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Biomedical subjects

David Gozal

Publications and source records attributed to David Gozal.

At least 109 records · Page 6Linked to original sources
PubMed2004

Neurobehavioral implications of habitual snoring in children.

OBJECTIVE: Current guidelines for the treatment of children with obstructive sleep apnea (OSA) suggest that primary snoring (PS) in children is benign. However, PS has not been well evaluated, and it is unknown whether PS is associated with serious morbidity. This study investigated whether PS is associated with neurobehavioral deficits in children. METHODS: Parents of 5- to 7-year-old snoring children in public schools were surveyed about their child's sleeping habits. Children with a history of snoring and nonsnoring children were invited for overnight polysomnographic assessment and a battery of neurobehavioral tests. Only children who did not have a history of attention-deficit/hyperactivity disorder and were not considered hyperactive by parental report were tested. RESULTS: Children with a history of snoring, an obstructive apnea index of <1/hour of total sleep time (hrTST), an apnea/hypopnea index <5/hrTST, and no gas exchange abnormalities were classified as PS (n = 87). Control subjects were defined as children without a history of snoring, an obstructive apnea index <1/hrTST, an apnea/hypopnea index <5/hrTST, and no gas exchange abnormalities (n = 31). Although means for both groups were in the normal range, the PS children were found to perform worse on measures related to attention, social problems, and anxious/depressive symptoms. In addition, although within the normal range, both overall cognitive abilities and certain language and visuospatial functions were significantly lower for the PS group than for the control subjects. CONCLUSIONS: PS seems to be associated with significant neurobehavioral deficits in a subset of children, possibly related to increased susceptibility to sleep fragmentation. Larger studies are urgently required because current guidelines for treatment of snoring in children may require reevaluation.

Attention Deficit and Disruptive Behavior Disorder↗
PubMed2004

The effect of chronic or intermittent hypoxia on cognition in childhood: a review of the evidence.

OBJECTIVE: A review of the evidence concerning the effect of chronic or intermittent hypoxia on cognition in childhood was performed by using both a systematic review of the literature and critical appraisal criteria of causality. Because of the significant impact of behavioral disorders such as attention-deficit/hyperactivity disorder on certain cognitive functions as well as academic achievement, the review also included articles that addressed behavioral outcomes. METHODS: Both direct and indirect evidence were collected. A structured Medline search was conducted from the years 1966-2000 by using the OVID interface. Both English- and non-English-language citations were included. Significant articles identified by the reviewers up to 2003 were also included. To be included as direct evidence, an article needed to be an original report in a peer-reviewed journal with data on cognitive, behavioral, or academic outcomes in children up to 14 years old, with clinical conditions likely to be associated with exposure to chronic or intermittent hypoxia. Indirect evidence from other reviews and publications in closely related fields, including experimental studies in adults, was used to help formulate conclusions. Two reviewers screened abstracts and titles. Each article included as direct evidence received a structured evaluation by 2 reviewers. Adjudication of differences was performed by a group of 2 reviewers and a research consultant. After this review, tables of evidence were constructed that were used as the basis for group discussion and consensus development. Indirect evidence assigned by topic to specific reviewers was also presented as part of this process. A formal procedure was used to rank the studies by design strength. The critical appraisal criteria for causation described in Evidence Based Pediatrics and Child Health (Moyer V, Elliott E, Davis R, et al, eds. London, United Kingdom: BMJ Books; 2000:46-55) were used to develop consensus on causality. RESULTS: A total of 788 literature citations were screened. For the final analysis, 55 articles met the criteria for inclusion in the direct evidence. Of these, 43 (78.2%) reported an adverse effect. Of the 37 controlled studies, 31 (83.8%) reported an adverse effect. Adverse effects were noted at every level of arterial oxygen saturation and for exposure at every age level except for premature newborns. The studies were classified into 5 clinical categories: congenital heart disease (CHD), sleep-disordered breathing (SDB), asthma, chronic ventilatory impairment, and respiratory instability in infants. Two of these categories, CHD and SDB, which accounted for 42 (76.4%) of the included articles, fulfilled the Evidence Based Pediatrics and Child Health criteria for causation. The indirect evidence included 8 reviews, 1 meta-analysis, and 10 original reports covering the fields of adult anoxia, animal research, SDB in adults, natural and experimental high-altitude studies, perinatal hypoxic-ischemic encephalopathy, anemia, and carbon-monoxide poisoning. The studies of high-altitude and carbon-monoxide poisoning provided evidence for causality. CONCLUSIONS: Adverse impacts of chronic or intermittent hypoxia on development, behavior, and academic achievement have been reported in many well-designed and controlled studies in children with CHD and SDB as well as in a variety of experimental studies in adults. This should be taken into account in any situation that may expose children to hypoxia. Because adverse effects have been noted at even mild levels of oxygen desaturation, future research should include precisely defined data on exposure to all levels of desaturation.

Adolescent↗
PubMed2003

Differential control over postganglionic neurons in rat cardiac ganglia by NA and DmnX neurons: anatomical evidence.

In previous single-labeling experiments, we showed that neurons in the nucleus ambiguous (NA) and the dorsal moto nucleus of the vagus (DmnX) project to intrinsic cardiac ganglia. Neurons in these two motor nuclei differ significantly in the size of their projection fields, axon caliber, and endings in cardiac ganglia. These differences in NA and DmnX axon cardiac projections raise the question as to whether they target the same, distinct, or overlapping populations of cardiac principal neurons. To address this issue, we examined vagal terminals in cardiac ganglia and trace injection sites in the brain stem using two different anterograde t ace s 1,1-dioleyl-3,3,3,3-tetramethylindocarbocyanine methanesulfonate and 4-[4-(dihexadecylamino)-styryl]-N-methylpyridinium iodide] and confocal microscopy in male Sprague-Dawley rats. We found that 1) NA and DmnX neurons innervate the same cardiac ganglia, but these axons target separate subpopulations of principal neurons and 2) axons arising from neurons in the NA and DmnX in the contralateral sides of the brain stem enter the cardiac ganglionic plexus through separate bundles and preferentially innervate principal neurons near their entry regions, providing topographic mapping of vagal motor neurons in left and right brain stem vagal nuclei. Because the NA and DmnX project to distinct populations of cardiac principal neurons, we propose that they may play different roles in controlling cardiac function.

Animals↗
PubMed2003

Attenuation of baroreflex sensitivity after domoic acid lesion of the nucleus ambiguus of rats.

The nucleus ambiguus (NA) and the dorsal motor nucleus of the vagus (DmnX) innervate distinct populations of cardiac ganglionic principal neurons. This anatomic evidence suggests that these two nuclei play different roles (Cheng Z and Powley TL, Soc Neurosci Abstr 26: 1189, 2000). However, lesion of the DmnX does not attenuate baroreflex sensitivity (Cheng Z, Guo SZ, Lipton AJ, and Gozal D, J Neurosci 22: 3215-3226, 2002). The present study tested the functional role of the NA in baroreflex control of heart rate (HR). Domoic acid (DA) was injected into the left NA of Sprague-Dawley rats to lesion the NA. The neuronal loss was assessed using retrograde labeling and confocal microscopy. HR changes induced by phenylephrine and sodium nitroprusside administration and after electrical stimulation of the left vagal trunk were measured at 15 days, and HR responses to left NA microinjection of L-glutamate were determined at 180 days postlesion. Compared with vehicle injections, DA lesions significantly reduced the population of NA motor neurons by approximately 68% (P < 0.01) and attenuated baroreflex sensitivity by approximately 83% (P < 0.01) at 15 days. Similarly, electrical stimulation of the vagal trunk of DA-lesioned animals led to attenuated decreases in HR responses. NA neuronal counts were reduced by approximately 81% (P < 0.01) and mean HR responses to l-glutamate injection into the lesioned NA were attenuated by approximately 65% (P < 0.01) at 180 days. Therefore, the NA plays a major role in baroreflex control of HR, and the integrity of the NA is critically important for the normal baroreflex control. In addition, NA lesions produce long-term anatomic and functional dysfunction of the nucleus, and thus it may provide an useful model for functional assessment of respective roles of the NA and DmnX.

Animals↗
PubMed2003

Regulation of catecholamines by sustained and intermittent hypoxia in neuroendocrine cells and sympathetic neurons.

Chronic intermittent hypoxia, a characteristic feature of sleep-disordered breathing, induces hypertension through augmented sympathetic nerve activity and requires the presence of functional carotid body arterial chemoreceptors. In contrast, chronic sustained hypoxia does not alter blood pressure. We therefore analyzed the biosynthetic pathways of catecholamines in peripheral nervous system structures involved in the pathogenesis of intermittent hypoxia-induced hypertension, namely, carotid bodies, superior cervical ganglia, and adrenal glands. Rats were exposed to either intermittent hypoxia (90 seconds of room air alternating with 90 seconds of 10% O2) or to sustained hypoxia (10% O2) for 1 to 30 days. Dopamine, norepinephrine, epinephrine, dihydroxyphenylacetic acid, and 5-hydroxytyptamine contents were measured by high-performance liquid chromatography. Expression of tyrosine hydroxylase and its phosphorylated forms, dopamine beta-hydroxylase, phenylethanolamine N-methyltransferase, and GTP cyclohydrolase-1 were determined by Western blot analyses. Both sustained and intermittent hypoxia significantly increased dopamine and norepinephrine content in carotid bodies but not in sympathetic ganglia or adrenal glands. In carotid bodies, both types of hypoxia augmented total levels of tyrosine hydroxylase protein and its phosphorylation on serines 19, 31, 40, as well as levels of GTP cyclohydrolase-1. However, the effects of intermittent hypoxia on catecholaminergic pathways were significantly smaller and delayed than those induced by sustained hypoxia. Thus, attenuated induction of catecholaminergic phenotype by intermittent hypoxia in carotid body may play a role in development of hypertension associated with sleep-disordered breathing. The effects of both types of hypoxia on expression of catecholaminergic enzymes in superior cervical neurons and adrenal glands were transient and small.

Adrenal Glands↗
PubMed2003

Increased upper airway collapsibility in children with obstructive sleep apnea during wakefulness.

Upper airway collapsibility (UAC) is increased in children with sleep-disordered breathing (SDB), but during wakefulness, active neural processes preserve upper airway patency, such that measurement of upper airway dynamics using acoustic pharyngometry may contribute to diagnostic accuracy in snoring children. Upper airway cross-sectional area obtained from acoustic pharyngometry measurements was assessed in 247 children referred for evaluation of suspected SDB and control subjects, before and after application of cetacaine 1% spray to the pharyngeal introitus under visual inspection. UAC was determined from the precentage change in cross-sectional area after topical anesthesia. UAC measurements were reproducible 1 week apart in both control subjects and patients with SDB (p < 0.005). A UAC less than or equal to -30% exhibited high sensitivity and specificity in identification of all children with obstructive apnea-hypopnea index greater than 5/hour total sleep time in a prospective initial sample of 54 children and in a subsequent post hoc sample of 94 snoring children. Thus, upper airway dynamic testing during wakefulness in response to a topical airway anesthetic may provide a useful clinical adjunct to the evaluation of snoring children, with more accurate identification of those children with SDB.

Adolescent↗
PubMed2003

Proteomic identification of a novel protein regulated in CA1 and CA3 hippocampal regions during intermittent hypoxia.

The CA1 and CA3 regions of the hippocampus markedly differ in their susceptibility to hypoxia in general, and more particularly to the intermittent hypoxia (IH) that characterizes sleep apnea. We used proteomic analysis to build a database of proteins expressed in normoxic CA1 and CA3. The current hippocampus protein database identifies 106 proteins. A hypothetical protein with accession number AK006737 (gimid R:12839969) was strongly upregulated in the CA1, but not CA3 hippocampal region. Bioinformatic analysis revealed that the unknown protein contained a high stringency protein kinase e binding site. Domain analysis demonstrated the presence of a conserved sequence indicative of macrophage scavenger receptors. Using proteomic analysis we have previously demonstrated that acute (6 h) IH-mediated CA1 injury results from complex interactions between pathways involving increased metabolism, induction of stress-induced proteins and apoptosis, and ultimately disruption of structural proteins and cell integrity. The current findings identify a hypothetical protein that may play a key role in the response of CA1 to IH. These findings provide initial insights into mechanisms underlying differences in susceptibility to hypoxia in neural tissue and demonstrate how proteomic analysis can be used to generate new hypotheses, which define neuronal adaptation to IH.

Animals↗
PubMed2003

Responses to hypoxia during early development.

Sustained hypoxia evokes a predictable cascade of ventilatory, neurochemical, and metabolic responses. Responses in immature animals are characterized by earlier and more marked depression of ventilation than fully mature animals. Ventilation during hypoxia reflects a collective system output, incorporating a number of compensatory mechanisms (stimulation or depression) from multiple systems. The time course of these responses is clearly developmentally regulated. When hypercapnia interacts with hypoxia, the ventilatory responses are enhanced but other responses are apparently unchanged. We propose a model in which responses to intermittent stimuli vary according to the point within the sequence of a single response where the stimulus interruption occurs. An intermittent stimulus may be seen as 'continuous' if the recurrence frequency exceeds a certain threshold, whereas application of slower cycles below such threshold may elicit discordant recruitment of the compensatory responses. Indeed, experimental observations on intermittent (hypercapnic or poikylocapnic) hypoxia show excitatory or depressant effects that are dictated by the cycle duration. Subject to further testing, this model may help explain how detrimental effects of hypoxic events in infancy only affect selected groups.

Animals↗
PubMed2003

Hypoxia induces an autocrine-paracrine survival pathway via platelet-derived growth factor (PDGF)-B/PDGF-beta receptor/phosphatidylinositol 3-kinase/Akt signaling in RN46A neuronal cells.

In neurons, hypoxia activates intracellular death-related pathways, yet the antiapoptotic mechanisms triggered by hypoxia remain unclear. In RN46A neuronal cells, minimum media growth conditions induced cell death as early as 12 h after the cells were placed in these conditions (i.e., after removal of B-27 supplement). However, apoptosis occurred in hypoxia (1% O2) only after 48 h, and in fact hypoxia reduced the apoptosis associated with trophic factor withdrawal. Furthermore, hypoxia induced time-dependent increases in expression of platelet-derived growth factor (PDGF) B mRNA and protein, as well as PDGF-beta receptor phosphorylation. Although exogenous PDGF-BB induced only transient Akt activation, hypoxia triggered persistent activation of Akt for up to 24 h. Inhibition of phosphatidylinositol 3-kinase (PI3K) or of PDGF-beta receptor phosphorylation abrogated both hypoxia-induced and exogenous PDGF-BB-induced Akt phosphorylation, and it completely abolished hypoxia-induced protection from media supplement deprivation, which suggests that the long-lasting activation of Akt during hypoxia and the prosurvival induction were due to endogenously generated PDGF-BB. Furthermore, these inhibitors decreased hypoxia-inducible factor 1alpha (HIF-1alpha) DNA binding, which suggests that the PDGF/PDGF-beta receptor/Akt pathway induces downstream HIF-1alpha gene transcription. We conclude that in RN46A neuronal cells, hypoxia activates an autocrine-paracrine antiapoptotic mechanism that involves up-regulation of PDGF-B and PDGF-beta receptor-dependent activation of the PI3K/Akt signaling pathway to induce downstream transcription of survival genes.

Apoptosis↗
PubMed2003

Cyclooxygenase 2 and intermittent hypoxia-induced spatial deficits in the rat.

Intermittent hypoxia (IH) during sleep, a critical feature of sleep apnea, induces significant neurobehavioral deficits in the rat. Cyclooxygenase (COX)-2 is induced during stressful conditions such as cerebral ischemia and could play an important role in IH-induced learning deficits. We therefore examined COX-1 and COX-2 genes and COX-2 protein expression and activity (prostaglandin E2 [PGE2] tissue concentration) in cortical regions of rat brain after exposure to either IH (10% O2 alternating with 21% O2 every 90 seconds) or sustained hypoxia (10% O2). In addition, the effect of selective COX-2 inhibition with NS-398 on IH-induced neurobehavioral deficits was assessed. IH was associated with increased COX-2 protein and gene expression from Day 1 to Day 14 of exposure. No changes were found in COX-1 gene expression after exposure to hypoxia. IH-induced COX-2 upregulation was associated with increased PGE2 tissue levels, neuronal apoptosis, and neurobehavioral deficits. Administration of NS-398 abolished IH-induced apoptosis and PGE2 increases without modifying COX-2 mRNA expression. Furthermore, NS-398 treatment attenuated IH-induced deficits in the acquisition and retention of a spatial task in the water maze. We conclude that IH induces upregulation and activation of COX-2 in rat cortex and that COX-2 may play a role in IH-mediated neurobehavioral deficits.

Analysis of Variance↗
PubMed2003

Sleep disturbances in children with attention deficit hyperactivity disorder.

The objective of the study was to compare polysomnographic patterns in two groups of preadolescent children with attention deficit hyperactivity disorder (ADHD) (a sleep clinic referral sample and a community sample) with control children. A prospective and observational study in the sleep clinic and the community was undertaken. Forty-seven ADHD children referred to the sleep clinic (ADHDcl), 53 ADHD children from a community survey (ADHDcom), and 49 control children underwent overnight polysomnography. Significant differences between the groups were observed for rapid-eye-movement (REM) sleep latency and percentage, and periodic limb movement index with associated arousals (PLMa). REM sleep latency was shorter in controls than ADHDcl and ADHDcom (p < 0.01) and REM% was highest in controls and lowest in ADHDcl (p < 0.001). PLMa was higher in ADHDcl than the other groups (p < 0.001), but there were no differences in PLMa between ADHDcom and controls. ADHD children display significant alterations in their sleep patterns, and ADHDcl are more likely to have an elevated PLMa than ADHDcom. In addition, REM sleep is affected by ADHD. We postulate that ADHDcl may represent a subset of children with ADHD at high risk for hyperactivity during sleep.

Attention Deficit Disorder with Hyperactivity↗
PubMed2003

VEGF-induced activation of the PI3-K/Akt pathway reduces mutant SOD1-mediated motor neuron cell death.

The increased oxidative stress induced by mutant SOD1 is associated with motor neuron degeneration in both human ALS and transgenic mice expressing mutant SOD1. Vascular endothelial growth factor (VEGF) is neurotrophic and also protects from hypoxia-induced neuronal injury. The potential role of VEGF in preventing mutant SOD1-mediated motor neuron cell death was examined using a mouse NSC34 motor neuron-like cell culture system. Infection with adenovirus containing mutant G93A-SOD1, but not vector control or wild-type SOD1, increased cellular oxidative stress and motor neuron-like cell death. However, NSC34 cells pretreated with VEGF displayed a dose-dependent resistance to oxidative damage from hydrogen peroxide, TNF-alpha, and mutant G93A-SOD1. VEGF activated both PI3-K and MAPK activities in mouse NSC34 motor neuron-like cells. Pharmacological inhibitors and constitutively active as well as dominant negative mutants of MAPK and PI3-K revealed that the protective effects of VEGF were mediated via the PI3-K activity, and that MAPK activation was not associated with NSC34 cell survival. Furthermore, VEGF-induced downstream Akt activation promoted motor neuron-like NSC34 cell survival in the presence of mutant G93A-SOD1. Thus, VEGF protected mouse NSC34 motor neuron-like cell death from mutant G93A-SOD1 effects via PI3-K/Akt activation.

Amyotrophic Lateral Sclerosis↗
PubMed2003

Spatial pre-training attenuates hippocampal impairments in rats exposed to intermittent hypoxia.

Intermittent hypoxia (IH), such as occurs in sleep apnea, is associated with increased apoptosis and neurobehavioral impairments in rats. To determine whether pre-training (P) modifies the effect of IH on spatial learning, adult male rats were trained in a spatial version of the water maze, exposed to IH or room air (RA) for 14 days, and then trained in a novel spatial task. P-RA had lower initial pathlengths than naive RA (N-RA), which were similar in P-IH and N-IH, indicating an adverse effect of IH on retention of behavioral strategies to solve the maze. However, P-IH acquired the later spatial task faster than N-IH. Pre-training was associated with increased phosphorylation of the cAMP-response element binding protein (CREB) in the hippocampus. Further, IH-induced decreases in CREB phosphorylation were attenuated by pre-training. We conclude that prior exposure to the water maze behavioral requirements attenuates the behavioral deficits occurring after IH exposure.

Animals↗
PubMed2003

Respiratory effects of gestational intermittent hypoxia in the developing rat.

Intermittent hypoxia (IH), one of the hallmarks of obstructive sleep apnea, occurs more frequently during pregnancy. We hypothesized that IH may lead to persistent postnatal changes in respiratory responses to acute hypoxia and may also lead to adverse effects on spatial function learning as revealed by the Morris water maze. To examine this issue, time-pregnant Sprague-Dawley rats were exposed to IH and room air (IHRA; 21 and 10% O2 alternations every 90 seconds) or to normoxia (RARA) until delivery. Ventilatory and metabolic responses to a 20-minute acute hypoxic challenge (10% O2) were conducted at postnatal ages 5, 10, 15, and 30 days. In addition, spatial task learning was assessed in the water maze at 1 and 4 months of age. Normoxic ventilation was higher at all time points in IHRA rats than in RARA rats (p < 0.01). Peak hypoxic ventilatory responses were attenuated in IHRA rats at 5 days of age and hypoxic ventilatory depression was accentuated at this age as well. However, ventilatory equivalents (minute ventilation/oxygen consumption) revealed significant reductions in peak hypoxic ventilatory responses of IHRA rats and hypoxic ventilatory depression at all postnatal ages (p < 0.01). Acquisition and retention of a spatial task were similar in the IHRA and RARA groups at both 1 and 4 months of age. We conclude that gestational intermittent hypoxia elicits long-lasting alterations in the control of breathing. We postulate that such IH-induced respiratory plasticity may create selective vulnerability to hypoxia during development.

Animals↗
PubMed2003

Intermittent hypoxia is associated with oxidative stress and spatial learning deficits in the rat.

In the adult rat, exposure to intermittent hypoxia (IH), such as occurs in sleep-disordered breathing, is associated with neurobehavioral impairments and increased apoptosis in the hippocampal CA1 region and cortex. We hypothesized that the episodic hypoxic-reoxygenation cycles of IH would induce oxidant stress, and the latter may underlie the IH-associated spatial learning and retention deficits. Adult male rats were therefore exposed to IH (90-second alternations of 10% oxygen and 21% oxygen) or room air (RA) for 7 days, and received twice-daily injections of either 3 mg/kg of the antioxidant PNU-101033E (PNU) or vehicle (V). Rats were then trained in a standard place-training task in the water maze. V-IH displayed significant impairments of spatial learning in the water maze, which were attenuated by PNU-101033E. Post hoc analyses further revealed that V-IH had significantly longer latencies and pathlengths to locate the hidden platform than PNU-IH, V-RA, or PNU-RA, indicating that PNU-101033E treatment reduced the behavioral impairments associated with IH. In addition, treatment with PNU-101033E markedly attenuated the increase in lipid peroxidation, and isoprostane concentrations associated with exposure to IH. Collectively, these findings indicate that the IH exposure is associated with increased oxidative stress, which is likely to play an important role in the behavioral impairments observed in a rodent model of sleep-disordered breathing.

Animals↗
PubMed2003

Intermittent hypoxia induces time-dependent changes in the protein kinase B signaling pathway in the hippocampal CA1 region of the rat.

Intermittent hypoxia (IH) during sleep induces temporally defined increases in apoptosis within vulnerable brain regions such as the hippocampal CA1 region in rats. Protein kinase B (AKT) has emerged as major signal transduction protein underlying inhibition of apoptosis and consequent increases in cell survival. Sprague Dawley adult male rats were exposed during sleep to IH or to normoxia (RA) for periods ranging from 0 to 30 days, and expression of total and phosphorylated AKT, of forkhead family members FKHR and FKHRL1, and of glycogen synthase kinase 3beta (GSK3beta) was assessed. Decreases in phosphorylation occurred as early as 1 h IH exposure, reached a nadir at 6 h-3 days, and then progressively returned to baseline levels at 14-30 days. Phosphorylated AKT and GSK3beta were intensely expressed and highly colocalized within neuronal cells (Neu-N positive) in the CA1 region. Thus, IH induces time-dependent biphasic changes in AKT survival pathways within the CA1 region that are temporally correlated with the initial increases and subsequent decreases in neuronal apoptosis.

Animals↗
PubMed2003

Kinetics of anaerobic metabolism in human skeletal muscle: influence of repetitive high-intensity exercise on sedentary dominant and non-dominant forearm. A 31P NMR study.

Potential differences were assessed between the dominant (D) and non-dominant (ND) forearms of sedentary subjects during anaerobic exercise. Subjects performed voluntary concentric contractions of D and ND forearm muscle during a series of three high-intensity (60% of the maximal voluntary contraction force (MVC)) exercise bouts. The time-dependent changes in intracellular pH (pH(i)), Pi, and PCr concentrations, and their relation to muscular work were examined using 31P magnetic resonance spectroscopy (MRS) techniques, and revealed that D forearm metabolic kinetics in sedentary individuals are improved during repetitive high-intensity exercise compared to their respective ND forearm muscle. We postulate that the more regular and preferential utilization of the D limb leads to a "trained-like" condition.

Adult↗