Academic literature on the topic 'Stretch (Physiology) Stretching exercises'

Skeletal muscle contraction increases glucose uptake via an insulin-independent mechanism. Signaling pathways arising from mechanical strain are activated during muscle contractions, and mechanical strain in the form of passive stretching stimulates glucose uptake. However, the exact mechanisms regulating stretch-stimulated glucose uptake are not known. Since nitric oxide synthase (NOS) has been implicated in the regulation of glucose uptake during ex vivo and in situ muscle contractions and during exercise, and NO is increased with stretch, we examined whether the increase in muscle glucose uptake during stretching involves NOS. We passively stretched isolated extensor digitorum longus muscles (15 min at ~100–130 mN) from control mice and mice lacking either neuronal NOSµ (nNOSµ) or endothelial NOS (eNOS) isoforms, as well as used pharmacological inhibitors of NOS. Stretch significantly increased muscle glucose uptake appoximately twofold ( P < 0.05), and this was unaffected by the presence of the NOS inhibitors NG-monomethyl-l-arginine (100 µM) or NG-nitro-l-arginine methyl ester (100 µM). Similarly, stretch-stimulated glucose uptake was not attenuated by deletion of either eNOS or nNOSµ isoforms. Furthermore, stretching failed to increase skeletal muscle NOS enzymatic activity above resting levels. These data clearly demonstrate that stretch-stimulated skeletal muscle glucose uptake is not dependent on NOS. NEW & NOTEWORTHY Passive stretching is known to activate muscle glucose uptake through mechanisms that partially overlap with contraction. We report that genetic knockout of endothelial nitric oxide synthase (NOS) or neuronal NOS or pharmacological NOS inhibition does not affect stretch-stimulated glucose uptake. Passive stretch failed to increase NOS activity above resting levels. This information is important for the study of signaling pathways that regulate stretch-stimulated glucose uptake and indicate that NOS should be excluded as a potential signaling factor in this regard.

Effects of passive static stretching intensity on recovery from unaccustomed eccentric exercise of right knee extensors was investigated in 30 recreationally active males randomly allocated into 3 groups: high-intensity (70%–80% maximum perceived stretch), low-intensity (30%–40% maximum perceived stretch), and control. Both stretching groups performed 3 sets of passive static stretching exercises of 60 s each for hamstrings, hip flexors, and quadriceps, over 3 consecutive days, post-unaccustomed eccentric exercise. Muscle function (eccentric and isometric peak torque) and blood biomarkers (creatine kinase and C-reactive protein) were measured before (baseline) and after (24, 48, and 72 h) unaccustomed eccentric exercise. Perceived muscle soreness scores were collected immediately (time 0), and after 24, 48, and 72 h postexercise. Statistical time × condition interactions observed only for eccentric peak torque (p = 0.008). Magnitude-based inference analyses revealed low-intensity stretching had most likely, very likely, or likely beneficial effects on perceived muscle soreness (48–72 h and 0–72 h) and eccentric peak torque (baseline–24 h and baseline–72 h), compared with high-intensity stretching. Compared with control, low-intensity stretching had very likely or likely beneficial effects on perceived muscle soreness (0–24 h and 0–72 h), eccentric peak torque (baseline–48 h and baseline–72 h), and isometric peak torque (baseline–72 h). High-intensity stretching had likely beneficial effects on eccentric peak torque (baseline–48 h), but likely had harmful effects on eccentric peak torque (baseline–24 h) and creatine kinase (baseline–48 h and baseline–72 h), compared with control. Therefore, low-intensity stretching is likely to result in small-to-moderate beneficial effects on perceived muscle soreness and recovery of muscle function post-unaccustomed eccentric exercise, but not markers of muscle damage and inflammation, compared with high-intensity or no stretching.

The aim of this mini-review is to describe the present state of knowledge regarding the effects of chronic changes in the patterns of muscle use (defined as changes lasting >1 wk), including muscle stretching, strengthening, and others, on the passive mechanical properties of healthy human skeletal muscles. Various forms of muscle stretch training and some forms of strength training (especially eccentric training) are known to strongly impact the maximum elongation capacity of muscles in vivo (i.e., maximum joint range of motion), largely by increasing our ability to tolerate higher stretch loads. However, only small effects are observed in the passive stiffness of the muscle-tendon unit (MTU) or the muscle itself, although a reduction in muscle stiffness has been observed in the plantar flexors after both stretching and eccentric exercise interventions. No changes have yet been observed in viscoelastic properties such as the MTU stress-relaxation response, although a minimum of evidence indicates that hysteresis during passive stretch-relaxation cycles may be reduced by muscle stretching training. Importantly, data exist for relatively few muscle groups, and little is known about the effects of age and sex on the adaptive process of passive mechanical properties. Despite the significant research effort afforded to understanding the effects of altered physical activity patterns on the maximum range of motion at some joints, further information is needed before it will be possible to develop targeted physical activity interventions with the aim of evoking specific changes in passive mechanical properties in individuals or in specific muscles and muscle groups.

The exercise pressor reflex is composed of two components, namely the muscle mechanoreflex and the muscle metaboreflex. The afferents evoking the two components are either thinly myelinated (group III) or unmyelinated (group IV); in combination they are termed “thin fiber afferents.” The exercise pressor reflex is often studied in unanesthetized, decerebrate rats. However, the relationship between the magnitude of this reflex and the number of thin fiber afferents stimulated by muscle contraction is unknown. This lack of knowledge prompted us to test the hypothesis that the magnitude of the exercise pressor reflex was directly proportional to the amount of muscle mass activated. Muscle mechanoreceptors were stimulated by stretching the calcaneal tendon. Likewise, muscle metaboreceptors were stimulated by injecting lactic acid into the arterial supply of the hindlimb muscles. In addition, both muscle mechanoreceptors and metaboreceptors were stimulated by statically contracting the hindlimb muscles. We found that simultaneous bilateral (both hindlimbs) stimulation of thin fiber afferents with stretch, lactic acid, and static contraction evoked significantly greater pressor responses than did unilateral (one hindlimb) stimulation of these afferents. In addition, the magnitude of the pressor responses to bilateral simultaneous stimulation of thin fiber afferents evoked by stretch, lactic acid, and contraction was not significantly different from the magnitude of the sum of the pressor responses evoked by unilateral stimulation of these afferents by stretch, lactic acid, and contraction. We conclude that the magnitude of the exercise pressor reflex and its two components is dependent on the number of afferents stimulated.

Warm-up: A case study on maximal oxygen consumption as it relates to acute stretchingThe aim of this study was to determine the acute effects of static and Proprioceptive Neuromuscular Facilitation (PNF) stretches on maximal oxygen consumption (VO2max). Ten physically active men (mean ± SD, 23.80 ± 1.54 years, 70.60 ± 9.70 kg, 1.74.60 ± 5.23 m), who were healthy students volunteered to take part in the study. The participants were subjected to Static and PNF stretching exercises. After the interventions, the Bruce treadmill protocol was applied to measure VO2max values. The expired gases were collected and analyzed continuously using the Cortex Metalyzer II. Analysis of variance showed significant main effects for interventions (F(2,18)=10.74, p<.05) on VO2max. The main result of this study showed that both static and PNF stretching exercises improved VO2max values.

AbstractThe aim of this study was to examine the long-term effects of static stretching of the plantar-flexor muscles oneccentric and concentric torque and ankle dorsiflexion range of motion in healthy subjects. Seventy five healthy malevolunteers, with no previous history of trauma to the calf that required surgery, absence of knee flexion contracture andno history of neurologic dysfunction or disease, systemic disease affecting the lower extremities were selected for thisstudy. The participants were divided into three equal groups. The control group did not stretch the plantar-flexormuscles. Two Experimental groups (trained and untrained) were instructed to perform static stretching exercise of 30second duration and 5 repetitions twice daily. The stretching sessions were carried out 5 days a week for 6 weeks. Thedorsiflexion range of motion was measured in all subjects. Also measured was the eccentric and concentric torque ofplantar-flexors at angular velocities of 30 and 120o/s pre and post stretching. Analysis of variance showed a significantincrease in plantar-flexor eccentric and concentric torque (p < 0.05) of trained and untrained groups, and an increase indorsiflexion range of motion (p < 0.05) at both angular velocities for the untrained group only. The static stretchingprogram of plantar-flexors was effective in increasing the concentric and eccentric plantarflexion torque at angularvelocities of 30 and 120o/s. Increases in plantar-flexors flexibility were observed in untrained subjects.

Patients with type-2 diabetes mellitus (T2DM) have exaggerated sympathetic activity and blood pressure responses to exercise. However, the underlying mechanisms for these responses, as well as how these responses change throughout disease progression, are not completely understood. For this study, we examined the effect of the progression of T2DM on the exercise pressor reflex, a critical neurocardiovascular mechanism that functions to increase sympathetic activity and blood pressure during exercise. We also aimed to examine the effect of T2DM on reflexive cardiovascular responses to static contraction, as well as those responses to tendon stretch when an exaggerated exercise pressor reflex was present. We evoked the exercise pressor reflex and mechanoreflex by statically contracting the hindlimb muscles and stretching the Achilles tendon, respectively, for 30 s. We then compared pressor and cardioaccelerator responses in unanesthetized, decerebrated University of California Davis (UCD)-T2DM rats at 21 and 31 wk following the onset of T2DM to responses in healthy nondiabetic rats. We found that the pressor response to static contraction was greater in the 31-wk T2DM [change in mean arterial pressure (∆MAP) = 39 ± 5 mmHg] but not in the 21-wk T2DM (∆MAP = 24 ± 5 mmHg) rats compared with nondiabetic rats (∆MAP = 18 ± 2 mmHg; P < 0.05). Similarly, the pressor and the cardioaccelerator responses to tendon stretch were significantly greater in the 31-wk T2DM rats [∆MAP = 69 ± 6 mmHg; change in heart rate (∆HR) = 28 ± 4 beats/min] compared with nondiabetic rats (∆MAP = 14 ± 2 mmHg; ∆HR = 5 ± 3 beats/min; P < 0.05). These findings suggest that the exercise pressor reflex changes as T2DM progresses and that a sensitized mechanoreflex may play a role in exaggerating these cardiovascular responses. NEW & NOTEWORTHY This is the first study to provide evidence that as type-2 diabetes mellitus (T2DM) progresses, the exercise pressor reflex becomes exaggerated, an effect that may be due to a sensitized mechanoreflex. Moreover, these findings provide compelling evidence suggesting that impairments in the reflexive control of circulation contribute to exaggerated blood pressure responses to exercise in T2DM.

Background A recent study found nonweightbearing stretching exercises specific to the plantar fascia to be superior to the standard program of weightbearing Achilles tendon-stretching exercises in patients with chronic plantar fasciitis. The present study used a cadaver model to demonstrate the influence of foot and ankle position on stretching of the plantar fascia. Methods Twelve fresh-frozen lower-leg specimens were tested in 15 different configurations representing various combinations of ankle and metatarsophalangeal (MTP) joint dorsiflexion, midtarsal transverse plane abduction and adduction, and forefoot varus and valgus. Measurements were recorded by a differential variable reluctance transducer (DVRT) implanted into the medial band of the plantar fascia, and primary measurement was a percent deformation of the plantar fascia (stretch) with respect to a reference position (90 degrees ankle dorsiflexion, 0 degrees midtarsal and forefoot orientation, and 0 degrees MTP dorsiflexion). Results Ankle and MTP joint dorsiflexion produced a significant increase (14.91%) in stretch compared to the position of either ankle dorsiflexion alone (9.31% increase, p < 0.001) or MTP dorsiflexion alone (7.33% increase, p < 0.01). There was no significant increase in stretch with positions of abduction or varus (2.49%, p = 0.27 and 0.55%, p = 0.79). Conclusion This study provides a mechanical explanation for enhanced outcomes in recent clinical trials using plantar fascia tissue-specific stretching exercises and lends support to the use of ankle and MTP joint dorsiflexion when employing stretching protocols for nonoperative treatment in patients with chronic proximal plantar fasciitis.

Purpose:To examine the acute effects of static stretching on countermovement vertical-jump (CMVJ) ability and monitor the time course of any stretch-induced changes.Methods:Once familiarized, 16 experienced jumpers completed 2 testing sessions in a randomized order. Each session consisted of a general warm-up, a pretreatment CMVJ assessment, a treatment, and multiple posttreatment CMVJ assessments. One treatment included lower-body static stretching, and the second treatment, involving no stretching, was the control. Posttreatment CMVJ measures occurred immediately, 3, 6, 12, and 24 minutes posttreatment. Stretching consisted of 3 static-stretching exercises, with each exercise repeated 3 times and each repetition held for 30 s.Results:Prestretch CMVJ height equaled 47.1 (± 9.7) cm. CMVJ height immediately poststretch was 45.7 (± 9.2) cm, and it remained depressed during the 24-min follow-up period. Pre-no-stretch CMVJ height was 48.4 (± 9.8) cm, whereas immediately post-no-stretch CMVJ height equaled 46.8 (± 9.5) cm, and as in the stretch treatment, post-no-stretch CMVJ height remained lower than pre-no-stretch values. Although there was a significant main effect of time (P = .005), indicating that CMVJ was lower and remained impaired after both treatments, no significant interaction effect (P = .749) was observed.Conclusion:In comparison with the no-activity control, static stretching resulted in similar reductions in CMVJ ability when examined over the same time course, so athletes preparing for CMVJ should avoid periods of inactivity, as well as static stretching.

Alveolar epithelial cells effect edema clearance by transporting Na+ and liquid out of the air spaces. Active Na+ transport by the basolaterally located Na+-K+-ATPase is an important contributor to lung edema clearance. Because alveoli undergo cyclic stretch in vivo, we investigated the role of cyclic stretch in the regulation of Na+-K+-ATPase activity in alveolar epithelial cells. Using the Flexercell Strain Unit, we exposed a cell line of murine lung epithelial cells (MLE-12) to cyclic stretch (30 cycles/min). After 15 min of stretch (10% mean strain), there was no change in Na+-K+-ATPase activity, as assessed by86Rb+uptake. By 30 min and after 60 min, Na+-K+-ATPase activity was significantly increased. When cells were treated with amiloride to block amiloride-sensitive Na+ entry into cells or when cells were treated with gadolinium to block stretch-activated, nonselective cation channels, there was no stimulation of Na+-K+-ATPase activity by cyclic stretch. Conversely, cells exposed to Nystatin, which increases Na+ entry into cells, demonstrated increased Na+-K+-ATPase activity. The changes in Na+-K+-ATPase activity were paralleled by increased Na+-K+-ATPase protein in the basolateral membrane of MLE-12 cells. Thus, in MLE-12 cells, short-term cyclic stretch stimulates Na+-K+-ATPase activity, most likely by increasing intracellular Na+ and by recruitment of Na+-K+-ATPase subunits from intracellular pools to the basolateral membrane.

This study examined the short-term training effects of two volumes of a dynamic warm up performed 4 days per week over a 3 1/2-week period. A total of 25 Division III wrestlers volunteered for the study. Three participants either dropped out or were unable to attend post-testing, resulting in 22 total participants completing the study. Groups were divided into control, low volume, and high volume groups. All participants completed pre and poststudy performance tests including the standing long jump, proagility, start-stop-cut, and 30- meter sprint. The low and high volume training groups each performed the same dynamic warm up prior to each pre-season captain's practice. The control group did not participate in an organized warm up. The low volume group performed one set of each warm up exercise, and the high volume group performing two sets of each warm up exercise. Data analysis indicated significant increases in performance for the standing long jump (p = .011) and start-stop-cut (p = .000) measures among the entire sample population. However, there was no significant difference between the groups in these measures. No significant results were found either for the sample as a whole or between groups for the proagility and 30-meter measures. The increased performance of all groups, including the control group, fails to provide evidence for the effectiveness of training with either warm up volume. Further research is needed to address limitations of this study to determine effectiveness of various warm up volumes.

Les étirements sont aujourd'hui une pratique courante dans les milieux sportifs et de réadaptation. Ils sont habituellement recommandés dans le but de contribuer à la prévention des blessures (Willson et al. 1991 ;Pope et al. 2000), à l’amélioration de la performance sportive lorsque celle-ci nécessite une amplitude articulaire importante (Heyters, 1985 ;Hortobagyi et al. 1985) et à la récupération de la mobilité articulaire dans le cadre d’un programme de réadaptation (Magnusson et al. 1996b). Ces méthodes, qui se sont développées ces dernières années, font classiquement appel à l’étirement passif et aux étirements neurofacilités (PNF), présentés initialement par Kabat (1958). Plus récemment, un intérêt particulier a été porté au travail musculaire excentrique. Des études ont montré que celui-ci permettait également d’augmenter l’amplitude articulaire (Willson et al. 1991 ;Nelson et Bandy, 2004).

Dans une première partie de ce travail, il nous a semblé intéressant de comparer les effets de l’étirement passif à ceux des étirements PNF par "contracté-relâché" et "contracté de l’antagoniste". Si les modalités d'application de chaque étirement sont différentes, elles présentent un intérêt majeur. De fait, elles permettent de faire varier les conditions d'allongement des différentes structures du système myotendineux, en modulant l'activité volontaire des musculatures agoniste ou antagoniste. En effet, si l’étirement passif s'effectue sans activation volontaire, l’étirement par "contracté-relâché" consiste à faire précéder l'étirement passif, d'une contraction volontaire maximale isométrique de la musculature agoniste. L’étirement par "contracté de l’antagoniste" associe à l'allongement de la musculature agoniste, une contraction volontaire maximale de la musculature antagoniste. Si de nombreuses études s'intéressent encore actuellement à caractériser leurs effets respectifs, elles ont déjà permis de montrer que ceux-ci avaient au moins deux origines distinctes, l'une neurophysiologique et l'autre mécanique (Taylor et al. 1990 ;Hutton, 1993). Au plan neurophysiologique, il est bien accepté que ces méthodes induisent une modulation de l'activité réflexe tonique facilitant le relâchement musculaire et par conséquent l’amplitude articulaire (Guissard et al. 1988 ;2001). Il est également bien admis que l’importance de ces effets sur la musculature est variable selon la méthode employée (Guissard et Duchateau, 2006). Au plan mécanique, des études menées chez l’animal ont montré que l’étirement passif modifie les caractéristiques viscoélastiques des tissus (Taylor et al. 1990), et de fait favorise l’allongement des tissus myotendineux (McHugh et al. 1992). Chez le sujet humain, plusieurs expérimentations ont montré que l’étirement par "contracté-relâché" permet d’obtenir un allongement myotendineux et un gain d’amplitude articulaire plus important que par étirement passif (Moore et Hutton, 1980). D’autres études ont montré que l’étirement par "contracté de l’antagoniste" permet de majorer encore les gains obtenus par l’étirement "contracté-relâché" (Osternig et al. 1990). Une première question posée dans ce travail est de savoir si la contribution des processus neurophysiologiques et mécaniques se traduit d’une manière spécifique sur le rapport de compliance des tissus de l’unité myotendineuse. Le développement de techniques d’investigation, telles que l’échographie, permet désormais d’observer le comportement de l’unité myotendineuse, d’une manière non invasive (Fukunaga et al. 1992 ;Herbert et Gandevia, 1995 ;Kuno et Fukunaga, 1995 ;Maganaris et al. 1998). Elle permet ainsi d’étudier les effets d’un étirement ou d’une contraction (Fukunaga et al. 1996) sur le rapport de compliance des structures musculaires et des tissus tendineux.

S’il était intéressant d’étudier la spécificité de ces trois méthodes d’étirement classiques par rapport à leurs effets sur les tissus myotendineux, il nous paraissait pertinent d’observer celle d’un travail musculaire excentrique. En effet, la particularité de celui-ci est de soumettre l’unité myotendineuse préalablement activée, à un allongement. En réadaptation, le travail excentrique est généralement proposé dans le but d’améliorer plus rapidement la symptomatologie d’une tendinopathie (Stanish et al. 1986 ;Alfredson et al. 1998). Des études récentes ont indiqué qu’il peut également être proposé pour augmenter l'amplitude articulaire (Nelson et Bandy, 2004). Toutefois, ses effets sur les tissus myotendineux ne sont pas clairement définis dans la littérature. Chez l’animal, Heinemeier et al. (2007) ont comparé les effets d’un entraînement en contractions concentriques et excentriques sur les tissus de l’unité myotendineuse. Leurs résultats indiquent que si les tissus tendineux sont sensibles aux deux modes de contraction pour leurs effets favorisant la synthèse de collagène, les structures musculaires sont spécifiquement sensibles au mode excentrique. Chez le sujet humain, Crameri et al. (2004) ont observé une série de contractions excentriques d’intensité maximale augmente la synthèse de collagène au sein de l’ensemble des tissus de l’unité myotendineuse. Ces résultats montrent que les effets de ce travail ne se limitent pas aux tissus tendineux, tels que certains protocoles thérapeutiques le suggéraient, et que le tissu musculaire doit désormais être associé à la discussion des effets de ce travail musculaire. Dans ce contexte, la deuxième question que nous avons posée est de savoir si l’étirement de l’unité myotendineuse préalablement activée, telle que se caractérise une contraction excentrique, modifie le rapport de compliance des tissus myotendineux par rapport aux méthodes classiques. Autrement dit, si l’étirement de l’unité myotendineuse activée favorise spécifiquement l’allongement de l’un des tissus de l’unité myotendineuse.

Dans une troisième partie, il nous a paru intéressant d'étudier le comportement à l’étirement de l’unité myotendineuse, dont la compliance était modifiée suite à une désadaptation à long terme. L’hypertonie spastique, qui caractérise une majorité de sujets parétiques spastiques, est généralement caractérisée par une augmentation anormale des résistances opposées à l'étirement passif (Carey et Burghart, 1993). L’origine de ces résistances peut être attribuée à des adaptations tant neurophysiologiques (Pierrot-Deseilligny et Mazières, 1985) que mécaniques et structurelles des tissus de l'unité myotendineuse (Berger et al. 1984 ;Tardieu et al. 1989). Il n’existe pourtant pas encore dans la littérature de consensus les définissant clairement (Fridén et Lieber, 2003). En outre, l’étude récente de Lieber et Fridén (2002) a mis en évidence des modifications de l’architecture des muscles fléchisseurs du carpe. Contrairement à ce qui est généralement proposé au sujet de la longueur des fascicules spastiques (Tardieu et al. 1982), Lieber et Fridén (2002) n’ont pas mis en évidence de raccourcissement de ces derniers. Ainsi, l’hypothèse de Tardieu et al. (1982), selon laquelle le raccourcissement des fascicules est à l’origine de l’augmentation des résistances à l’allongement, ne peut plus être soutenue. Il nous paraissait ainsi intéressant d’associer, à l’observation du comportement des fascicules, celui des tissus tendineux, dans le but de déterminer si l’une de ces deux structures présente des caractéristiques particulières, susceptibles d’expliquer le développement plus important de ces résistances à l’allongement. La troisième question que nous avons posée dans ce travail est de savoir comment se caractérise, à l’étirement, le rapport de compliance des tissus musculaire et tendineux dans un contexte de spasticité.

Outre le fait que la réponse à ces différentes questions soit fondamentale pour mieux comprendre et spécifier la pratique des méthodes d’étirement, l’objectif de notre travail est non seulement de mettre en évidence le tissu dont l’allongement est spécifiquement favorisé par l’une ou l’autre méthode, mais également de contribuer à différencier celui qui limite l’étirement global du système myotendineux. Dans ce contexte, il sera intéressant de pouvoir recommander la pratique d’une méthode particulière, en fonction des besoins spécifiques de chacun.

Doctorat en Sciences de la motricité
info:eu-repo/semantics/nonPublished

Thesis (M. Phil.)--University of Sydney, 2009.
Title from title screen (viewed September 25, 2009) Submitted in fulfilment of the requirements for the degree of Master of Philosophy to the Faculty of Medicine. Includes bibliographical references. Also available in print form.

Thesis (Ph.D.)--University of Toledo, 2004.
Typescript. "A dissertation [submitted] as partial fulfillment of the requirements of the Doctor of Philosophy degree in Exercise Science." Bibliography: leaves 72-77.

[Truncated abstract] First metatarsophalangeal joint (MTPJ1) motion is an important factor in normal weight transference during walking. Disruptions to normal range can influence joints both proximal and distal to the MTPJ1, potentially leading to pain and dysfunction. Whilst the MTPJ1 has been investigated significantly, the numerous methodologies described to quantify range of motion can be questioned and makes comparisons difficult. Range of MTPJ1 motion is commonly assessed in a clinical setting to determine pathology as well as to make decisions on appropriate intervention. The anatomical and biomechanical influence of tendo Achilles load and MTPJ1 motion has been well described; however few studies measuring MTPJ1 range control for Achilles load or describe ankle joint positioning. Further to this the effects of reducing tendo Achilles stiffness on MTPJ1 extensions has yet to be investigated. The purpose of this study was to describe a technique to quantify passive MTPJ1 extension and to determine the influence of ankle joint position on joint range. Secondly the effect of calf muscle stretching on MTPJ1 range was also investigated. The information gathered will assist both research and clinical protocols for quantifying MTPJ1 range, and provide a greater understanding of the anatomic and biomechanical relationship between tendo Achilles load and MTPJ1 extension. In order to fulfil the purposes of the study it was necessary to establish a reliable methodology to quantify non weight bearing MTPJ1 extension. Reliability testing was undertaken in three parts. '...' The results demonstrated a statistically significant increase in joint range immediately following a one minute stretch for variables ankle joint range of motion as well as MTPJ1 extension for ankle joint plantar flexed at 10 Newton's and ankle joint neutral and plantar flexed at 30 Newtons. No significant differences were noted in ankle or MTPJ1 range of motion in either the control group on immediate re-testing, or in both groups after a one week stretch program. The findings of this study support those documented in the literature pertaining to the ankle joint position, tendo Achilles load and plantar fascial stiffness to MTPJ1 range of motion. Increased stiffness at the MTPJ1 was noted dependant on ankle joint position from ankle joint plantar flexion through to ankle joint dorsiflexion. This appears most likely due to increases in tendo Achilles load and subsequent forces transmitted to the plantar aponeurosis. The present study also demonstrated a trend towards increased joint extensibility and limb dominance. The study also supports previous literature into gender differences and joint extensibility, with a positive trend towards increased MTPJ1 range evident in the female subjects tested. The study also demonstrated the immediate effect of calf muscle stretching on ankle and MTPJ1 range of motion. It remains however unclear as to the exact mechanisms involved in producing increased joint range be it reflex inhibition or actual changes to the viscoelastic properties of the soft tissues. Despite this, no changes were evident following a one week stretching program, which supports previous literature describing a short lag time before soft tissues revert to baseline length properties following a single stretch session.