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Biomedical subjects

J M Soares

Publications and source records attributed to J M Soares.

17 recordsLinked to original sources
PubMed1999

Exercise-induced signs of muscle overuse in children.

Signs of overuse after intense muscular exertion are well described in adults, while little research has been conducted in children. The aim of the study was to investigate some indirect markers of muscle damage in 13 years old boys following two different protocols of one-leg stepping exercise to exhaustion. This stepping exercise was performed by two experimental groups with different contributions of concentric and eccentric contractions in a 1:1 vs 1:2 ratio of timing. Subjective soreness perception and maximum voluntary isometric force of the knee extensor muscles were measured immediately prior to and immediately following the exercise, and at 1, 3, 24, 48, 72, 96 hours post exercise. Metabolic markers of exercise stress were taken at similar time intervals and included plasma glutathione concentrations as a marker for oxidative stress, circulating leukocyte numbers, and plasma creatine kinase (CK) activity. All parameters studied demonstrated a higher level of muscular exertion, with more evident signs of overuse in the group with the more eccentric contribution. Complete recovery was achieved between 72 and 96 hours after exertion. However, in this group of boys, the CK activity did not show the typical adult-like increase. Therefore the wide use of CK as an indicator of intense muscle exertion was not supported in this group of children. It can be concluded that children, like adults, experience similar degrees of muscle disturbances following intense exercise and that they may recover more quickly from such exercise.

Adolescent↗
PubMed1998

The impact of soccer training on the immune system.

OBJECTIVE: The aim of this study was to evaluate whether the level of some immune markers changed in soccer players during pre-season and during playing-season. DESIGN: An observational study for one soccer season (one year). SETTING: Professional soccer players. PARTICIPANTS: Thirteen professional soccer players (age: 26.3 +/- 3.7 years). MEASURES: The effect of 11 months of soccer training sessions and matches on circulating leukocyte and lymphocyte subpopulations was investigated. Blood samples were taken before the season and also 6 weeks, 6 months and 11 months later. All samples were taken at 08:00 h. RESULTS: Total lymphocyte counts did not change in all samples. During the pre-season, however, the concentrations of some inflammatory lymphocyte subpopulations were changed: CD4CD45RA+ was elevated and CD57 and CD8CD57 showed a significant decrease (p < 0.05), At the competitive period, CD4 and CD8 were increased. At the end of the season there were significant changes in some immune cells: total leukocyte and neutrophil number and CD8+ cell concentration was increased compared to pre-season values and the CD4/CD8 ratio was decreased. CONCLUSIONS: The results suggest that athletes exposed to a long-term training periods can exhibit variations in some immune cells. The clinical significance of these variations requires more detailed investigation.

Adult↗
PubMed1997

Supplementation of vitamin E may attenuate skeletal muscle immobilization atrophy.

The aim of this study was to investigate whether oxidative stress contributes to the development of atrophy in immobilized muscles, and, under this assumption, whether the administration of an antioxidant has beneficial effects to attenuate immobilization atrophy. One hindlimb of rats was immobilized for eight days, the contralateral leg served as control. One experimental group was supplemented with vitamin E. In the soleus muscle, the glutathione content as an indicator for oxidative stress was measured, and muscle fiber diameters were evaluated to estimate muscle atrophy. The biochemical results indicate no pronounced oxidative stress in the immobilized muscles and even less oxidative stress in the vitamin E supplemented muscles (with and without immobilization). Eight days of immobilization lead to a 35% atrophy, while with vitamin E the muscles atrophied only by 12%. This difference can be attributed to the action of vitamin E as a scavenger for free radicals and, on the other hand, to an atrophy promoting effect of oxidative stress. Oxidative stress is hypothesized to exist during the initial phase, but to disappear after some days of immobilization. It is suggested that oxidative stress plays a role in initiating muscle atrophy, and supplementation of vitamin E prior to and during the early phase of immobilization is recommended. Moreover, such may also be useful during remobilization to avoid additional oxidative stress with rehabilitative exercise.

Animals↗
PubMed1997

Forensic nursing in Pakistan. Bridging the gap between victimized women and health care delivery systems.

1. Women's issues tend to be more pronounced in developing countries, where they include extreme limited resources, poor communication, vast distances, individual and community poverty, and lack of education. 2. Empowerment of victimized women depends on support, information, resources, creativity, and positive self-concept. 3. Through support, understanding, effort, and determination, the forensic nurse and Pakistani women can translate a vision into reality by the integration of victimized women into all aspects of society.

Female↗
PubMed1997

Administration of tourniquet. I. Are edema and oxidative stress related to each other and to the duration of ischemia in reperfused skeletal muscle?

One hindlimb of mice was subjected to 60, 90 and 120 min ischemia by application of a tourniquet followed by a 60-min reperfusion period. An additional experimental group received a tourniquet for 90 min without subsequent reperfusion. The soleus muscle (from the contralateral side also as control) was removed and evaluated for muscle weight, protein weight, protein content, and glutathione concentrations. Ischemia alone without subsequent reperfusion did not produce significant changes. With postischemic reperfusion, the protein content and muscle weight increased, probably because of an increased capillary permeability, leading to muscle edema. Oxidative stress was also present during reperfusion, correlating well with the changes in protein content. The intensity of these alterations appeared to depend on the period of ischemia.

Animals↗
PubMed1997

Administration of tourniquet. II. Prevention of postischemic oxidative stress can reduce muscle edema.

An experimental group of mice were subjected to a hindlimb tourniquet for 90 min followed by 60 min postischemic reperfusion (ischemia/reperfusion, I/R). Two further groups with the same experimental procedure received allopurinol to inhibit endothelial xanthine oxidase to produce oxygen free radicals (I/R-allo) or vitamin E as a radical scavenger (I/R-vitE). The soleus muscle was examined, and the contralateral muscle served as control. Glutathione (both reduced and oxidized forms, GSH and GSSG) concentrations and the relative protein content were measured. Additionally, the muscles were examined under the electron microscope for pathological alterations. The results showed: (i) the existence of much oxidative stress in the I/R group, but not in the I/R-allo and I/R-vitE groups; (ii) an increased protein content indicative for high capillary permeability in the I/R group, but not in the I/R-allo and I/R-vitE groups; (iii) considerably fewer capillary endothelial disturbances in the I/R-allo and I/R-vitE groups than in the I/R group. We conclude that allopurinol and vitamin E diminished the occurrence of oxidative stress and of edema in postischemic skeletal muscle.

Animals↗
PubMed1997

[Is autonomic control of the heart rate at rest altered by detraining? A study of heart rate variability in professional soccer players after the pretraining period and after the preparatory period for competitions].

The aim of this study was to assess the influence of detraining and training on the autonomic control of heart rate (HR), using time and frequency (spectral analysis) domain components of heart rate variability. Sixteen professional football players (26.7 +/- 3.8 years; 74.9 +/- 4.1 kg; 177 +/- 6.3 cm) were analysed at the end of a 1 month holiday (detraining) and after a 6 week training period (training). HR was recorded over 15 minutes with Holter equipment. The athletes rested in a supine position, in a quiet place and all test were performed between 8 and 10 AM. The subjects were requested to refrain from meals or caffeine for 12 hours before testing. In spite of the high intensity of the training period, there was no significant change in results from detraining condition to training condition. These results can have two possible explanations: (i) the high level of cardiovascular capacity in the detraining trial originated by the recreative physical activity that the players underwent during their holidays, and/or (ii) the training period was not long enough to promote any relevant effect on the autonomic control of HR.

Adaptation, Physiological↗
PubMed1994

Do invading leucocytes contribute to the decrease in glutathione concentrations indicating oxidative stress in exercised muscle, or are they important for its recovery?

Mice were subjected to one session of strenuous running exercise and their soleus muscles were examined in respect of changes in ultrastructure and to their concentration of reduced glutathione [GSH] which are indicators of oxidative stress. It was hypothesized that invading leucocytes contributed to oxidative stress and they were functionally inhibited in one experimental group by the administration of colchicine. Exercise led to an immediate decrease in [GSH] of about 60%, which slowly recovered during 96 h after exercise. With the administration of colchicine after exercise, [GSH] was higher than in the untreated exercise group 48 h after exercise, indicating an inhibition of the ability of leucocytes to produce oxidative stress. However, at 96 h after exercise, [GSH] was lower in the treated exercise group than in the untreated group. The morphological evaluation of the percentage of affected fibres showed that the invasion of leucocytes increased muscle fibre damage. The results suggested that invading leucocytes enhanced production of reactive species of oxygen that may have participated in inducing muscle damage. However, inhibition of leucocyte invasion did not permit their scavenger action of removing cell debris, which appeared to produce even more oxidative stress in the muscle.

Animals↗
PubMed1993

Skeletal muscle damage during tourniquet-induced ischaemia. The initial step towards atrophy after orthopaedic surgery?

Muscle biopsies from the vastus lateralis muscle of patients who had undergone anterior cruciate ligament surgery under conditions of tourniquet-induced ischaemia were examined under the electron microscope at different periods of time up to 90 min of ischaemia. The severity of the alterations in ultrastructure appeared to depend on the period of ischaemia. The pathological changes consisted of accumulation of lysosomes, persistent intrafibre oedema, and some extracellular oedema. Signs of fibre necrosis were found after 90 min of ischaemia. Capillary ultrastructure was only altered with regard to some swelling of the endothelium and marked thickening of the basement membrane. It was concluded that skeletal muscle could be severely affected even during relatively short periods of ischaemia, which might facilitate the development of muscle atrophy during immobilization after orthopaedic surgery.

Adult↗
PubMed1993

The possible role of intracellular Ca2+ accumulation for the development of immobilization atrophy.

Little is known about the cellular mechanisms which induce the development of skeletal muscle immobilization atrophy. Initial disturbances in cellular homeostasis seem to occur very early during immobilization. The aim of the study was to investigate whether loss of calcium homeostasis might be of etiological importance for atrophy. Therefore a calcium channel blocker (nifedipine) was administered to mice immobilized for four days, and their soleus muscle was investigated comparatively to immobilized animals without nifedipine. The immobilized muscles showed an atrophy of about 15% which was not the case in nifedipine-treated immobilized muscles. Ultrastructural alterations (lysosomes, mitochondrial damage) were found predominantly in the immobilized muscles, but rarely with nifedipine. It was concluded that nifedipine protected the muscle fibers probably against calcium overload, thereby avoiding an autophagic response and an impairment of mitochondrial respiratory function.

Animals↗
PubMed1993

Endothelium-derived oxidative stress may contribute to exercise-induced muscle damage.

In exercise-induced muscle damage, oxidative stress derived from the liberation of reactive oxygen species (ROS) is assumed to be of etiological importance. Xanthine oxidase (XO) located in capillary endothelium is one of the possible sources for ROS, mainly investigated so far under conditions of ischemia/reperfusion. XO can be inhibited by allopurinol. To investigate the contribution of XO for the oxidative stress-induced development of muscle damage, mice were subjected to a single bout of exhaustive running exercise. Another exercised group received allopurinol. The reduced form of glutathione (GSH) was measured to estimate the amount of oxidative stress in soleus muscle, and the same muscle was examined in the light and electron microscope at different periods of time (0, 48, 96 h) after exercise. While exercise alone resulted in a marked reduction of GSH indicative for oxidative stress, which only recovered at 96 h, the administration of allopurinal to exercised animals induced a complete recovery already at 48 h after exercise. Muscle damage was more pronounced in the exercised animals which had not been treated with allopurinol. It is concluded that endothelium-derived ROS contribute reasonably to oxidative stress to exercised muscle and to fiber and capillary damage.

Allopurinol↗
PubMed1992

Nifedipine diminishes exercise-induced muscle damage in mouse.

The purpose of this study was to evaluate the effects of a calcium channel blocker (nifedipine) on the severity of muscle damage induced by intensive exercise. Male Charles River mice were assigned to four groups (8 mice/group): normal control (C), nifedipine (N), nifedipine and exercise (N + E) and exercise (E). The animals of the C group were not submitted to any exercise nor to drug administration. The animals of the N group received 1 mg.kg-1 per day of nifedipine (Adalat 10 mg, Bayer AG), per os, during 3 days. The mice of the N + E group were submitted to a treadmill run (0 degree slope) at 1000 m.h-1 (80% of their maximal speed) for 1 hour. In this group, the administration of the drug was under the same conditions as for the N group. The administration started 24 h before the run. The E group was submitted to the same exercise protocol as the animals of N + E group. The soleus muscle was excised for light and electron microscopic evaluation using routine histological techniques. In the C and N groups no morphological alterations were detected. In the E group the number of alterations of striated pattern was twice that in the N + E group. The number of fibres with central nuclei was 35% in the E group but only 8% in the N + E group. The total number of damaged fibres was significantly higher in the E group. The results suggest that nifedipine may give protection to exercise-induced skeletal muscle damage in mouse, probably because the blocking of channels impaired Ca2+ influx; and the results of this study therefore confirm earlier contentions about the possible role of calcium ions in producing muscle damage after work.

Animals↗
PubMed1992

Exercise, muscle damage and fatigue.

Fatigue as a functional sign and muscle damage as a structural sign can be observed after prolonged exercise like marathon running or after strenuous exercise, especially with the involvement of eccentric contractions. For fatigue due to prolonged exercise, hypoxic conditions and the formation of free oxygen radicals seem to be of aetiological importance, resulting in an elevated lysosomal activity. Eccentric exercise of high intensity rather results in a mechanical stress to the fibres. Although these different mechanisms can be discerned experimentally, both result in similar impairments of muscle function. A good training status may attenuate the clinical signs of fatigue and muscle damage. The symptoms and events occurring during delayed onset of muscle soreness (DOMS) can be explained by a cascade of events following structural damage to muscle proteins.

Animals↗
PubMed1992

Effects of training on muscle capillary pattern: intermittent vs continuous exercise.

The effects of two exercise regimens (intermittent and continuous endurance) on the fiber area, and capillarization of mice skeletal muscle (gastrocnemius) was studied. The training programs had a duration of 30 days, 5 days/week, and was performed on a motor-driven treadmill. The intermittent group performed the exercise at 16 m.min-1 with a slope of 5%. The continuous group performed the exercise at 16 m.min-1 with 0%. The fiber area and the capillarization was evaluated in the white portion of the gastrocnemius. A high degree of hypertrophy was observed, and a significant increase in the capillary density, capillary to fiber ratio, and in the number of capillaries sectioned obliquely and/or longitudinally was found. The results suggest that the endurance training, intermittent or continuous, induce cell hypertrophy, and an increase in capillarization especially, based on an alteration of the structural pattern.

Animals↗
PubMed1991

Effects of training and an anabolic steroid on murine red skeletal muscle. A stereological analysis.

The purpose of this study was the evaluation of changes induced by training (swimming 1 h/day, 5 days/week, 6 weeks) and an anabolic hormone (nandrolone decanoate, intramuscular injections of 15 mg.kg-1 per week) on fiber size, capillarization and mitochondrial fraction of murine soleus muscle. The animals (n = 32) were divided into 4 groups: a control group (C), that received the arachis oil carrier; a steroid group (S), that received the hormone; a training group (T), and a group that was submitted to training and to the administration of hormone (S + T). The soleus muscle was selected for quantitative light- and electron-microscopic evaluation. The muscle fiber size was increased in group T and decreased in groups S and S + T. The axial length of capillaries per unit volume of muscle decreased significantly in groups S and T. The number of capillaries per number of fibers showed a significant decrease in groups S and S + T and an increase in group T. The mitochondrial content decreased in group S, which suggested that anabolic steroids can be harmful for these organelles. This hypothesis was confirmed by histological evaluation at the electron-microscopic level. Many swollen and disrupted mitochondria were found in groups S and S + T. The results suggest that administration of nandrolone decanoate may have some deleterious effects on the muscle respiratory system (capillaries and mitochondria).

Animals↗