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

Heat stress promotes intramyocyte calcium concentration ([Ca²⁺]i) 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 [Ca²⁺]i via TRPV1, further impairing [Ca²⁺]i homeostasis. Spinotrapezius muscles of adult Wistar rats were exteriorized in vivo and loaded with the fluorescent Ca²⁺ 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. [Ca²⁺]i 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 [Ca²⁺]i 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 [Ca²⁺]i elevation (<2.8% accumulation during heat stress, P 0.05). In conclusion, this in vivo physiological model demonstrated that isometric muscle contraction(s) can suppress the phosphorylation response of TRPV1 and maintain [Ca²⁺]i homeostasis during heat stress. [ABSTRACT FROM AUTHOR]