Background: Deep dry needling (DDN) and ischemic compression technic (ICT) may be considered as interventions used for the treatment of Myofascial Pain Syndrome (MPS) in latent myofascial trigger points (MTrPs). The immediate effectiveness of both DDN and ICT on pressure pain threshold (PPT) and skin temperature of the latent MTrPs of the triceps surae has not yet been determined, especially in athletes due to their treatment requirements during training and competition. Objective: To compare the immediate efficacy between DDN and ICT in the latent MTrPs of triathletes considering PPT and thermography measurements. Method: A total sample of 34 triathletes was divided into two groups: DDN and ICT. The triathletes only received a treatment session of DDN (n = 17) or ICT (n = 17). PPT and skin temperature of the selected latent MTrPs were assessed before and after treatment. Results: Statistically significant differences between both groups were shown after treatment, showing a PPT reduction (p < 0.05) in the DDN group, while PPT values were maintained in the ICT group. There were not statistically significant differences (p > 0.05) for thermographic values before and treatment for both interventions. Conclusions: Findings of this study suggested that ICT could be more advisable than DDN regarding latent MTrPs local mechanosensitivity immediately after treatment due to the requirements of training and competition in athletes’ population. Nevertheless, further studies comparing both interventions in the long term should be carried out in this specific population due to the possible influence of delayed onset muscle soreness and muscle damage on PPT and thermography values secondary to the high level of training and competition.

Toll-like receptor 4, the receptor for bacterial lipopolysaccharide (LPS), drives inflammatory responses that protect against pathogens and boost the adaptive immunity. LPS responses are known to depend on calcium fluxes, but the molecular mechanisms involved are poorly understood. Here we present evidence that the transient receptor potential canonical channel 3 (TRPC3) is activated intracellularly during macrophage exposure to LPS and is essential for Ca2+ release from internal stores. In this way TRPC3 participates in cytosolic Ca2+ elevations, TLR4 endocytosis, activation of inflammatory transcription factors and cytokine upregulation. We also report that TRPC3 is activated by diacylglycerol (DAG) generated by the phosphatidic acid phosphatase lipin-1. In accord with this, lipin-1-deficient cells show reduced Ca2+ responses to LPS challenge. A cameleon indicator directed to the endoplasmic reticulum shows that this is the organelle from which TRPC3 mediates the Ca2+ release. Finally, pharmacological inhibition of TRPC3 reduces systemic inflammation induced by LPS in mice. Collectively, our study unveils a central component of LPS-triggered Ca2+ signaling that involves intracellular sensing of lipin-1-derived DAG by TRPC3.