Honors Project--Smith College, Northampton, Mass., 2010. / Includes bibliographical references (p. 43-46)

Achilles tendinopathy is a debilitating condition affecting the entire spectrum of society and a condition that increases the risk of tendon rupture. Effective therapies remain elusive, as anti-inflammatory drugs and surgical interventions show poor long-term outcomes. Eccentric loading of the Achilles muscle-tendon unit is an effective physical therapy for treatment of symptomatic human tendinopathy. Post-injury analgesia is often achieved with non-steroidal anti-inflammatory drugs such as ibuprofen; however, there is increasing evidence that NSAID usage may interfere with the healing process. The deposition of aggrecan/hyaluronan (HA)-rich matrix within the tendon body and surrounding peritenon impede tendon healing and result in compromised biomechanical properties. Herein, we present work investigating chemical, biological, and mechanical loading approaches to treating Achilles tendinopathy in a murine model. Our previously established TGF-ß1-induced murine model of Achilles tendinopathy was used to investigate the cellular mechanism by which ibuprofen (chemical) therapy might lead to a worsening of tendon pathology, potentially by interfering with the native inflammation phase of tendon healing. We conclude that the use of ibuprofen for pain relief during inflammatory phases of tendinopathy has detrimental effects on the turnover of a pro-inflammatory HA matrix produced ain response to soft-tissue injury, thus preventing the switch to cellular responses associated with functional matrix remodeling and eventual healing. We examined the therapeutic potential of a recombinant human hyaluronidase, rHuPH20 (biologic, FDA approved for reducing HA accumulation in tumors) in a novel Achilles tendinopathy and retrocalcaneal bursitis injury model. The potential of rHuPH20 to effectively clear the pro-inflammatory, HA-rich matrix within the retrocalcaneal bursa (RCB) and tendon strongly supports the future refinement of injectable glycosidase preparations as potential treatments to protect or regenerate tendon tissue by reducing inflammation and scarring in the presence of bursitis or other inducers of damage such as mechanical overuse. Finally, we developed a novel mouse model of hind limb muscle loading (mechanical) designed to achieve a tissue-targeted therapeutic exercise. When applied to a murine Achilles tendinopathy model, muscle loading led to a significant improvement in Achilles tendon biomechanical outcome measures, with a decrease in cross-sectional area and an increase in material properties, compared to untreated animals. Our model facilitates the future investigation of mechanisms whereby rehabilitative muscle loading promotes healing of Achilles tendon injuries. Overall, these findings enhance our understanding of the mechanisms of injury and treatment in Achilles tendinopathy injuries. / Doctor of Philosophy / Achilles tendinopathy is a chronic, overuse condition affecting the entire spectrum of society and a condition that increases the risk of tendon rupture. Therapies are limited, as anti-inflammatory drugs and surgical interventions show poor long-term outcomes. Drugs such as ibuprofen are commonly prescribed at the onset of injury to treat pain. Eccentric loading of the Achilles muscle-tendon unit is an effective physical therapy for treatment of human tendinopathy; however, the reasons driving the healing are not well understood. Characteristics of the disease include pain, increased tendon size, and disorganization of tendon fiber structure. Here, we present work investigating chemical, biological, and mechanical loading approaches to treating Achilles tendinopathy in a mouse model. Our mouse model of Achilles tendinopathy was used to investigate how ibuprofen (chemical) therapy might lead to a worsening of tendon by potentially interfering with the inflammation phase of tendon healing. We conclude that the use of ibuprofen for pain relief during inflammatory phases of tendinopathy has negative effects on the turnover of matrix produced in response to injury, affecting the transition to the next phase in the tendon healing response. We examined the potential of a recombinant human hyaluronidase, rHuPH20 (biologic, FDA approved for reducing HA accumulation in tumors) in a novel Achilles tendinopathy and retrocalcaneal bursitis injury model. The potential of rHuPH20 to effectively clear the proinflammatory, HA-rich matrix within the retrocalcaneal bursa (RCB) and tendon strongly supports the future refinement of injectable treatments as a potential to protect or regenerate tendon tissue by reducing inflammation and scarring in the presence of bursitis or other inducers of damage such as mechanical overuse. Finally, we developed a mouse model of hind limb muscle loading (mechanical) based on physical therapy exercises. This model led to an improvement in biomechanical measures compared to untreated animals. The model allows for investigation of the underlying mechanisms in which physical therapy promotes healing of Achilles tendon injuries. Overall, these findings enhance our understanding of the mechanisms of injury and treatment in Achilles tendinopathy injuries.

This diploma thesis deals with the Achilles tendinopathy, and particularly with its etiopatogenetics. The theoretical part includes information about the Achilles tendon, tendinopathy of Achilles tendon and a summary of dysfunctions of the locomotor system. We assumed that the dysfunction of the locomotor system is the main etiopatogenetic factor of the Achilles tendinopathy, and that it results in changes of its position and loading. In the practical part we tried to reveal these dysfunctions by examination of seven patients, and to prove its main etiopatogenetic influence by a successfull therapy. The aim of the thesis was to point out the importance of the examination as well as the therapy of the locomotor systems function. Powered by TCPDF (www.tcpdf.org)

Diss. (sammanfattning) Linköping : Linköpings universitet, 2008. / Härtill 4 uppsatser.

Diss. (sammanfattning) Linköping : Linköpings universitet, 2007. / Härtill 6 uppsatser.

(in English): Aim of present paper is to reconstruct and compare Aristotle's solution of Zeno's paradoxes of motion from Books VI and VIII of his Physics. Aristotle claims that there is difference between these two solutions. There is difference in charakter of question which is posed by Zeno. In book VI. the question is concerning the possibility of traversing infinite distance in finite time. In book VIII. this question is asked about time itself. It is here, in book VIII, where we should find the right solution to paradoxes of motion. In this paper I shall look into the nature of this difference between solution in book six and in book VIII, and I will find out if there si some consquence for Aristotle's conception of magnitudes.

Introdução: os estudos sobre flexibilidade vêm tentando compreender quais propriedades explicam o aumento da amplitude de movimento (ADM), além do aumento de extensibilidade muscular. Propriedades mecânicas passivas de outros tipos de tecido, como o tendão, vêm sendo avaliadas, para entender a sua interferência no aumento da ADM. Desenho do estudo: o estudo foi do tipo ensaio clínico randomizado. Objetivos: analisar, minuto a minuto, o deslocamento da junção miotendínea (JMT) do músculo gastrocnêmio medial com o tendão do calcâneo e o torque passivo durante uma sessão de 10 minutos de alongamento estático passivo de flexores plantares, e analisar a mudança destas e de outras propriedades passivas mecânicas da unidade músculo-tendínea (UMT) do tríceps sural antes e após essa intervenção, verificando se estas mudanças perduram após 15, 30, 45 e 60 minutos após o protocolo de alongamento. Métodos: 30 participantes saudáveis foram divididos em grupo controle, o qual permaneceu em repouso, e experimental, o qual realizou uma sessão de 10 minutos de alongamento estático passivo no dinamômetro isocinético. Os participantes realizaram os testes de ADM, torque passivo, deslocamento da JMT e histerese antes e após a intervenção (0, 15, 30, 45 e 60 minutos). A partir dessas variáveis, foram calculadas as medidas de rigidez tendínea, muscular e da UMT. Resultados: Cinco participantes não permaneceram relaxados durante os testes e foram excluídos após análise dos dados eletromiográficos. 25 participantes foram incluídos na análise. Os resultados foram divididos em dois estudos diferentes. No primeiro estudo, apenas os 12 participantes do grupo experimental foram incluídos e, ao longo da intervenção, foi encontrada uma redução significativa do torque passivo, com a principal diferença ocorrendo nos minutos cinco e sete. No segundo estudo, foram comparados os indivíduos do grupo controle (n=13) e do grupo experimental (n=12), com um período de follow up de 60 minutos após a intervenção. A ADM aumentou e permaneceu aumentada até uma hora após a intervenção em ambos os grupos. As variáveis de deslocamento da JMT, rigidez muscular e histerese aumentaram em alguns momentos ao longo do tempo, sem diferença entre os grupos. A rigidez tendínea não apresentou diferença nem para grupo e nem para tempo. As variáveis de torque passivo e rigidez da UMT apresentaram uma interação significativa entre grupo e tempo, com uma redução das duas ao longo do tempo no grupo experimental. Conclusões: há uma redução de torque passivo ao longo de uma sessão de alongamento estático de 10 minutos dos flexores plantares de tornozelo, e fazer parte do grupo experimental influenciou no comportamento do torque passivo e da rigidez da UMT, levando a uma maior redução das mesmas para o grupo que realizou o alongamento. A ADM aumentou e permaneceu aumentada até uma hora após a intervenção. / Background: studies on flexibility have attempted to understand which properties explain increased range of motion (ROM), in addition to increased muscle extensibility. Mechanical and passive properties of other types of tissue, such tendon tissue, have been evaluated in order to understand their interference in increased ROM. Study Design: randomized clinical trial. Objectives: to analyze, minute by minute, myotendinous junction (MTJ) displacement of the medial gastrocnemius muscle with Achilles tendon and passive torque during a 10-minute passive static stretching of the ankle plantar flexors. To analyze, also, the time course change of these and other muscle-tendon unit (MTU) mechanical properties of the triceps surae before and after the intervention, verifying if the changes persist after 15, 30, 45 and 60 minutes after the stretching protocol. Methods: 30 healthy participants were divided into a control group, which remained at rest, and an experimental group, which performed a 10-minute passive static stretching on the isokinetic dynamometer. Participants performed tests of ROM, passive torque, MTJ displacement and hysteresis before and after the intervention (0, 15, 30, 45 and 60 minutes). From these variables, the measures of tendinous, muscular and MTU stiffness were calculated. Results: Five participants did not remain relaxed during the test and were excluded after electromyographic data analysis. 25 participants were included in the analysis. Results were divided into two different studies. In the first one, only 12 participants of experimental group were included and during the intervention, a significant reduction of the passive torque was found, with the main difference occurring in minutes five and seven. In the second study, individuals from control group (n=13) and experimental group (n=12) were compared, with a 60 minute follow-up period after the intervention. ADM increased and remained increased up to one hour after the intervention. The variables of MTJ displacement, muscular stiffness and hysteresis increased at some moments over time, with no difference between the groups. The tendinous stiffness showed no difference neither for group nor for time. The variables of passive torque and MTU stiffness showed a significant interaction between group and time, with a reduction of the two over time in the experimental group. Conclusions: passive torque decreased throughout a 10-minute passive static stretching of the ankle plantar flexors, and being part of the experimental group influenced the behavior of the passive torque and the MTU stiffness, leading to a greater reduction of the same for the group who performed the stretching.

Epidemiologic data suggest 25% to 75% of all runners experience an overuse injury each year. Commonly cited biomechanical factors related to overuse injuries such as Achilles tendinopathy or medial tibial stress syndrome include excessive amounts or velocities of foot pronation. However, there is conflicting evidence in the literature supporting this theory. An alternative hypothesis suggests it is not necessarily the amount or velocity of pronation which is important for injury development; rather it is the duration the foot remains in a pronated position throughout stance that is the important variable. This project examined this hypothesis by first identifying biomechanical markers of prolonged pronation. Second, it assessed whether individuals currently symptomatic with injuries typically attributed to excessive pronation instead demonstrate the biomechanical markers of prolonged pronation. Finally, musculoskeletal modeling techniques were used to examine musculotendinous kinematics in injured and healthy runners, as well as healthy runners with prolonged pronation. The results suggest the two most robust measures for identifying individuals with prolonged pronation are the period of pronation and the eversion of the rear foot at heel off. Individuals with prolonged pronation can also be identified with a set of clinically feasible measures including higher standing tibia varus angles, reduced static hip internal rotation range of motion, and increased hip internal rotation during stance phase. Finally, individuals with prolonged pronation display a more medially located center of pressure trajectory during stance. Compared to healthy controls, individuals currently symptomatic with Achilles tendinopathy or medial tibial stress syndrome did not differ in the amount or velocity of pronation. However, they did demonstrate the biomechanical markers of prolonged pronation. Injured individuals also demonstrated greater average musculotendinous percent elongation than healthy controls, especially through mid and late stance. Currently healthy individuals demonstrating prolonged pronation exhibited musculotendinous percent elongations intermediate to the healthy and injured groups. As a whole, the results from this study suggest prolonged pronation may play a role in the development of common overuse running injuries. It is suggested future studies on injury mechanisms consider pronation duration as an important variable to examine. This dissertation includes unpublished co-authored material.

This paper addresses the causes and effects of grief within Homer's Iliad. In addition, this paper argues that error, both committed and suffered, is the primary cause of grief, and that grief is particularly transformative in regard to Achilles, both in his motivations and his physicality.

The research described in this thesis examined age- and strength training-related changes in Achilles tendon stiffness and plantarflexor force production in prepubertal children. The measurement of both Achilles tendon stiffness and muscular force production requires in vivo moment arm lengths to be known. Currently, this is possible only by using expensive and time-consuming medical imaging methodologies. Therefore, the predictability of the Achilles tendon moment arm from surface anthropometric measurements was assessed in the first experimental study (Chapter 3). The results demonstrated that a combination of foot length and the distance between the calcaneal tuberosity and 1st metatarsal head could explain 49% of the variability in Achilles tendon moment arm length in 5 – 12 year-old children. This was considered to be unacceptable for further use, thus an ultrasound-based method was decided upon for obtaining moment arm length in subsequent experimental studies. In the second and third experimental studies (Chapters 4 and 5), age-related changes in tendon mechanical and structural properties were documented and their relationship with changes in force production ability were examined in prepubertal children (5 – 12 years) and adult men and women. In Chapter 4, Achilles tendon stiffness was shown to increase with age through to adulthood, and that changes in tendon stiffness were strongly and independently associated with body mass (R2 = 0.58) and peak force production capacity (R2 = 0.51),which may provide the tendon with an increasing mechanical stimulus for growth and microadaptation. These increases in tendon stiffness were associated with a greater increase in tendon CSA (~105%) than that found for tendon length (~60%), in addition to an increase in Young’s modulus (~139%), suggesting that gross increases in tendon size as well as changes in its microstructure underpinned the increase in stiffness. In Chapter 5, the relationships between Achilles tendon stiffness and both electro-mechanical delay (EMD) and rate of force development (RFD) were determined during maximal isometric plantarflexion contractions. Moderate correlations were found between tendon stiffness and both EMD (r = -0.66) and RFD (r = 0.58). RFD was significantly better predicted when muscle activation (estimated as the rate of EMG rise) was included in a regression model. These data clearly show that increases in tendon stiffness with age through to adulthood are associated with decreases in EMD and increases in RFD, and that the rate of muscle activation has an additional influence on RFD during growth. Given that 1) Achilles tendon stiffness was lower in children than adults, 2) this lower stiffness was associated with a longer EMD and slower RFD, and 3) that strength training in adults had previously been shown to increase tendon stiffness and RFD, the adaptability of the developing Achilles tendon to a resistance training programme, and consequence of the potential changes on force production capacity were examined in the final experimental study (Chapter 6). Significant increases in Achilles tendon stiffness and Young’s modulus were found after 10 weeks of twice-weekly plantarflexor strength training in 8-9 year-old boys and girls, which demonstrates that the larger muscle force production provided a sufficient stimulus for tendon microadaptation. The training also resulted in a decrease in EMD, which was moderately correlated with the change in tendon stiffness (r = 55), but no change in RFD. Thus, the increasing tendon stiffness with training was associated with a decreasing EMD, but had no detectable effect on RFD. This would likely have a significant effect on the performance of tasks requiring rapid muscle force production. Together, the results of the present series of investigations demonstrate that the tendon loading experienced from both normal ageing and overloading (strength training) can increase tendon stiffness in children, and that these changes have a detectable effect on rapid force production.