H.-H. Dickhuth

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.

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 providesthermotolerance. We asked if two consecutive endurance runs 1 weekapart (CR1, CR2) and additional environmental heat stress affectHSP72‐expression in leukocytes of nonheat‐acclimated enduranceathletes. Twelve subjects were allocated randomly into two groups. Group HH completed both runs at 28°C ambient temperature, and groupNH performed CR1 at 18°C and CR2 at 28°C. HSP72‐expression wasdetermined by flow cytometry and RT‐PCR before and 0, 24, and 48 hafter exercise. Additionally, post‐exercise cells were exposed toin vitro heat shock (HS; 2 h, 42°C). The prolonged, high HSP72 protein level after CR1 in HH compared with NH may reflectthermotolerance induced by endurance exercise at high ambienttemperature. Adaptation of cardiocirculatory/thermoregulatory capacityafter CR2 in HH went along with a more rapid down‐regulation of HSP72compared with CR1. HSP72 mRNA demonstrated temperature‐related changesafter exercise. The reduced HS response in vitro after CR2may represent exercise‐related adaptation mechanisms. HSP72concentrations in leukocytes may indicate previous exercise‐ andtemperature‐related stress conditions and adaptation in immunocompetentcells.

Metabolic reaction after concentric and eccentric endurance-exercise of the knee and ankle.

PURPOSE Power training plays an essential part in many sport disciplines. The importance of eccentric power training remains a matter of controversial discussion. The objective of this study was therefore to investigate the difference in metabolic reaction between eccentric and concentric stress in comparable work. METHODS Sixty-four men between 22 and 60 yr of age performed maximum isokinetic 1-min endurance tests of the knee and ankle each in concentric (180 degrees.s-1) and eccentric (60 degrees.s-1) modes with comparable total area of contraction-time curve (NS). Higher strength values (mean peak torque, P < 0.01), lower fatigue (fatigue index, P < 0.001), lower increase in lactate (P < 0.01), and lower ammonia production (P < 0.01) were found in eccentric than in concentric exercise, independent of the joint. The eccentric form of stress showed lower decrease and thus age-dependence in maximum strength and in fatigue than the concentric form. RESULTS The results permit the conclusion that eccentric exercise leads to less fatigue and lower lactate and ammonia reaction than concentric exercise in comparable work levels. Variable visco-elastic properties of the muscle fibers themselves with additive passive strength in eccentric mode is considered as the cause. CONCLUSIONS It remains uncertain whether the lower metabolic stress might be useful during the training process. A greater scope of training and increased number of training stimuli might be applied in primarily eccentric forms of exercise.

Inverse response of leukocyte heat shock proteins and DNA damage to exercise and heat.

Elevated ambient temperature may exert an additional impact on the exercise-induced expression of heat shock proteins (HSP) and DNA damage in leukocytes. The protective functions of HSP include antioxidative and antiapoptotic effects and may prevent damage to DNA. Twelve athletes completed a continuous run (75% VO2max) on the treadmill, six at 28 degrees C and six at 18 degrees C room temperature. Leukocyte expression of HSP27 and inducible HSP70 was analyzed on mRNA- (RT-PCR) and protein-level (flow cytometry), while DNA damage was quantified by the comet assay. High ambient temperature induced an additional accumulation of HSP-mRNA and -protein in leukocytes compared with the exercise-induced expression at 18 degrees C. HSP27 showed a special heat sensitivity. Surprisingly, the increase of DNA damage was less pronounced after exercise at 28 degrees C compared to 18 degrees C although heat shock in vitro clearly induced DNA damage. The inverse relation between HSP and DNA damage may indicate functions of HSP which protect against exercise-induced DNA-damage in terms of thermotolerance or apoptosis.

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 · 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 · 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 × 109 · 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

Fibrinogen in patients with coronary heart disease: relationship to lipoproteins

Die Bedeutung des Fibrinogens als Gerinnungsfaktor, Akutphaseprotein, Co-Faktor in der Plattchenaggregation und rheologiebeeinflussender Faktor ist wohl bekannt [10]. In der Genese der Arteriosklerose spielt es eine bisher unterschatzte Rolle [6]. Erst seit 1983 ist das Fibrinogen als Risikofaktor bekannt [8], durch Ergebnisse von Yarnell et al. 1985 bestatigt [9] und seit 1987 aufgrund von Daten aus der Framingham-Studie als unabhangiger Risikofaktor etabliert [3]. Offensichtlich besteht auch ein Zusammenhang zwischen Fibrinogen und Gesamtcholesterin [4] bzw. zwischen Fibrinogen und niedrigem High density lipoprotein (HDL)- bzw. hohem Low density lipoprotein (LDL)-Cholesterin [7]. In der vorliegenden Studie wurde anhand eines Kollektivs mit manifester Arteriosklerose die Beziehung von Fibrinogen zu den Lipiden und Lipoproteinen untersucht.

Zur langfristigen Rückbildung der physiologischen Herzhypertrophie

Bisher liegen nur wenige Untersuchungen uber die Ruckbildungsfahigkeit der Herzhypertrophie und kardiozirkulatorischen Leistungsfahigkeit vor, die jedoch nicht quantifiziert werden konnten, da in der Regel die Herzgrose und Leistungsdaten aus der aktiven Zeit nicht vorlagen [3,4,5,6].