Biomedical subjects

A M Niess

Publications and source records attributed to A M Niess.

26 records · Page 2Linked to original sources

PubMed1999

[The significance of physical activity on the physiological stress reaction].

The extent of physical activity and the dynamic performance capacity show an inverse relationship to cardiovascular mortality, independent of the influence of other risk factors, but the underlying mechanism remains uncertain. Most concepts assume that the aerobic capacity of the peripheral musculature is increased by training, and thus improved cardiocirculatory regulation and especially a more favorable stress reaction pattern are attained. This adaptation is essentially an inverse adaptation mechanism as in established cardiocirculatory insufficiency. Based on an extended stress concept, it can be seen that training effects, especially in autonomic circulatory regulation, occur under physiological conditions to a lower degree in the renin-angiotensin-aldosterone system and in inflammatory reaction. The training effects depend on the form of exercise, the baseline condition, the extent of training, and genetic predisposition. It can be particularly demonstrated when the aerobic capacity has been sufficiently enlarged in an adequate proportion of the peripheral musculature. To what extent and under what conditions these training effects can be used under the pathophysiological conditions of established cardiocirculatory insufficiency is presently under investigation.

Adaptation, Physiological↗

PubMed1999

Expression of the antioxidant stress protein heme oxygenase-1 (HO-1) in human leukocytes.

Inducible heme oxygenase (HO-1) is an antioxidant stress protein, that is mainly induced by reactive oxygen species (ROS), cytokines and hyperthermia. By using flow cytometry the present investigation demonstrated a rise in the cytoplasmic expression of HO-1 in lympho- (L), mono- (M) and granulocytes (G) of 9 endurance-trained male subjects after a half marathon run. The expression was more pronounced in M (median: 98.3% HO-1 positive cells/4.31 mfc) and G (94.8%/1.93 mfc) than in L (80.1%/1.51 mfc) when measured 3 h post-exercise. Additionally the exercise protocol caused a rise in the plasma levels of myeloperoxidase, TNF alpha and interleukin-8 (IL-8), indicating an inflammatory response. We could detect a correlation between IL-8 and HO-1, directly after exercise, that was apparent in G (r = 0.67, p < .05) and L (r = 0.80, p < .05), but did not reach significance in M (r = 0.65, p = 0.06). An additional detection of HO-1 at rest in 12 untrained subjects showed a higher baseline expression of HO-1 compared to the athletes. The regulatory pathways leading to an increased expression of HO-1 after endurance exercise are not completely clear, but a causal involvement of a cytokine-mediated generation of ROS must be discussed. We supposed that the down-regulation of the baseline expression of HO-1 in athletes reflects an adaptional mechanism to regular exercise training.

Adaptation, Physiological↗

PubMed1999

Free radicals and oxidative stress in exercise--immunological aspects.

Reactive oxygen (ROS) and nitrogen species (RNS) are continuously generated in the biological system and play an important role in a variety of physiological and pathological processes. There is evidence that physical exercise augments the generation of ROS/RNS. The present review discusses and compares insights into the generation and function of ROS/RNS such as superoxide, hydrogen peroxide, hypochloric acid, and nitric oxide released by leukocytes in response to exercise. Emphasis is placed on: (a) mechanisms and regulation of ROS/RNS generation in immunocompetent cells with respect to acute exercise and regular training; (b) damaging effects of ROS/RNS in terms of oxidative stress which may be causally involved in features such as exercise-induced damage to muscle tissue and leukocyte DNA; (c) (immuno-) modulating effects of ROS/RNS which include activation of transcription factors; (d) responses of antioxidant stress proteins to acute exercise and regular training; and (e) effects of antioxidants on exercise-induced changes in immune function. Available data suggests that ROS/RNS are involved in the inflammatory response to heavy exercise and therefore exert damaging effects. Several immune functions are influenced by actions of ROS/RNS, and it is hypothesized that adaption to regular training is also modulated in part by free radicals. Furthermore, regular training seems to reduce the capacity of leukocytes for oxidant release and leads to an adaptation of antioxidative mechanisms, which may contribute to a limitation of exercise-induced oxidative stress.

Animals↗

PubMed1999

Role of heat shock proteins in the exercise response.

Heat shock proteins (HSP) are a characteristic set of highly conserved proteins that are synthesized shortly after the organism is exposed to external stress, including physical activity. HSP help to maintain cellular homeostasis and protein conformation, reactivate denatured or malformed proteins, and provide "housekeeping," translocase, and chaperone functions. Some of the conditions known to elicit the cellular stress reaction are similar to those experienced by cells in response to physical exercise. Hyperthermia, ischemia, oxidative, cytokine and muscular stress, glucose deprivation, and alterations in calcium and pH are potent inducers of HSP expression in different types of cells and tissues. This review provides an overview of the cellular heat shock response to exercise. The presently known exercise related HSP are introduced. Their possible roles in response to acute exercise, thermotolerance, adaptation to training, aging, and immunological reactions are discussed.

Adaptation, Physiological↗

PubMed1998

Predicting competition performance in long-distance running by means of a treadmill test.

PURPOSE: The purpose of this study was to examine the power of 16 parameters beside the individual anaerobic threshold (IAT) in predicting performance in various competition distances. METHODS: This study examined 427 competitive runners to test the prediction probability of the IAT and other parameters for various running distances. All runners (339 men, 88 women; ages, 32.5 +/- 10.14 yr; training, 7.1 +/- 5.53 yr; training distance, 77.9 +/- 35.63 km.wk-1) performed an increment test on the treadmill (starting speed, 6 or 8 km.h-1; increments, 2 km.h-1; increment duration, 3 min to exhaustion). The heart rate (HR) and the lactate concentrations in hemolyzed whole blood were measured at rest and at the end of each exercise level. The IAT was defined as the running speed at a net increase in lactate concentration 1.5 mmol.L-1 above the lactate concentration at LT. RESULTS: Significant correlations (r = 0.88-0.93) with the mean competition speed were found for the competition distances and could be increased using stepwise multiple regression (r = 0.953-0.968) with a set of additional parameters from the training history, anthropometric data, or the performance diagnostics. CONCLUSIONS: The running speed at a defined net lactate increase thus produces an increasing prediction accuracy with increasing distance. A parallel curve of the identity straight lines with the straight lines of regression indicates the independence of at least a second independent performance determining factor.

Adult↗

PubMed1998

Effects of intensive endurance exercise on DNA damage in leucocytes.

OBJECTIVE: It has been shown that highly intensive anaerobic exercise induces DNA damage in leucocytes (LEU). The present study was designed to investigate whether intensive endurance exercise is capable of inducing comparable effects. EXPERIMENTAL DESIGN: A prospective study. PARTICIPANTS: Twelve men (aged 27.3 +/- 4.1 years) who undertook a regular training of different extent (running volume 45 +/- 25 km.week-1) volunteered in the study. INTERVENTIONS: The subjects competed in a half marathon (HM) of 21.1 km, 93.0 +/- 10.4 min. MEASUREMENTS: Blood was taken at rest, 1 and 24 hrs after HM for determination of creatine kinase, neutrophil (PMN), lymphocyte and monocyte counts. DNA damage in LEU at rest and 24 hrs after HM was quantified using the single cell gel-electrophoresis (SCG) assay. RESULTS: PMN increased from 2.81 +/- 0.69 to 13.13 +/- 2.91 1 hrs after HM (p < 0.01) and returned to 3.26 +/- 0.47 10(9) cells.l-1 by 24 hr recovery. DNA migration (image length, IL) reflecting the extent of DNA damage was elevated significantly in 10 of 12 subjects one day after HM. IL rose from 32.7 +/- 2.2 to 40.7 +/- 3.9 microns (p < 0.01). Correlation analysis revealed a relationship between DNA migration 24 hrs after HM and PMN count 1 hr post-exercise (r = 0.67, p < 0.05). CONCLUSIONS: The results confirm the hypothesis that DNA damage in LEU occurs after intensive endurance exercise. We suppose our observation of exercise-induced DNA damage in LEU is affected by reactive oxygen species which are released from PMN. It is quite unclear whether DNA damage in LEU is causal involved in exercise-induced modifications of the immune system.

Adult↗

PubMed1996

DNA damage after exhaustive treadmill running in trained and untrained men.

The single cell gel electrophoresis (SCG) assay was used to compare the occurrence of DNA damage in peripheral white blood cells in 6 trained (TR) and 5 untrained (UT) men after exhaustive exercise. The subjects completed an incremental treadmill test until exhaustion (maximal lactate: 12.9 +/- 1.7 in TR and 12.2 +/- 2.5 mmol.l-1 in UT). A clear and significant increase of DNA migration from 2.31 +/- 0.20 (TR) and 2.22 +/- 0.16 (UT) at rest to 2.65 +/- 0.30 (TR) and 3.00 +/- 0.41 tail moment (UT) was found 24 hours after exercise. Noteworthy is that the increase of DNA migration was significantly lower in TR (+ 18.7 +/- 6.8%) compared to UT (+ 35.7 +/- 8.9%). Plasma levels of malondialdehyde (MDA) were not significantly increased in TR and UT after exercise. At rest and 15 minutes after exercise MDA-values were significantly lower in TR compared to UT. In conclusion the present investigation demonstrates the occurrence of DNA damage in white blood cells following exhaustive exercise. This observation may be induced by oxidative stress. Our data suggest that adaptation to training seems to be capable of reducing free radical associated effects, such as DNA damage. Further investigations are needed to clarify the causal mechanisms and biological relevance of exercise-induced DNA damage.

Adaptation, Physiological↗

PubMed1995

Vitamin E prevents exercise-induced DNA damage.

The single cell gel test (SCG test or comet assay) was used to study DNA damage in peripheral white blood cells (WBC) of humans after a single bout of exhaustive exercise and the effect of vitamin supplementation. Human subjects were asked to run on a treadmill until exhaustion and blood samples were taken before and 24 h after the run. A clear increase in DNA strand breakage was observed in the 24-h sample of all probands. A short-term application of multivitamin pills or vitamin E (3 x 800 mg) resulted in a significantly smaller increase of DNA effects in WBC of some probands. When the volunteers were given a supplement of vitamin E (1200 mg daily) for 14 days prior to a run, exercise-induced DNA damage was clearly reduced in all probands. In four out of five subjects, vitamin supplementation completely prevented the induction of DNA damage after exhaustive exercise. Intake of vitamin E for 14 days led to a clear increase in vitamin E serum concentrations. Malondialdehyde (MDA), a marker of lipid peroxidation, was measured in the serum of probands in tests with and without vitamin supplementation for 14 days. MDA concentrations were significantly decreased following vitamin E supplementation but not significantly changed 15 min and 24 h after a run. Our results demonstrate that vitamin E prevents exercise-induced DNA damage and indicate that DNA breakage occurs in WBC after exhaustive exercise as a consequence of oxidative stress.

Adult↗