Altered Triceps Surae Muscle-Tendon Unit Properties after 6 Months of Static Stretching.

INTRODUCTION: This study examined the effects of 24 wk of daily static stretching of the plantarflexors (unilateral 4 × 60-s stretching, whereas the contralateral leg served as a control; n = 26) on joint range of motion (ROM), muscle-tendon unit morphological and mechanical properties, neural activation, and contractile function. METHODS: Torque-angle/velocity was obtained in passive and active conditions using isokinetic dynamometry, whereas muscle-tendon morphology and mechanical properties were examined using ultrasonography. RESULTS: After the intervention, ROM increased (stretching, +11° ± 7°; control, 4° ± 8°), and passive torque (stretching, -10 ± 11 N·m; control, -7 ± 10 N·m) and normalized EMG amplitude (stretching, -3% ± 6%; control, -3% ± 4%) at a standardized dorsiflexion angle decreased. Increases were seen in passive tendon elongation at a standardized force (stretching, +1.3 ± 1.6 mm; control, +1.4 ± 2.1 mm) and in maximal passive muscle and tendon elongation. Angle of peak torque shifted toward dorsiflexion. No changes were seen in tendon stiffness, resting tendon length, or gastrocnemius medialis fascicle length. Conformable changes in ROM, passive dorsiflexion variables, tendon elongation, and angle of peak torque were observed in the nonstretched leg. CONCLUSIONS: The present findings indicate that habitual stretching increases ROM and decreases passive torque, altering muscle-tendon behavior with the potential to modify contractile function.

Oral Treatment with the Ghrelin Receptor Agonist HM01 Attenuates Cachexia in Mice Bearing Colon-26 (C26) Tumors.

The gastrointestinal hormone ghrelin reduces energy expenditure and stimulates food intake. Ghrelin analogs are a possible treatment against cancer anorexia-cachexia syndrome (CACS). This study aimed to investigate whether oral treatment with the non-peptidergic ghrelin receptor agonist HM01 counteracts CACS in colon-26 (C26) tumor-bearing mice. The C26 tumor model is characterized by pronounced body weight (BW) loss and muscle wasting in the absence of severe anorexia. We analyzed the time course of BW loss, body composition, muscle mass, bone mineral density, and the cytokines interleukin-6 (IL-6) and macrophage-inhibitory cytokine-1 (MIC-1). Moreover, we measured the expression of the muscle degradation markers muscle RING-finger-protein-1 (MuRF-1) and muscle atrophy F-box (MAFbx). After tumor inoculation, MIC-1 levels increased earlier than IL-6 and both cytokines were elevated before MuRF-1/MAFbx expression increased. Oral HM01 treatment increased BW, fat mass, and neuronal hypothalamic activity in healthy mice. In tumor-bearing mice, HM01 increased food intake, BW, fat mass, muscle mass, and bone mineral density while it decreased energy expenditure. These effects appeared to be independent of IL-6, MIC-1, MuRF-1 or MAFbx, which were not affected by HM01. Therefore, HM01 counteracts cachectic body weight loss under inflammatory conditions and is a promising compound for the treatment of cancer cachexia in the absence of severe anorexia.