Effect of caffeine supplementation on the extracellular heat shock protein 72 response to exercise

2006 ◽  
Vol 101 (4) ◽  
pp. 1222-1227 ◽  
Author(s):  
Martin Whitham ◽  
Gary J. Walker ◽  
Nicolette C. Bishop
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
High Performance ◽  
Prolonged Exercise ◽  
Venous Blood ◽  
Plasma Catecholamines ◽  
Important Mediator ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Exercise In Humans

The stimulus for the release of 72-kDa heat shock protein (HSP72) during exercise in humans is currently unclear. Recent evidence in an animal model is suggestive of an involvement of catecholamines. The present study, therefore, investigated the effect of caffeine supplementation, a known stimulator of sympathetic activity, on the extracellular (e)HSP72 response to prolonged exercise. Ten healthy male endurance-trained cyclists were recruited (age: 21 ± 1 yr, maximum O2 uptake 61.1 ± 1.7 ml·kg−1·min−1, mean ± SE). Each subject was randomly assigned to ingest either 6 mg/kg body mass of caffeine (Caff) or placebo (Pla) 60 min before one of two 90-min bouts of cycling at 74 ± 1% maximum O2 uptake. Trials were performed at least 7 days apart in a counterbalanced design. Venous blood samples were collected by venepuncture at pretreatment, preexercise, postexercise, and 1 h postexercise. Serum caffeine and plasma catecholamines were determined using a spectrophotometric assay and high-performance liquid chromatography, respectively. Plasma HSP72 and cortisol were determined by ELISA. Serum caffeine concentrations were significantly increased throughout Caff, while no increases were detected in Pla. Caffeine supplementation and exercise was associated with a greater eHSP72 response than exercise alone (postexercise Caff 8.6 ± 1.3 ng/ml; Pla 5.9 ± 0.9 ng/ml). This greater eHSP72 response was associated with a greater epinephrine response to exercise in Caff. There was a significant increase in norepinephrine and cortisol, with no intertrial differences. The present data suggest that, in humans, catecholamines may be an important mediator of the exercise-induced increase in eHSP72 concentration.

scholarly journals Statins Attenuate the Increase in P-Selectin Produced by Prolonged Exercise

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Amanda Zaleski ◽  
Jeffrey Capizzi ◽  
Kevin D. Ballard ◽  
Christopher Troyanos ◽  
Aaron Baggish ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Inflammatory Response ◽  
Inflammatory Markers ◽  
Prolonged Exercise ◽  
Venous Blood ◽  
Serum Levels ◽  
Blood Samples ◽  
Boston Marathon ◽  
Exercise Induced ◽  
Response To Exercise

Strenuous endurance exercise increases inflammatory markers and acutely increases cardiovascular risk; however, statins may mitigate this response. We measured serum levels of p-selectin in 37 runners treated with statins and in 43 nonstatin treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) as well as within 1 hour after (FINISH) and 24 hours after (POST) the race. The increase in p-selectin immediately after exercise was lower in statin users (PRE to FINISH: 20.5 ± 19.4 ng/mL) than controls (PRE to FINISH: 30.9 ± 27.1 ng/mL;P<0.001). The increase in p-selectin 24 hours after exercise was also lower in statin users (PRE to POST: 21.5 ± 26.6 ng/mL) than controls (PRE to POST: 29.3 ± 31.9 ng/mL;P<0.001). Furthermore, LDL-C was positively correlated with p-selectin at FINISH and POST (P<0.01andP<0.05, resp.), irrespective of drug treatment, suggesting that lower levels of LDL-C are associated with a reduced inflammatory response to exercise. We conclude that statins blunt the exercise-induced increase in p-selectin following a marathon and that the inflammatory response to a marathon varies directly with LDL-C levels.

Heat Shock Protein 72 Response to Exercise in Humans

2008 ◽  
Vol 38 (9) ◽  
pp. 715-733 ◽  
Author(s):  
Paulette Yamada ◽  
Fabiano Amorim ◽  
Pope Moseley ◽  
Suzanne Schneider
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 72 ◽  
Response To Exercise ◽  
Exercise In Humans

scholarly journals L-NAME Treatment Enhances Exercise-induced Content of Myocardial Heat Shock Protein 72 (Hsp72) in Rats

2011 ◽  
Vol 27 (5) ◽  
pp. 479-486 ◽  
Author(s):  
Wellington Lunz ◽  
Luciano S.A. Capettini ◽  
Ana P.C. Davel ◽  
Carolina D. Munhoz ◽  
Josiane F. da Silva ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 72 ◽  
Exercise Induced

scholarly journals Exercise protects against doxorubicin-induced oxidative stress and proteolysis in skeletal muscle

2011 ◽  
Vol 110 (4) ◽  
pp. 935-942 ◽  
Author(s):  
Ashley J. Smuder ◽  
Andreas N. Kavazis ◽  
Kisuk Min ◽  
Scott K. Powers
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Oxidative Damage ◽  
Muscle Fibers ◽  
Muscular Exercise ◽  
Protease Activation ◽  
Exercise Induced

Doxorubicin (Dox) is a potent antitumor agent used in cancer treatment. Unfortunately, Dox is myotoxic and results in significant reductions in skeletal muscle mass and function. Complete knowledge of the mechanism(s) by which Dox induces toxicity in skeletal muscle is incomplete, but it is established that Dox-induced toxicity is associated with increased generation of reactive oxygen species and oxidative damage within muscle fibers. Since muscular exercise promotes the expression of numerous cytoprotective proteins (e.g., antioxidant enzymes, heat shock protein 72), we hypothesized that muscular exercise will attenuate Dox-induced damage in exercise-trained muscle fibers. To test this postulate, Sprague-Dawley rats were randomly assigned to the following groups: sedentary, exercise, sedentary with Dox, or exercise with Dox. Our results show increased oxidative stress and activation of cellular proteases (calpain and caspase-3) in skeletal muscle of animals treated with Dox. Importantly, our findings reveal that exercise can prevent the Dox-induced oxidative damage and protease activation in the trained muscle. This exercise-induced protection against Dox-induced toxicity may be due, at least in part, to an exercise-induced increase in muscle levels of antioxidant enzymes and heat shock protein 72. Together, these novel results demonstrate that muscular exercise is a useful countermeasure that can protect skeletal muscle against Dox treatment-induced oxidative stress and protease activation in skeletal muscles.

Exercise-induced stimulation of K+ transport in human erythrocytes

1999 ◽  
Vol 87 (6) ◽  
pp. 2157-2167 ◽  
Author(s):  
Michael I. Lindinger ◽  
Peggy L. Horn ◽  
Simon P. Grudzien
Keyword(s):  
Venous Blood ◽  
Plasma Osmolality ◽  
Exercise Bout ◽  
Plasma Composition ◽  
Human Red Blood Cells ◽  
Exercise Induced ◽  
Induced Changes ◽  
Response To Exercise ◽  
Human Rbcs

The hypothesis was tested that exercise-induced changes in plasma composition stimulate unidirectional K+ transport ( J inK) in human red blood cells (RBCs). Ten men performed two 30-s high-intensity leg-cycling tests separated by 4 min of rest. Antecubital venous blood was sampled before exercise and at the end of the second exercise bout. RBCs were separated from true exercise plasma,42K was added to plasma, and RBC K+ transport was studied in vitro at 37°C. In the second part of the study, blood from nine healthy men studied in vitro at 37°C was used to test the hypothesis that exercise-simulated (ES) plasma stimulates net K+ transport and J inK (measured using 86Rb) in human RBCs. The J inK of resting RBCs added to true exercise plasma was 1,574 ± 200 (SE) μmol ⋅ h−1 ⋅ l−1vs. 1,236 ± 256 μmol ⋅ h−1 ⋅ l−1in true resting plasma at 2 min (controls). In true exercise and ES plasma, J inK was increased through activation of the ouabain-sensitive Na+-K+pump and the bumetanide-sensitive Na+-K+-2Cl−cotransporter. Increases in plasma osmolality and K+, H+, and epinephrine concentrations independently and in combination stimulated K+ transport into human RBCs. In a third series of experiments, in which ES plasma K+ concentration was continuously measured during the first 5 min of incubation of RBCs, a 1.6 ± 0.3 mmol/l decrease in plasma K+concentration occurred during the first 2 min. It is concluded that RBCs transport K+ at elevated rates in response to exercise-induced changes in plasma composition.

Heat shock protein expression protects against cerebral ischemia and monoamine overload in rat heatstroke

1999 ◽  
Vol 276 (6) ◽  
pp. H1961-H1967 ◽  
Author(s):  
Yi-Ling Yang ◽  
Mao-Tsun Lin
Keyword(s):  
Cerebral Ischemia ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
High Performance ◽  
Chemical Stress ◽  
Microdialysis Probe ◽  
Neural Damage ◽  
Heat Shock Protein Expression ◽  
The Moment ◽  
The Brain

This study attempted to ascertain whether the ischemic damage to neurons and monoamine overload in brain that occur during rat heatstroke can be attenuated by heat shock protein (HSP) 72 induction. Effects of heatstroke on mean arterial pressure (MAP), cerebral blood flow (CBF), brain dopamine (DA) and serotonin (5-HT) release, and neural damage score were assayed in rats 0, 16, or 48 h after heat shock (42°C for 15 min) or chemical stress (5 mg/kg sodium arsenite ip). Brain HSP 72 in rats after heat shock or chemical stress was detected by Western blot, and brain monoamine was determined by a microdialysis probe combined with high-performance liquid chromatography. Heatstroke was induced by exposing the animal to a high ambient temperature (43°C); the moment at which MAP and CBF decreased from their peak values was taken as the time of heatstroke onset. Prior heat shock or chemical stress conferred significant protection against heatstroke-induced hyperthermia, arterial hypotension, cerebral ischemia, cerebral DA and 5-HT overload, and neural damage and correlated with expression of HSP 72 in brain at 16 h. However, at 48 h, when HSP 72 expression returned to basal values, the above responses that occurred during the onset of heatstroke were indistinguishable between the two groups (0 h vs. 48 h). These results lead to the hypothesis that the brain can be preconditioned by thermal or chemical injury, that this preconditioning will induce HSP 72, and that HSP 72 induction will correlate quite well with anatomic, histochemical, and hemodynamic protection in rat heatstroke.

scholarly journals Experience affects exercise-induced changes in catecholamines, glucose, and FFA

1989 ◽  
Vol 256 (1) ◽  
pp. R169-R173 ◽  
Author(s):  
A. J. Scheurink ◽  
A. B. Steffens ◽  
G. H. Dreteler ◽  
L. Benthem ◽  
R. Bruntink
Keyword(s):  
Metabolic Response ◽  
Plasma Catecholamines ◽  
Plasma Free Fatty Acid ◽  
Blood Component ◽  
Experimental Conditions ◽  
Glucose Levels ◽  
Exercise Induced ◽  
Induced Changes ◽  
Response To Exercise ◽  
First Time

The interference of the experimental conditions on the exercise-induced alterations in plasma catecholamines, plasma free fatty acids, and glucose and insulin concentrations was investigated in rats. Exercise consisted of strenuous swimming against a countercurrent (0.22 m/s) for 15 min in a pool with water of 33 degrees C. Before, during, and after swimming, blood samples were taken through a permanent heart catheter. The blood component levels in rats that were confronted with exercise for the very first time were compared with the levels in rats that were well accustomed to the exercise conditions. The very first time rats swam caused an enhanced release of epinephrine from the adrenal medulla and a reduced output of norepinephrine from the sympathetic nerve endings. Furthermore, in the first time swim group, blood glucose levels were higher and plasma free fatty acid concentrations were lower compared with the well-accustomed animals. There were no differences in plasma insulin concentrations. It is concluded that the experimental conditions may interfere considerably with the hormonal and metabolic response to exercise. Furthermore the results reinforce the idea that the two parts of the sympathoadrenal system are functionally and metabolically dissociated.

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