Role of TRPV1 in High Temperature-Induced Mitochondrial Biogenesis in Skeletal Muscle: A Mini Review

Abstract

Transient receptor potential vanilloid 1 (TRPV1) is a protein that is susceptible to cell environment temperature. High temperatures of 40–45°C can activate the TRPV1 channel. TRPV1 is highly expressed in skeletal muscle and located on the sarcoplasmic reticulum (SR). Therefore, TRPV1 activated by high-temperature stress releases Ca2+ from the SR to the cytoplasm. Cellular Ca2+ accumulation is a key event that enhances TRPV1 activity by directly binding to the N-terminus and C-terminus. Moreover, Ca2+ is the key messenger involved in regulating mitochondrial biogenesis in skeletal muscle. Long-term activation of TRPV1 may promote mitochondrial biogenesis in skeletal muscle through the Ca2+-CaMKII-p38 MAPK-PGC-1α signaling axis. The discovery of the TRPV1 channel highlights the potential mechanism for high-temperature stress improving muscle mitochondrial biogenesis. The appropriate hot stimulus in thermal environments might be beneficial to the muscular mitochondrial adaptation for aerobic capacity. However, the investigation of TRPV1 on mitochondrial biogenesis is at an early stage. Further investigations need to examine the role of TRPV1 in response to mitochondrial biogenesis in skeletal muscle induced by different thermal environments.

Effects of Capsaicin and Capsiate on Endurance Performance: A Meta-Analysis

“…There are several possible physiological explanations for the ergogenic effect of capsaicin/capsiate on muscular endurance. As mentioned previously, the activation of TRPV1 may lead to an increase in calcium ion release in the sarcoplasmic reticulum, thus influencing the interaction between the actin-myosin filaments and enhancing force output [ 5 , 6 ]. Capsaicin and capsiate may alter motor neuron excitability and motor unit recruitment [ 31 ].…”

“…Activation of TRPV1 leads to the sensation of heat and an increase in energy expenditure and fat oxidation [ 1 ]. Furthermore, TRPV1 is also highly expressed in skeletal muscle (located on the sarcoplasmic reticulum) and its activation may also influence muscle contractility [ 5 , 6 ]. TRPV1 activation following capsaicin ingestion may increase calcium ion release from the sarcoplasmic reticulum, subsequently influencing the interaction between the actin-myosin filaments resulting in an increase in force output [ 5 , 6 ].…”

“…Furthermore, TRPV1 is also highly expressed in skeletal muscle (located on the sarcoplasmic reticulum) and its activation may also influence muscle contractility [ 5 , 6 ]. TRPV1 activation following capsaicin ingestion may increase calcium ion release from the sarcoplasmic reticulum, subsequently influencing the interaction between the actin-myosin filaments resulting in an increase in force output [ 5 , 6 ]. Consumption of capsaicin has also been reported to reduce pain perception and rating of perceived exertion (RPE), factors that may contribute to improvement in exercise performance [ 4 , 7 ].…”

Informing the Cannabis Conjecture: From Life’s Beginnings to Mitochondria, Membranes and the Electrome—A Review

“…In terms of compartmentalisation, mitochondria and the ER are in close contact via mitochondrial-associated membrane (MAM) complexes, which transport metabolites, including lipids and signalling moieties, such as calcium [165]. As an example, it seems that activation of TRPV1 in muscle by high temperatures may well be important in stimulating mitochondrial biogenesis [166], which suggests how various stressors can upregulate metabolism. In short, TRPV1 channels are key in hormesis.…”

Contribution of transient receptor potential vanilloid 1 (TRPV1) channel to cholinergic contraction of rat bladder smooth muscle

“…TRPV1, like many other TRP channels, can be localized and function not only in the plasma membrane but also in the intracellular membranes, including the endoplasmic/sarcoplasmic reticulum (ER/SR) and the mitochondria (Dong et al., 2010; Zhao & Tsang, 2017). In the skeletal muscle, for instance, TRPV1 might operate as a temperature‐sensitive SR Ca 2+ ‐leakage channel involved in crosstalk with the ryanodine receptor (RyR1) Ca 2+ ‐release channel (Lotteau et al., 2013; Xin et al., 2005; Xu et al., 2022). In airway smooth muscle cells, activation of SR‐localized TRPV1 was shown to contribute to the maintenance of muscarinic receptor‐mediated calcium oscillations and the force of contraction (Yocum et al., 2017), and even sensory dorsal root ganglion (DRG) neurons express ectopic but functional TRPV1 channels in the ER (Gallego‐Sandín et al., 2009).…”