In vivo cooling-induced intracellular Ca2+ elevation and tension in rat skeletal muscle.

Abstract

It is an open question as to whether cooling‐induced muscle contraction occurs in the in vivo environment. In this investigation, we tested the hypotheses that a rise in intracellular Ca²⁺ concentration ([Ca²⁺]i) and concomitant muscle contraction could be evoked in vivo by reducing muscle temperature and that this phenomenon would be facilitated or inhibited by specific pharmacological interventions designed to impact Ca²⁺‐induced Ca²⁺‐release (CICR). Progressive temperature reductions were imposed on the spinotrapezius muscle of Wistar rats under isoflurane anesthesia by means of cold fluid immersion. The magnitude, location, and temporal profile of [Ca²⁺]i were estimated using fura‐2 loading. Caffeine (1.25–5.0 mM) and procaine (1.6–25.6 mM) loading were applied in separatum to evaluate response plasticity by promoting or inhibiting CICR, respectively. Lowering the temperature of the muscle surface to ~5°C produced active tension and discrete sites with elevated [Ca²⁺]i. This [Ca²⁺]i elevation differed in magnitude from fiber to fiber and also from site to site within a fiber. Caffeine at 1.25 and 5.0 mM reduced the magnitude of cooling necessary to elevate [Ca²⁺]i (i.e., from ~5°C to ~8 and ~16°C, respectively, both p < 0.05) and tension. Conversely, 25.6 mM procaine lowered the temperature at which [Ca²⁺]i elevation and tension were detected to ~2°C (p < 0.05). Herein we demonstrate the spatial and temporal relationship between cooling‐induced [Ca²⁺]i elevation and muscle contractile force in vivo and the plasticity of these responses with CICR promotion and inhibition.