Effect of Heat Shock Preconditioning on ROS Scavenging Activity in Rat Skeletal Muscle after Downhill Running

Shima, Yosuke; Kitaoka, Katsuhiko; Yoshiki, Yumiko; Maruhashi, Yoshinobu; Tsuyama, Takeshi; Tomita, Katsuro

doi:10.2170/physiolsci.rp004808

Cited by 14 publications

(10 citation statements)

References 36 publications

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“…It is known that downhill running is an effective whole body preconditioning strategy (Shima et al, 2008; Touchberry et al, 2012; Isanejad et al, 2015), consequently, an acute preconditioning trial featuring both stressors (hot environmental conditions and downhill running; hot downhill running) was selected in the current experimental design to maximize stimuli to initiate the HSR and subsequent cellular preconditioning. This was compared to a temperate flat trial (flat running in a temperate environment) where no change in leukocyte Hsp72 and Hsp90α mRNA has been previously observed (Tuttle et al, 2015) and thus no preconditioning effect was hypothesized to occur.…”

Section: Methodsmentioning

confidence: 99%

The Hsp72 and Hsp90α mRNA Responses to Hot Downhill Running Are Reduced Following a Prior Bout of Hot Downhill Running, and Occur Concurrently within Leukocytes and the Vastus Lateralis

et al. 2017

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The leukocyte heat shock response (HSR) is used to determine individual's thermotolerance. The HSR and thermotolerance are enhanced following interventions such as preconditioning and/or acclimation/acclimatization. However, it is unclear whether the leukocyte HSR is an appropriate surrogate for the HSR in other tissues implicated within the pathophysiology of exertional heat illnesses (e.g., skeletal muscle), and whether an acute preconditioning strategy (e.g., downhill running) can improve subsequent thermotolerance. Physically active, non-heat acclimated participants were split into two groups to investigate the benefits of hot downhill running as preconditioning strategy. A hot preconditioning group (HPC; n = 6) completed two trials (HPC1HOTDOWN and HPC2HOTDOWN) of 30 min running at lactate threshold (LT) on −10% gradient in 30°C and 50% relative humidity (RH) separated by 7 d. A temperate preconditioning group (TPC; n = 5) completed 30 min running at LT on a −1% gradient in 20°C and 50% (TPC1TEMPFLAT) and 7 d later completed 30 min running at LT on −10% gradient in 30°C and 50% RH (TPC2HOTDOWN). Venous blood samples and muscle biopsies (vastus lateralis; VL) were obtained before, immediately after, 3, 24, and 48 h after each trial. Leukocyte and VL Hsp72, Hsp90α, and Grp78 mRNA relative expression was determined via RT-QPCR. Attenuated leukocyte and VL Hsp72 (2.8 to 1.8 fold and 5.9 to 2.4 fold; p < 0.05) and Hsp90α mRNA (2.9 to 2.4 fold and 5.2 to 2.4 fold; p < 0.05) responses accompanied reductions (p < 0.05) in physiological strain [exercising rectal temperature (−0.3°C) and perceived muscle soreness (~ −14%)] during HPC2HOTDOWN compared to HPC1HOTDOWN (i.e., a preconditioning effect). Both VL and leukocyte Hsp72 and Hsp90α mRNA increased (p < 0.05) simultaneously following downhill runs and demonstrated a strong relationship (p < 0.01) of similar magnitudes with one another. Hot downhill running is an effective preconditioning strategy which ameliorates physiological strain, soreness and Hsp72 and Hsp90α mRNA responses to a subsequent bout. Leukocyte and VL analyses are appropriate tissues to infer the extent to which the HSR has been augmented.

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Section: Methodsmentioning

confidence: 99%

The Hsp72 and Hsp90α mRNA Responses to Hot Downhill Running Are Reduced Following a Prior Bout of Hot Downhill Running, and Occur Concurrently within Leukocytes and the Vastus Lateralis

et al. 2017

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“…In addition, activation of HSP72 by thermal stress conditioning is also shown to improve antioxidant capacity and this was associated with reduced muscle injury in rats following downhill running (589). The precise stimuli and mechanisms required for the induction of HSP72 during exercise requires further investigation as well as the molecular underpinnings mediating the therapeutic benefit of HSP72 elevation.…”

Section: Mechanisms Of Insulin Resistancementioning

confidence: 99%

Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training

Roberts

Hevener

Barnard

2013

Comprehensive Physiology

467

425

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Metabolic syndrome (MS) is a collection of cardiometabolic risk factors that includes obesity, insulin resistance, hypertension, and dyslipidemia. Although there has been significant debate regarding the criteria and concept of the syndrome, this clustering of risk factors is unequivocally linked to an increased risk of developing type 2 diabetes and cardiovascular disease. Regardless of the true definition, based on current population estimates, nearly 100 million have MS. It is often characterized by insulin resistance, which some have suggested is a major underpinning link between physical inactivity and MS. The purpose of this review is to: (i) provide an overview of the history, causes and clinical aspects of MS, (ii) review the molecular mechanisms of insulin action and the causes of insulin resistance, and (iii) discuss the epidemiological and intervention data on the effects of exercise on MS and insulin sensitivity.

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“…This class of protein has been involved in the preservation of mitochondrial function through inhibition of mPTP opening (He and Lemasters 2003). They are synthesized in response to a wide variety of cellular stresses amongst which heat exposure is of particular interest since it increases cytoplasmic levels of inducible heat shock protein 72, a protein involved in cross-tolerance (Maloyan et al 1999;Shima et al 2008). Cross-tolerance results from multiple cellular and molecular adaptations and confers protection to the tissues against a stress of diVerent nature.…”

Section: Introductionmentioning

confidence: 99%

“…Cross-tolerance results from multiple cellular and molecular adaptations and confers protection to the tissues against a stress of diVerent nature. At a whole body level, prior heat exposure protects against decrements in muscle performance following eccentric exercise (Nosaka et al 2007;Saga et al 2008;Shima et al 2008) although the mechanism remains unclear. Heat exposure might then have the potential to limit mitochondrial respiration impairment observed in response to muscle eccentric contraction by modulating mPTP sensitivity to calcium levels.…”

Section: Introductionmentioning

confidence: 99%

Heat exposure does not alter eccentric exercise-induced increases in mitochondrial calcium and respiratory dysfunction

et al. 2011

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Eccentric exercise can lead to muscle damage including dramatic changes to mitochondrial calcium content (MCC) and impaired respiratory function. Heat acclimation can create a cross-tolerance to a number of stresses including eccentric exercise but little is known about any protection to mitochondria. We hypothesised that intermittent heat exposure will lead to improved control of MCC and to preserved mitochondrial function following eccentric exercise. Sprague-Dawley rats were exposed to 3 weeks of intermittent heat exposure (36°C, 40% relative humidity, 6 h/day, 5 days a week) or kept in cool conditions (20°C). Animals were then assigned to a control or exercise group (-14°C decline treadmill exercise for 90 min). MCC, mitochondrial respiration and mitochondrial permeability transition pore opening (mPTP) were measured in mitochondria isolated from the red quadriceps in animals killed immediately, 2 h and 48 h post-exercise. Results showed that heat exposure was associated with lower plasma creatine kinase levels (p < 0.05) post-exercise suggesting lower levels of muscle damage. There was a significant (~500%) rise in MCC (p < 0.001) and a reduction in mitochondrial respiratory control ratio (p < 0.001) 48 h post-exercise. mPTP displayed increased (p < 0.05) sensitivity to calcium immediately and 48 h post-exercise. Thus, decline running led to significant impairment of mitochondria respiration and calcium loading which was more pronounced 48 h post-exercise compared with earlier time points. MCC levels and mitochondrial function were not altered by heat exposure. In conclusion, intermittent heat exposure does not appear to provide protection against mitochondrial dysfunction resulting from eccentric exercise.

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Effect of Heat Shock Preconditioning on ROS Scavenging Activity in Rat Skeletal Muscle after Downhill Running

Cited by 14 publications

References 36 publications

The Hsp72 and Hsp90α mRNA Responses to Hot Downhill Running Are Reduced Following a Prior Bout of Hot Downhill Running, and Occur Concurrently within Leukocytes and the Vastus Lateralis

The Hsp72 and Hsp90α mRNA Responses to Hot Downhill Running Are Reduced Following a Prior Bout of Hot Downhill Running, and Occur Concurrently within Leukocytes and the Vastus Lateralis

Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training

Heat exposure does not alter eccentric exercise-induced increases in mitochondrial calcium and respiratory dysfunction

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