thresholds are sensitive to muscle length (Pasquet, Carpentier, & Duchateau, 2005). The muscle spindle is the primary sensory receptor that detects changes in muscle length and through 1a afferent feedback the efferent alpha motor neuron activity is regulated. Through the use of tendonvibration in this study to alter 1a afferent feedback the differential change in motor unit activity between heads indicates that the length dependent phenomenon is activated through 1a afferent spinal connections. The differential connectivity within the spinal cord might be governed through the rate at which the 1a afferent sends feedback to the spinal cord. Unlike the tibialis anterior which is a multipennate muscle with a singular origin and insertion the BB is a fusiform muscle that has two unique heads with independent origin and insertion points. The SBB and LBB originate on the coracoid process and supraglenoid tubercle of the scapula, respectively. Recent cadaveric studies of the BB have shown that the SBB and LBB also have unique insertion points on the distal radial tuberosity and proximal radial
A secondary finding of the present study was that a significant decrease in maximal voluntary force produc- tion was observed for at least 1 h in STIM but not STIM + Vib. It is important to note that these results were not influenced by the values obtained prior to the application of the electrical stimulation protocols (MVIC PRE), as these values were not statistically different (p = 0.19) and reliable between days (ICC = 0.95). This result showed an advantage of the superimposed tendonvibration that prevented the significant fatigue-induced decline in MVIC. Thus, in the clinical context, tendonvibration may provide a benefit of reduced voluntary muscle fatigue when compared to moderate-frequency, wide-pulse width NMES that could allow for further re- habilitation work or improved performance of activities of daily living and occupational tasks in the hours after a rehabilitation session. It is not clear from the present data how the vibration provided a fatigue-attenuation benefit. Speculatively, it may have reduced the synchrony of the motor unit activity during NMES, which may have then reduce the rate of muscle fatigue [45, 71]. This might occur if ongoing facilitation of fatigue-resistant motor units was provided due to the generation of trains of Ia afferent signals into the spinal cord, inducing an excitation of homonymous motor neurons through the development of persistent inward calcium (Ca 2+ ) or sodium (Na + ) currents (PIC) at their dendritic trees [45, 71]. Such a mechanism would evoke a tonic vibra- tory reflex influencing both spinal and supraspinal pathways [45, 71]. Tendonvibration-induced primary muscle spindle endings (i.e. Ia afferent activation) might also substitute for the fusimotor-driven Ia dis- charge and α-motor output decline that usually occurs during sustained voluntary contractions [49, 72]. This would have attenuated the muscle fatigue response ob- served in our study by continuing the Ia afferent activation response. Regardless of the potential mechanism, there seems to be a reversal of central drive failure when tendonvibration is superimposed onto wide-pulse width NMES, but further tests are needed to confirm this theory. How- ever, the levels of muscle voluntary isometric fatigue ob- served in the present study (−8% after STIM) were somewhat smaller than the 22–30% reported by other studies [20, 73, 74]. This discrepancy may be attributed to the use of biphasic wide-pulse width NMES, the use of a lower stimulation frequency (30 vs. 75 Hz) or different duty cycle ratio (2–2 vs. 5–15 s), or that muscles were activated to only 20% of MVIC (with ‘fatigue’ being 60% of this value) in comparison to maximal tolerable levels of MVIC used by others [20, 74, 75]. Further explanation of these possibilities is required to accurately explain the differences in voluntary fatigue.
and incomplete lesions to the spinal cord [58, 59]. A similar inter-individual variability in response to wide- pulse width NMES has also been suggested to originate from a difference in monoamine levels between individ- uals  and could be one reason for the different re- sponse to patellar tendonvibration superimposed onto wide-pulse width NMES observed in the current study. This difference in monoamine levels could be exacer- bated by the altered neuromuscular system in people with spinal cord injuries , such as changes in the ex- citability of the motor neurone , fibre type trans- formation towards fast-fatigable  and high levels of muscle atrophy . Another factor that could have de- creased the stretch reflex and thus prevented the forma- tion of PICs is the use of antispasmodic medications, such as Baclofen . On the other hand, the increased TTI in positive responders to patellar tendonvibration might be attributable to the development of tonic vibra- tion reflexes (TVR) which increase muscle force contribu- tions between the evoked muscular contractions [47, 64]. However, the activation of already hyper-excitable sensory pathways by the use of patellar tendonvibration in people suffering from a spinal cord injury may have either trig- gered episodes of intrinsic phasic spasticity in some partic- ipants , whilst attenuated spasticity symptoms in others , and thus may have increased the variability in the response to wide-pulse width NMES and patellar ten- don vibration observed in the present study. These hy- potheses will need to be explored in further studies investigating explicitly the pathophysiological responses (i.e. spasticity) of paralysed muscles to tendonvibration superimposed onto wide-pulse width NMES.
Recent research shows that vibration training may improve neuro-muscular performance (Bosco et al., 1999; Cardinale and Bosco, 2003; Cardinale and Lim, 2003; Cardinale and Wakeling, 2005). This improvement may result from recruitment of previously inactive motor units (Mischi and Cardinale, 2009), enhanced motor excitability (Cardinale and Bosco, 2003; Delecluse et al., 2003), increased muscle temperature and blood flow (Bosco et al., 1999) as well as facilitating neural functions resulting from tonic vibration reflex (Lapole and Perot, 2010). Tonic vibration is known to attenuate inhibitory effects of tendon reflex stem from SS. In order to address the controversy of using SS in pre-competition warm- up protocols, we added vibration with SS to observe if vibration might diminish the negative effects of SS. Therefore, we aimed to investigate the potential effects of tendonvibration on effects of SS on vertical jump performance.
This experimental study was conducted to find out the effect of Achilles tendonvibration on gait performance in ambulatory stroke patients of 20. This Study showed that 25, 55 and 20 of the respondents belonged to age group 30-45 years, 46-60 years and more than 60 years respectively. Similar findings have been highlighted in many others studies of Keenan MA, Kollen B and Hesse SA et. al editors. 18- 20 Study showed that the mean age of the respondents was
In a room maintained at 25.1 ± 0.2°C, each subject stayed in a semi-reclined position in a chair in which body position could be maintained, while the left elbow was kept at a 90° angle on a padded armrest with the wrist attached to an arm lever by a Velcro strap. The subjects rested for at least 20 minutes before data collec- tion began. After baseline data were collected for 5 min- utes, subjects performed: static elbow flexion at 35% MVC without vibration of the biceps tendon for 2 min- utes (EX); and static elbow flexion at 35% MVC with vi- bration of the biceps tendon for 2 minutes (EX + VIB). Each exercise period was followed by a recovery period of 1 minute. Static elbow flexion was produced using the same dynamometer that was used to measure the MVC (VINE), with visual feedback of the achieved force pro- vided via an oscilloscope display. For EX + VIB, tendonvibration was initiated 1 minute before starting exercise and continued during the exercise. Immediately after ex- ercise, subjects read instructions for the 6 to 20 rating of perceived exertion (Overall RPE) category scale devel- oped by Borg  and instructions for rating muscle fa- tigue sensation (Arm RPE) on a scale of 1 to 10 . In all trials, subjects regulated their respiratory frequency at 10 or 15 breaths/minute using a metronome, because exercise movement and respiratory cycle influence sym- pathetic nervous system activity. EX and EX + VIB were performed randomly, and the rest period between the two conditions was at least 20 minutes.
Treatment of chronic Achilles tendon rupture is still a challenge for most orthopedic surgeons. It is different from the acute Achilles tendon rupture as there are large gaps that will be bridged by scar tissue and muscle becomes infiltrated with fat, so ankle will be weak affecting the gait. Several techniques for chronic Achilles tendon reconstruction have been described, including turndown flap, tendon transfer, tendon graft, and augmentation with synthetic materials . In cases of neglected chronic tendo-Achilles ruptures, augmented tendo-Achilles repair provides stronger reconstruction and provides more biomechanical stability to the repair. Central gastro-soleus aponeurosis flap repair is superior to standard Kessler repair by virtue of its strength. Augmentation to the repair site allows earlier mobility, weight-bearing and a more aggressive rehabilitation program with reduction in the incidence of re-rupture for both acute and neglected Achilles tendon re- rupture. Lo et al.  reviewed the literature on the treatment of Achilles tendon rupture and identified 742operative cases and 248 cases managed conservatively. The overall rate of re-rupture was 3% for those managed operatively and 12% for those managed non-operatively.
Methods: A systematic review was carried out between May to July 2013 in the electronic databases: CINAHL, WOK, Medline, Scopus, PEDro, IME (CSIC) and Dialnet. The keywords used were: 1) in English: chronic, supraspinatus “ long head of the biceps tendon ” , biceps, rotator cuff, tendinosis, tendinopathy, evaluation, examination; 2) in Spanish: supraespinoso, biceps, tendinopatía. Inclusion criteria of the articles included subjects with a previously diagnosed chronic pathology of rotator cuff (RC) without previous surgery or any other pathologies of the shoulder complex. The total number of articles included in the study were five.
isometric ramp contraction, according to the principles previously described by Maganaris and colleagues (Maganaris, 2002; Maganaris and Paul, 2002). In brief, the ultrasound probe was placed over the distal myotendinous junction of the GM muscle in the sagittal plane. An external marker fixed to the skin, which cast a shadow on the ultrasound images, served as a reference position. The participants then conducted an isometric maximum voluntary plantarflexion contraction (MVC) at a joint angle of 0deg as detailed in ‘Dynamometric measurements’ below. The displacement of the myotendinous junction induced by the muscular contraction was recorded during the entire contraction and measured by evaluating the ultrasound images corresponding to 0, 20, 40, 60, 80 and 100% of MVC. The images were analysed with publicly available imaging software (ImageJ 1.43b, NIH, Bethesda, MD, USA). To prevent overestimation of the tendon elongation due to unintentional joint rotation during isometric contraction (Arampatzis et al., 2008), the displacement of the myotendinous junction induced by passive motion of the foot was measured by sonography. The amount of erroneous joint rotation during isometric contraction was determined using an electrogoniometer (K100, Biometrics Ltd, Cwmfelinfach, UK) attached to the ankle. This allowed the correction of the tendon elongation data for ankle joint rotation.
Results: Chronic inflammation was noted in only two of 26 specimens, and no specimen demonstrated acute inflammation. Tenocyte enlargement and proliferation, characterized by increased roundness and size of the cell and nucleus with proteoglycan matrix expansion and myxoid degenerative changes, was found in all 26 specimens. Abundant ground substance, collagen bundle changes, and increased vascularization were visualized in all samples. Conclusion: Anterior shoulder pain attributed to the biceps tendon does not appear to be due to an inflammatory process in most cases. The histologic findings of the extra-articular portion of the LHB tendon and synovial sheath are similar to the pathologic findings in de Quervain tenosynovitis at the wrist, and may be due to a chronic degenerative process similar to this and other tendinopathies of the body.
Our current study demonstrates unequivocally that the structures we observed between the arte- rial roots fail to correspond to the classic micro- scopic description of the tendon of a muscle. Ac- cording to Montes et al. , a tendon is a white shiny fibrous cord, varying in length and thickness, sometimes round and sometimes flattened, and devoid of elasticity. The most common type of dense connective tissue, and the densest form of collage- nous tissue, is that of the tendon. It consists al- most entirely of white fibrous tissues, the fibrils of which have an undulating course and which are firmly united. These bundles are separated by a small quantity of amorphous intracellular sub- stance. The collagen bundles of tendons aggregate into larger bundles that are enveloped by loose con- nective tissue containing blood vessels and nerves. Externally, a tendon is surrounded by a sheath of dense connective tissue. When boiled in water the tendon is almost completely converted into gela- tin, the white fibres being composed of the albu- minoid collagen, which is often regarded as the anhydride of gelatin.
For most injections, 1 percent lidocaine or 0.25 to 0.5 percent bupivacaine is mixed with a corticosteroid preparation. The dose of anes- thetic varies from 0.25 mL for a flexor tendon sheath (trigger finger) to 5 to 8 mL for larger joints. On rare occasions, patients exhibit signs of anesthetic toxicity, including flushing, hives, chest or abdominal discomfort, and nausea. It can take as long as 20 to 30 minutes following the injection for these symptoms to present. For this reason, and to monitor for allergic reac- tions, patients should be observed in the office for at least 30 minutes following the injection.
Tendons and ligaments are unique forms of connective tissue that are considered an integral part of the musculo- skeletal system. The ultimate function of tendon is to connect muscles to bones and to conduct the forces generated by muscle contraction into movements of the joints, whereas ligaments connect bone to bone and provide joint stabilization. Unfortunately, the almost acellular and collagen I–rich structure of tendons and ligaments makes them very poorly regenerating tissues. Injured tendons and ligaments are considered a major clinical challenge in orthopedic and sports medicine. This Review discusses the several factors that might serve as molecular targets that upon activation can enhance or lead to tendon neoformation.
To identify the impact of elastic modulus on tenogen- esis, alginate hydrogels were designed to mimic the elas- tic modulus of embryonic tendon at specific developmental stages . Alginate hydrogels function- alized with arginyl-glycyl-aspartic acid (RGD), to enable cell attachment, were tuned using a combination of al- ginate concentration and calcium crosslinking density to have nanoscale elastic moduli from 3.4 to 20.1 kPa, representing the nanoscale elastic moduli of embryonic chick tendon from prior to E5.5 and up to E17 . Tendon progenitor cells isolated from E11 chick calca- neal tendons were encapsulated in the 3D alginate hydrogels and cultured for 7 days in vitro. Scleraxis and Col XII gene expression increased at the highest elastic modulus (representing late stage embryonic tendon). Col I expression was downregulated at elastic moduli repre- senting middle and later embryonic stages, whereas tenomodulin and Col III were not affected by elastic modulus . This model suggests that embryonic ten- don mechanical properties impact tenogenic markers, but additional factors may be needed, as late stage ten- don markers (tenomodulin) were not affected. It is also possible that embryonic magnitudes of elastic moduli are not fully representative of the tenogenic environ- ment. Tendon formation continues throughout postnatal development with increases in differentiation markers , collagen content, and mechanical properties [26, 59]. For example, linear region elastic modulus of post- natal mouse Achilles tendon increases from approxi- mately 87 MPa at P4 to 544 MPa at P28, and toe region elastic modulus increases from 25 MPa to 72 MPa . Elastic modulus of postnatal tendon can serve as a tem- plate for models aiming to mimic the complete develop- ing tendon environment. As the stress-strain relationship in tendon is non-linear , the elastic modulus (e.g., toe region or linear) that impacts teno- genesis needs to be explored. Furthermore, tendon ma- terial properties can be evaluated at nano- and microscales (e.g., atomic force microscopy) or bulk scale (e.g., uniaxial tensile test), but how each scale impacts cells is unknown and challenging to uncouple. Model systems exploring the effects of bulk and cell-level ma- terial properties on tenogenesis are needed.
Studies in tendon development have revealed the complexity of tendon differentiation. As shown across several animal models, members of the transforming growth factor-β (TGF-β) superfamily are actively involved in tendon development and healing in a spatiotemporally specific manner. For example, mouse patellar tendon cells were found to respond to TGF-β signaling at developmental stages starting at gestation day 17.5 and ending at postnatal day 14 . Consistent with this finding, micromass culture of chick embryonic limb bud mesodermal cells with TGF-β demonstrated significant up-regulation of tendon markers, scleraxis (SCX) and tenomodulin (TNMD), with concurrent reduction in cartilage markers . Conversely, disruption of TGF-β signaling resulted in the loss of most tendons and ligaments in a SCX-GFP mouse model . When injured, high levels of TGF-β expression and activity were seen throughout the healing period [51, 177, 178]. However, TGF-β signaling is also known to play a crucial role in chondrogenesis . As is increasingly recognized, the tissue-specific bioactivity of TGF-β depends upon additional cues provided by the extracellular microenvironment [15, 159].
In Case 1, an incision along the laceration site was given and extended. After exploration of the wound retraction of the muscle-tendon unit was observed. The ruptured ends of both the tendons (SDFT and FCUT) were isolated, debrided and the uneven edg- es were excised (5 mm) to establish healthy tendon margins. The retraction of the muscle-tendon unit as well as excision of the irregular edges rendered it difficult to achieve apposition of the ruptured tendon ends. The tendons were released from the surrounding tissue to gain length and decrease ten- sion. The ruptured SDFT was apposed with a 2-0 polyester suture using a modified Kessler suture pattern which was then followed by reinforcement with interrupted horizontal mattress sutures with 3-0 monofilament polydioxanone. After that a su- turing gap formation was noticed on the carpus extension. To minimise this and provide additional strength, a fresh frozen Achilles tendon allograft (FFATA) was implanted to augment the injured ten- dons. The FFATA was thawed in crystalloid fluid at room temperature and cut (1 × 4 cm) so as to cover one third of the circumference of the tendon. Then, the FFATA was sutured using 3-0 monofila- ment polydioxanone in a simple interrupted pat-
Isolation and identification of rat TSCs were performed as previously described . Briefly, 0.3% pentobarbital sodium (Sigma, 30 mg/kg) was used for intraperitoneal anesthesia in rats. In sterile conditions, the tendon tis- sues were then removed, carefully dissected, cut into pieces, and digested in 3 mg/mL of type I collagenase (Sigma-Aldrich, St. Louis, MO, USA). After a 70-μm cell filter filtration, the suspension turned into a single cell suspension, which was then cultured in Dulbecco’s modified Eagle’s medium (Gibco, Invitrogen, NY, Invi- trogen Corporation, Grand Island, USA) containing 10% fetal bovine serum (Biological Industries, Kibbutz Beit- Haemek, Israel) and 1% penicillin-streptomycin anti- biotic mixture (Beyotime, Shanghai, China). Cells were subcultured at 80% confluence. Cells at passages three were incubated with fluorescein isothiocyanate- conjugated antibodies (anti-CD90, anti-CD105, anti- CD44, anti-CD11b, and anti-CD106) (Biolegend San Diego, CA, USA) through flow cytometry. The multiline- age differentiation potential of TSCs was determined by inducing the differentiation of cells in passage 3 into os- teocytes, adipocytes, and chondrocytes (all the differenti- ation media were from Cyagen).
Tendon also contains elastic fibres (approximately 4.4g / lOOg dry weight) (Grant & Prockop, 1972). Elastic fibres are composed of elastin. Elastin is a complex structure with a mechanical property of elasticity (the ability of a stretched material to return to its original resting state) due both to its biochemical composition and to the physical arrangement of its individual molecules (Hukins, 1984). Elastic fibres yield easily to stretching because they are composed of a network of randomly coiled chains joined by covalent cross links. These cross links impose a restriction on the elastic fibres such that, upon stretching, the individual chains are constrained and cannot slip past one another (Franzblau & Paris, 1981). However, the covalent interchain forces are weak and the cross links widely spaced. As a result, minimal unidirectional force can produce extensive elongation of chains before cross-links begin to restrict movement. Thus, similar to the collagenous fibres, elastic fibres allow extensibility until the slack and spacing between the chains are taken up (Franzblau & Paris, 1981). It seems the tendon is elastic because the collagen after it is extended returns to its original length, rather than due to the small percentage of elastic fibres. The amount of elastic fibres has not been found to vary much between different tendon types (Hukins, 1984).
paratenon defects; repairing only the PT defect; repairing only the paratenon defect; or leaving both the PT and paratenon unrepaired . The paratenon is juxtaposed to the bursal tissue on its anterior and posterior surfaces, and thus exhibits the potential to regenerate the tendon tissue within the defect . The surgical technique that we describe for a proximal medial, distal-lateral repair includes surgical repair of the paratenon. There have been many studies in the recent literature regarding the closure of the PT defect after BPTB graft harvest for ACL reconstruction. Histologically, the tissue growth in the non- reconstructed defect does not resemble normal tendon, but rather scar tissue made of poorly oriented collagen fibers [7, 8]. Aggressive scar tissue reaction with disorganized collagen networks may be secondary to exposure of the original tendon substance to stresses leading to overproduction of repair tissue and remodeling of the cross-sectional area . While defect closure may reduce the size of the gap, and therefore scar reaction, the closure has also been noted to be adversely affective to the remaining tendon. The tension in the defect closure may result in avascular degeneration, focal necrosis, and calcification of the proximal remaining tendon, which leads to an increased risk of PT rupture .