Uphill running improves rat Achilles tendon tissue mechanical properties and alters gene expression without inducing pathological changes.

Overuse Achilles tendinopathy is a common and challenging problem in sports medicine. Little is known about the etiology of this disorder, and the development of a good animal model for overuse tendinopathy is essential for advancing insight into the disease mechanisms. Our aim was to test a previously proposed rat model for Achilles tendon overuse. Ten adult male Sprague-Dawley rats ran on a treadmill with 10° incline, 1 h/day, 5 days/wk (17-20 m/min) for 12 wk and were compared with 12 control rats. Histological, mechanical, and gene-expression changes were measured on the Achilles tendons after the intervention, and local tendon glucose-uptake was measured before and after the intervention with positron emission tomography. No differences were detected between runners and controls in tissue histology or in glucose uptake, indicating that tendon pathology was not induced. Greater tendon tissue modulus (P < 0.005) and failure stress/body weight (P < 0.02) in runners compared with controls further supported that tendons successfully adapted to uphill running. Several genes of interest were regulated after 12 wk of running. Expression of collagen III and insulin-like growth factor I was increased, while collagen I was unchanged, and decreases were seen in noncollagen matrix components (fibromodulin and biglycan), matrix degrading enzymes, transforming growth factor-ß1, and connective tissue growth factor. In conclusion, the tested model could not be validated as a model for Achilles tendinopathy, as the rats were able to adapt to 12 wk of uphill running without any signs of tendinopathy. Improved mechanical properties were observed, as well as changes in gene-expression that were distinctly different from what is seen in tendinopathy and in response to short-term tendon loading.

Local NSAID infusion does not affect protein synthesis and gene expression in human muscle after eccentric exercise.

Unaccustomed exercise leads to satellite cell proliferation and increased skeletal muscle protein turnover. Several growth factors and cytokines may be involved in the adaptive responses. Non-steroidal anti-inflammatory drugs (NSAIDs) negatively affect muscle regeneration and adaptation in animal models, and inhibit the exercise-induced satellite cell proliferation and protein synthesis in humans. However, the cellular mechanisms eliciting these responses remain unknown. Eight healthy male volunteers performed 200 maximal eccentric contractions with each leg. To block prostaglandin synthesis locally in the skeletal muscle, indomethacin (NSAID) was infused for 7.5 h via microdialysis catheters into m. vastus lateralis of one leg. Protein synthesis was determined by the incorporation of 1,2-(13) C(2) leucine into muscle protein from 24 to 28 h post-exercise. Furthermore, mRNA expression of selected genes was measured in muscle biopsies (5 h and 8 days post-exercise) by real-time reverse transcriptase PCR. Myofibrillar and collagen protein synthesis were unaffected by the local NSAID infusion. Five hours post-exercise, the mRNA expression of cyclooxygenase-2 (COX2) was sixfold higher in the NSAID leg (P=0.016) compared with the unblocked leg. The expression of growth factors and matrix-related genes were unaffected by NSAID. Although NSAIDs inhibit the exercise-induced satellite cell proliferation, we observed only limited effects on gene expression, and on post-exercise protein synthesis.

Effect of administration of oral contraceptives on the synthesis and breakdown of myofibrillar proteins in young women.

Oral contraceptive (OC) treatment has an inhibiting effect on protein synthesis in tendon and muscle connective tissue. We aimed to investigate whether OC influence myofibrillar protein turnover in young women. OC-users (24±2 years; Lindynette® n=7, Cilest® n=4) and non-OC-users (controls, 24±4 years n=12) performed one-legged kicking exercise. The next day, the myofibrillar protein fractional synthesis rate (FSR) was measured using stable isotopic tracers ((13)C-proline) while the subjects were fed standardized nutrient drinks. Simultaneously, a marker for myofibrillar protein breakdown, 3-methyl-histidine (3-MH), was measured in the interstitial fluid of the vastus lateralis. Measurements were performed in both legs. In general, myofibrillar protein FSR was lower in OC-users (two-way analysis of variance, P<0.05), although the difference seemed to depend on the OC type. Interstitial 3-MH in the skeletal muscle was not different between groups and did not vary by OC type. Exercise did not change myofibrillar protein FSR or 3-MH concentrations. Serum androstenedione and bioavailability of testosterone were lower in OC-users. In conclusion, the results indicate that the use of OC has an inhibiting effect on myofibrillar protein synthesis and the magnitude of the effect may depend on the type of OC. In contrast, there was no effect of OC on myofibrillar protein breakdown in the fed state.

Local NSAID infusion inhibits satellite cell proliferation in human skeletal muscle after eccentric exercise.

Despite the widespread consumption of nonsteroidal anti-inflammatory drugs (NSAIDs), the influence of these drugs on muscle satellite cells is not fully understood. The aim of the present study was to investigate the effect of a local NSAID infusion on satellite cells after unaccustomed eccentric exercise in vivo in human skeletal muscle. Eight young healthy males performed 200 maximal eccentric contractions with each leg. An NSAID was infused via a microdialysis catheter into the vastus lateralis muscle of one leg (NSAID leg) before, during, and for 4.5 h after exercise, with the other leg working as a control (unblocked leg). Muscle biopsies were collected before and 8 days after exercise. Changes in satellite cells and inflammatory cell numbers were investigated by immunohistochemistry. Satellite cells were identified using antibodies against neural cell adhesion molecule and Pax7. The number of Pax7(+) cells per myofiber was increased by 96% on day 8 after exercise in the unblocked leg (0.14 +/- 0.04, mean +/- SE) compared with the prevalue (0.07 +/- 0.02, P < 0.05), whereas the number of Pax7(+) cells was unchanged in the leg muscles exposed to the NSAID (0.07 +/- 0.01). The number of inflammatory cells (CD68(+) or CD16(+) cells) was not significantly increased in either of the legs 8 days after exercise and was unaffected by the NSAID. The main finding in the present study was that the NSAID infusion for 7.5 h during the exercise day suppressed the exercise-induced increase in the number of satellite cells 8 days after exercise. These results suggest that NSAIDs negatively affect satellite cell activity after unaccustomed eccentric exercise.

Effect of administration of oral contraceptives in vivo on collagen synthesis in tendon and muscle connective tissue in young women.

Women are at greater risk than men for certain kinds of diseases and injuries, which may at least partly be caused by sex hormonal differences. We aimed to test the influence of estradiol in vivo on collagen synthesis in tendon, bone, and muscle. Two groups of young, healthy women similar in age, body composition, and exercise-training status were included. The two groups were either habitual users of oral contraceptives exposed to a high concentration of synthetic estradiol and progestogens (OC, n = 11), or non-OC-users tested in the follicular phase of the menstrual cycle characterized by low concentrations of estradiol and progesterone (control, n = 12). Subjects performed 1 h of one-legged kicking exercise. The next day collagen fractional synthesis rates (FSR) in tendon and muscle connective tissue were measured after a flooding dose of [(13)C]proline followed by biopsies from the patellar tendon and vastus lateralis in both legs. Simultaneously, microdialysis catheters were inserted in vastus lateralis and in front of the patellar tendon for measurement of insulin-like growth factor I (IGF-I) and its binding proteins. Serum NH(2)-terminal propeptide of type I collagen (PINP) and urine COOH-terminal telopeptides of type-I collagen (CTX-I) were measured as markers for bone synthesis and breakdown, respectively. Tendon FSR and PINP were lower in OC compared with control. An increase in muscle collagen FSR postexercise was only observed in control (P < 0.05). Furthermore, the results indicate a lower bioavailability of IGF-I in OC. In conclusion, synthetic female sex hormones administered as OC had an inhibiting effect on collagen synthesis in tendon, bone, and muscle connective tissue, which may be related to a lower bioavailability of IGF-I.

Novel methods for tendon investigations.

PURPOSE: Tendon structures have been studied for decades, but over the last decade, methodological development and renewed interest for metabolic, circulatory and tissue protein turnover in tendon tissue has resulted in a rising amount of investigations. METHOD: This paper will detail the various modern investigative techniques available to study tendons. RESULTS: There are a variety of investigative methods available to study the correlations between mechanics and biology in tendons. CONCLUSION: The available methodologies not only allow for potential insight into physiological and pathophysiological mechanisms in tendon tissue, but also, to some extent, allow for more elaborate studies of the intact human tendon.

Cyclo-oxygenase-2 mediated prostaglandin release regulates blood flow in connective tissue during mechanical loading in humans.

Mechanical loading is known to increase connective tissue blood flow of human tendons and to cause local release of vasodilatory substances. The present study investigated the importance of prostaglandins (PG) formed by cyclo-oxygenase isoforms (COX-1 and 2) for the exercise-related increase in blood flow in connective tissue. Healthy individuals (n = 24, age: 23-31 years) underwent 30 min of intermittent, isometric, plantarflexion with both calf muscles either without (n = 6, Control, C) or with blockade of PG formation, either COX-2 specific (n = 10, Celecoxib 2 x 100 mg day-1 for 3 days prior to the experiment) or COX unspecific (n = 8, indomethacin 100 mg (12 and 1 h pre-experiment) and acetyl salicylic acid 500 mg day-1 for 3 days pre-experiment). Prostaglandin E2 (PGE2) concentration was determined by microdialysis and blood flow by 133Xe washout. In C, interstitial PGE2 rose from (0.8 +/- 0.2 (rest) to 1.4 +/- 0.5 ng ml-1 (exercise), P < 0.05), whereas during unspecific COX inhibition, tissue PGE2 was completely inhibited at rest and during exercise. COX-2 specific blockade did not inhibit tissue PGE2 at rest, but totally abolished the exercise induced increase. Blood flow was similar in the three groups at rest (P > 0.05), whereas the increase in flow with exercise was reduced by 35 and 43 % with COX-2 specific blockade (3.2 +/- 0.7 to 6.1 +/- 1.5 ml (100 g tissue)-1 min-1 or COX unspecific blockade (3.0 +/- 0.8 to 7.6 +/- 1.6), respectively, compared to C (2.7 +/- 0.8 to 10.2 +/- 2.0)(P < 0.05). The findings indicate that COX-2 specific mechanisms are responsible for the exercise-induced increase in prostaglandin synthesis, and that increase in tissue prostaglandin plays an important role for blood flow in peritendinous connective tissue during physical loading in vivo.

Splanchnic blood flow and hepatic glucose production in exercising humans: role of renin-angiotensin system.

The study examined the implication of the renin-angiotensin system (RAS) in regulation of splanchnic blood flow and glucose production in exercising humans. Subjects cycled for 40 min at 50% maximal O(2) consumption (VO(2 max)) followed by 30 min at 70% VO(2 max) either with [angiotensin-converting enzyme (ACE) blockade] or without (control) administration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was estimated by indocyanine green, and splanchnic substrate exchange was determined by the arteriohepatic venous difference. Exercise led to an approximately 20-fold increase (P < 0.001) in ANG II levels in the control group (5.4 +/- 1.0 to 102.0 +/- 25.1 pg/ml), whereas this response was blunted during ACE blockade (8.1 +/- 1.2 to 13.2 +/- 2.4 pg/ml) and in response to an orthostatic challenge performed postexercise. Apart from lactate and cortisol, which were higher in the ACE-blockade group vs. the control group, hormones, metabolites, VO(2), and RER followed the same pattern of changes in ACE-blockade and control groups during exercise. Splanchnic blood flow (at rest: 1.67 +/- 0.12, ACE blockade; 1.59 +/- 0.18 l/min, control) decreased during moderate exercise (0.78 +/- 0.07, ACE blockade; 0.74 +/- 0.14 l/min, control), whereas splanchnic glucose production (at rest: 0.50 +/- 0.06, ACE blockade; 0.68 +/- 0.10 mmol/min, control) increased during moderate exercise (1.97 +/- 0.29, ACE blockade; 1.91 +/- 0.41 mmol/min, control). Refuting a major role of the RAS for these responses, no differences in the pattern of change of splanchnic blood flow and splanchnic glucose production were observed during ACE blockade compared with controls. This study demonstrates that the normal increase in ANG II levels observed during prolonged exercise in humans does not play a major role in the regulation of splanchnic blood flow and glucose production.

In situ microdialysis of intramuscular prostaglandin and thromboxane in contracting skeletal muscle in humans.

Arachidonic acid metabolites, especially prostacyclin I2, are regulators of vascular tone, and may be released from contracting muscle. In the present study, the influence of exercise on accumulation of prostaglandins and thromboxane in skeletal muscle was determined by the use of microdialysis technique using PGE2-3H as an internal reference. Interstitial tissue concentrations were determined both in m. gastrocnemius during intermittent static exercise (protocol A, 40 min, perfusion rate: 1 microL min-1) as well as in m. vastus lateralis during dynamic knee extension (protocol B, 20 W, 60 min, perfusion rate: 3 microL min-1). Relative recovery always rose with transition from rest to exercise (82 +/- 8% (A) and 75 +/- 7% (B), respectively) and returned to basal values during postexercise. Interstitial PGE2 concentrations rose 4-fold with dynamic exercise (0.95 +/- 0.26 ng mL-1 (rest) to 3.97 +/- 0.75 (exercise), P < 0.05), but where unchanged in response to intermittent static exercise. TXB2 decreased during intermittent static exercise, whereas intramuscular PGI2 (6-keto-PGF1alpha) concentration did not change with intermittent static exercise. The present study demonstrates measurable amounts of prostaglandins and thromboxanes in the interstitial space of skeletal muscle. Furthermore, the concentration of prostaglandin E2 is unchanged during static calf exercise and increased markedly with dynamic thigh muscle exercise, which together with an exercise induced increase in muscle blood flow indicate, that prostaglandin E2 is released from skeletal muscle during exercise in humans.

Age related blood flow around the Achilles tendon during exercise in humans.

Injuries due to the overuse of tendons increase with age, and it has been suggested that this correlates with hypovascularity of the tendon. In the present study, the peritendinous blood flow was determined using xenon-133 washout at rest and during standardised intermittent exercise of the calf-muscle (1.5 s contraction, 1.5 s rest, 40 min) in young (n = 6; 26 years), middle-aged (n = 6; 48 years), and older (n = 6; 74 years) individuals. At rest, the older individuals had a lower peritendinous blood flow compared with the two other age groups. During exercise, blood flow in all three groups rose 2.5-3.5-fold to reveal similar blood flows [2.7 (SEM 0.5) to 7.8 (SEM 1.0) ml.100 g tissue-1 min-1 (young group); 3.0 (SEM 0.4) to 7.3 (SEM 1.6) ml.100 g tissue-1 min-1 (middle-aged group); 1.6 (SEM 0.2) to 5.5 (SEM 1.1) ml 100 g tissue-1.min-1 (older group)]. The findings demonstrated that the peritendinous blood flow to the zone of the tendon with the highest incidence of injury from overuse is unaltered by age during exercise, and indicates that factors other than blood flow are important for the increased incidence with age of injuries from overuse.

Interstitial and arterial-venous [K+] in human calf muscle during dynamic exercise: effect of ischaemia and relation to muscle pain.

Changes in the concentration of interstitial K+ surrounding skeletal muscle fibres ([K+]I) probably play some role in the regulation of cardiovascular adjustments to muscular activity, as well as in the aetiology of muscle pain and fatigue during high-intensity exercise. However, there is very little information on the response of [K+]I to exercise in human skeletal muscle. Five young healthy subjects performed plantar flexion exercise for four 5 min periods at increasing power outputs ( approximately 1-6 W) with 10 min intervening recovery periods, as well as for two 5 min periods with ischaemia at approximately 1 and approximately 3 W. Microdialysis probes were inserted into the gastrocnemius medialis muscle of the right leg to measure [K+]I, and K+ release from the plantar flexors during and after incremental exercise was calculated from plasma flow and arterial-venous differences for K+. Calf muscle pain was assessed using a visual analogue scale. On average, [K+]I was 4.4 mmol l(-1) at rest and increased during minutes 3-5 of incremental exercise by approximately 1-7 mmol l(-1) as a positive function of power output. K+ release also increased as a function of exercise intensity, although there was a progressive increase by approximately 1-6 mmol l-1 in the [K+] gradient between the interstitium and arterial-venous plasma. [K+]I was lower during ischaemic exercise than control exercise. In contrast to this effect of ischaemia on [K+]I, muscle pain was relatively higher during ischaemic exercise, which demonstrates that factors other than changes in [K+]I are responsible for ischaemic muscle pain. In conclusion, this study has demonstrated that during 5 min of dynamic exercise, [K+]I increases during the later period of exercise as a positive function of exercise intensity, ischaemia reduces [K+]I during rest and exercise, and the increase in [K+]I is not responsible for muscle pain during ischaemic exercise.

In vivo studies of peritendinous tissue in exercise.

Soft tissue injury of tendons represents a major problem within sports medicine. Although several animal and cell culture studies have addressed this, human experiments have been limited in their ability to follow changes in specific tissue directly in response to interventions. Recently, methods have allowed for in vivo determination of tissue concentrations and release rates of substances involved in metabolism, inflammation and collagen synthesis, together with the measurement of tissue blood flow and oxygenation in the peritendinous region around the Achilles tendon in humans during exercise. It can be demonstrated that this region experiences an increase in blood flow during both static and dynamic exercise, and that exercise causes increased metabolic activity, accumulation of inflammatory mediators (prostaglandins) and increased formation of collagen type I in response to acute exercise. This coincides with a surprisingly marked drop in tissue pressure during contraction. With regards to both circulation, metabolism and collagen formation, peritendinous tissue represents a dynamic, responsive region that adapts markedly to acute muscular activity.

Time pattern of exercise-induced changes in type I collagen turnover after prolonged endurance exercise in humans.

Type I collagen is known to adapt to physical activity, and biomarkers of collagen turnover indicate that synthesis can be influenced by a single intense exercise bout, but the exact time pattern of these latter changes are largely undescribed. In the present study, 17 healthy young males had their plasma concentrations of the carboxyterminal propeptide of type I procollagen (PICP), a marker of collagen formation, and the immunoactive carboxyterminal cross-linked telopeptide (ICTP), a marker of collagen resorption, measured before and immediately postexercise, as well as 1, 2, 3, 4, 5, and 6 days after completion of a marathon run (42 km). Serum concentrations of creatine kinase (S-CK) were measured as an indicator of muscular breakdown in response to the exercise bout. After a transient decrease in collagen formation immediately after exercise (plasma PICP concentration: 176 +/- 17 microg/liter to 156 +/- 9 microg/liter)(P < 0.05), concentrations rose in the days following the marathon, peaked 72 hours after exercise (197 +/- 8 microg/liter)(P < 0.05 versus basal), and returned to basal values similar to those 5 days postexercise (170 +/- 10 microg/liter). Apart from a short increase immediately after exercise, collagen resorption did not change from basal levels throughout the remaining period (P > 0.05). Muscle breakdown was elevated during the days following the exercise and peaked 24 hours after the exercise (S-CK concentration: 3,133 +/- 579 U/liter). The findings in the present study indicate that type I collagen synthesis is accelerated in response to prolonged strenuous exercise, reaching a peak after 3 days and returning to preexercising levels 5 days after the completion of a marathon run.

Blood flow and oxygenation in peritendinous tissue and calf muscle during dynamic exercise in humans.

1. Circulation around tendons may act as a shunt for muscle during exercise. The perfusion and oxygenation of Achilles' peritendinous tissue was measured in parallel with that of calf muscle during exercise to determine (1) whether blood flow is restricted in peritendinous tissue during exercise, and (2) whether blood flow is coupled to oxidative metabolism. 2. Seven individuals performed dynamic plantar flexion from 1 to 9 W. Radial artery and popliteal venous blood were sampled for O2, peritendinous blood flow was determined by 133Xe-washout, calf blood flow by plethysmography, cardiac output by dye dilution, arterial pressure by an arterial catheter-transducer, and muscle and peritendinous O2 saturation by spatially resolved spectroscopy (SRS). 3. Calf blood flow rose 20-fold with exercise, reaching 44 +/- 7 ml (100 g)-1 min-1 (mean +/- s.e.m. ) at 9 W, while Achilles' peritendinous flow increased (7-fold) to 14 +/- 4 ml (100 g)-1 min-1, which was 18 % of the maximal flow established during reactive hyperaemia. SRS-O2 saturation fell both in muscle (from 66 +/- 2 % at rest to 57 +/- 3 %, P < 0.05) and in peritendinous regions (58 +/- 4 to 52 +/- 4 %, P < 0.05) during exercise along with a rise in leg vascular conductance and microvascular haemoglobin volume, despite elevated systemic vascular resistance. 4. The parallel rise in calf muscle and peritendinous blood flow and fall in O2 saturation during exercise indicate that blood flow is coupled to oxidative metabolism in both tissue regions. Increased leg vascular conductance accompanied by elevated microvascular haemoglobin volume reflect vasodilatation in both muscle and peritendinous regions. However, peak exercise peritendinous blood flow reaches only approximately 20 % of its maximal blood flow capacity.

Type I collagen synthesis and degradation in peritendinous tissue after exercise determined by microdialysis in humans.

1. Physical activity is known to increase type I collagen synthesis measured as the concentration of biomarkers in plasma. By the use of microdialysis catheters with a very high molecular mass cut-off value (3000 kDa) we aimed to determine local type I collagen synthesis and degradation in the peritendinous region by measuring interstitial concentrations of a collagen propeptide (PICP; 100 kDa) and a collagen degradation product (ICTP; 9 kDa) as well as an inflammatory mediator (PGE2). 2. Seven trained human runners were studied before and after (2 and 72 h) 3 h of running (36 km). Two microdialysis catheters were placed in the peritendinous space ventral to the Achilles' tendon under ultrasound guidance and perfused with a Ringer-acetate solution containing 3H-labelled human type IV collagen and [15-3H(N)]PGE2 for in vivo recovery determination. Relative recovery was 37-59 % (range of the s.e.m. values) for both radioactively labelled substances. 3. PICP concentration decreased in both interstitial peritendinous tissue and arterial blood immediately after exercise, but rose 3-fold from basal 72 h after exercise in the peritendinous tissue (55 +/- 10 microg l-1, mean +/- s.e.m. (rest) to 165 +/- 40 microg l-1 (72 h), P < 0.05) and by 25 % in circulating blood (160 +/- 10 microg l-1 (rest) to 200 +/- 12 microg l-1 (72 h), P < 0.05). ICTP concentration did not change in blood, but decreased transiently in tendon-related tissue during early recovery after exercise only. PGE2 concentration increased in blood during running, and returned to baseline in the recovery period, whereas interstitial PGE2 concentration was elevated in the early recovery phase. 4. The findings of the present study indicate that acute exercise induces increased formation of type I collagen in peritendinous tissue as determined with microdialysis and using dialysate fibre with a very high molecular mass cut-off. This suggests an adaptation to acute physical loading also in non-bone-related collagen in humans.

Negative interstitial pressure in the peritendinous region during exercise.

In the present study, tissue pressure in the peritendinous area ventral to the human Achilles tendon was determined. The pressure was measured during rest and intermittent isometric calf muscle exercise at three torques (56, 112, and 168 Nm) 20, 40 and 50 mm proximal to the insertion of the tendon in 11 healthy, young individuals. In all experiments a linear significant decrease in pressure was obtained with increasing torque [e.g., at 40 mm: -0.4 +/- 0.3 mmHg (rest) to -135 +/- 12 mmHg (168 Nm)]. No significant differences were obtained among the three areas measured. On the basis of these observations, microdialysis was performed in the peritendinous region with a colloid osmotic active substance (Dextran 70, 0.1 g/ml) added to the perfusate with the aim of counteracting the negative tissue pressure. Dialysate volume was found to be fully restored (100 +/- 4%) during exercise. It is concluded that a marked negative tissue pressure is generated in the peritendinous space around the Achilles tendon during exercise in humans. Negative tissue pressure could lead to fluid shift and could be involved in the increase in blood flow previously noted in the peritendinous tissue during exercise (H. Langberg, J. Bülow, and M. Kjaer. Acta Physiol. Scand. 163: 149-153, 1998; H. Langberg, J. Bülow, and M. Kjaer. Clin. Physiol. 19: 89-93, 1999).

Metabolism and inflammatory mediators in the peritendinous space measured by microdialysis during intermittent isometric exercise in humans.

1. The metabolic processes that occur around the tendon during mechanical loading and exercise are undescribed in man. These processes are important for understanding the development of overuse inflammation and injury. 2. A microdialysis technique was used to determine interstitial concentrations of glycerol, glucose, lactate, prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) as well as to calculate tissue substrate balance in the peritendinous region of the human Achilles tendon. Recovery of 48-62 % (range) at rest and 70-77 % during exercise were obtained for glycerol, glucose and PGE2. 3. Six young healthy humans were studied at rest, during 30 min of intermittent static plantar flexion of the ankle at a workload corresponding to individual body weight, and during 60 min of recovery. Microdialysis was performed in both legs with simultaneous determination of blood flow by 133Xe washout in the same area, and blood sampling from the radial artery. 4. With exercise, the net release of lactate as well as of glycerol from the peritendinous space of the Achilles tendon increased 2-fold (P < 0.05). Furthermore a 100 % increase in interstitial concentration of PGE2 and TXB2 was found, but it was only significant for TXB2(P < 0.05). As peritendinous blood flow increased 2- to 3-fold during intermittent static contractions, this indicates also that the output of these substances from the tissue increased during exercise. 5. This study indicates that both lipid and carbohydrate metabolism as well as inflammatory activity is accelerated in the peritendinous region of the human Achilles tendon with dynamic loading.

Conservative treatment of a partial Achilles tendon rupture with an intratendinous lesion.

The Achilles tendon is a common site of acute and overuse injuries in runners. A case is described here in which the diagnosis of a post-traumatic intratendinous lesion was based on clinical examination and magnetic resonance imaging (MRI), and where conservative treatment was given. After a 6 months follow-up, symptoms as well as the MRI verified that intra-tendinous structural abnormalities had disappeared. This case report demonstrates that conservative treatment may be sufficient to cure Achilles injury with severe structural changes inside the tendon.

[Bilateral Achilles tendon rupture in individuals with renal transplantation]. / Bilateral akillesseneruptur hos nyretransplanterede.

Increased incidence of tendinitis and tendon ruptures is reported in recipients of a kidney transplant. Two cases of bilateral achilles tendon rupture after minimal trauma are described. Tendon ruptures are more frequent in individuals with kidney disease in dialysis or after transplantation compared with patients receiving other organ transplantations. It is therefore more likely that tendon ruptures are related to metabolic changes associated with kidney disease rather than with transplantation or with glucocorticoid treatment per se. Clinical symptoms of achilles tendinitis should be considered as warning signs prior to tendon rupture and treated appropriately to avoid further morbidity. There is no contraindication towards surgical suturing of an achilles tendon rupture in patients receiving immunosuppressive treatment including glucocorticoids.