Skeletal muscle has a remarkable ability to respond to different physical stresses. Loading muscle through exercise, either anaerobic or aerobic, can lead to increases in muscle size and function while, conversely, the absence of muscle loading stimulates rapid decreases in size and function. A principal mediator of this load-induced change is focal adhesion kinase (FAK), a downstream non-receptor tyrosine kinase that translates the cytoskeletal stress and strain signals transmitted across the cytoplasmic membrane by integrins to activate multiple anti-apoptotic and cell growth pathways. Changes in FAK expression and phosphorylation have been found to correlate to specific developmental states in myoblast differentiation, muscle fiber formation and muscle size in response to loading and unloading. With the capability to regulate costamere formation, hypertrophy and glucose metabolism, FAK is a molecule with diverse functions that are important in regulating muscle cell health.

• ▶ muscle-tendon stiff ness • ▶ infl ammatory response • ▶ injury • ▶ therapeutic modality Instrument-assisted Soft Tissue Mobilization: Eff ects on the Properties of Human Plantar Flexorstion following eccentric exercise may be important components for the recovery of muscle tissue [ 20 ] . Though this research provides the most recent mechanistic example of the response to soft tissue mobilization in an animal model, the physiological diff erences to that of human subjects may limit its clinical applicability [ 11 , 35 ] . In contrast, the research fi ndings on IASTM often describe clinical markers such as range of motion (ROM) and functional measures, but are not derived from randomized controlled studies [ 15 ] . Collectively, however, it appears that soft tissue mobilization therapies may play a role in reducing infl ammation [ 6 ] . The purpose of this project was to evaluate the eff ects of IASTM on intramuscular infl ammation, pain, ROM and strength following muscle damage in a randomized controlled laboratory experiment. Materials and Methods ▼ Subjects11 healthy men (mean ± SD age = 23 ± 3 years; stature = 181 ± 7 cm; mass = 83 ± 11 kg) volunteered for this investigation. Each participant was screened Introduction ▼ According to the marketing information for Graston Technique ® , a form of instrument-assisted soft tissue mobilization (IASTM), more than 16 000 clinicians currently employ this technique for treating soft tissue ailments [ 17 ] . This does not include the number of clinicians and alternative medicine providers utilizing other forms of IASTM techniques such as sound-assisted soft tissue mobilization (SASTM), ASTYM ® , GuaSha, or others. Interestingly, the ability of IASTM to ameliorate loss of function, pain and infl ammation has yet to be clarifi ed. There are several physiological hypotheses as to how soft tissue mobilization works. These include increased blood fl ow, increased lymphatic drainage of toxins, reduced tissue stiff ness, alteration in neuromuscular activity and a decreased infl ammatory response [ 48 ] . However, the current literature fails to support these claims. Recently, studies have evaluated the eff ects of soft tissue mobilization on the recovery of muscular attributes following eccentric exercise-induced muscle damage [ 13 , 14 ] . Interestingly, it has been demonstrated that the intensity of the compressive load and the timing of applica-

Myokines are molecules produced and secreted by skeletal muscle to act in an auto-, para-and endocrine manner to alter physiological function of target tissues. The growing number of effects of myokines on metabolism of distant tissues provides a compelling case for crosstalk between skeletal muscle and other tissues and organs to regulate metabolic homoeostasis. In this review, we summarize and discuss the current knowledge regarding the impact on metabolism of several canonical and recently identified myokines. We focus specifically on myostatin, β-aminoisobutyric acid, interleukin-15, meteorin-like and myonectin, and discuss how these myokines are induced and regulated as well as their overall function. We also review how these myokines may serve as potential prognostic biomarkers that reflect whole-body metabolism and how they may be attractive therapeutic targets for treating muscle and metabolic diseases. K E Y W O R D Sinterleukin-15, metabolism, meteorin-like, myonectin, myostatin, β-aminoisobutyric acid

Heat shock proteins (HSPs) are chaperones that are known to have important roles in facilitating protein synthesis, protein assembly and cellular protection. While HSPs are known to be induced by damaging exercise, little is known about how HSPs actually mediate skeletal muscle adaption to exercise. The purpose of this study was to determine the effects of a heat shock pretreatment and the ensuing increase in HSP expression on early remodeling and signaling (2 and 48 h) events of the soleus (Sol) muscle following a bout of downhill running. Male Wistar rats (10 weeks old) were randomly assigned to control, eccentric exercise (EE; downhill running) or heat shock + eccentric exercise (HS; 41°C for 20 min, 48 h prior to exercise) groups. Markers of muscle damage, muscle regeneration and intracellular signaling were assessed. The phosphorylation (p) of HSP25, Akt, p70s6k, ERK1/2 and JNK proteins was also performed. As expected, following exercise the EE group had increased creatine kinase (CK; 2 h) and mononuclear cell infiltration (48 h) compared to controls. The EE group had an increase in p-HSP25, but there was no change in HSP72 expression, total protein concentration, or neonatal MHC content. Additionally, the EE group had increased p-p70s6k, p-ERK1/2, and p-JNK (2 h) compared to controls; however no changes in p-Akt were seen. In contrast, the HS group had reduced CK (2 h) and mononuclear cell infiltration (48 h) compared to EE. Moreover, the HS group had increased HSP72 content (2 and 48 h), total protein concentration (48 h), neonatal MHC content (2 and 48 h), p-HSP25 and p-p70s6k (2 h). Lastly, the HS group had reduced p-Akt (48 h) and p-ERK1/2 (2 h). These data suggest that heat shock pretreatment and/or the ensuing HSP72 response may protect against muscle damage, and enhance increases in total protein and neonatal MHC content following exercise. These changes appear to be independent of Akt and MAPK signaling pathways.