scholarly journals The effects of heat stress in redox balance and inflammatory signaling in porcine skeletal muscle

2013 ◽  
Author(s):  
Sandra Isabel Rosado Montilla
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Redox Balance ◽  
Inflammatory Signaling

scholarly journals Heat stress causes oxidative stress but not inflammatory signaling in porcine skeletal muscle

Temperature ◽  
2014 ◽  
Vol 1 (1) ◽  
pp. 42-50 ◽  
Author(s):  
Sandra I Rosado Montilla ◽  
Theresa P Johnson ◽  
Sarah C Pearce ◽  
Delphine Gardan-Salmon ◽  
Nicholas K Gabler ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Heat Stress ◽  
Inflammatory Signaling

scholarly journals Twelve hours of heat stress induces inflammatory signaling in porcine skeletal muscle

2016 ◽  
Vol 310 (11) ◽  
pp. R1288-R1296 ◽  
Author(s):  
Shanthi Ganesan ◽  
Carmen Reynolds ◽  
Katrin Hollinger ◽  
Sarah C. Pearce ◽  
Nicholas K. Gabler ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Heat Shock ◽  
Relative Abundance ◽  
Protein Abundance ◽  
Heat Shock Factor 1 ◽  
Activator Protein 1 ◽  
Inflammatory Signaling ◽  
Skeletal Muscle Dysfunction ◽  
Livestock Productivity

Heat stress causes morbidity and mortality in humans and animals and threatens food security by limiting livestock productivity. Inflammatory signaling may contribute to heat stress-mediated skeletal muscle dysfunction. Previously, we discovered increased circulating endotoxin and intramuscular oxidative stress and TNF-α protein abundance, but not inflammatory signaling following 24 and 72 h of heat stress. Thus the purpose of this investigation was to clarify the role of inflammatory signaling in heat-stressed skeletal muscle. Crossbred gilts ( n = 8/group) were assigned to either thermal neutral (24°C), heat stress (37°C), or pair-fed thermal neutral (24°C) conditions for 12 h. Following treatment, animals were euthanized, and the semitendinosus red (STR) and white (STW) were recovered. Heat stress did not alter inflammatory signaling in STW. In STR, relative heat shock protein abundance was similar between groups, as was nuclear content of heat shock factor 1. In whole homogenate, relative abundance of the NF-κB activator inhibitory κB kinase-α was increased by heat stress, although abundance of NF-κB was similar between groups. Relative abundance of phosphorylated NF-κB was increased by heat stress in nuclear fractions. Activator protein-1 (AP-1) signaling was similar between groups. While there were few differences in transcript expression between thermal neutral and heat stress, 80 and 56% of measured transcripts driven by NF-κB or AP-1, respectively, were increased by heat stress compared with pair-fed thermal neutral. Heat stress also caused a reduction in IL-6 transcript and relative protein abundance. These data demonstrate that short-term heat stress causes inflammatory signaling through NF-κB in oxidative, but not glycolytic, skeletal muscle.

scholarly journals Short-term heat stress alters redox balance in porcine skeletal muscle

2017 ◽  
Vol 5 (8) ◽  
pp. e13267 ◽  
Author(s):  
Olga Volodina ◽  
Shanthi Ganesan ◽  
Sarah C. Pearce ◽  
Nicholas K. Gabler ◽  
Lance H. Baumgard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Redox Balance ◽  
Short Term

scholarly journals Acute heat stress activated inflammatory signaling in porcine oxidative skeletal muscle

2017 ◽  
Vol 5 (16) ◽  
pp. e13397 ◽  
Author(s):  
Shanthi Ganesan ◽  
Olga Volodina ◽  
Sarah C. Pearce ◽  
Nicholas K. Gabler ◽  
Lance H. Baumgard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Inflammatory Signaling ◽  
Acute Heat Stress

scholarly journals PSVII-6 Effects of heat stress on proteolysis in dairy cattle skeletal muscle

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 168-168
Author(s):  
Melissa S Roths ◽  
Megan A Abeyta ◽  
Tori Rudolph ◽  
Brittany Wilson ◽  
Matthew B Hudson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Dairy Cattle ◽  
Electric Heating ◽  
Economic Loss ◽  
Urea Nitrogen ◽  
Plasma Urea ◽  
E3 Ligases ◽  
Acclimation Period ◽  
Milk Urea

Abstract Heat stress (HS) occurs when internal body temperatures are elevated above a thermoneutral zone in response to extreme environmental temperatures. In the U.S. dairy industry, HS results in economic loss due to decreased feed intake, milk quality, and milk yield. Previous work has demonstrated increased plasma urea nitrogen in heat stressed dairy cattle which is thought to originate from increased skeletal muscle proteolysis, however this has not been empirically established. The objective of this investigation was to determine the extent to which HS promotes proteolysis in skeletal muscle of dairy cattle. We hypothesized HS would increase activation of the calpain and proteasome systems in skeletal muscle. To test this hypothesis, following a 3-d acclimation period in individual box stalls, all lactating dairy cows were held under thermoneutral (TN) conditions for 4-d for collection of baseline measures and then exposed to TN or HS conditions for 7-d followed by a biopsy of semitendinosus (n=8/group). To induce HS, cattle were fitted with electric heating blankets, which they wore for the duration of the heating period. This approach increased rectal temperature 1.1°C (P< 0.05), respiratory rate by 33 bpm (P< 0.05), plasma urea nitrogen by 19% (P=0.08) and milk urea nitrogen by 26% (P< 0.05), and decreased dry matter intake by 32% (P< 0.05) and milk production by 26% (P< 0.05) confirming HS. Contrary to our expectations, we discovered that calpain I and II abundance and activation, and calpain activity were similar between groups. Likewise, protein expression of E3 ligases, MafBx and Murf1, were similar between groups as was total ubiquitinated proteins and proteasome activity. Collectively, and counter to our hypothesis, these results suggest skeletal muscle proteolysis is not increased following 7-d of HS. These data question the presumed dogma that increased blood urea nitrogen is due to elevated proteolysis in skeletal muscle.

scholarly journals Mitochondrial Oxidative Damage in Chicken Skeletal Muscle Induced by Acute Heat Stress

2007 ◽  
Vol 44 (4) ◽  
pp. 439-445 ◽  
Author(s):  
Ahmad Mujahid ◽  
Neil R. Pumford ◽  
Walter Bottje ◽  
Kiyotaka Nakagawa ◽  
Teruo Miyazawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Oxidative Damage ◽  
Acute Heat Stress ◽  
Mitochondrial Oxidative Damage ◽  
Chicken Skeletal Muscle

scholarly journals Heat stress enhances mTOR signaling after resistance exercise in human skeletal muscle

2011 ◽  
Vol 61 (2) ◽  
pp. 131-140 ◽  
Author(s):  
Ryo Kakigi ◽  
Hisashi Naito ◽  
Yuji Ogura ◽  
Hiroyuki Kobayashi ◽  
Norio Saga ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Resistance Exercise ◽  
Human Skeletal Muscle ◽  
Mtor Signaling

scholarly journals Some aspects of heat stress on the plasticity of skeletal muscle cells

2012 ◽  
Vol 1 (2) ◽  
pp. 197-204 ◽  
Author(s):  
Katsumasa Goto ◽  
Yoshitaka Ohno ◽  
Ayumi Goto ◽  
Akihiro Ikuta ◽  
Miho Suzuki ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

scholarly journals Skeletal muscle adaptations to heat therapy

2020 ◽  
Vol 128 (6) ◽  
pp. 1635-1642 ◽  
Author(s):  
Kyoungrae Kim ◽  
Jacob C. Monroe ◽  
Timothy P. Gavin ◽  
Bruno T. Roseguini
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Intracellular Signaling ◽  
Tissue Temperature ◽  
Whole Body ◽  
Therapeutic Effects ◽  
Muscle Disorders ◽  
Muscle Adaptations ◽  
Heat Therapy ◽  
Skeletal Muscle Adaptations

The therapeutic effects of heat have been harnessed for centuries to treat skeletal muscle disorders and other pathologies. However, the fundamental mechanisms underlying the well-documented clinical benefits associated with heat therapy (HT) remain poorly defined. Foundational studies in cultured skeletal muscle and endothelial cells, as well as in rodents, revealed that episodic exposure to heat stress activates a number of intracellular signaling networks and promotes skeletal muscle remodeling. Renewed interest in the physiology of HT in recent years has provided greater understanding of the signals and molecular players involved in the skeletal muscle adaptations to episodic exposures to HT. It is increasingly clear that heat stress promotes signaling mechanisms involved in angiogenesis, muscle hypertrophy, mitochondrial biogenesis, and glucose metabolism through not only elevations in tissue temperature but also other perturbations, including increased intramyocellular calcium and enhanced energy turnover. The few available translational studies seem to indicate that the earlier observations in rodents also apply to human skeletal muscle. Indeed, recent findings revealed that both local and whole-body HT may promote capillary growth, enhance mitochondrial content and function, improve insulin sensitivity and attenuate disuse-induced muscle wasting. This accumulating body of work implies that HT may be a practical treatment to combat skeletal abnormalities in individuals with chronic disease who are unwilling or cannot participate in traditional exercise-training regimens.

Sign in / Sign up

Export Citation Format

Share Document