effect independent of metabolism. In terms of muscle-oxygenation levels, stretch or massage during WBV may be more suitable as a recovery program than static or dynamic exercise. Furthermore, we found that the vasodilatation effect of WBV persisted at 1 minute after the recovery protocol (as reflected in increased tHb and increased O2Hb) compared with the active recovery and passive recovery conditions. Likewise, previous studies have found a vasodilatation effect after WBV training.2,32 Reduction of vasoconstrictor substances and increasing vasodilators may be preserved after vibration.2,5 The vasodilatation after WBV may well enhance blood flow to the muscle for longer, perhaps benefiting subsequent performances. Future research is required to investigate the post-WBV vasodilatation effect on performance recovery, particularly aerobic performance since enhanced oxygenation of the muscle tissue should have its greatest effect on aerobic metabolism. We acknowledge that a limitation of this study is the relatively small number of participants in the passive recovery group, which was lower than in the other 2 recovery groups. Initially, this study aimed to compare the effect of WBV recovery with conventional exercise recovery, but it became obvious that little information existed for NIRS data on passive recovery, so we asked the subjects to return for further passive recovery testing. Unfortunately, a number of participants had prior engagements and were unable to attend this testing. Accordingly, the results of the passive recovery testing should be considered hypothetical until substantiated with further research on a larger subject pool. A further limitation is that the PowerPlate device used in this study did not directly calculate the amplitude and acceleration values. These values were calculated from the peak-to-peak displacement and acceleration using information from Pel et al.14 Similarly, we did not measure acceleration of WBV when only part of body was placed on the platform (as in some of the exercises used in this study) and suggest that future studies investigate changes in these parameters when only part of the body is placed on the vibrating platform.
Practical Applications WBV has an effect on short-term explosive-performance recovery similar to that of conventional recovery protocols. The increase in muscle oxygenation found after WBV may assist recovery of aerobic metabolism, but the added cost and logistics of using WBV may overcome any potential benefits.
Conclusion Monitoring of muscle oxygenation levels revealed that the WBV recovery program improved muscle oxygenation without the subsequent increase in energy demand required by active recovery. However, the WBV and the active recovery program had similar effects on lactate recovery, power, strength, flexibility, rating of perceived exertion, and muscle pain after intensive exercise in rugby players.
Acknowledgments Special thanks to the athletes for their contribution and participation and the PowerPlate Company for supporting the vibration machine. The results of the current study do not constitute endorsement of the product by the authors or the journal.
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