Biomedical subjects

M D Delp

Publications and source records attributed to M D Delp.

At least 37 records · Page 2Linked to original sources

PubMed1998

Regulation of skeletal muscle perfusion during exercise.

For exercise to be sustained, it is essential that adequate blood flow be provided to skeletal muscle. The local vascular control mechanisms involved in regulating muscle perfusion during exercise include metabolic control, endothelium-mediated control, propagated responses, myogenic control, and the muscle pump. The primary determinant of muscle perfusion during sustained exercise is the metabolic rate of the muscle. Metabolites from contracting muscle diffuse to resistance arterioles and act directly to induce vasodilation, or indirectly to inhibit noradrenaline release from sympathetic nerve endings and oppose alpha-adrenoreceptor-mediated vasoconstriction. The vascular endothelium also releases vasodilator substances (e.g., prostacyclin and nitric oxide) that are prominent in establishing basal vascular tone, but these substances do not appear to contribute to the exercise hyperemia in muscle. Endothelial and smooth muscle cells may also be involved in propagating vasodilator signals along arterioles to parent and daughter vessels. Myogenic autoregulation does not appear to be involved in the exercise hyperemia in muscle, but the rhythmic propulsion of blood from skeletal muscle veins facilitates venous return to the heart and muscle perfusion. It appears that the primary determinants of sustained exercise hyperemia in skeletal muscle are metabolic vasodilation and increased vascular conductance via the muscle pump. Additionally, sympathetic neural control is important in regulating muscle blood flow during exercise.

Animals↗

PubMed1998

Differential effects of training on the control of skeletal muscle perfusion.

Endurance and high-intensity sprint training have been shown to alter skeletal muscle blood flow and factors that govern muscle perfusion under various conditions. Neither endurance nor sprint training alter skeletal muscle perfusion at rest but can result in an increase in muscle blood flow during the anticipation of exercise. The magnitude of the anticipatory increases in muscle blood flow is dependent on the intensity and duration of the prior training bouts and results from elevations in mean arterial pressure and decreases in vascular resistance in skeletal muscle. The decrements in skeletal muscle vascular resistance appear to be mediated through increases in muscle sympathetic cholinergic nerve activity or decreases in muscle sympathetic adrenergic nerve activity. During submaximal exercise, total muscle blood flow is either unchanged or slightly lower. However, a redistribution of muscle blood flow may occur following aerobic training, resulting in an enhanced perfusion of high-oxidative skeletal muscles and less flow going to low-oxidative muscles. The increased perfusion of the high-oxidative muscles may result from various factors including: a) increased recruitment of high-oxidative motor units, b) increased local release of metabolic vasodilator substances, c) qualitative changes in the metabolic substances released, d) decreased muscle sympathetic nerve activity, e) diminished sensitivity of the arterial vasculature to norepinephrine or other vasoconstrictor agents, f) enhanced endothelium-mediated dilation in the resistance vasculature, and g) an increased effectiveness of the skeletal muscle pump. Conversely, the decreases in blood flow to low-oxidative muscles may result from an enhanced autoregulatory responsiveness of the resistance vasculature. Endurance and sprint training increase muscle perfusion during exercise at VO2max: this primarily appears to be the result of an enhanced pumping capacity of the heart to increase in maximal cardiac output. Many of the training-induced alterations in muscle blood flow and vascular structure are localized in the muscles that are most active during the training bouts. Therefore, differences in muscle recruitment patterns that occur with low-intensity endurance exercise and high-intensity sprint exercise may account for differences observed between these two training regimens.

Animals↗

PubMed1998

Effects of hyperthyroidism on vascular contractile and relaxation responses.

Previous research has shown that skeletal muscle blood flow, at rest and during muscular contractions, is elevated in the hyperthyroid state. We hypothesized that reduced vascular contractile and enhanced endothelium-dependent relaxation responses contribute to these observations. To test these hypotheses, male rats were administered triiodothyronine (Hyper, n = 27; 300 micrograms/kg) for 6-12 wk. Compared with euthyroid control rats (Eut, n = 27), Hyper exhibited left ventricular hypertrophy (Eut, 2.01 +/- 0.04 mg/g body wt; Hyper, 2.70 +/- 0.06; P < 0.0005) and greater oxidative enzyme activity in several skeletal muscles (all P < 0.0005). Vascular rings, 2-3 mm in axial length, were prepared from abdominal aortas, and responses to vasoactive agents were determined in vitro. Compared with Eut, vascular rings with intact endothelium from Hyper exhibited reductions in contractile responses to norepinephrine (NE) across a range of NE concentrations (P < 0.05). Maximal tension developed in response to NE was reduced approximately 30% in hyperthyroidism (Eut, 3.8 +/- 0.2 g; Hyper, 2.6 +/- 0.4; P < 0.01). Contractile responses to NE were not different between Eut and Hyper in rings denuded of endothelium. Maximal vasorelaxation responses to acetylcholine (ACh), after precontraction with NE (10(-7) M), were enhanced in the hyperthyroid state (Eut, 65.1 +/- 4.8%; Hyper, 84.0 +/- 7.1; P < 0.05). Enhanced vasorelaxation to ACh was also observed when precontraction was induced by prostaglandin F2 alpha. These findings indicate that vascular contractile and relaxation responses are altered in male hyperthyroid rats.

Acetylcholine↗

PubMed1998

Ocular and regional cerebral blood flow in aging Fischer-344 rats.

Vascular remodeling and changes in vascular responsiveness occur in the rat cerebrum with old age. This includes reductions in cerebral arteriolar numerical density, cross-sectional area, distensibility, the relative proportion of distensible elements in the cerebral arteriolar wall, and reduced endothelium-dependent relaxation. The purpose of this study was to test the hypothesis that old age results in an increase in vascular resistance and, correspondingly, a decrease in blood flow to ocular, regional cerebral, and spinal tissue in the rat. Blood flow was measured in the eye, olfactory bulb, left and right cerebrum, pituitary gland, midbrain, pons, cerebellum, medulla, and spinal cord of juvenile (2-mo-old, n = 6), adult (6-mo-old, n = 7), and aged (24-mo-old, n = 7) male Fischer-344 rats. Arterial pressure and blood flow were used to calculate vascular resistance. Vascular resistance in the eye of aged rats (6.03 +/- 1.08 mmHg . ml-1 . min . 100 g) was higher than that in juvenile (3.83 +/- 0.38 mmHg . ml-1 . min . 100 g) and adult rats (3.12 +/- 0.24 mmHg . ml-1 . min . 100 g). Similarly, resistance in the pons of older rats (2.24 +/- 0.55 mmHg . ml-1 . min . 100 g) was greater than in juvenile (0.66 +/- 0.06 mmHg .ml-1 . min . 100 g) and adult rats (0.80 +/- 0.11 mmHg . ml-1 . min . 100 g). In contrast, vascular resistance in the pituitary gland was lower in the aged rats (juvenile, 3.09 +/- 0.22; adult, 2.79 +/- 0.42; aged, 1.73 +/- 0.32 mmHg . ml-1 . min . 100 g, respectively). Vascular resistance was not different in other cerebral tissues or in the spinal cord in the aged rats. These data suggest that regional cerebral and spinal blood flow and vascular resistance remain largely unchanged in conscious aged rats at rest but that elevations in ocular vascular resistance and, correspondingly, decreases in ocular perfusion with advanced age could have serious adverse effects on visual function.

Aging↗

PubMed1998

Effects of aging on cardiac output, regional blood flow, and body composition in Fischer-344 rats.

The purpose of this study was to determine the effects of maturation and aging on cardiac output, the distribution of cardiac output, tissue blood flow (determined by using the radioactive-microsphere technique), and body composition in conscious juvenile (2-mo-old), adult (6-mo-old), and aged (24-mo-old) male Fischer-344 rats. Cardiac output was lower in juvenile rats (51 +/- 4 ml/min) than in adult (106 +/- 5 ml/min) or aged (119 +/- 10 ml/min) rats, but cardiac index was not different among groups. The proportion of cardiac output going to most tissues did not change with increasing age. However, the fraction of cardiac output to brain and spinal cord tissue and to skeletal muscle was greater in juvenile rats than that in the two adult groups. In addition, aged rats had a greater percent cardiac output to adipose tissue and a lower percent cardiac output to cutaneous and reproductive tissues than that in juvenile and adult rats. Differences in age also had little effect on mass-specific perfusion rates in most tissues. However, juvenile rats had lower flows to the pancreas, gastrointestinal tract, thyroid and parathyroid glands, and kidneys than did adult rats, and aged rats had lower flows to the white portion of rectus femoris muscle, spleen, thyroid and parathyroid glands, and prostate gland than did adult rats. Body mass of juvenile rats was composed of a lower percent adipose mass and a greater fraction of brain and spinal cord, heart, kidney, liver, and skeletal muscle than that of the adult and aged animals. Relative to the young adult rats, the body mass of aged animals had a greater percent adipose tissue mass and a lower percent skeletal muscle and skin mass. These data demonstrate that maturation and aging have a significant effect on the distribution of cardiac output but relatively little influence on mass-specific tissue perfusion rates in conscious rats. The old-age-related alterations in cardiac output distribution to adipose and cutaneous tissues appear to be associated with the increases in percent body fat and the decreases in the fraction of skin mass, respectively, whereas the decrease in the portion of cardiac output directed to reproductive tissue of aged rats appears to be related to a decrease in mass-specific blood flow to the prostate gland.

Aging↗

PubMed1997

Time course of enhanced endothelium-mediated dilation in aorta of trained rats.

Previous work has demonstrated that 10 wk of exercise training enhances the responsiveness of rat abdominal aortas to acetylcholine (ACh), an endothelium-dependent vasodilator. The purpose of this study was to determine the time course for this training-induced adaptation of vascular endothelium. Additionally, the contribution of the cyclooxygenase and nitric oxide synthase mechanisms to the enhanced endothelium-mediated relaxation were examined. Male rats were divided into sedentary (SED) and exercise groups. Exercised animals were further subdivided into postexercise (POST-EX), 1 DAY, 1 WK, 2 WK, 4 WK and 10 WK groups. Exercise consisted of treadmill running at 30 m.min-1 (15 degrees incline) for 1 h.d-1 (5 d.wk-1 for the 1 WK, 2 WK, 4 WK, and 10 WK groups). Maximal vasodilator responses induced by 10(-4) M ACh (10(-7) M norepinephrine preconstriction) were determined on abdominal aortic rings in vitro immediately after a single exercise bout in POST-EX rats and 24 h after a single bout of exercise in 1 DAY animals. Maximal 10(-4) M ACh-induced dilation of aortas from 1 WK, 2 WK, 4 WK, and 10 WK animals was determined 24 h after the last exercise bout. Soleus muscle citrate synthase activity was greater in 2 WK (31 +/- 1 mumol.min-1.g wet wt-1), 4 WK (34 +/- 2), and 10 WK (36 +/- 1 mumol.min-1.g wet wt-1) rats than in SED (27 +/- 1 mumol.min-1.g wet wt.-1) animals. Maximal ACh-induced relaxation was greater in aorta from 4 WK (72 +/- 2%) and 10 WK (79 +/- 1%) rats than SED (61 +/- 2%) rats. ACh-mediated dilatory responses remained enhanced in the presence of the cyclooxygenase blocker indomethacin (10(-5) M), but were abolished by the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (300 microM). In addition, the expression of endothelial nitric oxide synthase (ecNOS) protein in aortas from 4 WK (P = 0.057) and 10 WK (P < 0.05) rats was greater than in aortas from SED animals. These data indicate that the enhanced endothelium-dependent, ACh-mediated dilation of the rat aorta is present by 4 wk of endurance exercise training. This adaptation appears to be mediated primarily through the nitric oxide synthase pathway and is associated with an increased expression of ecNOS.

Acetylcholine↗

PubMed1997

A review of effects of hypothyroidism on vascular transport in skeletal muscle during exercise.

Hypothyroidism is a common thyroid disease characterized by exercise intolerance. Both exercise capacity and endurance are compromised in the hypothyroid state. Studies involving rats performing treadmill running have shown that blood flows during exercise to high oxidative, extensor-type muscles are lower in hypothyroid rats compared with those in euthyroid rats. Abnormal cardiac and vascular function appear to contribute to this hypoperfusion. Experiments involving isolated arterial vessel segments have demonstrated that potential for constriction is normal in vessels from hypothyroid animals; however, reduced vasodilator potential is associated with hypothyroidism. Dysfunction of both endothelium and vascular smooth muscle appear to contribute to blunted potential for vasodilation. Altered ability to generate vasodilatory substances and/or changes in responses to these vasodilators may account for vascular dysfunction. It appears that impaired vascular function interacts with other factors such as poor myocardial function and changes in energy metabolism to compromise exercise tolerance.

Animals↗

PubMed1997

Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure.

One of the primary consequences of left ventricular dysfunction (LVD) after myocardial infarction is a decrement in exercise capacity. Several factors have been hypothesized to account for this decrement, including alterations in skeletal muscle metabolism and aerobic capacity. The purpose of this study was to determine whether LVD-induced alterations in skeletal muscle enzyme activities, fiber composition, and fiber size are 1) generalized in muscles or specific to muscles composed primarily of a given fiber type and 2) related to the severity of the LVD. Female Wistar rats were divided into three groups: sham-operated controls (n = 13) and rats with moderate (n = 10) and severe (n = 7) LVD. LVD was surgically induced by ligating the left main coronary artery and resulted in elevations (P < 0.05) in left ventricular end-diastolic pressure (sham, 5 +/- 1 mmHg; moderate LVD, 11 +/- 1 mmHg; severe LVD, 25 +/- 1 mmHg). Moderate LVD decreased the activities of phosphofructokinase (PFK) and citrate synthase in one muscle composed of type IIB fibers but did not modify fiber composition or size of any muscle studied. However, severe LVD diminished the activity of enzymes involved in terminal and beta-oxidation in muscles composed primarily of type I fibers, type IIA fibers, and type IIB fibers. In addition, severe LVD induced a reduction in the activity of PFK in type IIB muscle, a 10% reduction in the percentage of type IID/X fibers, and a corresponding increase in the portion of type IIB fibers. Atrophy of type I fibers, type IIA fibers, and/or type IIB fibers occurred in soleus and plantaris muscles of rats with severe LVD. These data indicate that rats with severe LVD after myocardial infarction exhibit 1) decrements in mitochondrial enzyme activities independent of muscle fiber composition, 2) a reduction in PFK activity in type IIB muscle, 3) transformation of type IID/X to type IIB fibers, and 4) atrophy of type I, IIA, and IIB fibers.

Animals↗

PubMed1996

Composition and size of type I, IIA, IID/X, and IIB fibers and citrate synthase activity of rat muscle.

A population of muscle fibers containing a myosin heavy-chain isoform IId (or 2x) has recently been identified in rat muscle. The purpose of this study was to histochemically determine the relative population and size of muscle fibers composed of type IID/X fibers as well as type I, IIA, and IIB fibers to estimate the absolute mass of the different types of fibers in rat muscle. In addition, muscle citrate synthase activity was measured to determine the relationship between fiber composition and muscle oxidative capacity. Seventy-six muscles or muscle parts from the face, neck, shoulder, arm, trunk, hip, thigh, and leg of three adult (4.5-5 mo of age) male Sprague-Dawley rats were removed, weighed, and frozen for histochemical and biochemical analyses. The data demonstrated that type IIB fibers make up 71% of the total muscle mass, type IID/X fibers 18%, type IIA fibers 5%, and type I fibers 6%. The mean cross-sectional area across all muscles was 5,078 +/- 175 microns 2 for type IIB fibers, 3,078 +/- 105 microns2 for type IID/X fibers, 2,045 +/- 80 microns2 for type IIA fibers, and 1,898 +/- 90 microns2 for type I fibers. Citrate synthase activity, an indicator of muscle mitochondrial content, was most closely related to the population of type IIA fibers and was in the rank order of type IIA > I > IID/X > IIB. NADH-tetrazolium reductase staining intensity also confirmed this order. These data demonstrate that type IID/X fibers make up a significant portion of the adult rat muscle mass and are intermediate to type IIA and IIB fibers in regard to fiber size and oxidative potential.

Aerobiosis↗

PubMed1995

Exercise training alters aortic vascular reactivity in hypothyroid rats.

Hypothyroidism induces a number of cardiovascular adaptations in rats, including decreases in blood flow to high-oxidative skeletal muscle and increases in total peripheral resistance. Conversely, exercise training results in elevations in blood flow to high-oxidative skeletal muscle and decreases in vascular resistance. The purpose of this study was to determine whether hypothyroidism induces changes in the vasomotor responses of arterial vessels and whether exercise training modifies these responses. Rats were divided into three groups, sedentary euthyroid (S-Eut), sedentary hypothyroid (S-Hypo), and exercise-trained hypothyroid (ET-Hypo). Responses to vasoactive compounds were examined in vitro using abdominal aortic rings. Maximal isometric contractile tension (g/mm2) evoked by KCl and norepinephrine (NE) were not different among groups. However, sensitivity to KCl [agonist concentration producing 50% of maximal vasoconstrictor response (EC50; in mM): S-Eut, 21.1 +/- 1.1; S-Hypo, 35.7 +/- 2.7; ET-Hypo, 43.8 +/- 2.0] and to NE [EC50 (in M): S-Eut, 4.0 x 10(-8) +/- 2.3 x 10(-8); S-Hypo, 8.3 x 10(-8) +/- 3.4 x 10(-8); ET-Hypo, 3.6 x 10(-7) +/- 1.1 x 10(-7)] was different among groups, and in the order S-Eut > S-Hypo > ET-Hypo. Maximal vasodilator responses induced by acetylcholine (10(-7) M NE preconstriction) were lower in rings from S-Hypo animals than those from S-Eut and ET-Hypo rats. Dilatory responses induced by sodium nitroprusside (SNP) with the same NE preconstriction were not different among groups. However, with a 10(-4) M NE preconstriction, maximal dilatory responses induced by SNP were lower in vessels from hypothyroid animals. Dilatory responses to forskolin (10(-4) M NE preconstriction) were not different among groups.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1995

Muscle blood flow during exercise in sedentary and trained hypothyroid rats.

Hypothyroidism is characterized by exercise intolerance. We hypothesized that active muscle blood flow during in vivo exercise is inadequate in the hypothyroid state. Additionally, we hypothesized that endurance exercise training would restore normal blood flow during acute exercise. To test these hypotheses, rats were made hypothyroid (Hypo) over 3-4 mo with propylthiouracil. A subset of Hypo rats was trained (THypo) on a treadmill at 30 m/min (15% grade) for 60 min/day 5 days/wk over 10-15 wk. Hypothyroidism was evidenced by approximately 80% reductions in plasma triiodothyronine levels in Hypo and THypo and by 40-50% reductions in citrate synthase activities in high oxidative muscles in Hypo compared with euthyroid (Eut) rats. Training efficacy was indicated by increased (25-100%) citrate synthase activities in muscles of THypo vs. Hypo. Regional blood flows were determined by the radiolabeled microsphere method before exercise and at 1-2 min of treadmill running at 15 m/min (0% grade). Preexercise muscle blood flows were generally similar among groups. During exercise, however, flows were lower in Hypo than in Eut for high oxidative muscles such as the red section of vastus lateralis [277 +/- 24 and 153 +/- 13 (SE) ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01] and vastus intermedius (317 +/- 32 and 187 +/- 20 ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01) muscles. Training (THypo) did not normalize these flows (168 +/- 24 and 181 +/- 24 ml.min-1.100 g-1 for red section of vastus lateralis and vastus intermedius muscles, respectively). Blood flows to low oxidative muscle, such as the white section of vastus lateralis muscle, were similar among groups (21 +/- 5, 25 +/- 4, and 34 +/- 7 ml.min-1.100 g-1 for Eut, Hypo, and THypo, respectively; P = NS). These findings indicate that hypothyroidism is associated with reduced blood flow to skeletal muscle during exercise, suggesting that impaired delivery of nutrients to and/or removal of metabolites from skeletal muscle contributes to the poor exercise tolerance characteristic of hypothyroidism.

Animals↗

PubMed1995

Rat aortic vasoreactivity is altered by old age and hindlimb unloading.

Prolonged bed rest in young adults leads to a number of cardiovascular alterations, including orthostatic intolerance and decreased exercise capacity. Similar changes occur with advanced age. These modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Using rat hindlimb unloading as an animal model of physical inactivity, this study was designed to determine whether prolonged decreases in weight-bearing activity induce changes in vascular reactivity that are similar to those occurring in senescent rats and whether the imposition of inactivity on old rats further modifies any age-related alterations in vasomotor responsiveness. Responses to vasoactive compounds were examined in vitro by using isolated abdominal aortic rings. Maximal isometric contractile force evoked by the vasoconstrictors KCl, norepinephrine (NE), and arginine vasopressin was lower in aortic segments from young hindlimb-unloaded (YHU), old control (OC), and old hindlimb-unloaded (OHU) rats compared with that from young control (YC) rats. Sensitivity [mean effective concentration (EC50)] to KCl was enhanced in segments from both old and unloaded animals compared with YC rats, but EC50 values for the other constrictors were not different among groups. Vasorelaxation responses induced by acetylcholine (10(-7) M NE preconstriction) were lower in vessel rings from OC (1 x 10(-7) to 3 x 10(-6) M), YHU (10(-7) to 10(-5) M), and OHU (10(-7) to 10(-5) M) rats than those from YC animals. In addition, vessel rings from OC, YHU, and OHU rats were less sensitive to sodium nitroprusside-induced relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1995

Thyroid status and exercise tolerance. Cardiovascular and metabolic considerations.

Both hypo- and hyperthyroidism are characterised by exercise intolerance. In hypothyroidism, inadequate cardiovascular support appears to be the principal factor involved. Insufficient skeletal muscle blood flow compromises exercise capacity via reduced oxygen delivery, and endurance through decreased delivery of blood-borne substrates. The latter effect results in increased dependence on intramuscular glycogen. Additionally, decreased mobilisation of free fatty acids from adipose tissue and, consequently, lower plasma free fatty acid levels compound the problem of reduced lipid delivery to active skeletal muscle in the hypothyroid state. In contrast, cardiovascular support is enhanced in hyperthyroidism, implicating other factors in exercise tolerance. Greater reliance on muscle glycogen appears to be the primary reason for decreased endurance. Biochemical changes with hyperthyroidism that would favour enhanced flux through glycolysis may account for this dependence on glycogen. Deviations from normal thyroid function, and the ensuing exercise tolerance, require appropriate medical therapy to attain euthyroid status.

Cardiovascular Physiological Phenomena↗

PubMed1995

Effects of exercise training on endothelium-dependent peripheral vascular responsiveness.

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 alpha 2-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.

Adaptation, Physiological↗

PubMed1994

Morphological changes during fiber type transitions in low-frequency-stimulated rat fast-twitch muscle.

This study investigates morphological adaptations of rat extensor digitorum longus muscle to chronic low-frequency stimulation (10 Hz, 10 h/d, up to 61 +/- 7d). During the early stimulation period (2-4 d), increased basophilia and accumulation of RNA were seen predominantly in type-IIB fibers. Putative satellite cell activation, as indicated by 3H-thymidine incorporation, was also evident during this phase. By 12 d, fiber composition remained unaltered, but there was a decrease in the cross-sectional area of the type-IIB fibers. Following 28 d of low-frequency stimulation, the percentage of type-IIB fibers decreased from 43 +/- 3% to 0%, while type-IID fibers increased from 30 +/- 3% to 60 +/- 6%. The fraction of type-IIA fibers tended to increase (controls 19 +/- 3%; stimulated 29 +/- 4%), whereas that of the type-I fibers was unaltered (4 +/- 1%). At this time, the cross-sectional area of type-IID fibers was unaltered, but that of type-IIA and type-I fibers increased. Further stimulation resulted in a return of type-IID fibers to control levels (23 +/- 5%), and a marked increase in type-IIA fibers (45 +/- 8%). The percentage of type-I fibers increased from 4 +/- 1% to 8 +/- 1%. Throughout each stage of chronic stimulation, there was no histological evidence of fiber degeneration and regeneration. These results indicate that, in contrast to the rabbit, chronic low-frequency stimulation-induced fiber conversion in the rat extensor digitorum longus muscle is entirely due to fiber transformation.

Adaptation, Physiological↗

PubMed1993

Elevations in rat soleus muscle [Ca2+] with passive stretch.

Previous work has demonstrated that muscular injury in rat soleus muscles resulting from eccentric contractions (downhill walking) is accompanied by elevations in mitochondrial [Ca2+] (MCC). Muscles are stretched during eccentric contractions, and there is evidence in the literature that stretch of the cell membrane induces Ca2+ influx in various tissues, including skeletal muscle. The purpose of this study was to determine if passive stretch of rat soleus muscles will induce increases in total muscle [Ca2+] (TCC) and MCC. Soleus muscles from female rats (51-122 g) were isolated and incubated in vitro for 2 h at resting length (Lo) or at the maximal in situ length (S). TCC (+62%) and MCC (+56%) were elevated in the S muscles. Also, there was a 63% reduction in maximal twitch tension in the S muscles. ATP concentration, phosphocreatine concentration, and lactate release between Lo and S muscles were the same, indicating that impaired metabolism was not responsible for the observed differences in [Ca2+] and force production between Lo and S muscles. Increases in TCC in the S condition indicate that stretch results in Ca2+ influx from the extracellular space, which is supported by the observation that when S muscles were incubated in Ca(2+)-free buffer, TCC and MCC did not increase. High concentrations of verapamil (0.25-0.75 mM) blocked the elevations in TCC and MCC in the S muscles, but the magnitude of the drug concentration required makes it questionable whether the effect resulted from specific blockade of slow voltage-sensitive Ca2+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Exercise training alters endothelium-dependent vasoreactivity of rat abdominal aorta.

We tested the hypothesis that adaptations in peripheral arterial vasoreactivity are induced by exercise training. Male rats were trained to run on a treadmill at 30 m/min (15 degrees incline) for 1 h/day 5 days/wk for 10-12 wk. Efficacy was indicated by a 51% increase (P < 0.05) in citrate synthase activity in soleus muscle of exercise-trained (ET) rats compared with that of sedentary (SED) control rats. Responses to vasoactive compounds were examined in vitro using rings of abdominal aorta. Maximal isometric contractile tension evoked by KCl, norepinephrine (NE), and phenylephrine were not different between groups; sensitivity to phenylephrine was also not different between groups. However, sensitivity was lower for both KCl and NE in vessels from ET animals. Endothelium removal did not influence KCl sensitivity but did abolish the difference in NE sensitivity of vessel segments between ET and SED animals. Maximal vasodilator responses induced by acetylcholine (ACh; NE or prostaglandin F2 alpha preconstriction) were greater in vessel rings from ET rats. However, dilatory responses by sodium nitroprusside (NE or prostaglandin F2 alpha preconstriction) and forskolin (NE preconstriction) were not different between groups, indicating that the augmented ACh-induced dilatory response resulted from an adaptation of the endothelium. Blockade of nitric oxide synthase activity diminished ACh-induced vasodilation by 79 and 100% in SED and ET rats, respectively. These results indicate that training alters vasomotor function in rat abdominal aortas through adaptations of both endothelium and smooth muscle.

Animals↗

PubMed1993

Vasoconstrictor properties of rat aorta are diminished by hindlimb unweighting.

Prolonged bed rest and exposure to weightlessness in humans result in cardiovascular alterations that are characterized by orthostatic intolerance and decreased exercise capacity. Modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Rat hindlimb unweighting (HU) was used as an animal model to determine whether prolonged decreases in weight-bearing activity induce changes in vasoreactivity of peripheral arterial vessels. Responses to vasoactive compounds were examined in vitro using isolated abdominal and thoracic aortic rings. Maximal isometric contractile tension evoked by the vasoconstrictors KCl (10-100 mM), norepinephrine (NE; 10(-9)-10(-4) M), phenylephrine (10(-9)-10(-4) M), arginine vasopressin (10(-13)-3 x 10(-5) M), and CaCl2 (10(-6)-10(-2) M) was lower in abdominal aortic rings from HU rats. Sensitivity [agonist concentration that produced 50% of maximal vasoconstrictor response (EC50)] to KCl was enhanced in segments from HU animals but was not different for the other constrictors. Maximal contractile responses of thoracic aortic rings to KCl (10-100 mM) and NE (10(-9)-10(-4) M) were also attenuated by HU. In abdominal aortic rings preconstricted with 10(-4) M NE, maximal vasodilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and 8-bromoguanosine 3',5'-cyclic monophosphate (10(-6)-10(-2) M) were greater in vessel rings from HU rats. However, with 10(-7) M NE preconstriction, maximal dilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and acetylcholine (10(-9)-10(-4) M) were not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗