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This study investigated how one bout ( 1EX) and three bouts ( 3EX) of strenuous resistance exercise affected the cross-sectional area ( CSA) and water content ( WC) of the quadriceps muscle and patella tendon ( PT), 4 h and 52 h after the last exercise bout. Ten healthy untrained male subjects performed 1EX with one leg and 3EX with the other leg. CSA and WC were measured with magnetic resonance imaging 10, 20 and 30 cm proximal to the tibia plateau ( TP) for the muscle, and at the proximal, central and distal site for the PT prior to exercise, and 4 h and 52 h after the last exercise bout. Ten centimeter above the TP, muscle CSA was significantly increased at 4 h ( 1EX: 13 ± 5%; 3EX: 13 ± 4%) and 52 h ( 1EX: 16 ± 5%; 3EX: 16 ± 5%) compared with baseline. Muscle WC was significantly increased at 4 h ( 1EX: 7 ± 1%; 3EX: 6 ± 2%) and 52 h ( 1EX: 8 ± 2%; 3EX: 8 ± 3%) compared to baseline. PT central CSA was significantly reduced at 52 h ( 3EX: 14 ± 2%) compared with baseline and ( 3EX: 13 ± 1%) compared with 4 h. Present data demonstrate that strenuous resistance exercise results in an acute increase in muscle WC and underlines the importance of ensuring sufficient time between the last exercise bout and the determination of anatomical dimensions in muscles. [ABSTRACT FROM AUTHOR]

Tendinopathy is often discovered late because the initial development of tendon pathology is asymptomatic. The aim of this study was to examine the potential role of mast cell involvement in early tendinopathy using a high-intensity uphill running ( HIUR) exercise model. Twenty-four male Wistar rats were divided in two groups: running group ( n = 12); sedentary control group ( n = 12). The running-group was exposed to the HIUR exercise protocol for 7 weeks. The calcaneal tendons of both hind limbs were dissected. The right tendon was used for histologic analysis using Bonar score, immunohistochemistry, and second harmonic generation microscopy ( SHGM). The left tendon was used for quantitative polymerase chain reaction ( qPCR) analysis. An increased tendon cell density in the runners were observed compared to the controls ( P = 0.05). Further, the intensity of immunostaining of protein kinase B, P = 0.03; 2.75 ± 0.54 vs 1.17 ± 0.53, was increased in the runners. The Bonar score ( P = 0.05), and the number of mast cells ( P = 0.02) were significantly higher in the runners compared to the controls. Furthermore, SHGM showed focal collagen disorganization in the runners, and reduced collagen density ( P = 0.03). IL-3 mRNA levels were correlated with mast cell number in sedentary animals. The qPCR analysis showed no significant differences between the groups in the other analyzed targets. The current study demonstrates that 7-week HIUR causes structural changes in the calcaneal tendon, and further that these changes are associated with an increased mast cell density. [ABSTRACT FROM AUTHOR]

Key points Loss of muscle and tendon function during periods of immobilisation and rehabilitation represents a challenge in clinical medicine., It is not known to what extent growth hormone (GH) supplementation is able to counteract the absence of mechanical loading during immobilisation in musculo-tendinous connective tissue., This study examines the effect of GH in musculo-tendinous connective tissue in humans during immobilisation and subsequent rehabilitation., The main study findings were the observation that GH supplementation stimulates collagen expression in musculo-tendinous tissue and abolishes the normal decline in tendon stiffness and lysyl oxidase during immobilisation. Furthermore, GH supplementation results in an increased tendon size and stiffness during rehabilitation., GH supplementation has a matrix-stabilising effect during periods of inactivity and rehabilitation in humans., Abstract We examined the effect of growth hormone (GH) on connective tissue of tendon and skeletal muscle during immobilisation and re-training in humans. Young men (20-30 years; n= 20) were randomly assigned to daily recombinant human GH (rhGH) (33-50 μg kg−1 day−1) or placebo (Plc), and had one leg immobilised for 2 weeks, followed by 6 weeks of strength training. The cross-sectional area (CSA), maximal muscle strength (maximal voluntary contraction, MVC) and biomechanical properties of the quadriceps muscle and patellar tendon were determined. Muscle and tendon biopsies were analysed for mRNA of collagen (COL1A1/3A1), insulin-like growth factors (IGF-1Ea/Ec), lysyl oxidase (LOX), matrix metalloproteases (MMP-2 and MMP-9), decorin and tenascin-C. Fibril morphology was analysed by transmission electron microscopy (TEM) to detect changes in the fibril diameter distribution. In muscle, CSA and MVC declined with immobilisation and recovered with rehabilitation similarly in both groups. Likewise, both groups showed increased IGF-1Ea/Ec and COL1A1/3A1 expression in muscle during re-training after immobilisation compared with baseline, and the increase was more pronounced when subjects received GH. The tendon CSA did not change during immobilisation, but increased in both groups during 6 weeks of rehabilitation (∼14%). A decline in tendon stiffness after immobilisation was observed only in the Plc group, and an increase during 6 weeks of rehabilitation was observed only in the GH group. IGF-1Ea and COL1A1/3A1 mRNA increased with immobilisation in the GH group only, and LOX mRNA was higher in the GH group than in the Plc group after immobilisation. Both groups showed an increase in MMP-2 with immobilisation, whereas no changes in MMP-9, decorin and tenascin-C were observed. The tendon fibril diameter distribution remained unchanged in both groups. In conclusion, GH stimulates collagen expression in both skeletal muscle and tendon, abolishes the normal inactivity-related decline in tendon stiffness and LOX, and results in increased tendon CSA and stiffness during rehabilitation. GH has a matrix-stabilising effect during periods of inactivity and rehabilitation in humans. [ABSTRACT FROM AUTHOR]

Collagen is the predominant structural protein in tendons and ligaments, and can be controlled by hormonal changes. In animals, injections of insulin-like growth factor I ( IGF-I) has been shown to increase collagen synthesis in tendons and ligaments and to improve structural tissue healing, but the effect of local IGF-I administration on tendon collagen synthesis in human has not been studied. The purpose of this study was to study whether local injections of IGF-I would have a stimulating effect on tendon collagen synthesis. Twelve healthy nonsmoking men [age 62 ± 1 years (mean ± SEM), BMI 27 ± 1] participated. Two injections of either human recombinant IGF-I (0.1 mL Increlex©) or saline (control) into each patellar tendon were performed 24-h apart, respectively. Tendon collagen fractional synthesis rate ( FSR) was measured by stable isotope technique in the hours after the second injection. Simultaneously, interstitial peritendinous ( IGF-I) and [procollagen type I N-terminal propeptide ( PINP)], as a marker for type I collagen synthesis, were determined by microdialysis technique. Tendon collagen FSR and PINP were significantly higher in the IGF-I leg compared with the control leg ( P < 0.05). In conclusion, local IGF-I administration can directly enhance tendon collagen synthesis both within and around the human tendon tissue. [ABSTRACT FROM AUTHOR]

Aim Exercise-induced adaptations of skeletal muscle are related to training mode and can be muscle fibre type specific. This study aimed to investigate heat shock protein expression in type I and type II muscle fibres in resting skeletal muscle of subjects with different training backgrounds. Methods Three groups of subjects were included: healthy active not engaged in any training programme ( ACT, n = 12), resistance trained ( RES, n = 6) and endurance trained ( END, n = 8). Biopsies were obtained from vastus lateralis, and immunohistochemistry was performed using monoclonal antibodies against myosin heavy chain I and IIA, α B-crystallin, HSP27, HSP60 and HSP70. Results In ACT and RES, but not in END, a fibre type-specific expression with higher staining intensity in type I than type II fibres was seen for α B-crystallin. The opposite ( II > I) was found for HSP27 in subjects from ACT (6 of 12 subjects) and RES (3 of 6), whereas all subjects from END displayed uniform staining. HSP60 showed no fibre-specific expression. HSP70 displayed a fibre-specific expression pattern (I > II) in ACT (4 of 12), but not in END or RES. Conclusion This study shows that the level of expression of the different HSPs in human skeletal muscle is influenced by muscle fibre phenotype. The fibre type-specific expression of HSP70 is influenced by resistance and endurance training, whereas those of α B-crystallin and HSP27 is influenced only by endurance training, suggesting the existence of a training-modality-specific action on the adaptive processes including heat shock proteins in human skeletal muscle. [ABSTRACT FROM AUTHOR]

Manipulating joint range of motion during squat training may have differential effects on adaptations to strength training with implications for sports and rehabilitation. Consequently, the purpose of this study was to compare the effects of squat training with a short vs. a long range of motion. Male students ( n = 17) were randomly assigned to 12 weeks of progressive squat training (repetition matched, repetition maximum sets) performed as either a) deep squat (0-120° of knee flexion); n = 8 (DS) or (b) shallow squat (0-60 of knee flexion); n = 9 (SS). Strength (1 RM and isometric strength), jump performance, muscle architecture and cross-sectional area (CSA) of the thigh muscles, as well as CSA and collagen synthesis in the patellar tendon, were assessed before and after the intervention. The DS group increased 1 RM in both the SS and DS with ~20 ± 3 %, while the SS group achieved a 36 ± 4 % increase in the SS, and 9 ± 2 % in the DS ( P < 0.05). However, the main finding was that DS training resulted in superior increases in front thigh muscle CSA (4-7 %) compared to SS training, whereas no differences were observed in patellar tendon CSA. In parallel with the larger increase in front thigh muscle CSA, a superior increase in isometric knee extension strength at 75° (6 ± 2 %) and 105° (8 ± 1 %) knee flexion, and squat-jump performance (15 ± 3 %) were observed in the DS group compared to the SS group. Training deep squats elicited favourable adaptations on knee extensor muscle size and function compared to training shallow squats. [ABSTRACT FROM AUTHOR]

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely consumed in relation to pain and injuries in skeletal muscle, but may adversely affect muscle adaptation probably via inhibition of prostaglandin synthesis. Induction of heat shock proteins (HSP) represents an important adaptive response in muscle subjected to stress, and in several cell types including cardiac myocytes prostaglandins are important in induction of the HSP response. This study aimed to determine the influence of NSAIDs on the HSP response to eccentric exercise in human skeletal muscle. Healthy males performed 200 maximal eccentric contractions with each leg with intramuscular infusion of the NSAID indomethacin or placebo. Biopsies were obtained from m. vastus lateralis before and after (5, 28 hrs and 8 days) the exercise bout from both legs (NSAID vs unblocked leg) and analysed for expression of the HSPs HSP70, HSP27 and αB-crystallin (mRNA and protein). NSAID did not affect the mRNA expression of any of the HSPs. Compared to pre values, the mRNA expression of all HSPs was increased; αB-crystallin, 3.6- and 5.4-fold; HSP70, 26- and 3.4-fold; and HSP27: 4.8- and 6.5-fold at 5 and 28 hrs post-exercise, respectively (all p < 0.008). Immunohistochemical stainings for αB-crystallin and HSP70 revealed increased staining in some samples but with no differences between legs. Changes in force-generating capacity correlated with both αB-crystallin and HSP70 mRNA and immunohistochemisty data. Increased expression of HSPs was observed on mRNA and protein level following eccentric exercise; however, this response was unaffected by local intramuscular infusion of NSAIDs [ABSTRACT FROM AUTHOR]