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Biomedical subjects

A M Niess

Publications and source records attributed to A M Niess.

At least 19 recordsLinked to original sources

The use of nutritional supplements among master athletes.

We assessed the use of nutritional supplements among master athletes focusing on their source of information and source of supply of nutritional supplements. 1560 standardized, anonymous questionnaires were distributed among participants of the World Masters Athletics Championships Indoors 2004. These questions were related to biometric parameters, social indicators, training parameters, illicit drugs, and nutritional supplements. Chi2-tests were computed to reveal meaningful associations between basic information (age, gender, family status, children, education, country of origin, disciplines, training years, smoking, and the use of alcohol, illicit drugs, and doping) and the intake of nutritional supplements. Descriptive information on the history of their use of nutritional supplements was also provided. 60.5 % of all participants reported the actual use of nutritional supplements. We found no significant differences between nutritional supplement users and non-users with regard to basic information. The substances predominantly used were vitamins (35.4 %) and minerals (29.9 %). In contrast to elite athletes who use nutritional supplements to increase their athletic performance, master athletes use these substances predominantly for health reasons and, thus, have a closer contact to the health care system. Physicians are their preferred source of information about nutritional supplements. More than half of the interviewed athletes obtain their nutritional supplements from pharmacies or physicians. The results of this study indicate that nutritional supplement users in master athletics show no specific user profile. Since it is not rare for nutritional supplements to contain trace contaminations of anabolic androgenic steroids or pro-hormones, physicians should also inform master competitive athletes of the dangers of testing positive for doping substances due to their intake of nutritional supplements and advise them accordingly.

Adult↗

Exercise intensity and duration affect blood soluble HSP72.

Soluble heat shock protein 72 (sHSP72) is suggested to play a role as a signalling molecule in the immune response to exercise. We were interested in whether duration and intensity of endurance running affect the level of inducible sHSP72 in the plasma/serum of endurance athletes. In the first part of the study, the influence of a continuous treadmill run of 60 min (CR) with an intensity of 75 % VO2max, a long treadmill run of 120 min (LR) with an intensity of 60 % VO2max, an extensive interval training program (IT; 10 x 1000 m, ca. 35 min, VO2max 88 %), and a competitive marathon run (MA) within 260 +/- 39 min (VO2max ca. 65 %) on the release of sHSP72 into the peripheral blood was tested. Blood samples were drawn before and directly after exercise, as well as 0.5, 1, 3, 24 h after exercise to determine sHSP72 levels. Secondly, we compared the effects of two exercise bouts with identical duration (23.7 +/- 7 min) but different intensities (Exhaustive exercise (ET) at 80 % VO2max vs. moderate exercise (MT) at 60 % VO2max) on sHSP72 concentration. The sHSP72 levels in plasma/serum were analyzed using an enzyme immunoassay specific for inducible HSP72 (Stressgen,Victoria, Canada). Early, significant increases of sHSP72 were detected immediately after all types of exercise with highest levels after MA. ET induced significantly higher levels of sHSP72 compared with MT. Long-lasting, competitive endurance exercise induced a more pronounced response of sHSP compared with more intensive but shorter exercise. Exercise intensity was also an important influencing factor. A duration- and intensity-dependent role for sHSP72 in the exercise-induced changes of the immune response may be assumed.

Adult↗

The World Anti-Doping Code 2003--consequences for physicians associated with elite athletes.

The purpose of the World Anti-Doping Code 2003 and the 2004 Prohibited List is to create a universal international standard to fight doping in competitive sports. The result of this is a whole series of changes for doctors with regard to their work with competitive athletes. The revised definition of doping now includes physicians in the group of persons who can fulfil the elements of a doping offence. Moreover, the mere possession of substances appearing on the Prohibited List represents a violation of anti-doping regulations. The 2004 Prohibited List includes several changes to the Olympic Movement List from 2003. Caffeine, for example, was removed from the list. Cannabinoids, on the other hand, are now prohibited in competition for all sports. The same is true for all forms of glucocorticosteroids. Therapeutic use exemptions in an abbreviated process are possible for the administration of glucocorticosteroids by non-systemic routes, as well as inhalative therapy with the beta-2-agonists formoterol, salbutamol, salmeterol, and termbutalin. In other cases, a therapeutic use exemption is possible using a standard application process. Further changes will become effective in the 2005 Prohibited List. In 2005, it is essential that beta-2-agonists are prohibited in and out of competition. HCG and LH are prohibited for all athletes. Dermatological preparations of glucocorticosteroids are no longer prohibited, and intravenous infusions will be a prohibited method in 2005, except as a legitimate acute medical treatment. In cases of violations of anti-doping regulations where it is permissible for the affected person to furnish proof of exoneration, the burden of proof is not higher than that required to prove the violation. The sanctions provided for in the World Anti-Doping Code follow a principle of rules and exceptions which at first glance seems difficult to understand. In the case of doping violations by physicians, the anti-doping code provides--as a general rule--for exclusion from sports associations for at least four years. Since several of the changes are questionable under constitutional aspects, it remains to be seen whether the World Anti-Doping Code 2003 will allow the achievement of a universal standard to combat doping.

Adrenergic beta-Agonists↗

Contaminated nutritional supplements--legal protection for elite athletes who tested positive: a case report from Germany.

A significant proportion of nutritional supplements manufactured worldwide contain non-listed contaminations with anabolic-androgenic steroids (AAS), whose ingestion may lead to positive doping test results. This will lead to the suspension of, and sanctions against, the athlete, since this group of active substances is prohibited by the anti-doping code of the World Anti-Doping Agency as well as by sports associations not connected with this agency. Considerable financial losses are often the consequence for a banned athlete. Based on an amendment to the law governing the manufacture and prescription of drugs (AMG) in Germany in 1997 and an increasingly extensive interpretation of the term "drug" by the Federal Supreme Court, preparations containing anabolic steroids or their precursors are to be classified as drugs and, therefore, are subject to compulsory declaration as stated by the AMG. If this obligation is not adhered to, the result may be a claim for damages by the athlete against the manufacturer of a preparation, if the athlete took the preparation thinking it was harmless as judged by the Anti-Doping regulations, but was then found to be positive in doping tests. The judges in the first case before the county court in Stuttgart decided in favour of the claim for damages with respect to lost bonuses, loss of earnings and accrued legal costs by a soccer player who tested positive and was therefore suspended. Based on the evidence presented, the court came to the decision that the soccer player's positive test result was due to the ingestion of nutritional supplements containing non-listed AAS. This procedure could set a precedent for other states to demonstrate that athletes who had tested positive due to contaminated nutritional supplements are not without legal protection.

Anabolic Agents↗

Antioxidant intervention does not affect the response of plasma erythropoietin to short-term normobaric hypoxia in humans.

Recent research has demonstrated that reactive oxygen species (ROS) participate in intracellular signaling processes initiated during hypoxia. We investigated the role of ROS in the response of plasma erythropoietin (Epo) to short-term normobaric hypoxia in humans. Twelve male subjects were exposed twice to 4 h of normobaric hypoxia (H; inspired oxygen fraction 12.5%) with a period of 6 wk between both experiments (H1 and H2). With the use of a randomized placebo-controlled crossover design, the subjects received orally a combination of the antioxidants all-rac-alpha-tocopherol (800 mg/day for 3 wk) and alpha-lipoic acid (600 mg/day for 2 wk) or placebo before H1 and H2, respectively. Three weeks before H1, the subjects underwent one control experiment in normoxia (N; inspired oxygen fraction 20.9%) without any treatment. Serum alpha-tocopherol was significantly higher after treatment with antioxidants compared with placebo. Capillary Po(2) declined during H without significant differences between antioxidants and placebo. Plasma peroxide levels were lower under antioxidant treatment but not affected by hypoxia. The response of Epo to H did not show significant differences between antioxidant [maximum increase (means, 95% confidence interval): +121%, +66 to +176%] and placebo conditions (+108%, +68 to +149%). Similarly, hypoxia-induced increase of Epo corrected for diurnal variations, as revealed during N, did not differ between antioxidants and placebo. Individual variability of Epo in response to H was not related to the individual degree of hypoxemia during H. Our results do not support the assumption that ROS play a major modulating role in the response of Epo to short-term normobaric hypoxia in humans.

Antioxidants↗

Impact of elevated ambient temperatures on the acute immune response to intensive endurance exercise.

To date, there has been little research examining how elevated ambient temperatures exert an additional effect on the acute immune response to endurance exercise. Seven endurance-trained, non-heat-acclimated men [mean (95% confidence interval): 29.7 (25.9-33.5) years, .VO(2max) 66.3 (61.3-71.3) ml.kg(-1).min(-1)] performed two 60-min treadmill runs (75% .VO(2max)) in two different environments (EX1: 18 degrees C/50% room temperature/relative humidity and EX2: 28 degrees C/50% room temperature/relative humidity) with a 7-day interval between the runs. Blood samples were drawn at rest and 0, 0.5, 3, 24, and 48 h after exercise. Compared to EX1, exercise-induced increases in core temperature, sweating rate, heart rate, plasma norepinephrine, cortisol, human growth hormone, and neutrophil and monocyte counts were significantly (5% level) more pronounced after EX2. In contrast, responses of plasma epinephrine, myeloperoxidase, interleukin (IL)-6 as well as lymphocyte counts were similar in EX1 and EX2. Plasma concentrations of IL-8 and C-reactive protein were affected by neither exercise nor by additional heat exposure. Our results suggest that the additional impact of elevated ambient temperatures on stress responses to endurance exercise in trained subjects seems to affect primarily the cardiocirculatory and hormonal systems, and resulting changes in neutrophil and monocyte cell-trafficking. In contrast, heat stress does not seem to exert large additional effects on the acute immune response to endurance exercise as performed in the present study.

Acute-Phase Reaction↗

Influence of different types of exercise on the expression of haem oxygenase-1 in leukocytes.

Haem-oxygenase-1 (HO-1) is an antioxidant stress protein that is mainly induced by reactive oxygen species, inflammatory cytokines and hyperthermia. We assessed the influence of different types of exercise on HO-1 expression in leukocytes of the peripheral blood in three groups of male participants: a short exhaustive run above the lactate steady state (n = 15), eccentric exercise (n = 12) and an intensive endurance run (half-marathon, n = 12). Blood samples were taken at rest and up to 24 h after exercise. Blood lactate concentration after exercise was 9.0 +/- 2.1, 3.8 +/- 1.6 and 5.1 +/- 2.2 mmol x l(-1) (mean +/- s) for the exhaustive run, eccentric exercise and half-marathon groups, respectively (P < 0.05). Creatine kinase concentration was highest 24 h after exercise: 133 +/- 91, 231 +/- 139 and 289 +/- 221 U x l(-1) for the exhaustive run, eccentric exercise and half-marathon groups, respectively (P < 0.05). The maximal increase in leukocyte counts after exercise was 11.5 +/- 19.2, 6.2 +/- 1.4 and 14.7 +/- 2.1 x 10(9) x l(-1). There was no change in HO-1 as a result of the short exhaustive run or the eccentric exercise, whereas the half-marathon had a significant stimulatory effect on HO-1-expression in lymphocytes, monocytes and granulocytes (P < 0.001) using flow cytometry analyses. In conclusion, eccentric exercise alone or short-term heavy exercise are not sufficient to stimulate the antioxidative stress protein HO-1 in peripheral leukocytes

Adult↗

Individual differences in self-reported heat tolerance. Is there a link to the cardiocirculatory, thermoregulatory and hormonal response to endurance exercise in heat?

AIM: Tolerance to exercise in heat exhibits great interindividual variability. We questioned whether individual differences in self-reported heat tolerance within a group of endurance trained athletes are linked to the cardiocirculatory, thermoregulatory and hormonal response to endurance exercise in heat. METHODS: Using a rating scale to assess the individual degree of tolerance to exercise in heat we allocated 12 non-heat-acclimated trained runners into two groups of 5 highly heat tolerant (HHT) and 7 less heat tolerant (LHT) athletes. Both groups performed a 60-min treadmill run (velocity 90% of individual anaerobic threshold, room temperature and humidity 28 inverted exclamation mark C and 50%, respectively). RESULTS: Sweating rate did not differ between HHT (mean +/- SEM: 0.44+/-0.02) and LHT (0.40+/-0.02 ml x kg(-1) x min(-1)). Compared to LHT, exercise-induced rises in core temperature (39.3+/-0.2/40.0+/-0.2 inverted exclamation mark C), heart rate, plasma norepinephrine and cortisol were significantly lower in HHT, while epinephrine did not exhibit differences between the groups. In contrast, response of human growth hormone (hGH) was significantly more pronounced in HHT. CONCLUSION: Our initial results, obtained in a small group of endurance-trained runners, show that self-reported tolerance to exercise in heat is associated with an attenuated rise in body core temperature during prolonged exercise under elevated ambient temperatures. This finding in heat tolerant athletes is paralleled by a lower stress response as reflected by lower rises in heart rate and stress hormones such as norepinephrine and cortisol. The functional significance (i.e. with respect to sweating function) of the more pronounced response of hGH in heat tolerant athletes warrants further research.

Body Temperature↗

Microarray technology--the future analyses tool in exercise physiology?

Microarray analysis offers a set of analytical platforms that provide rapid, affordable and substantial information at the DNA, RNA or protein level. It enables the analysis of thousands of genes simultaneously in a parallel manner across samples derived from various biological sources and treatment regimens. This development became possible as a result of the combination of three technological advances achieved at the beginning of the 1990's, namely parallelism, miniaturization and automation. In regular physical checkups the microarray technology could be used to supplement the current spectrum of tests and therefore enhance the quality of the data obtained. Arrays for analyses of RNA expression will allow gene expression profiling also in exercise physiology. DNA chips may also be used for genetic screening and diagnostics to analyze polymorphisms and mutations which may underlie genetic diseases or interindividual variations between subjects. Using microarrays in exercise physiology will provide new insights into the complex molecular mechanisms of the exercise-induced stress response, adaptation to training and modulation of immune function. Gene expression profiling and genetic screening will probably help to characterize and predict the individually variable response to and efficiency of training.

Exercise↗

Basal expression of leukocyte iNOS-mRNA is attenuated in moderately endurance-trained subjects.

Nitric oxide (NO) is generated in immunocompetent cells by inducible NO-synthase (iNOS), and plays an important role in host defense. However, when produced in large amounts, NO can also exert damaging effects, a scenario that is observed during several inflammatory processes. In the study presented here, we investigated the impact of moderate endurance training (running volume: mean 53.1 km x week(-1), 95% confidence interval 41.2-65.1 km week(-1)) on the leukocyte expression of iNOS mRNA. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis was used to examine iNOS mRNA expression in total leukocyte samples from 12 male trained subjects (TR) and a control group of 12 untrained men (UT) at rest. Relative iNOS mRNA levels (iNOS/beta-actin) were higher in UT (0.88, 0.73-1.03) when compared with TR (0.34, 0.09-0.58, P<0.001). iNOS mRNA was not detectable in 5 of the 12 TR subjects. These initial results show that the basal expression of iNOS mRNA is downregulated by moderate endurance training. Further research should clarify whether regular training also affects the responsiveness of leukocyte iNOS gene expression to stimulatory signals. It would be of interest to establish whether moderate training can exert a suppressive and therefore therapeutic effect on the elevated levels of expression of iNOS observed in, for example, several inflammatory disorders.

Adult↗

Effects of RRR-alpha-tocopherol on leukocyte expression of HSP72 in response to exhaustive treadmill exercise.

Previous research revealed an increased expression of HSP72 in leukocytes after vigorous endurance exercise. We questioned whether more intensive but shorter exercise also induces leukocyte HSP72 synthesis. To delineate the role of reactive oxygen species (ROS) in exercise-related HSP72 induction, we additionally examined the effect of RRR-alpha-tocopherol (alpha-toc) on HSP72 expression using a double-blind placebo (P) controlled cross-over design. After supplementation with alpha-toc (500 I.U. daily) or P for 8 days, 9 male subjects performed a combined exhaustive treadmill protocol (total duration 29.4 +/- 2.0 min). HSP72 was assessed on mRNA (RT-PCR) and protein levels (flow cytometry). HSP72 mRNA rose 3 h after exercise only in the P group, but individual differences (alpha-toc - P) did not reveal significant treatment effects. A moderate but significant rise of HSP72 protein occurred in granulocytes up to 48 h after exercise. Three hours post-exercise, granulocyte HSP72 protein was lower when subjects received alpha-toc, but this effect vanished 24 and 48 h post-exercise. Exhaustive treadmill exercise augments HSP72 mRNA in leukocytes and induced a moderate but prolonged response of granulocyte HSP72 protein. These exercise effects are lower when compared to earlier findings obtained after vigorous endurance exercise. ROS seem to be involved, but do not play the major role in the induction of granulocyte HSP72 synthesis after exhaustive exercise.

Adult↗

Utilisation of intramyocellular lipids (IMCLs) during exercise as assessed by proton magnetic resonance spectroscopy (1H-MRS).

Recently, a 1H-MRS method became available to quantify intramyocellular lipids (IMCL) non-invasively. Currently, little is known about the regulation of this lipid pool. During prolonged exercise of moderate intensity, non-plasma-derived fatty acids play an important role as an energy source; lipids located within the skeletal muscle are considered to be a major source for these fatty acids. To see whether IMCL are reduced by exercise, 12 male runners were studied before and after exercising at different workloads and duration. Six subjects participated in a non-competitive run (NCR), three runners in a competitive half marathon (HM, 21 km) and another three in a competitive marathon (M, 42 km). Intra- and extramyocellular lipids were quantified by 1H-MR spectroscopy in the tibialis anterior (TA) and soleus (SOL) muscles prior to and after the exercise bout. Moderate intensity (MI; 60-70% VO2max in NCR) with a mean exercise time (MET) ranging between 105-110 min decreased IMCL by 10 - 36% in both muscles. Prolonged MI exercise (MET 210-240 min; 68-70% VO2max in M) reduced IMCL by 42-57% in TA and 27 - 56% in SOL. In contrast, high intensity exercise (HI; MET 80-120 min; 83-85% VO2max in HM) did not alter IMCL in either muscle. Extramyocellular lipids (EMCL) did not show any significant change in any group. The data show that one bout of moderate-intensity (60-70% VO2max) aerobic exercise markedly reduces the IMCL in TA and SOL muscles in a time-dependent fashion as assessed by 1H-MRS. However, exercise of similar duration but higher workload (> 80% VO2max) does not reduce IMCL. These data suggest that both exercise duration and workload are important factors in determining the reduction of IMCL.

Adult↗

Changes of HSP72-expression in leukocytes are associated with adaptation to exercise under conditions of high environmental temperature.

Overexpression of the heat shock protein HSP72 provides thermotolerance. We asked if two consecutive endurance runs 1 week apart (CR1, CR2) and additional environmental heat stress affect HSP72-expression in leukocytes of nonheat-acclimated endurance athletes. Twelve subjects were allocated randomly into two groups. Group HH completed both runs at 28 degrees C ambient temperature, and group NH performed CR1 at 18 degrees C and CR2 at 28 degrees C. HSP72-expression was determined by flow cytometry and RT-PCR before and 0, 24, and 48 h after exercise. Additionally, post-exercise cells were exposed to in vitro heat shock (HS; 2 h, 42 degrees C). The prolonged, high HSP72 protein level after CR1 in HH compared with NH may reflect thermotolerance induced by endurance exercise at high ambient temperature. Adaptation of cardiocirculatory/thermoregulatory capacity after CR2 in HH went along with a more rapid down-regulation of HSP72 compared with CR1. HSP72 mRNA demonstrated temperature-related changes after exercise. The reduced HS response in vitro after CR2 may represent exercise-related adaptation mechanisms. HSP72 concentrations in leukocytes may indicate previous exercise- and temperature-related stress conditions and adaptation in immunocompetent cells.

Adaptation, Physiological↗

Physical exercise-induced expression of inducible nitric oxide synthase and heme oxygenase-1 in human leukocytes: effects of RRR-alpha-tocopherol supplementation.

This study evaluated the effects of RRR-alpha-tocopherol (500 IU/day, 8 days) on in vivo cytokine response and cytoplasmic expression of inducible nitric oxide synthase (iNOS) and the antioxidant stress protein heme oxygenase-1 (HO-1) in human leukocytes after exhaustive exercise. Thirteen men were investigated in a double-blind, placebo-controlled, cross-over study with a wash-out period of 28 days. The exercise procedure consisted of an incremental treadmill test followed by a continuous run until exhaustion at 110% of the individual anaerobic threshold (total duration 28.5 +/- 0.8 min). HO-1 and iNOS protein were assessed in mono- (M), lympho-, and granulocytes (G) using flow cytometry. Plasma interleukin-6 (IL-6) and IL-8 were measured by ELISA. IL-6 rose significantly whereas IL-8 did not exhibit significant changes after exercise. Changes of IL-6 were not affected by RRR-alpha-tocopherol. Exercise induced an increase of iNOS protein primarily in M and G. A small, but significant, increase of HO-1 protein was measured in M and G. RRR-alpha-Tocopherol did not show any significant effects on cytoplasmic expression of iNOS and HO-1 at rest and after exercise. In conclusion, exhaustive exercise induces expression of iNOS and HO-1 in human leukocytes by a mechanism that is not sensitive to RRR-alpha-tocopherol supplementation.

Adult↗

HSP expression in human leukocytes is modulated by endurance exercise.

PURPOSE: Temperature increase, oxidative stress, and inflammatory reactions after endurance exercise were expected to stimulate the synthesis of heat shock proteins (HSP) in peripheral blood leukocytes. Furthermore, it was of interest whether regular endurance training influences HSP expression. METHODS: The expression of HSP27, HSP60, HSP70, constitutive HSC70, and HSP90 in the cytoplasma and surface of lymphocytes, monocytes, and granulocytes of 12 trained athletes was analyzed by flow cytometry before and after (0, 3, and 24 h) a half marathon. Twelve untrained persons at rest were included as control. RESULTS: After the race, there was a significantly greater percentage of leukocytes expressing cytoplasmic HSP27, HSP60, and HSP70 (P < 0.01), whereas HSC70 and HSP90 remained unchanged. The fluorescence intensity increased significantly in monocytes for HSP27 (0 and 3 h) and HSP70 (0, 3, and 24 h) and in granulocytes, only 24 h postexercise for HSP70. The percent values of trained athletes at rest were significantly lower compared with untrained persons (P < 0,01). CONCLUSIONS: Strenuous exercise increased HSP expression in blood immediately after the run, indicating a protective function of HSP in leukocytes of athletes to maintain function after heavy exercise. The downregulation of HSP-positive cells in trained athletes at rest seems to be a result of adaptation mechanisms to regular endurance training.

Adaptation, Physiological↗

Expression of the inducible nitric oxide synthase (iNOS) in human leukocytes: responses to running exercise.

INTRODUCTION: We examined the influence of two different bouts of vigorous running exercise on the expression of the inducible nitric oxide synthase (iNOS) in leukocytes (LE). METHODS: In study 1, 10 trained runners competed in a half marathon (HM) lasting 90.5 +/- 11.0 min. In study 2, 8 untrained subjects performed a graded treadmill test followed by a continuous run (CR) until exhaustion (11.3 +/- 1.3 min). iNOS mRNA levels were assessed by RT/PCR at rest, 0, 3, and 24 h after HM and CR. In study 2, iNOS was additionally analyzed at the protein level in lympho- (L), mono- (M), and granulocytes (G) by flow cytometry at rest and up to 48 h after CR. RESULTS: Analysis revealed a rise of the iNOS transcript directly after the HM in 8 of 10 subjects. In study 2, the expression of iNOS protein at rest differed between L (mean +/- SE: 30.9 +/- 4.5% iNOS positive cells), M (91.3 +/- 4.0%), and G (64.9 +/- 10.3%): 3 h after CR, expression of iNOS increased in L (67.3 +/- 7.4%) and G (90.3 +/- 2.9%) and was still elevated 48 h post-exercise. However, our measurements failed to detect significant changes of leukocyte iNOS mRNA in response to CR. After the HM, our findings were paralleled by elevated plasma levels of interleukin-8, myeloperoxidase (MPO), and partly of TNF-alpha, whereas CR only induced a low rise of MPO. CONCLUSION: Our investigations revealed an increased expression of iNOS at the transcriptional and translational level in response to vigorous exercise. This reflects an inflammatory response and may contribute to an exercise-induced rise of endogenous nitric oxide production. It remains unclear if these effects serve an in-vivo immunoregulatory or cell-damaging role.

Adult↗

Transcriptional and translational regulation of heat shock proteins in leukocytes of endurance runners.

Heat shock proteins (HSP) represent cell-protective and antioxidant systems that may be induced by reactive oxygen species, cytokines, and hyperthermia. In the present study, we evaluated the influence of heavy endurance exercise and training on HSP27 and HSP70 in peripheral leukocytes of 12 athletes (before and at 0, 3, and 24 h after a half-marathon) and 12 untrained controls on protein and mRNA levels by flow cytometry and RT/PCR, respectively. HSP transcripts increased significantly immediately after acute exertion accompanied by elevated levels of corresponding proteins. HSP protein expression remained high until 24 h postexercise. Significant increases of plasma interleukin-8, myeloperoxidase, and creatine kinase occurred after exercise. Basal HSP expression was usually lower in trained compared with untrained subjects. Applying in vitro heat shock to resting blood samples of all subjects significantly stimulated HSP mRNA, showing higher increases in trained individuals. The exercise-induced alterations indicate that immunocompetent cells became activated. In addition to heat stress, other exercise-associated stress agents (oxidants, cytokines) may have also participated in stimulation of HSP expression in leukocytes. The expression pattern of HSP due to training status may be attributed to adaptive mechanisms.

Actins↗