scholarly journals Human skeletal muscle HSP70 response to training in highly trained rowers

1999 ◽  
Vol 86 (1) ◽  
pp. 101-104 ◽  
Author(s):  
Yuefei Liu ◽  
Sabine Mayr ◽  
Alexandra Opitz-Gress ◽  
Claudia Zeller ◽  
Werner Lormes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Protein 70 ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Human Muscle ◽  
Muscle Sample ◽  
Exercise Induced ◽  
The Right

Previous studies have demonstrated exercise-induced heat shock protein 70 (HSP70) in animals. The purpose of this study was to investigate human skeletal muscle HSP70 response to rowing training. Ten male rowers trained for 4 wk with different forms, durations, and intensities of exercise. Biopsy was performed in the right musculus vastus lateralis before training and at the end of each week. HSP70 in 5 μg of total protein from the muscle sample was determined by using Western blot and immunodetection with chemiluminescence technique, by means of laser densitometer referring to a series of known standard HSP70. Compared with pretraining (100%), HSP70 increased during training (181, 405, 456, and 363% from the first to fourth training week, respectively) with the maximum HSP70 production at the end of second training week. Thus HSP70 is induced in highly trained human muscle by long-term training.

Reduced carbohydrate availability enhances exercise-induced p53 signaling in human skeletal muscle: implications for mitochondrial biogenesis

2013 ◽  
Vol 304 (6) ◽  
pp. R450-R458 ◽  
Author(s):  
Jonathan D. Bartlett ◽  
Jari Louhelainen ◽  
Zafar Iqbal ◽  
Andrew J. Cochran ◽  
Martin J. Gibala ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
Repeated Measures ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Oxidative Capacity ◽  
Pyruvate Dehydrogenase Kinase ◽  
Repeated Measures Design ◽  
P53 Signaling ◽  
Exercise Induced

The mechanisms that regulate the enhanced skeletal muscle oxidative capacity observed when training with reduced carbohydrate (CHO) availability are currently unknown. The aim of the present study was to test the hypothesis that reduced CHO availability enhances p53 signaling and expression of genes associated with regulation of mitochondrial biogenesis and substrate utilization in human skeletal muscle. In a repeated-measures design, muscle biopsies (vastus lateralis) were obtained from eight active males before and after performing an acute bout of high-intensity interval running with either high (HIGH) or low CHO availability (LOW). Resting muscle glycogen (HIGH, 467 ± 19; LOW, 103 ± 9 mmol/kg dry wt) was greater in HIGH compared with LOW ( P < 0.05). Phosphorylation (P-) of ACCSer79 (HIGH, 1.4 ± 0.4; LOW, 2.9 ± 0.9) and p53Ser15 (HIGH, 0.9 ± 0.4; LOW, 2.6 ± 0.8) was higher in LOW immediately postexercise and 3 h postexercise, respectively ( P < 0.05). Before and 3 h postexercise, mRNA content of pyruvate dehydrogenase kinase 4, mitochondrial transcription factor A, cytochrome- c oxidase IV, and PGC-1α were greater in LOW compared with HIGH ( P < 0.05), whereas carnitine palmitoyltransferase-1 showed a trend toward significance ( P = 0.09). However, only PGC-1α expression was increased by exercise ( P < 0.05), where three-fold increases occurred independently of CHO availability. We conclude that the exercise-induced increase in p53 phosphorylation is enhanced in conditions of reduced CHO availability, which may be related to upstream signaling through AMPK. Given the emergence of p53 as a molecular regulator of mitochondrial biogenesis, such nutritional modulation of contraction-induced p53 activation has implications for both athletic and clinical populations.

Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans

2006 ◽  
Vol 100 (5) ◽  
pp. 1679-1687 ◽  
Author(s):  
Christian P. Fischer ◽  
Natalie J. Hiscock ◽  
Samar Basu ◽  
Bengt Vessby ◽  
Anders Kallner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ascorbic Acid ◽  
Heat Shock ◽  
Protein Content ◽  
Vastus Lateralis ◽  
Placebo Control ◽  
Plasma Vitamin ◽  
Maximal Power Output ◽  
Exercise Induced ◽  
Response To Exercise

Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR-α-tocopherol 400 IU/day + ascorbic acid (AA) 500 mg/day (CEα), RRR-α-tocopherol 290 IU/day + RRR-γ-tocopherol 130 IU/day + AA 500 mg/day (CEαγ), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50% of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, α-tocopherol, γ-tocopherol, AA, and 8-iso-prostaglandin-F2α(8-PGF2α). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF2α, increased from 0 h to 3 h in all groups, however, markedly less ( P < 0.05) in CEα. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold ( P < 0.05) and serum HSP72 protein increased 4-fold ( P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed ( P = 0.07). In CEα, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CEαγ. The results indicate that γ-tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.

Effects of exercise on insulin binding to human muscle

1985 ◽  
Vol 248 (4) ◽  
pp. E403-E408 ◽  
Author(s):  
A. Bonen ◽  
M. H. Tan ◽  
P. Clune ◽  
R. L. Kirby
Keyword(s):  
Skeletal Muscle ◽  
Linear Relationship ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Experimental Period ◽  
Insulin Binding ◽  
Bicycle Ergometer ◽  
Human Muscle ◽  
O2 Consumption ◽  
Blood Samples

A procedure was developed to measure insulin binding to human skeletal muscle obtained via the percutaneous muscle biopsy technique. With this method the effects of exercise on insulin binding were investigated. Subjects (n = 9) exercised for 60 min on a bicycle ergometer at intensities ranging from 20-86% maximum O2 consumption (VO2max). Blood samples were obtained before, during, and after exercise and analyzed for glucose and insulin. Muscle samples (250 mg) for the vastus lateralis were obtained 30 min before exercise, at the end of exercise, and 60 min after exercise. Two subjects rested during the experimental period. There was no linear relationship between exercise intensities and the changes in insulin binding to human muscle. At rest (n = 2) and at exercise intensities below 60% VO2max (n = 5) no change in insulin binding occurred (P greater than 0.05). However, when exercise occurred at greater than or equal to 69% VO2max (n = 4), a pronounced decrement in insulin binding (30-50%) was observed (P less than 0.05). This persisted for 60 min after exercise. These results indicate that insulin binding in human muscle is not altered by 60 min of exercise at less than or equal to 60% VO2max but that a marked decrement occurs when exercise is greater than or equal to 69% VO2max.

scholarly journals Angiogenesis-related ultrastructural changes to capillaries in human skeletal muscle in response to endurance exercise

2015 ◽  
Vol 119 (10) ◽  
pp. 1118-1126 ◽  
Author(s):  
Oliver Baum ◽  
Jennifer Gübeli ◽  
Sebastian Frese ◽  
Eleonora Torchetti ◽  
Corinna Malik ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cross Sections ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Capillary Density ◽  
Volume Density ◽  
Ultrastructural Changes ◽  
Vastus Lateralis Muscle ◽  
Before And After ◽  
Exercise Induced

The ultrastructure of capillaries in skeletal muscle was morphometrically assessed in vastus lateralis muscle (VL) biopsies taken before and after exercise from 22 participants of two training studies. In study 1 (8 wk of ergometer training), light microscopy revealed capillary-fiber (C/F) ratio (+27%) and capillary density (+16%) to be higher ( P ≤ 0.05) in postexercise biopsies than in preexercise biopsies from all 10 participants. In study 2 (6 mo of moderate running), C/F ratio and capillary density were increased (+23% and +20%; respectively, P ≤ 0.05) in VL biopsies from 6 angiogenesis responders (AR) after training, whereas 6 nonangiogenesis responders (NR) showed nonsignificant changes in these structural indicators (−4%/−4%, respectively). Forty capillary profiles per participant were evaluated by point and intersection counting on cross sections after transmission electron microscopy. In study 1, volume density (Vv) and mean arithmetic thickness (T) of endothelial cells (ECs; +19%/+17%, respectively) and pericytes (PCs; +20%/+21%, respectively) were higher ( P ≤ 0.05), whereas Vv and T of the pericapillary basement membrane (BM) were −23%/−22% lower ( P ≤ 0.05), respectively, in posttraining biopsies. In study 2, exercise-related differences between AR and NR-groups were found for Vv and T of PCs (AR, +26%/+22%, respectively, both P ≤ 0.05; NR, +1%/−3%, respectively, both P > 0.05) and BM (AR, −14%/−13%, respectively, both P ≤ 0.05; NR, −9%/−11%, respectively, P = 0.07/0.10). Vv and T of ECs were higher (AR, +16%/+18%, respectively; NR, +6% /+6%, respectively; all P ≤ 0.05) in both groups. The PC coverage was higher (+13%, P ≤ 0.05) in VL biopsies of individuals in the AR group but nonsignificantly altered (+3%, P > 0.05) in those of the NR group after training. Our study suggests that intensified PC mobilization and BM thinning are related to exercise-induced angiogenesis in human skeletal muscle, whereas training per se induces EC-thickening.

Time course and differential responses of the major heat shock protein families in human skeletal muscle following acute nondamaging treadmill exercise

2006 ◽  
Vol 101 (1) ◽  
pp. 176-182 ◽  
Author(s):  
James P. Morton ◽  
Don P. M. MacLaren ◽  
Nigel T. Cable ◽  
Thomas Bongers ◽  
Richard D. Griffiths ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Time Course ◽  
Human Skeletal Muscle ◽  
Treadmill Running ◽  
Vastus Lateralis Muscle ◽  
Exercise Protocol ◽  
Running Exercise ◽  
Αb Crystallin ◽  
Exercise Induced

The exercise-induced expression of heat shock proteins (HSPs) in rodent models is relatively well defined. In contrast, comparable data from human studies are limited and the exercise-induced stress response of human skeletal muscle is far from understood. This study has characterized the time course and magnitude of the HSP response in the skeletal muscles of a healthy active, but untrained, young male population following a running exercise protocol. Eight subjects performed 45 min of treadmill running at a speed corresponding to their lactate threshold (11.7 ± 0.5 km/h; 69.8 ± 4.8% maximum O2 uptake). Muscle biopsies were obtained from the vastus lateralis muscle immediately before and at 24 h, 48 h, 72 h, and 7 days postexercise. Exercise induced a significant ( P < 0.05) but variable increase in HSP70, heat shock cognate (HSC) 70, and HSP60 expression with peak increases (typically occurring at 48 h postexercise) to 210, 170, and 139% of preexercise levels, respectively. In contrast, exercise did not induce a significant increase in either HSP27, αB-crystallin, SOD 2 (MnSOD) protein content, or the activity of SOD and catalase. When examining baseline protein levels, HSC70, HSP27, and αB-crystallin appeared consistently expressed between subjects, whereas HSP70 and MnSOD displayed marked individual variation of up to 3- and 1.5-fold, respectively. These data are the first to define the time course and extent of HSP production in human skeletal muscle following a moderately demanding and nondamaging running exercise protocol. Data demonstrate a differential effect of aerobic exercise on specific HSPs.

Exercise increases phosphorylation of the putative mTORC2 activity readout NDRG1 in human skeletal muscle

2021 ◽  
Author(s):  
Jonas Roland Knudsen ◽  
Kaspar W Persson ◽  
Jaroslawna Meister ◽  
Christian Strini Carl ◽  
Steffen H Raun ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Ex Vivo ◽  
Vastus Lateralis ◽  
Published Data ◽  
Vastus Lateralis Muscle ◽  
Mouse Muscle ◽  
Exercise Induced ◽  
Stimulation Of

In mice, exercise is suggested to activate the mechanistic target of rapamycin complex 2 (mTORC2) in skeletal muscle, and mTORC2 is required for normal muscle glucose uptake during exercise. Whether this translates to human skeletal muscle and what signaling pathways facilitate the exercise-induced mTORC2 activation is unknown but important to determine given the important role of mTORC2 in metabolism. We herein tested the hypothesis that exercise increases mTORC2 activity in human skeletal muscle and investigated if β2-adrenergic receptor (AR) activation mediates exercise-induced mTORC2 activation. We examined several mTORC2 activity readouts (p-NDRG1 Thr346, p-Akt Ser473, p-mTOR S2481, and p-Akt Thr450) in human skeletal muscle biopsies after uphill walking or cycling exercise. In mouse muscles, we assessed mTORC2 activity readouts following acute activation of muscle β2-adrenergic or Gs signaling and during in vivo and ex vivo muscle contractions. Exercise increased phosphorylation of NDRG1 Thr346 in human soleus, gastrocnemius, and vastus lateralis muscle, without changing p-Akt Ser473, p-Akt Thr450, and p-mTOR Ser2481. In mouse muscle, stimulation of β2-adrenergic or Gs signaling and ex vivo contractions failed to increase p-NDRG1 Thr346, while in vivo contractions were sufficient to induce p-NDRG1 Thr346. In conclusion, the mTORC2 activity readout p-NDRG1 Thr346 is a novel exercise-responsive signaling protein in human skeletal muscle. Notably, contraction-induced p-NDRG1 Thr346 appears to require a systemic factor. Unlike exercise, and in contrast to published data obtained in cultured muscles cells, stimulation of β2-adrenergic signaling is not sufficient to trigger NDRG1 phosphorylation in mature mouse skeletal muscle.

scholarly journals Metabolic adaptations in skeletal muscle after 84 days of bed rest with and without concurrent flywheel resistance exercise

2017 ◽  
Vol 122 (1) ◽  
pp. 96-103 ◽  
Author(s):  
José M. Irimia ◽  
Mario Guerrero ◽  
Paula Rodriguez-Miguelez ◽  
Joan A. Cadefau ◽  
Per A. Tesch ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Human Skeletal Muscle ◽  
Citrate Synthase ◽  
Glycogen Synthase ◽  
Vastus Lateralis ◽  
Bed Rest ◽  
Metabolic Adaptations

As metabolic changes in human skeletal muscle after long-term (simulated) spaceflight are not well understood, this study examined the effects of long-term microgravity, with and without concurrent resistance exercise, on skeletal muscle oxidative and glycolytic capacity. Twenty-one men were subjected to 84 days head-down tilt bed rest with (BRE; n = 9) or without (BR; n = 12) concurrent flywheel resistance exercise. Activity and gene expression of glycogen synthase, glycogen phosphorylase (GPh), hexokinase, phosphofructokinase-1 (PFK-1), and citrate synthase (CS), as well as gene expression of succinate dehydrogenase (SDH), vascular endothelial growth factor (VEFG), peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1α), and myostatin, were analyzed in samples from m. vastus lateralis collected before and after bed rest. Activity and gene expression of enzymes controlling oxidative metabolism (CS, SDH) decreased in BR but were partially maintained in BRE. Activity of enzymes regulating anaerobic glycolysis (GPh, PFK-1) was unchanged in BR. Resistance exercise increased the activity of GPh. PGC-1α and VEGF expression decreased in both BR and BRE. Myostatin increased in BR but decreased in BRE after bed rest. The analyses of these unique samples indicate that long-term microgravity induces marked alterations in the oxidative, but not the glycolytic, energy system. The proposed flywheel resistance exercise was effective in counteracting some of the metabolic alterations triggered by 84-day bed rest. Given the disparity between gene expression vs. enzyme activity in several key metabolic markers, posttranscriptional mechanisms should be explored to fully evaluate metabolic adaptations to long-term microgravity with/without exercise countermeasures in human skeletal muscle.

scholarly journals Effect of ionizing radiation on human skeletal muscle precursor cells

2013 ◽  
Vol 47 (4) ◽  
pp. 376-381 ◽  
Author(s):  
Mihaela Jurdana ◽  
Maja Cemazar ◽  
Katarina Pegan ◽  
Tomaz Mars
Keyword(s):  
Skeletal Muscle ◽  
Stress Response ◽  
Ionizing Radiation ◽  
Human Skeletal Muscle ◽  
Long Term Effects ◽  
Post Irradiation ◽  
Acute Response ◽  
Proliferation Capacity ◽  
Myoblast Proliferation

Abstract Background. Long term effects of different doses of ionizing radiation on human skeletal muscle myoblast proliferation, cytokine signalling and stress response capacity were studied in primary cell cultures. Materials and methods. Human skeletal muscle myoblasts obtained from muscle biopsies were cultured and irradiated with a Darpac 2000 X-ray unit at doses of 4, 6 and 8 Gy. Acute effects of radiation were studied by interleukin - 6 (IL-6) release and stress response detected by the heat shock protein (HSP) level, while long term effects were followed by proliferation capacity and cell death. Results. Compared with non-irradiated control and cells treated with inhibitor of cell proliferation Ara C, myoblast proliferation decreased 72 h post-irradiation, this effect was more pronounced with increasing doses. Post-irradiation myoblast survival determined by measurement of released LDH enzyme activity revealed increased activity after exposure to irradiation. The acute response of myoblasts to lower doses of irradiation (4 and 6 Gy) was decreased secretion of constitutive IL-6. Higher doses of irradiation triggered a stress response in myoblasts, determined by increased levels of stress markers (HSPs 27 and 70). Conclusions. Our results show that myoblasts are sensitive to irradiation in terms of their proliferation capacity and capacity to secret IL-6. Since myoblast proliferation and differentiation are a key stage in muscle regeneration, this effect of irradiation needs to be taken in account, particularly in certain clinical conditions.

scholarly journals Microwave hyperthermia treatment increases heat shock proteins in human skeletal muscle * COMMENTARY

2007 ◽  
Vol 41 (7) ◽  
pp. 453-455 ◽  
Author(s):  
Y. Ogura ◽  
H. Naito ◽  
T. Tsurukawa ◽  
N. Ichinoseki-Sekine ◽  
N. Saga ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Human Skeletal Muscle ◽  
Hyperthermia Treatment ◽  
Shock Proteins ◽  
Microwave Hyperthermia

scholarly journals Exercise, heat shock proteins and insulin resistance

2017 ◽  
Vol 373 (1738) ◽  
pp. 20160529 ◽  
Author(s):  
Ashley E. Archer ◽  
Alex T. Von Schulze ◽  
Paige C. Geiger
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Metabolic Effects ◽  
Diabetic Patients ◽  
Alcoholic Fatty Liver ◽  
Insulin Resistant ◽  
Exercise Induced ◽  
Shock Proteins

Best known as chaperones, heat shock proteins (HSPs) also have roles in cell signalling and regulation of metabolism. Rodent studies demonstrate that heat treatment, transgenic overexpression and pharmacological induction of HSP72 prevent high-fat diet-induced glucose intolerance and skeletal muscle insulin resistance. Overexpression of skeletal muscle HSP72 in mice has been shown to increase endurance running capacity nearly twofold and increase mitochondrial content by 50%. A positive correlation between HSP72 mRNA expression and mitochondrial enzyme activity has been observed in human skeletal muscle, and HSP72 expression is markedly decreased in skeletal muscle of insulin resistant and type 2 diabetic patients. In addition, decreased levels of HSP72 correlate with insulin resistance and non-alcoholic fatty liver disease progression in livers from obese patients. These data suggest the targeted induction of HSPs could be a therapeutic approach for preventing metabolic disease by maintaining the body's natural stress response. Exercise elicits a number of metabolic adaptations and is a powerful tool in the prevention and treatment of insulin resistance. Exercise training is also a stimulus for increased HSP expression. Although the underlying mechanism(s) for exercise-induced HSP expression are currently unknown, the HSP response may be critical for the beneficial metabolic effects of exercise. Exercise-induced extracellular HSP release may also contribute to metabolic homeostasis by actively restoring HSP72 content in insulin resistant tissues containing low endogenous levels of HSPs. This article is part of the theme issue ‘Heat shock proteins as modulators and therapeutic targets of chronic disease: an integrated perspective’.

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