Women will do it in the long run.
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Competitive Behavior↗
Biomedical subjects
R Beneke
Publications and source records attributed to R Beneke.
Experiment and computer-aided simulation: complementary tools to understand exercise metabolism.
During the last two decades the concept of the MLSS (maximal lactate steady state) has been established. The MLSS detects the highest level of the BLC (blood lactate concentration) and the corresponding workload (MLSS workload) that can be maintained over time without continual BLC accumulation. In spite of a lack of experimental and/or theoretical foundation, it has been speculated that the level of the MLSS may decrease with increasing performance capacity. The potential inter-relationship between performance capacity and BLC response to prolonged constant workload will be analysed based on a recent study, which provided evidence that the MLSS is independent of performance whereas MLSS workload increases with performance capacity, and by a computer-aided simulation. The simulated model modifies and combines previous theories put forward to explain the response of BLC to exercise and incorporates a theory about limiting factors of oxygen transport to the muscle cell. Simulations consider the BLC response to selected prolonged constant workloads while paying special respect to changes in body structure and substrate utilization, which are generally accepted as limiting factors of performance capacity. This complex modulation of appearance and disappearance of lactate during constant prolonged exercise seems to support the experimental results, which indicated independence between MLSS and performance capacity.
Adult↗
How anaerobic is the Wingate Anaerobic Test for humans?
The Wingate Anaerobic Test (WAnT) is generally used to evaluate anaerobic cycling performance, but knowledge of the metabolic profile of WAnT is limited. Therefore the energetics of WAnT was analysed with respect to working efficiency and performance. A group of 11 male subjects [mean (SD), age 21.6 (3.8) years, height 178.6 (6.6) cm, body mass 82.2 (12.1) kg] performed a maximal incremental exercise test and a WAnT. Lactic and alactic anaerobic energy outputs were calculated from net lactate production and the fast component of the kinetics of post-exercise oxygen uptake. Aerobic metabolism was determined from oxygen uptake during exercise. The WAnT mean power of 683 (96.0) W resulted from a total energy output above the value at rest of 128.1 (23.2) kJ x 30 s(-1) [mean metabolic power=4.3 (0.8) kW] corresponding to a working efficiency of 16.2 (1.6)%. The WAnT working efficiency was lower (P < 0.01) than the corresponding value of 24.1 (1.7)% at 362 (41) W at the end of an incremental exercise test. During WAnT the fractions of the energy from aerobic, anaerobic alactic and lactic acid metabolism were 18.6 (2.5)%, 31.1 (4.6)%, and 50.3 (5.1)%, respectively. Energy from metabolism of anaerobic lactic acid explained 83% and 81% of the variance of WAnT peak and mean power, respectively. The results indicate firstly that WAnT requires the use of more anaerobically derived energy than previously estimated, secondly that anaerobic metabolism is dominated by glycolysis, thirdly that WAnT mechanical efficiency is lower than that found in aerobic exercise tests, and fourthly that the latter finding partly explains discrepancies between previously published and the present data about the metabolic profile of WAnT.
Adult↗
Markers of coagulation, fibrinolysis and angiogenesis after strenuous short-term exercise (Wingate-test) in male subjects of varying fitness levels.
It was the aim of the study to analyse the haemostatic system during a high standardized intensive short-term (30 s) exercise (anaerobic Wingate test). Blood samples were taken from 15 male subjects before (t0 ), and within 2 (t1 ), 9 (t2 ) and 30 min (t3 ) after the test. We found that the partial thromboplastin time was markedly shortened, whereas the prothrombin time increased slightly from t0 to t1 (p < 0.002) and remained elevated (t3, p < 0.046). Factor VIII increased from t0 to t1 (p < 0.001) and remained elevated as well (t3, p < 0.001). Fibrin monomers were approximately 15 times higher immediately post-exercise (t1, p < 0.001) and continued to be elevated (t3, p < 0.004). The tissue plasminogen activator increased by 4 times after exercise (t1, p < 0.001) and remained elevated (t3, p < 0.002). The d-dimers increased from t0 to t1 (p < 0.001) as well and remained elevated (t3, p < 0.005). Thrombopoietin concentrations were unchanged, whereas the vascular endothelial growth factor increased immediately post-exercise (t0 to t1, p < 0.011 resp. at t2 p < 0.019) and returned to the control level at t3 (p < 0.878). In conclusion, it was found that prothrombotic markers and, even more pronounced, those of the fibrinolytic system were increased. The study provides evidence that due to intensive short-term exercise the balance of the haemostatic system is shifted to a higher equilibrium. Theoretically, the data show that in the case of a subject with risk factors such as impaired fibrinolysis, unfavourable conditions cannot be excluded.
Adult↗
Inhibition of poly(ADP-ribose) polymerase activity accelerates T-cell lymphomagenesis in p53 deficient mice.
Cells that lack PARP-1 activity are limited in their ability to repair DNA single strand breaks and respond to DNA damage with a strong accumulation of p53 and enhanced rates of apoptotic cell death. We have generated combinatorial mutant mice that both lack p53 and PARP-1 activity due to the expression of a dominant negative PARP-1 allele targeted to T-cells by the lck promoter. Here we report that these double mutant mice develop T-cell lymphoma at a significantly reduced latency period compared to single p53 null mice that are already cancer prone. We demonstrate that the absence of p53 does not only protect T-cells from lck-PARP-DBD transgenic mice from apoptosis but also abrogates the DNA damage induced cell cycle arrest in the G1 phase. T-cells from double mutant mice continue to proliferate after the induction of DNA strand breaks, are limited in their DNA repair capacity and cannot be eliminated by apoptosis. These results indicate that PARP-1 and p53 cooperate in the suppression of tumorigenesis by maintaining genomic integrity after DNA damage through the activation of a G1/S cell cycle checkpoint the initiation of DNA repair and the induction of cell death.
Animals↗
Exercise-induced changes in blood levels of alpha-tocopherol.
Levels of alpha-tocopherol (alphaT) in plasma and red blood cells (RBC) are assumed to be modulated by exercise. The mechanisms involved remain to be established. We examined the influence of different running bouts on the content of alphaT in RBC (alphaT(RBC)), the concentration in plasma (alphaTplasma), and their relationship with lipolysis, as indicated by changes (delta) in plasma glycerol concentration ([glycerol]). Eleven healthy runners [mean (SD) age 35 (9) years, height 177.3 (7.6) cm, body mass 69.6 (9.4) kg, and peak oxygen consumption, VO2peak, 57.8 (4.8) ml.kg(-1).min(-1)] performed an incremental treadmill test [duration 17 (2) min, peak velocity, vpeak 4.8 (0.4) m.s(-1)], a training run [173 (12) min, 57 (4)% vpeak] and a marathon [197 (24) min, 75 (5)% vpeak]. Before (pre) and after (post) each run, haematological and lipid parameters, alphaT(RBC) and alphaTplasma were determined. Haemoconcentration was observed after each run. delta[glycerol] was +0.10 (0.10) mmol.l(-1), +0.40 (0.14) mmol.l(-1) and +0.51 (0.15) mmol.l(-1) in the treadmill test, training run and marathon, respectively. When corrected for haemoconcentration, values of alphaTplasma decreased [-5.4 (7.5)%, P< 0.05] in the treadmill test, were unchanged [+0.7 (8.7)%] in the training run and increased [+7.8 (8.3)%, P<0.05] in the marathon. alphaT(RBC) decreased [pre vs post: 22.7 (3.2) nmol.g haemoglobin(-1) (nmol.g Hb(-1)) vs 18.9 (3.8) nmolg Hb(-1), P < 0.05] in the treadmill test and was not significantly changed in either the training run [20.8 (1.9) nmol.g Hb(-1) vs 19.1 (3.0) nmol.g Hb(-1)] or the marathon [21.6 (2.9) nmol.g Hb(-1) vs 23.4 (2.7) nmol.g Hb(-1)]. deltaalphaT(RBC) and deltaalphaTplasma were positively related to delta[glycerol]. The reduction in alphaTRBC and alphaTplasma after short-lasting heavy exercise indicates the consumption of alphaT, whereas the association between deltaalphaT and delta[glycerol] suggests mobilisation of alphaT, especially in long-lasting exercises. However, although alphaT appears to be influenced by exercise, the results suggest a well-balanced regulation of alphaT during exercise resulting in small, and only in part, significant deltaalphaT in blood.
Adult↗
Measured fraction of carboxyhaemoglobin depends on oxygen saturation of haemoglobin.
The use of the OSM3 oximeter for measurement of the fraction of carboxyhaemoglobin (FCOHb) in blood allows for estimation of total circulating haemoglobin mass (Hb(tot)) by using the carbon monoxide rebreathing method. To ensure high accuracy of Hb(tot) estimation, potential sources of analytical errors should be identified and adjusted for. Based on observed differences in results of measured FCOHb between simultaneously sampled, arterialized and venous blood samples we investigated the influence of haemoglobin oxygen saturation (sO2) on results of measured FCOHb. Blood from nine healthy non-smokers was tonometered with gas mixtures containing 94% N2 or air and 6% CO2. The resulting oxygenated and deoxygenated specimens were mixed in different proportions to obtain varying sO2 values in the same blood. sO2, fractions of dyshaemoglobins, pO2, pCO2 and pH were measured at each step. FCOHb was significantly (p<0.001) higher in oxygenated (median, range: 0.6%, 0.4-0.9%) compared to deoxygenated (-0.2%, -0.5-0.0%) blood. Regression analysis identified the sO2 as the most important factor explaining 86% of the variance in observed changes in FCOHb. The observed sO2 effect has important implications on calibration procedure of OSM3, accuracy of measured FCOHb, and FCOHb dependent calculations such as estimation of Hb(tot) and related quantities. If the highest accuracy of FCOHb measurement is needed, an sO2 effect on results of measured FCOHb has to be considered and adjusted for.
Carbon Dioxide↗
Dependence of the maximal lactate steady state on the motor pattern of exercise.
BACKGROUND: Blood lactate concentration (BLC) can be used to monitor relative exercise intensity. The highest BLC representing an equilibrium between lactate production and elimination is termed maximal lactate steady state (MLSS). MLSS is used to discriminate qualitatively between continuous exercise, which is limited by stored energy, from other types of exercise terminated because of disturbance of cellular homoeostasis. AIM: To investigate the hypothesis that MLSS intraindividually depends on the mode of exercise. METHODS: Six junior male rowers (16.5 (1.4) years, 181.7 (3.1) cm, 69.8 (3.3) kg) performed incremental and constant load tests on rowing and cycle ergometers. Measurements included BLC, sampled from the hyperaemic ear flap, heart rate, and oxygen uptake. MLSS was defined as the highest BLC that increased by no more than 1.0 mmol/l during the final 20 minutes of constant workload. RESULTS: In all subjects, MLSS was lower (p < or = 0.05) during rowing (2.7 (0.6) mmol/l) than during cycling (4.5 (1.0) mmol/l). No differences between rowing and cycling were found with respect to MLSS heart rate (169.2 (9.3) v 172.3 (6.7) beats/min), MLSS workload (178.7 (29.8) v 205.0 (20.7) W), MLSS intensity expressed as a percentage (63.3 (6.6)% v 68.6 (3.8)%) of peak workload (280.8 (15.9) v 299.2 (28.4) W) or percentage (76.4 (3.4)% v 75.1 (3.0)%) of peak oxygen uptake (60.4 (3.4) v 57.2 (8.6) ml/kg/min). CONCLUSIONS: In rowing and cycling, the MLSS but not MLSS workload and MLSS intensity intraindividually depends on the motor pattern of exercise. MLSS seems to decrease with increasing mass of the primarily engaged muscle. This indicates that task specific levels of MLSS occur at distinct levels of power output per unit of primarily engaged muscle mass.
Adolescent↗
Measurable amount of glutathione in blood is influenced by oxygen saturation of hemoglobin.
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Glutathione↗
Determination of circulating hemoglobin mass and related quantities by using capillary blood.
PURPOSE: A standardized carbon monoxide (CO) rebreathing procedure with measurements of CO-hemoglobin, hemoglobin concentration ([Hb]), and hematocrit (Hct) enables to determine total Hb mass (Hb(tot)), blood, erythrocyte, and plasma volume (BV, EV, and PV). These calculations are normally based on venous blood samples. However, micromethods also allow determinations from capillary blood. METHODS: The accuracy of using capillary blood for Hb(tot), BV, EV, and PV determination was evaluated in 42 men (age: 25.1 +/- 4.0 yr, body mass: 80.3 +/- 9.6 kg) by comparison of capillary and venous data. RESULTS: Capillary Hb(tot) (962 +/- 110 g) did not differ from venous values (959 +/- 106 g). Hb(tot) values were highly correlated (r = 0.987, P < 0.001, SEE 18 g). Also, capillary and venous BV, PV, and EV were highly correlated (0.94 < r < 0.98), but slightly different (-2.7 to 0.9%) because of higher capillary than venous [Hb] and Hct. Coefficients of variation of repeated Hb(tot), EV, PV, and BV measurements (3.0-5.2%) were similar in capillary and venous blood. CONCLUSION: Calculation of Hb(tot) using capillary blood is as accurate and reliable as using venous blood.
Adult↗
Maximal lactate-steady-state independent of performance.
PURPOSE: The maximal lactate steady state (MLSS) corresponds to the highest workload that can be maintained over time without a continual blood lactate accumulation. MLSS and MLSS intensity have been speculated to depend on performance. Experimental proof of this hypothesis is missing. METHODS: 33 male subjects (age: 23.7 +/- 5.5 yr, height: 181.2 +/- 5.3 cm, body mass: 73.4 +/- 6.4 kg) performed an exhausting incremental load test to measure peak workload and three to six 30-min constant load tests on a cycle ergometer to determine MLSS. RESULTS: MLSS (4.9 +/- 1.4 mmol x L(-1)) was independent of MLSS workload (3.4 +/- 0.6 W x kg(-1)) and peak workload (4.8 +/- 0.6 W x kg(-1)). MLSS intensity (71.1 +/- 6.7%) did not correlate with peak workload or MLSS (P > 0.05). A positive correlation was found between peak workload and MLSS workload (r = 0.82, P < 0.001). CONCLUSIONS: MLSS and MLSS intensity are independent of performance but subjects with higher maximum performance have higher MLSS workloads. The combination of various fitness related effects on both, the production and the disappearance of lactate during exercise, may explain that different MLSS workloads coincide with similar levels of MLSS and MLSS intensity.
Adolescent↗
DNA excision repair and DNA damage-induced apoptosis are linked to Poly(ADP-ribosyl)ation but have different requirements for p53.
Poly(ADP-ribose) polymerase (PARP) is a DNA binding zinc finger protein that catalyzes the transfer of ADP-ribose residues from NAD(+) to itself and different chromatin constituents, forming branched ADP-ribose polymers. The enzymatic activity of PARP is induced upon DNA damage and the PARP protein is cleaved during apoptosis, which suggested a role of PARP in DNA repair and DNA damage-induced cell death. We have generated transgenic mice that lack PARP activity in thymocytes owing to the targeted expression of a dominant negative form of PARP. In the presence of single-strand DNA breaks, the absence of PARP activity correlated with a strongly increased rate of apoptosis compared to cells with intact PARP activity. We found that blockage of PARP activity leads to a drastic increase of p53 expression and activity after DNA damage and correlates with an accelerated onset of Bax expression. DNA repair is almost completely blocked in PARP-deficient thymocytes regardless of p53 status. We found the same increased susceptibility to apoptosis in PARP null mice, a similar inhibition of DNA repair kinetics, and the same upregulation of p53 in response to DNA damage. Thus, based on two different experimental in vivo models, we identify a direct, p53-independent, functional connection between poly(ADP-ribosyl)ation and the DNA excision repair machinery. Furthermore, we propose a p53-dependent link between PARP activity and DNA damage-induced cell death.
Animals↗
Regulation of MAC-1 (CD11b/CD18) expression on circulating granulocytes in endurance runners.
PURPOSE: We tested the hypothesis that degranulation of granulocytes and upregulation of the granulocyte integrin MA-1 (CD11b/CD18) are related to exercise duration and/or intensity. We also investigated whether or not the expression of MAC-1 would be influenced by body temperature or dehydration. Moreover, we tested the hypothesis that changes in leukocyte counts and changes in MAC1 expression with endurance exercise are independently regulated. METHODS: In eight amateur runners, MAC-1 (CD11b/CD18) surface expression on granulocytes was determined by fluorescent antibody cell sorting, before and after an incremental maximal treadmill test, a moderate 3-h run, and a competitive marathon race. RESULTS: Expression CD11b on granulocytes was increased by 10+/-9.6% (P < 0.05) after the maximal treadmill test and by 84+/-76% (P < 0.01) after the marathon run. There was no change in CD11b expression after the moderate 3-h run. CD18 expression was not significantly changed after any of the exercise protocols. CONCLUSION: Expression of CD11b on granulocytes is increased with intense endurance exercise, either incremental maximal treadmill testing or competitive marathon running, but not in moderate endurance training. Thus, exhaustive exercise may be one mechanism for the upregulation of integrin adhesive receptors on granulocytes. This phenomenon could be in part responsible for increased adhesion of granulocytes to endothelial cells and could facilitate tissue infiltration after endurance exercise.
Adult↗
Red cell membrane skeletal changes in marathon runners.
Hemolysis in endurance exercise may be related to structural changes in red blood cell (RBC) membrane skeletal proteins. To test this hypothesis, we studied 13 male subjects before and after a marathon race. RBC membrane skeletons were observed with scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Plasma haptoglobin was measured. RBCs were affixed on poly-l-lysine coated glass supports for SEM and copper grids with formvar were prepared for TEM. Cytoplasmatic materials and lipid membranes were extracted with Triton-X-100 solution. TEM specimens were negatively stained and air dried. For SEM, the remaining RBC membrane skeletons were fixed, postfixed and sputtered with platinum. RBC membrane skeletal areas on SEM micrographs were measured by digitizer table planimetry. No RBC changes were observed with TEM. On the other hand, SEM showed disrupted RBC membrane skeletons. Furthermore, there appeared to be a loss of membrane material in RBC after the race, compared to RBC before the race. RBC membrane skeletal areas were increased by 30% (p<0.01). Hemolysis was indicated by a 57% decrease in plasma haptoglobin values (p<0.001). Thus, structural changes in RBC membrane skeletons occur after a marathon race. These changes can be identified with SEM but not with TEM. They may be related to increased susceptibility to chemical and physical stress and may contribute to hemolysis in endurance exercise.
Adult↗
Predictors of response to exercise training in severe chronic congestive heart failure.
We prospectively assessed whether baseline central hemodynamics and exercise capacity can predict improvement of VO2 at ventilatory threshold (VT) after exercise training in patients with severe chronic congestive heart failure. Eighteen patients (mean +/- SEM; age 52 +/- 2 years), half of them listed for transplant, underwent 3 weeks of exercise training (interval cycle and treadmill walking; 5 x/week) and 3 weeks of activity restriction in a random-order crossover trial. Baseline data were not significantly different for groups with exercise training first and activity restriction first: cardiac index at rest (2.1 +/- 0.1 L/m2/min), maximum cardiac index (3.1 +/- 0.2 L/m2/min) (Fick), and echocardiographic ejection fraction (21 +/- 1%). The same was true for cardiopulmonary exercise data (cycle ergometry; up 12.5 W/min): VO2 at VT (9.3 +/- 0.4 ml/kg/min), maximum VO2 (12.2 +/- 0.7 ml/kg/min), VT in percentage of predicted maximum VO2 (31 +/- 2%), heart rate at VT (95 +/- 4 beats/min), and decrease of dead space-to-tidal volume ratio from rest to VT (33 +/- 1 --> 29 +/- 1). Improvement of VO2 at VT after training (2.2 +/- 0.4 ml/kg/min; p <0.001) was not related to baseline central hemodynamics (r = <0.10 for each), but was greater in patients with a lower baseline VO2 at VT (r = -0.65; p <0.01), peak VO2 (r = -0.66; p <0.01), VT in percentage of predicted maximum VO2 (r = -0.74; p <0.001), heart rate at VT (r = -0.63; p <0.01), and smaller decrease of dead space-to-tidal volume ratio from rest to VT (r = 0.65; p <0.01). Ejection fraction after exercise training (24 +/- 2%) and activity restriction (23 +/- 2%) did not differ significantly compared with baseline, and patient status (heart failure and cardiac rhythm) remained stable. Three parameters accounted for 84% of the variance of improvement in VO2 at VT: VO2 at VT in percent predicted maximum VO2, decrease of dead space-to-tidal volume ratio, and heart rate at VT. The findings suggest that there was a greater increase in VO2 at VT after exercise training in patients with greater peripheral deconditioning at baseline. The improvement was unrelated to central hemodynamics. Clinically stable patients with severe chronic congestive heart failure, potential heart transplant candidates, and those awaiting transplantation may benefit from involvement in a short-term exercise training program.
Exercise↗
Walking performance and economy in chronic heart failure patients pre and post exercise training.
The effect of a 3-week exercise programme on performance and economy of walking was analysed in 16 male patients with chronic heart failure [mean age 51.8 (SD 6.9) years, height 174.9 (SD 6.3) cm, body mass 75.3 (SD 11.5) kg, ejection fraction 20.8 (SD 5.0)%]. They were submitted to a cardiopulmonary exercise test on a cycle ergometer and a 6-min walking test on a treadmill before and after the period of exercise training. The training programme consisted of interval cycle (five times a week for 15 min), and treadmill ergometer training (three times a week for 10 min) at approximately 70% cycling peak oxygen uptake (VO2peak) and supplementary exercises (three times a week for 20 min). Compared to the pre values cycling VO2peak [11.9 (SD 2.9) vs 14.0 (SD 2.3) ml. kg-1.min-1], maximal self paced walking speed [0.68 (SD 0.33) vs 1.16 (SD 0.30) m.s-1], and net walking power [2.16 (SD 0.89) vs 2.73 (SD 0.91) W.kg-1] had increased (P < 0.01) while net energy cost [3.31 (SD 0.66) vs 2.33 (SD 0.38) J.kg-1. m-1] had decreased (P < 0.001) after the training period. Approximately 42% of the increase of walking speed resulted from a higher walking power output, whereas approximately 58% corresponded to a positive effect on walking economy. The improvement in walking economy was a function of an increase in walking velocity itself and a result of a more efficient walking technique. These results would indicate that in patients with marked exercise intolerance, adequate exercise training programmes could contribute to favourable metabolic changes with positive effects on the economy of motion.
Cardiac Output, Low↗
Moderate exercise leads to decreased expression of beta1 and beta2 integrins on leucocytes.
Intravascular adhesion of leucocytes plays a role in the pathogenesis of acute and chronic vascular disease. Regular aerobic exercise seems to protect against vascular disease. Since leucocyte adhesion is mediated by integrins, we tested the hypothesis that surface expression of the integrin adhesive receptors LFA-1 (cd11a/cd18), MAC-1 (cd11b/cd18), gp 150/95 (cd11c/cd18), and VLA-4 (cd29/cd49) is decreased by moderate endurance exercise. Surface expression of integrins was measured by FACS analysis in 19 healthy subjects (16 males, 3 females, 36.6 +/- 8.7 years, 177.1 +/- 7.5 cm, 70.3 +/- 8.1 kg) before and after submaximal exercise (3 h run) using monoclonal antibodies against cd11a, cd11b, cd11c, cd18, cd29 and cd49. In addition, we compared resting integrin expression in this group with a group of sedentary subjects (19 males, 6 females, 29.3 +/- 5.3 years). White blood cell count increased from 5300 ml(-1) to 9740 ml(-1) during exercise (P < 0.001). Nevertheless, the expression (indicated by the mean log fluorescence) of cd11a (94 +/- 24 vs. 78 +/- 14) and cd18 (128 +/- 31 vs. 102 +/- 21) on lymphocytes and of cd11a (104 +/- 25 vs. 85 +/- 16), cd11c (497 +/- 171 vs. 408 +/- 126) cd29 (109 +/- 16 vs. 89 +/- 16), cd49 (69 +/- 8 vs. 54 +/- 11) on monocytes was decreased after exercise (all P < 0.05). In contrast, integrin expression on granulocytes was not altered by exercise. Comparison of exercising and sedentary subjects showed a significantly decreased expression of integrins in exercising subjects. Our results demonstrate that moderate exercise leads to decreased expression of integrin receptors on leucocytes. This decreased expression of adhesion molecules may result in decreased adhesion and infiltration of leucocytes into the vessel wall. This phenomenon may play a role in the beneficial effect of moderate exercise in prevention of acute and chronic vascular disease.
Adult↗