Accumulation of intramyocyte TRPV1-mediated calcium during heat stress is inhibited by concomitant muscle contractions

• Published in: Journal of applied physiology (1985) 2019-03, Vol.126 (3), p.691-698
• Main Authors: Ikegami, Ryo, Eshima, Hiroaki, Mashio, Takuro, Ishiguro, Tomosada, Hoshino, Daisuke, Poole, David C, Kano, Yutaka
• Format: Article
• Language: English
• Subjects: Accumulation; Calcium; Calcium (intracellular); Calcium homeostasis; Calcium ions; Capsaicin receptors; Capsazepine; Fluorescence; Fluorescence microscopy; Heat stress; Heat tolerance; Homeostasis; In vivo methods and tests; Muscle contraction; Muscles; Muscular function; Phosphorylation; Stress concentration; Surface temperature; Transient receptor potential proteins; Western blotting
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00668.2018

Heat stress promotes intramyocyte calcium concentration ([Ca ] ) accumulation via transient receptor potential vanilloid 1 (TRPV1) channels. We tested the hypothesis that muscle contractile activity concomitant with heat stress would accelerate the increase in [Ca ] via TRPV1, further impairing [Ca ] homeostasis. Spinotrapezius muscles of adult Wistar rats were exteriorized in vivo and loaded with the fluorescent Ca probe fura 2-AM. Heat stress (muscle surface temperature 40°C) was used as TRPV1 activator. An isometric contraction (100 Hz, 5-10 V, 30 s) was induced electrically concomitant with heat stress. [Ca ] was determined for 20 min using in vivo fluorescence microscopy, and the phosphorylation response of TRPV1 was determined by Western blotting. Heat stress induced a significant [Ca ] increase of 18.5 ± 8.1% at 20 min and TRPV1 phosphorylation (+231%), which was inhibited by addition of the TRPV1 inhibitor (capsazepine). However, contrary to expectations, the heat stress and isometric contraction condition almost completely inhibited TRPV1 phosphorylation and the consequent [Ca ] elevation ( 0.05). In conclusion, this in vivo physiological model demonstrated that isometric muscle contraction(s) can suppress the phosphorylation response of TRPV1 and maintain [Ca ] homeostasis during heat stress. NEW & NOTEWORTHY This investigation is the first document the dynamics of intramyocyte calcium concentration ([Ca ] ) increase in the myoplasm of skeletal muscle fibers in response to heat stress where the muscle blood flow is preserved. Heat stress at 40°C drives a myoplasmic [Ca ] accumulation in concert with transient receptor potential vanilloid 1 (TRPV1) phosphorylation. However, muscle contraction caused TRPV1 channel deactivation by dephosphorylation of TRPV1. TRPV1 inactivation via isometric contraction(s) permits maintenance of [Ca ] homeostasis even under high imposed muscle temperature.