摘要:

The impact of long-term (6-month) moderate exercise on the iron status of previously sedentary women was determined by randomly assigning 62 college-age women into one of the following four groups: 1) 50 mg.d-1iron supplement, low iron diet (N= 16); 2) Placebo, free choice diet (N= 13); 3) Meat supplement to achieve 15 mg.d-1iron intake (N= 13); and 4) Control, free choice diet (N= 20). All groups except the Control group exercised 3 d.wk-1at 60%–75% of their heart rate reserve. VO2maxwas measured at baseline and week 24. Blood was sampled at baseline and every 4 wk thereafter for 24 wk to measure iron status and to elucidate the causes for alterations in iron status. Subjects had depleted iron stores throughout the study as indicated by their serum ferritin levels (<15 ng.ml-1). Serum iron, total iron binding capacity and transferrin saturation were not compromised with exercise. Mean hemoglobin level in the Placebo/Ex group was significantly (P< 0.05) lower than the 50 Fe/Ex and the Meat/Ex groups by week 24. However, changes in serum albumin, haptoglobin, and erythropoietin data from the study cannot explain these changes.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

We examined the acute and chronic effects of changes in training volume and intensity on the blood lymphocyte percentages and immunoglobulin levels in runners. Twelve runners participated in four 10-d phases of low volume/low intensity (LV/LI), high volume/low intensity (HV/LI), or high volume/high intensity (HV/LI) running. Subjects were assigned to one of two different training group orders: 1) LV/LI, HV/LI, LV/LI, HV/HI; or 2) LV/LI, HV/HI, LV/LI, HV/LI. Venous blood was drawn at rest on days 1, 4, and 7; and 5 min post-exercise on days 1 and 7 of each 10-d phase. Lymphocyte subsets were determined by flow cytometry for CD3+, CD4+, CD8+, and HLA-DR+, IgA, IgG, and IgM levels were obtained by ELISA analysis. Immunoglobulin, CD8+ and HLA-DR+ levels, and pre-exercise plasma cortisol concentrations were not significantly affected by alterations in volume or intensity. A transient decrease (P< 0.05) was observed in CD4+ and the CD4/CD8 ratio 5 min post-exercise during the HV/LI and HV/HI phases. Results indicate that the exercise-induced lymphocyte subset reduction is transient and suggest that it is more dependent upon training intensity than volume, and the training order of exposure to the high-intensity stimulus may determine the magnitude of subsequent responses.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Clenbuterol is a recently popular drug used by athletes in many sports for its purported anabolic effects and reduction of subcutaneous fat. It is a beta-2 (β2) agonist prescribed overseas as a bronchodilator, but not approved for use in this country. It is on the banned substance list of the United States Olympic Committee. To avoid any erosion of confidence, physicians caring for athletes need accurate information regarding clenbuterol. Such information is unavailable within the routine medical environs. A review of the literature of animal husbandry reveals that this drug, when administered in doses far greater than those required for bronchodilation, does indeed increase the deposition rate of lean mass and retard adipose gain. There are no human studies available. Animal studies were conducted on laboratory and slaughter stock. No investigation into long-term cardiovascular side effects has been undertaken. The rate of extrapolation from animal studies to unsupervised human usage is alarming. If this category of drugs does preserve lean mass in humans, there are legitimate medical applications. Trials of efficacy and safety are needed.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

There is extensive vasodilation of arterial vasculature in heart and active skeletal muscle during exercise. Considerable knowledge concerning mediators of this vasodilation which act directly on vascular smooth muscle has been acquired. Less well-understood is the role that mediators that act via vascular endothelium may play in exercise-induced vasodilationin vivo. Nonetheless, many studies have been conducted, both on blood vesselsin vitroand in resting animalsin vivo, since the discovery of endothelial-derived relaxing factor (EDRF) in 1980. In fact, several EDRF have been defined, of which nitric oxide (NO) appears to be most important. Release of NO from vascular endothelium can be induced by two general classes of stimuli, pharmacologic and physical. Of the former class, a physiologically relevant example is norepinephrine. In the latter class, elevated shear stress due to increased blood flow associated with exercise could be a stimulus for NO release. This symposium examines the role that endothelium may play in vasodilation of the coronary and skeletal muscle circulations during acute exercise. It also addresses the question of whether exercise training modifies this role of vascular endothelium.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Nitric oxide (NO) is a vasodilator produced under normal physiologic conditions primarily by the vascular endothelium lining all blood vessels. The primary stimulus for the production of nitric oxide by the constitutive endothelial nitric oxide synthase (ECNOS, Type II) found in blood vessels is most likely the shear stress, the frictional force, caused by blood flowing through blood vessels. During exercise there is an increase in cardiac output and redistribution of blood flow to increase blood flow in skeletal muscle and in the coronary circulation. These adjustments provide increased oxygen delivery to support aerobic energy production and to sustain the exercise response. NO may be involved in the regulation of vascular tone in exercising skeletal and cardiac muscle by promoting, enhancing the metabolic vasodilation. In addition, the production of NO by capillary endothelium may regulate oxygen consumption by mitochondria through chemical interactions between NO and the iron-sulfur center of these enzymes. Finally, brief exercise training may alter the gene expression for the enzyme, the constitutive endothelial NO synthase, which forms NO and may be part of the vascular adaptation seen after aerobic exercise training. Furthermore, if there is a genetic predisposition to produce NO, as in world class athletes or animals bred to race, NO may contribute to spectacular exercise performance. These three potential roles of NO will be discussed and data presented to support each of these in our review.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The purpose of this paper is to examine the role of endothelium-derived relaxing factors in the control of coronary vascular resistance in conditioned subjects (i.e., after exercise training for a period of time sufficient to complete adaptation processes). Results from studies with exercise trained (EX) dogs, miniature swine, and rats are summarized. Since the relative importance of vascular control mechanisms differ in various segments of the coronary arterial tree, the effects of EX on conduit arteries and the coronary arterial microcirculation are discussed separately. Results indicate that endothelium-mediated vasodilator responses are normal in conduit coronary arteries of EX dogs, miniature swine, and rats. It is proposed that endothelium-mediated vasodilation of conduit coronary arteries is enhanced early in the exercise-adaptive process but returns to normal as adaptation to EX is complete, when structural adaptations produce a relative decrease in coronary shear during exercise. EX miniature swine manifest enhanced endothelium-mediated vasodilation stimulated by bradykinin and flow in isolated coronary resistance arteries and appear to have increased expression of NO synthase (ecNOS). Brief training also appears to increase the expression of ecNOS. The role of endothelium-mediated vasodilation in regulation of coronary blood flow in EX animals remains uncertain.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Blood flow (BF) to active muscle increases dramatically during exercise. This increase in BF is permitted by relaxation of smooth muscle (and ensuing vasodilation) in the vasculature of muscle tissue. Recently, attention has focused on the possible role of the endothelium-derived relaxing factor nitric oxide (EDNO) in the vasodilation of muscle vasculature during exercise. A variety of experimental approaches have been used in elucidating the role of EDNO. These include isolated vessel, isolated muscle or muscle group, and conscious exercising animal preparations. Studies utilizing isolated vessels have shown that arterioles from muscle dilate, in an endothelium-dependent manner, to stimuli present during exercise (e.g., increased flow rates). A limitation of such studies, however, is that only the potential for EDNO-induced vasodilation is indicated. The isolated muscle/muscle group approach has consistently demonstrated a role for EDNO in determining resting BF. Findings for muscle BF during contractions are equivocal. A limitation of this approach is that exercise is simulated by stimulating the motor neuron of the muscle of interest. Since this type of muscle activity elicits a relatively small active hyperemia, it may be that a role for EDNO in exercise-induced hyperemia is masked. Findings from exercising animals are equivocal. Some studies demonstrate a role for EDNO in permitting increased muscle blood flow during exercise, while others show no impact of inhibition of EDNO synthesis. Some studies suggest that the importance of EDNO may vary with the muscle (and its fiber type composition) studied. Additional research is needed to clarify the role of EDNO in mediating increased BF to skeletal muscle during exercise.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Endurance training results in peripheral vascular adaptations in skeletal muscle which enhance perfusion and vascular flow capacity. These adaptations could result from structural modifications of the vasculature and/or alterations in the control of vascular tone. One potential mechanism through which vascular control may be modified is through adaptive changes in the intrinsic responsiveness of vascular endothelium. Experiments have demonstrated that vascular responsiveness to endothelium-dependent vasodilators are enhanced in exercise-trained animals. The enhanced endothelium-dependent relaxation appears to be mediated through elevations in the formation of endothelium-derived nitric oxide. Training also results in a decreased sensitivity to the vasoconstrictor effects of norepinephrine. This alteration appears to be due to an endothelium-dependent mechanism involving α2-adrenergic receptors. One stimulus that appears to be important in initiating the adaptation of the endothelium to training is the increase in muscle blood flow and shear stress which occurs during exercise. However, other factors associated with exercise may be necessary to induce endothelial adaptations produced by endurance training. Further research is needed to determine the significance of changes in endothelium-dependent vascular responsiveness and whether this is associated with training-induced increases in muscle perfusion and vascular flow capacity.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The coordination of blood flow control in exercising skeletal muscle is exemplified by the interaction among muscle fibers, nerves, and the smooth muscle and endothelial cells which comprise the resistance vasculature. During functional hyperemia in active muscle, maximal flow exceeds resting values by 10− to 50-fold, according to muscle fiber type and recruitment pattern. The control of muscle blood flow is coordinated among many vessel branches, encompassing the resistance arteries external to the muscle and the arteriolar network embedded within the tissue. As motor unit recruitment and metabolic demand increase with exercise intensity, the locus of blood flow control “ascends” from distal arterioles, which govern capillary perfusion and flow distribution, into the proximal arterioles and feed arteries, which control the volume of flow into a muscle. The organization of vasomotor responses within and among resistance vessels can be explained by the spread of electrical, chemical, and physical signals between endothelial and smooth muscle cells. These signals are triggered by substances released from muscle fibers and nerve terminals and by changes in transmural pressure and luminal flow. Thus, from several perspectives, cell-to-cell communication coordinates blood flow control in accord with the metabolic demands of active muscle fibers.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The endothelium has been shown to contribute to the modulation of vascular smooth muscle tone. Using digital imaging microscopy, we measured calcium in endothelial cells of isolated skeletal muscle arterioles. First-order arterioles (N= 6) were isolated from rat cremaster muscle and cannulated. All vessels developed spontaneous tone (99.4 μm; 60%–80% of passive diameter). Endothelial cells were loaded with Fura-2-AM (5 μM), a ratiometric calcium-sensitive fluorescent dye. The Fura-2-AM was placed in the lumen of the vessel for approximately 10 min and removed. Fluorescent images of endothelial cells were acquired following excitation at 340− and 380-nm wavelengths and the data expressed as the 340/380 ratio which is directly proportional to intracellular calcium. Acetylcholine (Ach; 10-6M), an endothelium-dependent dilator, caused significant dilation (132% of control) and increased calcium to 186% of control. Adenosine (Adn; 10-4M), an endothelium-independent agent, produced similar dilation (127% of control) but did not alter endothelial cell calcium. Increasing intraluminal pressure produced a myogenic constriction with no change in endothelial calcium. Flow, induced by a 20 cm H2O pressure gradient, failed to dilate the arterioles and produced no increase in endothelial cell calcium. However, flow induced by a 40 cm H2O pressure difference did increase endothelial cell calcium prior to a significant arteriolar dilation. Removal of the endothelium by physically rubbing the intimal surface eliminated both the dilation and increase in calcium to Ach or flow (40 cm H2O) while the response to Adn remained unchanged. Endothelial cell fluorescence was absent in denuded arterioles and residual fluorescence was less than 10% of the fluorescence in endothelium-intact vessels. These results demonstrate that endothelium-dependent dilation involves an increase in cell calcium that precedes actual vessel dilation. This increase in endothelial cell calcium could be initiated by agonist or changes in shear stress at the lumenal surface of the endothelial cell membrane. Furthermore, this implied mechanism may play an important part in the ability of skeletal muscle to increase blood flow during exercise.

ISSN:0195-9131    

出版商:OVID    

年代:1995

数据来源: OVID