Alterations to skeletal muscle architecture, which typically occur after intense exercise training, include primary or secondary sarcolemmal disruption, swelling or disruption of the sarcotubular system, distortion of the myofibrils' contractile components, cytoskeletal damage, and extracellular myofiber matrix abnormalities (21). The mechanical stimuli from intense exercise training lead to a cascade of cellular processes (i.e., muscle protein turnover, inflammation), which increase muscle soreness and discomfort. Skeletal muscle disruptions resulting from exercise training are known as exercise-induced muscle damage (EIMD) (39). Exercise-induced muscle damage typically occurs during the initial phases of an exercise training program and when the training principles of overload, variety, periodization, or increased volume (frequency, duration) are adopted (39). Symptoms of EIMD include muscle and joint stiffness, acute inflammation and swelling, a decrease in muscle force production, and delayed onset muscle soreness (DOMS) (12,39). Exercise-induced muscle damage can be quantified by assessing the concentrations of skeletal troponin I, myoglobin, and myosin heavy chain (12,40) but is more commonly assessed by plasma creatine kinase levels (CK) (4). Typically, an increase in CK after intense muscle contraction represents muscle fiber damage (2). During exercise, especially with eccentric muscle contractions, alterations to the normal binding pattern or alignment of muscle fibers occur, which results in CK release (2) into the lymphatic system and eventually the blood stream (12).
Two central theories exist that may help explain EIMD during exercise training. The mechanical stress model is theorized to be the primary cause of EIMD (12) and is characterized by eccentric or forced-lengthening muscle contractions (21). High-tension eccentric contractions stretch or disrupt Z line and sarcomere structure (11,21), resulting in greater EIMD. High-tension eccentric contractions typically result in a 50–65% loss of force-generating capacity (12) and significant muscle soreness, which may be caused by increased calcium-activated neutral proteases (21), lysosomal proteases (21), and prostaglandin E2 (PGE-2), a main regulator of inflammation (34). It is well established that eccentric contractions produce higher muscle force compared with concentric, isokinetic, or isometric muscle contractions per unit of muscle (39), possibly because of the greater mechanical stress per muscle fiber (39) and greater muscle hypertrophy (19). Alternatively, the metabolic stress theory suggests that EIMD may be the product of metabolic deficiencies within the working muscle, which causes the muscle to become vulnerable to mechanical and oxidative stress (12,39). Specifically, the inability of Ca2+ -adenosine triphosphatase (ATPase) to function properly is implicated in the metabolic stress theory (39). The decreased action of Ca2+ ATPase compromises the removal of Ca2+ from the cytosol, which may result in muscle fiber degeneration with subsequent training sessions.
Delayed onset muscle soreness is classified as a type I muscle strain injury (11,24), and may lead to an irregular maintenance of a training program for athletes and exercising individuals (36), possibly because of muscle aches and pain, discomfort, and inflammation (2,4,11). Delayed onset muscle soreness is generally concentrated in the distal portions of skeletal muscle and peaks around 24–48 hours postexercise (4,11,12). Mechanistically, localized muscle soreness has been attributed to a higher concentration of pain receptors in the connective tissue in the myotendinous regions (11). The myotendinous junction is a membrane that is extensively folded and integrated into the skeletal muscle cells. The oblique arrangement of muscle fibers just before the myotendinous region reduces the ability of the muscle to withstand intense mechanical stimuli (11), leading to microscopic damage and inflammation (12). Inflammatory signaling compounds such as PGE-2 are upregulated and may blunt the muscle protein synthetic response after exercise (16) because PGE-2 decreases the stimulation of the mammalian target of rapamycin signaling pathway (23). Subsequently, increased levels of the proinflammatory cytokines interleukin-6, tumor necrosis factor-α, and C-reactive protein, which upregulate the synthesis of PGE-2, have been linked to increased inflammation (22,32,33). Cytokines target the site of muscle disruption and act as mediators by either facilitating or impeding the influx of inflammatory cells into the injured tissue (12). Exercise that results in substantial muscle damage leads to a well-organized recovery response for the repair and regeneration of damaged tissues, known as the acute response phase (17). Because of the loss of muscle function, which is the end result of EIMD and DOMS, it is important to minimize muscle damage to increase muscle recovery for subsequent exercise training sessions. Emerging research suggests that vibration be considered as a strategy to possibly reduce muscle soreness in relation to exercise training.
Fundamentals of Whole-Body Vibration
Vibration is any motion that repeats itself after a given period of time (35). Free vibration occurs if a system, independent of external forces, moves on its own (e.g., pendulum), whereas forced vibration occurs when a system is subjected to an external force (often a repeating type of force) (35). Vibrations can be either deterministic or random and are characterized by frequency and amplitude. Frequency is the number of cycles per unit time (generally per second) and is typically measured in the hertz (8,30). Amplitude is the half difference between the maximum and the minimum value of the periodic oscillation (30). One hertz is 1 cycle per second (43); therefore, when a subject is exposed to a vibration of 30 Hz, the targeted muscles receive 30 cycles of vibration per second, which makes the muscles contract and relax 30 times in the same period. To activate the muscle most effectively, the vibration frequency should be in the range of 30–50 Hz (30). Depending on the desired outcome, different frequencies may be required. The duration and kinetics of the recovery period are determined by a number of factors (e.g., age, muscle volume, fiber type, prior fatigue level, years of training, prior vibration training) (13). In day-to-day life, people are exposed to many different forms of vibration. Everyday transportation vehicles such as boats, cars, bicycles, planes, helicopters, and trains exert vibrations on the human body (31). Even musical instruments cause vibrations through sound waves (35). Many sporting activities also have high levels of vibration. Sports such as alpine skiing, off-road cycling, surfing, inline skating, and horseback riding, and also simply running and jumping create oscillatory motion that leads to vibratory effects (31).
Whole-body vibration is a neuromuscular training technique that uses low to moderate multidimensional mechanical oscillations on both sides of a fulcrum that pivot to produce vibration, either vertically or horizontally, which triggers the tonic vibration reflex (TVR) (1,25,44). Biomechanical parameters influencing the intensity of mechanical stimulus are determined primarily by the frequency and amplitude of the vibration and, to a lesser degree, by the number of deflections per minute (10). Frequencies studied range from 15 to 44 Hz, amplitudes from 3 to 10 mm, and gravitational loads from 3.5 to 15g (10). Whole-body vibration–induced physiological changes have been suggested to be similar to those after several weeks of resistance training (5). The main variables that determine the magnitude of response to WBV include (a) vibration direction (i.e., vertical vs. oscillatory), (b) vibration amplitude (millimeters), (c) vibration frequency (Hertz), (d) vibration acceleration (gravitational units, 1.0g = 9.81 m·s−2), and (e) body position on the platform.
Whole-body vibration training involves an individual standing, sitting, or laying on a vibrating platform performing a static or dynamic exercise at various frequencies (42). The vibration can be applied to individual body segments, eliciting involuntary reflex contractions through the TVR (6,9). During vibration, the TVR is continually activated causing multiple muscle contractions (42), possibly because of greater motor neuron activation (7) and recruitment (44) and by increased synchronization of synergist muscles (6,10,40). Whole-body vibration is theorized to increase the amount of gravitational load placed on the neuromuscular system (5,10), resulting in greater muscle cross-sectional area and force-generating capacity (14,20).
Whole-Body Vibration as a Recovery Modality
Recovery modalities such as massage, cryotherapy, stretching, and ultrasound have not been proven to be consistent in alleviating symptoms of DOMS (11,28,36). Over the past few years, research indicates that WBV should be considered as a potential intervention to accelerate muscle recovery after exercise training (2,4,28,36). Whole-body vibration increases muscle spindle activity and muscle preactivation (i.e., lower firing threshold), which results in greater background tension and less disruption to excitation-contraction coupling (2,4,28). Theoretically, with an increase in muscle preactivation, a greater number of motor units and muscle fibers would be recruited, which may reduce myofibrillar stress during repeated muscle contractions leading to accelerated recovery (6). For example, using a crossover experimental design to determine the effects of single-limb vibration (6 minutes, 65 Hz) 30 minutes after eccentric exercise (10 sets of 6 maximal contractions) on DOMS in young men, Lau and Nosaka (28) observed a significant decrease in muscle soreness (18–30%) of the vibration-treated limb compared with the control limb. Serum CK activity increased in both limbs after exercise by ∼60%, but after 4 days of recovery, CK activity was decreasing at a faster rate with vibration. Potentially, vibration therapy may have influenced the activation of afferent input from sensory units in muscle fibers and attenuated pain sensation associated with exercise or increased lymphatic blood flow and the removal of metabolic wastes (H+) (28). Furthermore, untrained adults (N = 15) who maintained a static half-squat position for 60 seconds on a WBV platform (35 Hz) before performing 6 sets of 10 maximal voluntary isokinetic eccentric (60°·s−1) knee extensors contractions experienced a decrease in muscle damage (i.e., CK) and soreness compared with participants who did not perform WBV before exercise (2). Creatine kinase levels were 46% higher in the control group 24 hours postexercise and remained elevated for up to 7 days. Participants in the control group also experienced greater muscle soreness in the days after the exercise bout. The authors speculate that WBV performed before exercise may have increased recruitment of slow-twitch muscle fibers and broadened the contractile stimulus over a larger number of muscle fibers (i.e., fast twitch and slow twitch combined), resulting in less muscle damage (2). In examining the potential effects of WBV (35 Hz) on DOMS, Rhea et al. (36) showed that young untrained adults who performed WBV (90 seconds of static stretching of the gastrocnemius, hamstring, and quadriceps) immediately after eccentric resistance training (4 sets of 8–10 repetitions; exercises: squat, leg extension, leg curl, calf raise, and deadlift) and sprinting exercise (10 maximal 40-yard sprints) experienced a significant reduction in muscle pain (visual analogue scale, 22–61%) for up to 72 hours postexercise compared with subjects who performed the same stretches without WBV. These results suggest that WBV is an effective intervention to attenuate muscle pain after intense exercise training, possibly by stimulating skeletal blood flow (29) and increasing metabolic waste disposal (15) or by inhibiting pain sensory receptors (36). Finally, in assessing the effects of lower-limb vibration therapy (quadriceps, hamstrings, and calf; 50 Hz for 1 minute) before walking downhill (treadmill, 10° decline at 4 km·h−1 for 30 minutes) in young adults, Bakhtiary et al. (4) discovered that WBV resulted in a significant reduction in muscle soreness and subsequent decrease in plasma CK levels postexercise compared with subjects who did not perform WBV. In contrast, WBV (12 Hz, 2 × 15–minute sessions) performed after high-intensity interval training (3-km time trial, 8 × 400–m sprints) in 9 well-trained male runners had no effect on exercise performance or muscle damage. The authors suggest that the lower hertz (12 Hz) used may not have been frequent enough to produce meaningful results (15). Bullock et al. (8) suggest that a frequency of ≤30 Hz and an amplitude of 4 mm is too small of a stimulus to produce meaningful benefits in elite athletes, possibly because of advanced training status and neuromuscular adaptations. For example, well-trained athletes and exercising individuals have high muscle strength, motor neuron excitability, reflex sensitivity, and fast-twitch fiber recruitment, which may diminish the effects of WBV compared with untrained individuals (2). Rønnestad (38) suggests that the optimal frequency for trained individuals is 50 Hz, as the knee extensors reach maximum force output around 50–60 impulses per second. A vibration frequency of 50 Hz would potentially cause muscle spindles to fire at a rate of 50 impulses per second and increase the excitatory stimulus to the motor neuron pool compared with lower frequencies (38). However, 50 Hz coupled with the amplitude of 4–6 mm may be too strong of a stimulus for untrained individuals (27).
As with any form of training, one must consider the principles of progressive overload: training frequency, volume, and intensity (3). Lamont et al. (27) suggest that is more practical to periodize vibration exposure starting at lower frequencies and amplitudes before progressing to higher frequencies and amplitudes with shorter exposure time. The gradual increase in vibration intensity may lead to greater neuromuscular, skeletal, and exercise performance benefits over time (18,27).
Safety of Whole-Body Vibration
Among the potential positive aspects of WBV, research is limited regarding the safety of vibration. Exclusion criteria for most studies reviewed include kidney or bladder stones, arrhythmia, pregnancy, epilepsy, seizures, cancer, a pacemaker, untreated orthostatic hypotension, recent implants (e.g., joint, corneal, or cochlear), recent surgery, recently placed intrauterine devices or pins, acute thrombosis or hernia, acute rheumatoid arthritis, serious cardiovascular disease, severe diabetes, or migraines (41). A clinical trial investigating the effects of passive standing and WBV among individuals with spinal cord injuries reported adverse effects including pain, pressure sores on the feet, autonomic dysreflexia, and dizziness, which were largely attributed to the passive standing portion of the intervention (41). Whole-body vibration may cause inner-ear problems, dizziness, headache, lower-limb spasticity, fracture (especially among those with severe osteoporosis), or hardware loosening (plates or screws as a result of surgery) over the long term (41).
The majority of adverse effects from vibration occur in occupational settings (26). Occupational vibrations typically come from electrical tools or heavy machinery, with frequencies ranging from 80 to 100 Hz (29). Long-term occupational vibrations have been shown to negatively affect peripheral nerves, blood vessels, joints, and perceptual function (26,41). Because of the potential health hazards of occupational vibrations, the International Organization of Standards created guidelines limiting occupational exposure to vibration (37). The frequency and magnitude of occupational vibrations differ from those used with WBV as an exercise training modality (26,41). Overall, very little is documented or published regarding adverse effects or serious adverse effects as a result of WBV exposure. Among published literature, several studies using a low-magnitude, high-frequency WBV stimulus among populations with physical or neurological impairments have reported no adverse reactions (41), although it is important to keep in mind that shock and vibration are potentially harmful, in particular to the soft tissue organs in the head and chest (37).
Muscle soreness after exercise training may eventually jeopardize training status for athletes and exercising individuals. In addition to traditional therapies, WBV shows promise for alleviating symptoms of muscle soreness, which may in turn allow athletes to exercise more frequently leading to an increase in sporting performance over time. Evidence suggests that vibration therapy both before and after exercise, especially after eccentric contractions, is beneficial, although little is known regarding the timing of application. Future research should investigate the effects of the timing of vibration therapy (i.e., before vs. after exercise) on indices of muscle biology. Furthermore, long-term application of vibration therapy on bone biology should also be considered.
1. Abercromby A, Amonette W, Layne C, McFarlin B, Hinman M, Paloski W. Vibration exposure and biodynamic responses during whole-body vibration training. Med Sci Sports Exerc 39: 1794–1800, 2007.
2. Aminian-Far A, Hadian M, Olyaei G, Talebian S, Bakhtiary AH. Whole-body vibration and the prevention and treatment of delayed onset muscle soreness. J Athl Train 46: 43–49, 2011.
3. Baechle TR, Earle RW. Essentials of Strength Training and Conditioning (3rd ed.). Windsor, ON: Human Kinetics, 2008.
4. Bakhtiary AH, Safavi-Farokhi Z, Aminian-Far A. Influence of vibration on delayed onset muscle soreness following eccentric exercise. Br J Sports Med 41: 145–148, 2007.
5. Bosco C, Cardinale M, Tsarpela O. Influence of vibration on mechanical power and electromyogram activity in human arm flexor muscles. Eur J Appl Physiol 79: 306–311, 1999.
6. Bosco C, Colli R, Introini E, Cardinale M, Tsarpela O, Madella A, Tihanyi J, Viru A. Adaptive responses of human skeletal muscle to vibration exposure. Clin Physiol 19: 183–187, 1999.
7. Bosco C, Iacovelli M, Tsarpela O, Cardinale M, Bonifazi M, Tihanyi J, Viru M, De Lorenzo A, Viru A. Hormonal responses to whole-body vibration in men. Eur J Appl Physiol 81: 449–454, 2000.
8. Bullock N, Martin DT, Ross A, Rosemond CD, Jordan MJ, Marino F. Acute effect of whole-body vibration on sprint jumping performance in elite skeleton athletes
. J Strength Cond Res 22: 1371–1374, 2008.
9. Burke D, Hagbarth KE, Lofstedt L, Wallin BG. The responses of human muscle spindle endings to vibration during an isometric contraction. J Physiol 261: 695–711, 1976.
10. Cardinale M, Bosco C. The use of vibration as an exercise intervention. Exerc Sport Sci Rev 31: 3–7, 2003.
11. Cheung K, Hume PA, Maxwell L. Delayed onset muscle soreness: Treatment strategies and performance factors. Sports Med 33: 145–164, 2003.
12. Clarkson PM, Hubal MJ. Exercise induced muscle damage in humans. Am J Phys Med Rehabil 81: S52–S69, 2002.
13. Da Silva-Grigoletto ME, Vaamonde DM, Castillo E, Poblador MS, García-Manso JM, Lancho JL. Acute and cumulative effects of different times of recovery from whole body vibration exposure on muscle performance. J Strength Cond Res 23: 2073–2082, 2009.
14. Duchateau J, Enoka RM. Neural adaptations with chronic activity patterns in able-bodied humans. Am J Phys Med Rehabil 81: S17–S27, 2002.
15. Edge J, Mündel T, Weir K, Cochrane DJ. The effects of acute whole body vibration as a recovery modality following high-intensity interval training in well-trained, middle aged runners. Eur J Appl Physiol 105: 421–428, 2009.
16. Evans WJ. Skeletal muscle loss: Cachexia, sarcopenia, and inactivity. Am J Clin Nutr 91: 1123S–1127S, 2010.
17. Evans WJ, Cannon JG. The metabolic effects of exercise-induced muscle damage. Exerc Sport Sci Rev 19: 99–126, 1991.
18. Fagnani F, Giombini A, Di Cesare A, Pigozzi F, Di Salvo V. The effects of a whole-body vibration program on muscle performance and flexibility in female athletes
. Am J Phys Med Rehabil 85: 956–962, 2006.
19. Farthing JP, Chilibeck PD. The effects of eccentric and concentric training at different velocities on muscle hypertrophy. Eur J Appl Physiol 89: 578–586, 2003.
20. Fitts RH, Riley DR, Widrick JJ. Functional and structural adaptations of skeletal muscle to microgravity. J Exp Biol 204: 3201–3208, 2001.
21. Fridén J, Lieber RL. Structural and mechanical basis of exercise induced muscle injury. Med Sci Sports Exerc 24: 521–530, 1991.
22. Gokhale R, Chandrashekara S, Vasanthakumar KC. Cytokine response to strenuous exercise in athletes
—An adaptive response. Cytokine 40: 123–127, 2007.
23. Greig CA, Atherton PJ, Rennie MJ. Can an NSAID a day keep muscle wasting away? J Physiol 15: 5799–5800, 2009.
24. Gulick DT, Kimura IF. Delayed onset of muscle soreness: What is it and how do we treat it? J Sport Rehabil 5: 234–243, 1996.
25. Hazell TJ, Kenno KA, Jakobi JM. Evaluation of muscle activity for loaded and unloaded dynamic squats during vertical whole-body vibration. J Strength Cond Res 24: 1860–1865, 2010.
26. Jordan MJ, Norris SR, Smith DJ, Herzog W. Vibration training: An overview of the area, training consequences, and future considerations. J Strength Cond Res 19: 459–466, 2005.
27. Lamont HS, Cramer JT, Bemben DA, Shehab RL, Anderson MA, Bemben MG. Effects of a 6-week periodized squat training program with or without whole-body vibration on jump height and power output following acute vibration exposure. J Strength Cond Res 23: 2317–2325, 2009.
28. Lau WY, Nosaka K. Effect of vibration treatment on symptoms associated with eccentric exercise-induced muscle damage. Am J Phys Med Rehabil 90: 648–657, 2011.
29. Lohman EB, Petrofsky JS, Maloney-Hinds C, Betts-Schwab H, Thorpe D. The effect of whole body vibration on lower extremity skin blood flow in normal subjects. Med Sci Monit 13: CR71–CR76, 2007.
30. Luo J, McNamara B, Moran K. The use of vibration training to enhance muscle strength and power. Sports Med 35: 23–41, 2005.
31. Mester J, Spitzenfeil P, Schwarzer J, Seifriz F. Biological reaction to vibration—Implications for sport. J Sci Med Sport 2: 211–226, 1999.
32. Pedersen BK. Exercise and cytokines. Immunol Cell Biol 78: 532–535, 2000.
33. Pedersen BK, Steensberg A, Fischer C, Keller C, Keller P, Plomgaard P, Wolsk-Petersen E, Febbraio M. The metabolic role of IL-6 produced during exercise: Is IL-6 an exercise factor? Proc Nutr Soc 63: 263–267, 2004.
34. Rainsford KD. Ibuprofen: Pharmacology, efficacy and safety. Inflammopharmacology. 17: 275–342, 2009.
35. Rao SS. Mechanical Vibrations (4th ed.). Upper Saddle River, NJ: Pearson Education, Inc., 2004.
36. Rhea MR, Bunker D, Marín PJ, Lunt K. Effect of iTonic whole-body vibration on delayed-onset muscle soreness among untrained individuals. J Strength Cond Res 23: 1677–1682, 2009.
37. Rittweger J. Vibration as an exercise modality: How it may work, and what its potential may be. Eur J Appl Physiol 108: 877–904, 2010.
38. Rønnestad BR. Acute effects of various whole-body vibration frequencies on lower body power in trained and untrained subjects. J Strength Cond Res 23: 1309–1315, 2009.
39. Tee JC, Bosch AN, Lambert MI. Metabolic consequences of exercise-induced muscle damage. Sports Med 37: 827–836, 2007.
40. Torvinen S, Kannus P, Sievanen H, Harvinen TA, Pasanen M, Kontulainen S, Järvinen TL, Järvinen M, Oja P, Vuori I. Effect of four-month vertical whole body vibration on performance and balance. Med Sci Sports Exerc 34: 1523–1528, 2002.
41. Totosy de Zepetnek JO, Giangregorio LM, Craven BC. Whole-body vibration as potential intervention for people with low bone mineral density and osteoporosis: A review. J Rehabil Res Dev 46: 529–542, 2009.
42. Vela CA. Whole-body vibration training: Shake up clients' work-puts with this low-impact training method. IDEA Fit 2: 23–25, 2005.
43. Wallace RH. Understanding and Measuring Vibrations. London, EN: Taylor & Francis Ltd., 1970.
44. Wilcock I, Whatman C, Harris N, Keogh J. Vibration training: Could it enhance the strength, power, or speed of athletes
? J Strength Cond Res 23: 593–603, 2009.