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Resistance training is associated with periods of acute intracellular hypoxia with increased [H.sup.+] production and low intramuscular pH. The aim of this study was to investigate the possible adaptive response in muscle carnosine ([beta]-alanyl-L-histidine) in bodybuilders. Extracts of biopsies of m. vastus lateralis of 6 national-level competitive bodybuilders and 6 age-matched untrained but moderately active healthy subjects were analyzed by high-performance liquid chromatography. Significant differences were shown in carnosine (p < 0.001) and histidine (p < 0.05). Muscle carnosine in bodybuilders was twice that in controls. The carnosine contents measured are the highest recorded in human muscle and represent a 20% contribution to muscle buffering capacity. Taurine was 38% lower in bodybuilders, though the difference was not significant. Possible causes for the changes observed are prolonged repetitive exposure to low muscle pH, change of diet or dietary supplement use, or the use of anabolic steroids. The increase in buffering capacity could influence the ability to carry out intense muscular activity. Key Words. bodybuilders, histidine, taurine, buffering

Inhibitor of differentiation-2 (Id2) is a basic helix-loop-helix protein that acts as a negative regulator of the myogenic regulatory transcription factor family, but Id2 has also been implicated in apoptosis in several cell lines. In this study, we tested the hypothesis that Id2 has a role in both apoptosis-associated muscle atrophy and muscle hypertrophy. A weight corresponding to 12% of the body weight was attached to one wing of Japanese quail to induce hypertrophy in the patagialis (PAT) muscle. Birds in group I were killed after 5 (n = 8), 7 (n = 10), or 14 days (n = 10) of loading. The left wing was loaded for 14 days in group 2 birds, and then the weight was removed and the PAT was examined after 7 (n = 10), 14 (n = 10), or 21 (n = 5) days of unloading. A time-released bromodeoxyuridine (BrdU) pellet was implanted subcutaneously with wing weighting to identify activated satellite cells during loading. The left wing was loaded for 14 days, unloaded for 14 days, and then the weight was reattached for a subsequent 7 (n = 10) or 14 days (n = 10) in group 3 birds. BrdU was implanted on the second loading phase in this group. Id2 mRNA as measured by kinetic PCR increased by 3.9-, 2.7-, and 1.6-fold, relative to control levels after 7, 14, and 21 days of unloading (group 2). Id2 protein as estimated by Western blots increased by 1.5-, 1.4-, and 0.75-fold after 7, 14, and 21 days of unloading (group 2). Muscle unloading induced apoptosis, because poly(ADP-ribose) polymerase-(PARP)-positive nuclei increased and caspase 8 levels increased by 2.6- and 1.7-fold after 7 or 14 days of unloading, respectively (group 2). Although BrdU-positive nuclei increased during loading (groups 1 and 3), 50% failed to survive during unloading (group 2). Id2 mRNA increased by 2.2- and 1.8-fold after 5 and 7 days of loading, respectively, but decreased to control levels by 14 days of loading in group 1. Id2 protein levels increased 2.1-fold after 5 days of loading (group 1). In contrast, Id2 did not increase in reloaded muscles of group 3 birds. These data suggest that Id2 may have a role in apoptosis-associated atrophy of skeletal muscles, but its role in muscle hypertrophy is less clear. muscle atrophy; muscle hypertrophy; MyoD; myogenin

The effect of the initial muscle length (Li) on intrinsic tone (IT) in electrically stimulated guinea pig has been studied. The research seeks to find out if the amplitude of relaxation can determine the amount of intrinsic tone and measure the relationship between the active isometric force and the initial length. Experiments were done on tracheal segments of Hartley guinea pigs weighing 300 to 350 grams. Results show that Li regulates IT and the maximum extent of relaxation. It has also been observed that relaxation indicates a transient and incomplete inhibition of intrinsic tone.

Research shows that the intrinsic viscoelastic tension of relaxed skeletal and cardiac myofibrils in rabbit muscle is caused by a combination of passive force and dynamic stiffness. Contrary to the popular hypothesis that weak cross-bridges are formed through low-ionic strength, titin filaments are thought to involved in the creation of sarcomere length and frequency dependence.

The ileal tone and phasic intestinal motility of normal human subjects were analyzed to determine effects of lipids, glycochenodeoxycholic acid (GDCA) and short-chain fatty acids (SCFA) on ileal tonic activity. Analysis of ileal tonic activity by electronic barostat techniques indicated the role of triglycerides and GDCA on ileal relaxation. Infusions of SCFA also increased ileal tone and promoted propulsive ileal contractions in the human subjects.

The role of anion exchange in the regulation of pH-induced muscle contraction was investigated in canine basilar arteries. The arteries were exposed to a pH increase from 7.4 to 7.8 to induce muscle contraction. Intracellular pH and muscle tension were monitored. There were no changes in intracellular pH or muscle tension in the presence of Na+/H+ exchange blockers, but pH decreased in response to anion exchange blockers. This suggests that anion exchange is involved in the maintenance of muscle tone in the basilar artery.

The role of epinephrine and endothelium in pressure-sensitive myogenic response in skeletal muscle venules were investigated using first-order venules of rat gracilis muscle. The venules showed increases in diameter in response to perfusion pressure (PP). In passive conditions, the pressure-diameter curve shifted upwards, but shifted downwards in the presence of norepinephrine (NE). The removal of endothelium caused a marked decrease in venular diameters. These results suggest that NE is involved in the regulation of myogenic tone in rat skeletal muscle.

Extracellular calcium (Ca2+) stores and stretch-activated channels (SACs) contribute to the hypotonic cell swelling-induced Ca2+ increase (HICI) in the rat pituitary GH3 cell line. This HICI is suppressed by the L-type Ca2+ channel blocker, nifedipine, and the nonspecific SAC blocker, Gd3. The inhibition of HICI through spider venom indicates that the L-type Ca2+ channel is insufficient for HICI, and that SACs elicit HICI through direct activity or via depolarization-induced Ca2+ channel activation.

Endothelial-dependent relaxation of vascular smooth muscle cells evoked by a number of agonists, including cholinomimetics and substance P, is often accompanied by an increase (repolarization and/or hyperpolarization) in the membrane potential. This change in membrane potential appears predominately to reflect the action of an endothelial-derived hyperpolarizing factor (EDHF), which is distinct from NO (or endothelial-derived relaxing factor), and is discussed in this article by Chris Garland and colleagues. In large conducting arteries, EDHF may provide a secondary system to NO, which assumes primary importance in some disease states such as pulmonary hypertension and atherosclerosis. However, in small resistance arteries (100-300 [[micro]meter]), EDHF appears to be a major determinant of vascular calibre under normal conditions, and may therefore be of primary importance in the regulation of vascular resistance.

A noninvasive method, which combines the new high-resolution echo-tracking system for determining systolic/diastolic arterial diameter changes and the Finapres system for measuring instantaneous systolic/ diastolic pressure-diameter in human heart, indicates that sympathetic activation reduces radial arterial compliance in the human heart. Mental stress and cold pressor tests during sympathetic activation increase the mean arterial pressure and pulse pressure and decrease the stroke change in diameter, while radial arterial mean diameter remains constant. The variations in radial arterial smooth muscle tone and those in distending blood pressure interact to mediate the decrease in arterial compliance.

Three of the estimates made by a nonuniform hypothesis were tested. It was proposed that the extension of active muscles is not distributed evenly between sarcomeres. Some are extended beyond overlap while others are not extended at all. A small number of the overextended sarcomeres may reinterdigitate with relaxation. This results in several alterations in the mechanical functions of the muscle.

While some forms of brain-damage are considered to be static, a close examination of case records reveals that many so-called ''static'' encephalopathies (dysfunctions of the brain) do, in fact, progress. In particular, it is clear that dyskinesias (disorders of voluntary movement) may progress to severe dystonia (abnormal muscle tone and distorted movement) years after the original injury. Such delayed-onset dystonia has been shown to occasionally follow birth injury as well as head injury and stroke. Few such cases involving childhood encephalopathies have been described in the medical literature, however. The authors describe the cases of 10 patients who experienced delayed-onset dystonia. In all 10 cases, the only feature to which the neurologic impairment can be attributed is perinatal or early childhood asphyxia (insufficient oxygen). In six cases, there was some developmental delay following the asphyxia, while in the remainder development was normal. Seven of the patients are at least intellectually normal on IQ testing. The age of onset was highly variable, ranging from 5 to 21 years. It is clear, however, that attributing the dystonia to an episode of asphyxia which occurred years earlier is a diagnosis of exclusion, and care must be taken to exclude head injury, tumors, the use of neuroleptic drugs, as well as conditions such as Wilson's disease. It is also clear that if dystonia may, in some cases, result from asphyxia, these cases still represent only a minority of the cases of dystonia. Nevertheless, it may be possible to gain a greater understanding of the causes of dystonia in general if the ''static'' brain lesions that can give rise to delayed-onset dystonia are elucidated. (Consumer Summary produced by Reliance Medical Information, Inc.)

Recent experimental studies have shown significant alterations of the vascular smooth muscle (VSM) tone when an artery is subjected to an elevation in pressure. Therefore, the VSM participates in the adaptation process not only by means of its synthetic activity (fibronectins and collagen) or proliferative activity (hypertrophy and hyperplasia) but also by adjusting its contractile properties and its tone level. In previous theoretical models describing the time evolution of the arterial wall adaptation in response to induced hypertension, the contribution of VSM tone has been neglected. In this study, we propose a new biomechanical model for the wall adaptation to induced hypertension, including changes in VSM tone. On the basis of Hill's model, total circumferential stress is separated into its passive and active components, the active part being the stress developed by the VSM. Adaptation rate equations describe the geometrical adaptation (wall thickening) and the adaptation of active stress (VSM tone). The evolution curves that are derived from the theoretical model fit well the experimental data describing the adaptation of the rat common carotid subjected to a step increase in pressure. This leads to the identification of the model parameters and time constants by characterizing the rapidity of the adaptation processes. The agreement between the results of this simple theoretical model and the experimental data suggests that the theoretical approach used here may appropriately account for the biomechanics underlying the arterial wall adaptation. arterial wall; remodeling; myogenic response; theoretical model; Hill's model; biomechanics

The in vivo and in vitro study of the interaction of NO with thiol groups in proteins and peptides using chemiluminescence methods shows the presence of excess glutathione in human lung alveoli. NO reacts with glutathione to form S-nitroso (SNO)-glutathione. SNO-glutathione is more stable than NO, having a half-life of several hours rather than seconds. SNO-glutathione reduces NO toxicity and relaxes the smooth vascular epithelium in human airways. SNO-cysteine is an even more potent vasorelaxant due to its rapid decomposition.