Endurance training attenuates exercise-induced oxidative stress in erythrocytes in rat

The aim of this study was to investigate whether endurance training reduces exercise-induced oxidative stress in erythrocytes. Male rats (n=54) were divided into trained (n=28) and untrained (n=26) groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h·day^–1, 5 days a week for 8 weeks, reaching the speed of 2.1 km·h^–1 at the fourth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km·h^–1 at the 95th min, 10% uphill, and was continued until exhaustion. Acute exhaustive exercise increased the erythrocyte malondialdehyde level in sedentary but not in trained rats compared with the corresponding sedentary rest and trained rest groups, respectively. While acute exhaustive exercise decreased the erythrocyte superoxide dismutase activity in sedentary rats, it increased the activity of this enzyme in trained rats. On the other hand, acute exhaustive exercise increased the erythrocyte glutathione peroxidase activity in sedentary rats; however, it did not affect this enzyme activity in trained rats. Erythrocyte glutathione peroxidase activity was higher in trained groups compared with untrained sedentary group. Neither acute exhaustive exercise nor treadmill training affected the erythrocyte total glutathione level. Treadmill training increased the endurance time in trained rats compared with sedentary rats. The results of this study suggest that endurance training may be useful to prevent acute exhaustive exercise-induced oxidative stress in erythrocytes by up-regulating some of the antioxidant enzyme activities and may have implications in exercising humans.     

Lack of fibrin formation in exercise-induced activation of coagulation.

Strenuous physical exercise leads to a significant shortening of blood clotting in various test systems. Such short times are also characteristic of those observed in sedentary patients with thrombosis or disseminated intravascular coagulation, and of those observed in experimental animals after thrombin infusion. The patients exhibit an increase in circulating fibrinopeptide A, which is attributed to thrombin action on circulating fibrinogen, and to an increase of fibrinogen degradation products, which is thought to indicate reactive fibrinolysis. To check whether physical exercise leads to fibrinemia, 10 healthy male volunteers were subjected to strenuous exercise on a bicycle ergometer. Blood samples were taken immediately before and on completion of the exercise period. Despite a significant shortening of the activated partial thromboplastin time, the thrombin time, and the Reptilase time, no increase of fibrinopeptide A could be demonstrated and the ethanol gelation test remained consistently negative. Simultaneously, the euglobulin lysis time was significantly shortened, whereas the fibrin(ogen) degradation products did not increase. The results indicate that the shortening of the coagulation times associated with physical exercise must be explained by mechanisms other than thrombin-mediated conversion of fibrinogen to fibrin.     

Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats

Even though exhaustive exercise-induced oxidative stress increases the risk of tissue damage, regular endurance training is widely assumed to improve cardiac function and protects against heart disease. We tested the hypothesis that an endurance training program prevents exhaustive exercise-induced increases in cardiac dysfunction and apoptosis in left ventricle (LV). Thirty-two male Sprague-Dawley rats were randomly divided into four groups: sedentary control (C), trained (T), exhaustively exercised (E), and trained plus exhaustively exercised (TE). Rats in T and TE groups ran on a motorized treadmill for 12 weeks. Rats in groups E and TE performed an exhaustive running test on a treadmill. The main effects of training were indicated by increased running time to exhaustion (80 ± 5 and 151 ± 13 min for groups E and TE, respectively, P = 0.0001), myocardial hypertrophy (0.38% and 0.47% for untrained and trained rats, respectively, P = 0.0002), decreased LV ejection fraction (88% and 71% for untrained and trained rats, respectively, P < 0.0001), accelerated mitochondrial DNA 4834-bp large deletion (mtDNA⁴⁸³⁴ deletion), and up-regulated protein levels of heat shock protein-70, cytochrome C, cleaved capsase-3, and cleaved PARP in LV following a bout of exhaustive exercise. Contrary to our hypothesis, these results suggest that endurance training induced significant impairment of regional systolic and diastolic LV myocardial function and ejection fraction in rats. Our findings show that endurance training accelerates exhaustive exercise-induced mtDNA⁴⁸³⁴ deletion and apoptosis in the LV.     

Endurance training regimen based upon arterial blood lactate: Effects on anaerobic threshold

Summary The purpose of this investigation was to assess the effect of endurance training based upon the intensity as determined by the arterial blood lactate concentration (LA). Seven healthy male college students performed endurance training on a Monark bicycle ergometer for 15 min on 3 days/week for 8 weeks, at an intensity corresponding to 4 mmol·l⁻¹ arterial blood LA determined during an incremental exercise test (25 watts increment every minute on a bicycle at 50 rpm). Another six male students served as the control group. To assess the training effect, both an incremental exercise test and a submaximal exercise test were performed before and after the endurance training. In the incremental exercise test, at , anaerobic threshold (AT), and the onset of respiratory compensation for metabolic acidosis (RCMA) were measured. AT was determined as the point at which arterial LA rose above the resting value, and RCMA was determined as the point at which Paco₂ decreased during the incremental exercise test. After training, AT increased significantly (37% increment expressed in ,p<0.05). There was a significant increase (p<0.05) in RCMA (17%) and (14%). This training decreased (4%), (15%), heart rate (10%), respiratory exchange ratio (5%), and LA (23%) significantly (p<0.05) during the submaximal exercise test after training. On the other hand, there were no significant changes in the control group through the period when the training group performed their training. These results showed that the endurance training intensity corresponding to 4 mmol·l₋₁ arterial blood LA was effective for the improvement in AT as well as . It is suggested that the present training regimen could delay the onset of anaerobic glycolysis, thus shifting AT to the higher workload and decreasing LA at a given submaximal exercise after training.     

Endurance training reduces exercise-induced acidosis and improves muscle function in a mouse model of sickle cell disease

Sickle cell disease (SCD) mice (Townes model of SCD) presented exacerbated exercise-induced acidosis and fatigability as compared to control animals. We hypothesize that endurance training could represent a valuable approach to reverse these muscle defects. Endurance-trained HbAA (HbAA-END, n = 10), HbAS (HbAS-END, n = 11) and HbSS (HbSS-END, n = 8) mice were compared to their sedentary counterparts (10 HbAA-SED, 10 HbAS-SED and 9 HbSS-SED mice) during two rest – exercise – recovery protocols during which muscle energetics and function were measured. In vitro analyses of some proteins involved in muscle energetics, pH regulation and oxidative stress were also performed. Exercise-induced acidosis was lower in HbSS-END mice as compared to their sedentary counterparts during both moderate (p < 0.001) and intense (p < 0.1) protocols. The total force production measured during both protocols was higher in trained mice compared to sedentary animals. In vitro analyses revealed that enolase/citrate synthase ratio was reduced in HbSS-END (p < 0.001) and HbAS-END (p < 0.01) mice compared to their sedentary counterparts. In addition, malondialdehyde concentration was reduced in trained mice (p < 0.05). In conclusion, endurance training would reverse the more pronounced exercise-induced acidosis, reduce oxidative stress and ameliorate some of the muscle function parameters in SCD mice.     

The effect of running training on exercise-induced asthma

A running training program had no effect upon the severity of exercise-induced asthma, however, it appeared as if the children benefitted not only from a decrease in the frequency and duration of asthma in daily life, but also by improvement in self-confidence and ability to participate in group activities.     

The influence of intrinsic coagulation pathway on blood platelets activation by oxidized cellulose

Oxidized cellulose is an effective hemostat that works naturally to aid in blood coagulation. The mechanism of its action is not very well understood. Little effect on blood coagulation, but a pronounce decrease in platelet count has been reported upon the addition of the oxidized cellulose to the whole blood. As a marker of platelet activation and aggregation we used serotonin release reaction and turbidity changes in time. We found that oxidized cellulose did not activate washed platelets reconstituted in plasma-free medium or plasma-free medium with fibrinogen; no reduction of platelet count was observed. Serotonin release in platelet-rich plasma incubated with oxidized cellulose started in the range from 5 to 10 min. Serotonin release from platelets reconstituted in plasma deficient in either coagulation factor V, VIII, IX, or XII was delayed. Blood platelets activation by oxidized cellulose requires calcium ions present in dispersion of oxidized cellulose. Factor XIII deficiency had no influence on blood platelets activation by oxidized cellulose. Our results clearly indicate the significance of intrinsic coagulation pathway activation on blood platelets activation by oxidized cellulose and so indirectly on the hemostyptic effect of oxidized cellulose.     

Adsorption of coagulation proteins from whole blood on to polymer materials: relation to platelet activation.

A combination of methods, immunoassays of plasma proteins and platelet release of beta-thromboglobulin and chromogenic substrates for enzymatically active coagulation factors, was used to measure the reactions of coagulation proteins upon contact between whole blood and artificial surfaces as a function of time and surface material. Four types of well-known polymer surfaces, polyvinylchloride, polytetrafluoroethylene, polyurethane and silicone rubber, were investigated to elucidate if a simple and fast in vitro experimental set-up can be of guidance in the selection of materials for use in vivo. Platelets were activated at the polymer surfaces whereas the coagulation enzymes showed little activity on the polymer surfaces tested. There was a correlation between the adsorption of adhesins (fibrinogen, fibronectin and factor VIII-related antigen) at the surfaces and the release of beta-thromboglobulin from platelets, suggesting that adsorption of adhesins is a major determinant of blood compatibility of polymer materials. Significant differences between the surfaces were seen--polyurethane being the surface with the least protein adsorbed and least platelet activation initiated. This study shows that it is possible to make a first in vitro choice of possible blood compatible artificial surfaces before expensive and cumbersome in vivo experiments.     

Hydroxyapatite formed on/in agarose gel induces activation of blood coagulation and platelets aggregation

We reported earlier that hydroxyapatite (HA) formed on/in agarose gels (HA/agarose) produced by alternate soaking process is a bone-filling material possessing osteoconductive and hemostatic effects. This process could allow us to make bone-like apatite that was formed on/in organic polymer hydrogel matrices. Here, we investigated the mechanism of hemostasis induced by HA/agarose and found that HA/agarose, but not agarose or HA powder, significantly shortened activated partial thromboplastin time (APTT). While HA/agarose did not show significant platelet aggregation, it markedly enhanced adenosine diphosphate (ADP)-induced platelet aggregation. Moreover, Western blot analysis revealed selective adsorption of vitronectin onto HA/agarose. We also observed marked differences between HA powder and HA/agarose in their XRD patterns. The crystallinity of HA powder was much higher compared to that of HA/agarose. Furthermore, 50-100 nm of tube-form aggregations was observed in HA powder on the other hand 100-200 nm of particles was observed in HA/agarose by SEM observation. Thus 100-200 nm of low crystallized particles on the surface structure of HA/agarose may play an important role in hemostasis. Our results demonstrated a crucial role of HA/agarose in the mechanism of hemostasis and suggested a potential role for HA/agarose as a bone-grafting material.     

Interoceptive regulation of blood coagulation

Summary In the majority of cases injection of horse serum into the perfusate of the carotid sinus of normal dogs causes no reflex change of coagulation time. However, if the same stimulus is administered to previously sensitized dogs a reflex increase of coagulation time takes place. This prolongation is most pronnounced in 10 minutes. In a number of cases, this delay in blood coagulation is replaced by its acceleration. Preliminary vagotomy removes reflex delay of blood coagulation.Presented by Active Member AMN SSSR V. N. Chernigovskii     

Interoceptive control of blood coagulation

Summary Nicotine or acetylcholine stimulation of the carotid sinus in dogs shortens the coagulation time of the blood. The time of clotting is the shortest 20–30 minutes after the start of stimulation. Perfusion of the carotid sinus with the sinus nerve intact and no stimuli applied, as well as the injection into the denervated zone of nicotine or acetylcholine caused no reflex change of the clotting time. Experiments with the celiac nerve indicate that the secretion of adrenalin by the adrenal glands is an important, though not the sole factor in the reflex effect of the carotid sinus chemoreceptors on the blood coagulation time.Presented by Prof. V. N. Chernigovsky, Active Member of the AMS USSR     

The effect of substrate molecular mobility on surface induced immune complement activation and blood plasma coagulation

Changing the length of the alkyl ester side chain in poly(alkyl methacrylates) provides a unique opportunity to systematically vary the mobility of the polymer chains, or in other words vary the glass transition temperature (T(g)), without greatly affect the solid surface energy (gamma(s)) of the polymer. A series of poly(alkyl methacrylate) coatings was therefore analysed with regard to the human immune complement (IC) activation and the surface associated blood plasma coagulation cascade (CC) properties. For the IC and CC measurements we used a quartz crystal microbalance (QCM) where we modified the chemistry of the sensor surface by applying 10-30 nm thick poly(alkyl methacrylate) coatings. The surface energy was calculated from water contact angles and small differences between the coatings were observed. The surface chemistry of the coatings, as determined with X-ray photoelectron spectroscopy (XPS), showed no deviation from expected compositions. Tapping mode atomic force microscopy (TM-AFM) measurements revealed that all coatings displayed similar morphology and the roughness was in the range of 0.7-0.9 nm. Increased polymer mobility correlated with a decrease in IC activation, measured as a decreased C3c deposition at the surface. The surface induced CC, measured as fibrin clot formation at the surface, was different between the different coatings but no correlation with molecular mobility was observed. Thus, the molecular mobility of the polymer chains had a major effect on both the IC and the CC and it seems that different aspects of the chemistry of the solid surface regulate activation of the IC and the CC.