ArticleCell stress & chaperones2018
Heat acclimation increases mitochondrial respiration capacity of C2C12 myotubes and protects against LPS-mediated energy deficit.
Article in Cell stress & chaperones, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Short-term endurance training in the cold with layered clothing mitigates perceptual strain during exercise in the heat.European journal of applied physiology · 2026Article
- Respiratory efficiency and thermoregulatory responses of L-citrulline-supplemented broiler chickens under acute and chronic stress conditions.Frontiers in physiology · 2026Article
- Mitochondrial adaptations from heat acclimation - A narrative review.Journal of thermal biology · 2025Review
- Heat acclimation improves exercise performance in hot conditions and increases heat shock protein 70 and 90 of skeletal muscles in Thoroughbred horses.Physiological reports · 2024Article
- Temperate performance and metabolic adaptations following endurance training performed under environmental heat stress.Physiological reports · 2021Article
- Impacts of previous heatstroke history on physiological parameters eHSP72 and biomarkers of oxidative stress in military working dogs.Cell stress & chaperones · 2019Article
- Heat acclimation increases inflammatory and apoptotic responses to subsequent LPS challenge in C2C12 myotubes.Cell stress & chaperones · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This work investigated the effect of a 6-day heat acclimation (HA) protocol on myotube metabolic responses at baseline and in response to a subsequent lipopolysaccharide (LPS) challenge. C2C12 myotubes were incubated for 2 h/day at 40 °C for 6 days (HA) or maintained at 37 °C (C). Following 24-h recovery, myotubes were challenged with 500 ng/ml LPS for 2 h, then collected for analysis of protein markers of mitochondrial biogenesis and macronutrient storage. Functional significance of these changes was confirmed with mitochondrial respiration and glycolytic measurements on a Seahorse XF-96 analyzer. HA stimulated mitochondrial biogenesis and increased indicators of mitochondrial content [SIRT1 (+ 62%); PGC-1α (+ 57%); NRF-1 (+ 40%); TFAM (+ 141%); CS (+ 25%); CytC (+ 38%); all p < 0.05]. Altered lipid biosynthesis enzymes [p-ACCa:ACC (+ 59%; p = 0.04) and FAS (- 86%; p < 0.01)] suggest fatty acid generation may have been downregulated, whereas increased GLUT4 (+ 69%; p < 0.01) and LDH-B (+ 366%; p < 0.01) suggest aerobic glycolytic capacity may have been improved. Mitochondrial biogenesis signaling in HA myotubes was suppressed by 500 ng/ml LPS (PGC-1α, NRF-1, TFAM; all p > 0.05) but increased LDH-B (+ 30%; p = 0.02) and CPT-1 (+ 55%; p < 0.01) suggesting improved catabolic function. Basal respiration was increased in HA myotubes (+ 8%; p < 0.01) and HA myotubes maintained elevated basal respiration during LPS challenge (+ 8%; p < 0.01). LPS reduced peak respiration in C myotubes (- 6%; p < 0.01) but did not impair peak respiration in HA myotubes (p > 0.05). Oxidative reliance was elevated in HA over that in control (+ 25%; p < 0.01) and in HA + LPS over C + LPS (+ 30%; p < 0.01). In summary, HA stimulated mitochondrial biogenesis in C2C12 myotubes. HA myotubes exhibited (1) elevated basal/peak mitochondrial respiration capacities; (2) greater oxidative reliance; and (3) protection against LPS-mediated respiration impairment. Collectively, these data suggest HA may improve aerobic metabolism in skeletal muscle and protect against LPS-mediated energy deficit.
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