Abstract
The transient receptor potential vanilloid 1 (TRPV1) belongs to the transient receptor potential superfamily of sensory receptors. TRPV1 is a non-selective cation channel permeable to Ca2+ that is capable of detecting noxious heat temperature and acidosis. In skeletal muscles, TRPV1 operates as a reticular Ca2+-leak channel and several TRPV1 mutations have been associated with two muscle disorders: malignant hyperthermia (MH) and exertional heat stroke (EHS). Although TRPV1−/− mice have been available since the 2000s, TRPV1’s role in muscle physiology has not been thoroughly studied. Therefore, the focus of this work was to characterize the contractile phenotype of skeletal muscles of TRPV1-deficient mice at rest and after four weeks of exercise. As MS and EHS have a higher incidence in men than in women, we also investigated sex-related phenotype differences. Our results indicated that, without exercise, TRPV1−/− mice improved in vivo muscle strength with an impairment of skeletal muscle in vitro twitch features, i.e., delayed contraction and relaxation. Additionally, exercise appeared detrimental to TRPV1−/− slow-twitch muscles, especially in female animals.
Highlights
Transient receptor potential (TRP) channels form the ion channel family with the greatest variety of selectivity and activation mechanisms [1]
Since heat and acidosis [7,8] are both physiological parameters modified during muscle contraction and exercise, they can activate transient receptor potential vanilloid 1 (TRPV1), and it is clear that
malignant hyperthermia (MH) and exertional heat stroke (EHS) are the two main triggered hyperthermia types regarded as phenotypes of a latent skeletal muscle disorder, as they share several hallmarks [23,24,25,26]
Summary
Transient receptor potential (TRP) channels form the ion channel family with the greatest variety of selectivity and activation mechanisms [1]. MH and EHS are the two main triggered hyperthermia types regarded as phenotypes of a latent skeletal muscle disorder, as they share several hallmarks [23,24,25,26]. Both clinically present a dysregulation of muscle contraction, leading to an increase in body temperature and potentially to multiorgan failure. MH and EHS can lead to patient death Both diseases are linked to mutations of proteins involved in the sarcoplasmic reticulum. A thorough knowledge of TRPV1’s role in skeletal muscle is essential for developing new therapeutic strategies against skeletal muscle diseases as MH or EHS
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