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PubMed1996

Effects of physical activity and age on mitochondrial function.

It has been proposed that ageing results from the accumulation of mitochondrial DNA mutations with age which interfere with respiratory chain ATP production. Insufficient ATP production impairs cell function, and tissue dysfunction ensues, leading to morbidity, decline and eventually death. Supporting this theory, mitochondrial DNA mutations accumulate with age and respiratory chain function declines dramatically in human skeletal muscle. However, the extent of decline in respiratory chain function is greater (50%) than anticipated from the low levels of mitochondrial DNA mutations (< 1%) observed in aged muscle. We hypothesized that an age-related reduction in physical activity could be an important factor in this decline and thus studied the influence of chronological age on muscle mitochondria in subjects matched for levels of physical activity. In this carefully selected group, there was little correlation between oxidative metabolism and age. However, several parameters of respiratory chain function did correlate with markers of physical activity (activity score and handgrip strength). Our results suggest that reduced physical activity is a major contribution to the decline in mitochondrial oxidations during ageing. Physical activity ameliorates and may even mask mitochondrial 'ageing' in muscle.

Adult↗

PubMed2006

Cardiomyopathy in motor neuron diseases.

OBJECTIVE: Myocardial involvement in motor neuron diseases (MND) is an uncommon feature. In amyotrophic lateral sclerosis (ALS) abnormalities of the autonomic nervous system affecting cardiac function have been described, for the hereditary spastic paraplegias (HSP) comparable manifestations are unknown. This study observed ALS and HSP patients with coexisting cardiomyopathy without major cardial risk factors. METHODS: Four patients with definite ALS and two pHSP patients. In all patients detailed clinical, cardiological, electrophysiological and laboratory data were analysed. In two ALS patients skeletal muscle biopsy was performed. RESULTS: In all investigated MND patients cardiomyopathy was present. Beside hyperlipoproteinaemia and mild hypertension in one case, none of the patients showed major cardiovascular risk factors. There was no evidence for a secondary cause of cardiomyopathy like coronary heart disease, myocarditis, or mitochondrial damage mimicking MND. CONCLUSION: This report could not conclude that the occurrence of cardiomyopathy is rare logically. Although an underlying pathophysiological cause was not obvious, it is proposed that in all MND patients a routine cardiological evaluation should be performed.

Aged↗

PubMed1995

Volkmann's ischemic contracture of the foot and ankle: evaluation and treatment of established deformity.

Fibrotic contracture of skeletal muscle can follow weeks or months after the severe ischemic insult of compartment syndrome. Commonly known as Volkmann's ischemic contracture, the affected limb often becomes dysfunctional and painful, and may lose sensibility. The pathogenesis of the muscle contracture includes prolonged ischemia, myonecrosis, fibroblastic proliferation, contraction of the cicatrix, and myotendinous adhesion formation. Resultant shortening or overpull of involved muscles leads to stiffness and deformity. Simultaneously, nerve injury from initial ischemia or subsequent soft tissue fibrotic compression leads to muscle paresis or paralysis of the involved compartment and of those muscles more distally innervated. The resultant deformity is thus a combination of varying degrees of contracture and weakness depending on which muscles and nerves are affected. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by many factors, including: (1) which leg compartment, if any, has been affected and to what degree extrinsic flexor or extensor overpull is exhibited, (2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles (3) which foot compartment, if any, has been affected and to what degree intrinsic overpull is exhibited, and (4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Therefore, a variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Treatment is based on an appreciation of the pathoanatomy of the deformity. Nonoperative therapy is aimed at obtaining or preserving joint mobility, increasing strength, and providing corrective bracing and accommodative footwear. Operative management is usually reserved for treatment of residual nerve compression or severe and problematic deformities. Established surgical protocols are performed in a stepwise fashion, to include: (1) release of residual or secondary nerve compression, (2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy, (3) tendon transfers or arthrodesis to increase function, and (4) ostectomy or amputation for severe, refractory deformities.

Ankle Joint↗

PubMed1992

Central hemodynamic response to exercise in patients with chronic heart failure.

Although the pathophysiology of exercise intolerance in patients with chronic heart failure (CHF) is not fully understood, it appears that the cardiac output response plays an important role in limiting exercise in this disorder. Although previous studies have demonstrated that peak VO2 is not related to left ventricular (LV) ejection fraction, studies have consistently identified peak exercise cardiac output as an important predictor of peak VO2. It is likely that a reduced cardiac output to work rate relationship in CHF causes hypoperfusion of both working skeletal muscle and visceral organs, which leads to early anaerobic metabolism and fatigue. Several factors may influence the cardiac output response in patients with severe systolic LV dysfunction, including heart rate, diastolic LV function, and the mitral regurgitation fraction. Although stroke volume increases through use of the Frank-Starling mechanism in many patients with severe systolic LV dysfunction, some patients with this disorder may not increase stroke volume during exercise due to diastolic LV dysfunction or pericardial constraint. The finding that this latter group has more severe exercise intolerance suggests that diastolic dysfunction may further decrease peak VO2 in this disorder. Variations in the mitral regurgitation fraction also have been found to have an important effect on exercise stroke volume in some patients with CHF. Therefore, the finding that LV ejection fraction at rest or during exercise is not related to peak VO2 in patients with systolic LV dysfunction does not necessarily indicate that central hemodynamics do not play a role in exercise intolerance. Rather, it is likely that variability in the LV ejection fraction with exercise, which does not take variable increases in LV end-diastolic volume or mitral regurgitation into account, plays only a modest role in determining the stroke volume and cardiac output response to exercise in patients with severe systolic dysfunction.

Chronic Disease↗

PubMed1999

Properties of ventricular myocytes isolated from the hypertrophied and failing hearts of spontaneously hypertensive rats.

OBJECTIVE: To investigate how the morphological and physiological properties of single myocytes isolated from the hypertrophied, failing left ventricles (LV) differ from those of normal or hypertrophied not failing ventricles. METHOD: Single myocytes were isolated separately from right (RV) and left ventricles (LV) of male spontaneously hypertensive rats (SHR) or Wistar-Kyoto (WKY) rats at the age of 6 and 12 months and of SHRs which developed or not developed heart failure at the age of 20-24 months. We measured cells dimensions, range and kinetics of electrically stimulated or initiated by caffeine contractions and Ca2+ transients, and investigated the response of cells to thapsigargin. RESULTS: The transversal dimensions of the LV myocytes of 6 months old SHRs showed approximately 20% increase with respect to transversal dimensions of their RV myocytes and LV and RV myocytes of WKY rats. The difference did not change with progressing age and in the heart failure. The LV myocytes of 6 or 12 months old SHRs showed slowed kinetics of the Ca2+ transients and of contraction and relaxation and decreased contractile response to 2 s superfusion with 15 mM caffeine preceded by 5 mM Ni2+ used as an index of the sarcoplasmic reticulum (SR) Ca2+ content. Despite of this the range of shortening and relative contribution of the SR to contraction (assessed by measuring of the residual contractile response to electrical stimulation in cells poisoned with thapsigargin) or relaxation (assessed by calculation of the ratio of rate constants of the electrically stimulated and stimulated by 30 s superfusion with caffeine Ca2+ transients) was not altered in the hypertrophied myocytes. Properties of the LV myocytes of the 20-24 old SHRs with or without heart failure did not differ from those of LV myocytes of younger SHRs. The contractile response to caffeine of their RV myocytes dropped to the level of that in the LV myocytes. CONCLUSION: Our results suggest that transition from the compensated hypertrophy to the heart failure in 20-24 months old SHRs did not result from the further changes in properties of the surviving myocytes. Data from literature suggest that myocyte apoptosis and remodeling of the extramyocyte space is the more likely reason.

Animals↗

PubMed1999

[Pilot experience with skeletal muscles electrostimulation in rehabilitation of patients with complicated myocardial infarction].

AIM: To test electric stimulation of the skeletal muscles in rehabilitation of patients with complicated myocardial infarction. MATERIALS AND METHODS: 27 patients with macrofocal myocardial infarction (age 67 +/- 2.4 years) with persisting left ventricular insufficiency in the beginning of the subacute period. From day 3-4 all the patients were subjected to electrostimulation of large skeletal muscles (ESSM). The procedures were made daily for 2 hours using the Mioritm-040 unit. In the course of the first session the study was made of the changes in the intracardiac hemodynamics and doppler parameters of circulation in the popliteal artery. RESULTS: In the course of ESSM of 10-15 sessions none of the patients had anginal attacks, aggravation of dyspnea, arrhythmia episodes. After the course there was a marked increase in left ventricular ejection fraction and stroke volume. CONCLUSION: ESSM is safe in complicated myocardial infarction, prevent unwanted effects of long-term stay in bed, improves intracardiac hemodynamics.

Aged↗

PubMed2002

The health of the human skeletal system for weight bearing against gravity: The role of deloading the musculo-skeletal system in the development of musculoskeletal injury.

Musculo-skeletal disease is a major health problem which continues to increase in developed countries. A mechanism related hypothesis is presented to explain why most musculo-skeletal injury has an insidious onset and is not linked to a single traumatic event. The hypothesis predicts a close link between a dysfunction in the antigravity muscle system, which protects joints from injury, and the development of musculoskeletal disease patterns.

Journal Article↗

PubMed2000

The role of the levator ani muscle in evacuation, sexual performance and pelvic floor disorders.

This paper reviews the role of the levator ani muscle (LAM) in evacuation, sexual performance and pelvic floor disorders. The LAM fixes the vesical neck, anorectal junction and vaginal fornices to the side wall of the pelvis by means of the suspensory sling and hiatal ligament. On contraction it shares in the mechanism of evacuation (urination, defecation). During the sexual act vaginal distension by the erect penis evokes the vaginolevator and vaginopuborectalis reflexes, with a resulting LAM contraction. The LAM also contracts upon stimulation of the clitoris or cervix uteri, an action mediated through clitoromotor and cervicomotor reflexes. LAM contraction leads to upper vagina ballooning, which acts as receptacle for semen collection, to uterine elevation and straightening and to elongation and narrowing of the vagina. These actions enhance the sexual response and prepare the uterus and vagina for the reproductive process. During ejaculation LAM contraction facilitates semen ejection. Levator subluxation and sagging leads to levator dysfunction syndrome, which may present as pudendal canal syndrome.

Female↗

PubMed2001

[Modern concept of peripheral erectile mechanisms].

The article describes the peripheral mechanisms of erection and control over them. This knowledge has been acquired as a result of the recent development of pharmacological research designed to study the regulation of erectile smooth muscle tone. Smooth muscle fibres of the corpora cavernosa and arteries supplying the penis relax in response to a reduction of intracellular calcium. This relaxation allows both an increase of the blood flow to the penis and opening of sinusoid spaces. Cyclic nucleotides, cGMP and cAMP, are intracellular messengers of the mediators acting on smooth muscle fibres and regulating these intracellular calcium movements. Nitric oxide (NO) increases the intracellular cGMP concentration that triggers relaxation. Other proerectile mediators, such as vasoactive intestinal polypeptide, prostaglandin E1, are of the secondary importance. In contrast, neurotransmitters of the sympathetic nervous system (norepinephrine), neuropeptide Y, and endothelin induce contraction of cavernous smooth muscle fibres, thereby opposing erection. Oxygenation of the cavernous tissue is also an important factor in the regulation of local mechanisms of erection. Regulation of calcium sensitivity as well as functioning of intracellulare contact--gap junction are of certain interest. A better understanding of the peripheral pharmacology of erection opens the way to new pathophysiological and therapeutic prospects in the broad context of erectile dysfunction.

Animals↗

PubMed1997

Tissue-specific cytokine production during experimental acute pancreatitis. A probable mechanism for distant organ dysfunction.

Our purpose was to determine if cytokines are produced systemically during acute pancreatitis. Proinflammatory cytokines are elevated during acute pancreatitis and have been implicated in the progression of pancreatitis-associated multiple organ dysfunction. Whether these mediators are produced within all tissues or very few specific organs is not known. Edematous pancreatitis was induced in adult male mice by IP injection of cerulein. Necrotizing pancreatitis was induced in young female mice by feeding a choline-deficient, ethionine supplemented diet. Animals were sacrificed as pancreatitis worsened, with multiple organs prepared for tissue mRNA and protein analysis by RT-PCR and immunoblotting. Pancreatitis severity was established by histologic grading and serum amylase and lipase. There was no cytokine mRNA or protein detectable prior to the induction of pancreatitis. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1 beta) mRNA and protein were detected within the pancreas early in the course of pancreatitis in both models, coinciding with the development of hyperamylasemia (both P < 0.001). Interleukin-6 was produced in the pancreas after pancreatitis was more fully developed (P < 0.001). IL-1 beta and TNF-alpha were subsequently produced in large amounts in lung, liver, and spleen but never within kidney, cardiac muscle, or skeletal muscle. A significant delay between pancreatic and distant organ cytokine production was always observed. It is concluded that proinflammatory cytokines are produced within the pancreas and within organs known to develop dysfunction during severe pancreatitis. Cytokine production is tissue specific, correlates with disease severity, and occurs within the pancreas first and subsequently within distant organs.

Actins↗

PubMed1998

Trafficking pathway of GLUT4 glucose transporters in muscle (review).

Skeletal muscle is a major glucose-utilizing tissue in the absorptive state and alterations in muscle insulin-stimulated glucose uptake lead to derangements in whole body glucose disposal. The major glucose transporter expressed in skeletal muscle is the GLUT4 isoform. In the muscle fiber, GLUT4 undergoes insulin-stimulated translocation to T-tubules and to sarcolemma and it represents a pharmacological target for the treatment of diabetes mellitus, insulin-resistant states or in cardiac dysfunction. We review recent studies describing the characterization of the cellular steps followed by GLUT4 in muscle and we propose several working models for an integrated structure of the GLUT4 trafficking pathway.

Animals↗

PubMed1988

Weight loss with physiologic impairment. A basic indicator of surgical risk.

It is a long held belief that weight loss is a basic indicator of surgical risk. Many experienced surgeons, however, think otherwise. We have investigated the proposition that weight loss is a risk factor for postoperative complications but only when associated with clinically obvious physiologic impairment. Before major surgery, 102 patients had a careful history taken to ascertain if there had been recent weight loss and a reduction in the capacity for activity. Physical examination included assessment of mood, skeletal muscle function, respiratory muscle function, and wound healing. Plasma albumin was also measured. Using this information the patients were placed into one of three groups. Group I (N = 43) were normal, group II (N = 17) had weight loss greater than 10% but no clinical evidence of physiologic impairment, and group III (N = 42) had weight loss greater than 10% with clear evidence of dysfunction of two or more organ systems. The patients in group III had significantly more postoperative complications (p less than 0.05). They also had more septic complications (p less than 0.02) including a higher incidence of pneumonia (p less than 0.05) and a longer hospital stay (p less than 0.05) than patients in each of the other two groups. Objective measurements of body stores of protein and liver, and psychologic, respiratory, and skeletal muscle function, confirmed the validity of the clinical classification into the risk groups. The results demonstrate that weight loss is a basic indicator of surgical risk in modern practice providing it is associated with clinically obvious impairment of organ function. They suggest that adequate body protein stores are necessary for normal body function and for minimizing the risks of surgery.

Affect↗

PubMed2000

A pilot study using magnetic resonance imaging to determine the pattern of muscle group recruitment by rowers with different levels of experience.

OBJECTIVE: To determine whether it was possible using magnetic resonance imaging (MRI) to define the pattern of muscle recruitment in a specific sport (rowing) and to see whether there were differences in this pattern between athletes of different experience. DESIGN AND METHOD: It has been shown that during vigorous exercise the water content of muscle increases transiently. This can be observed using MRI, where the prolonged T2 relaxation time of muscle can be demonstrated. In this study we have exploited the increase in signal seen in exercised muscle on short TI inversion recovery (STIR) sequences, to show how rowers of different experience use different muscle groups. RESULTS: We have shown that trained athletes recruit selected muscle groups to carry out a given task, which they carry out more efficiently than untrained or less experienced athletes. CONCLUSION: We have provided the basis of potential research to refine training methods, in order to develop specific muscle groups in athletes, in the hope of achieving a higher level of performance at an earlier stage in their training. We have also defined a technique that may be of clinical value in cases of muscle dysfunction.

Adult↗

PubMed2003

[What is different about muscle pain?].

BACKGROUND: The bulk of available knowledge about pain mechanisms is derived from studies on cutaneous pain. However, deep somatic pain (from muscle, fascia, tendon, joint) is clinically of much greater importance. The existing subjective differences between muscle and skin pain (e.g. muscle pain is poorly localized and shows referral) suggest that muscle and skin pain do not share the same mechanisms. AIMS OF THE STUDY: To answer the question if the nociceptive information from muscle has neuroanatomical connections and mechanisms that are distinct from those of cutaneous nociception. MATERIALS AND METHODS: The results were obtained partly in animal experiments on anaesthetised rats, partly in studies with healthy subjects or fibromyalgia patients. RESULTS: 1. At the spinal level, the excitatory effects of unmyelinated afferent fibres from muscle are subject to a strong segmental inhibition by myelinated afferent fibres, which is largely absent in the effects of cutaneous C fibres. 2. At the cortical level, experimental muscle pain excites other regions than does cutaneous pain. 3. At the level of descending pain-modulating pathways, interruption of the activity in these pathways leads to higher activity of nociceptive neurones caudal to the site of interruption. The activity was higher in neurones with input from deep nociceptors than in cells mediating cutaneous nociception. CONCLUSIONS: The data demonstrate that at all central nervous levels the connections and processing of nociceptive information from muscle and skin are different. The findings regarding descending pain-modulating pathways suggest that a dysfunction of this system could lead to chronic deep pain as in fibromyalgia.

Humans↗

PubMed2000

[Role of microcirculation in multiorgan failure of infectious origin].

The normal host response to infection is a complex process which serves to localize and control bacterial invasion and to initiate repair of injured tissue. This inflammatory process is accompanied by activation of circulating and fixed phagocytic cells and generation of pro-inflammatory and anti-inflammatory mediators. Sepsis results when the prerequisite inflammatory response to infection becomes generalized, and thereby extends to involve otherwise normal tissue which is remote from the initial site of injury or infection. Sepsis is typically associated to cardiovascular alterations that have been characterized by increases in oxygen delivery to the tissues. Paradoxically, the host's systemic inflammatory response syndrome may simultaneously disturb the ability to adequately match tissue oxygen needs and availability at a time when tissue oxygen needs are typically increased. Depressed tissue oxygen availability relative to augmented needs may result from dysfunction at all of the central, regional, and microregional levels of the circulation. Significant dysregulation in the process by which oxygen availability is usually matched to changing tissue oxygen needs is typical associated with changes the microvascular blood flow behavior, vascular reactivity and endothelial and leukocyte activation. Specific tools developed to explore the microcirculation have been applied in the setting of both human and animal models sepsis. Abnormalities observed in the septic microvasculature are characterized by reductions in cutaneous and skeletal muscle blood flow and in mucosal intestinal ischemia and hypoxia. Regarding the skeletal muscle organ system, microvascular abnormalities were further characterized by an impairment of blood flow to increase in response to oxygen need increase. Also, microvascular abnormalities in the intestine were associated with evidence of endothelial and leukocyte activation leading to epithelial dysfunction. Thus, sepsis appears to be associated with early onset microvascular dysfunction. The relationship between microvascular dysfunction and endothelial and leukocyte activation leading to organ failure has been suggested by numerous studies.

Blood Flow Velocity↗

PubMed1996

Accumulation of somatic nucleotide substitutions in mitochondrial DNA associated with the 3243 A-to-G tRNA(leu)(UUR) mutation in encephalomyopathy and cardiomyopathy.

To understand the pathogenesis of mitochondrial encephalomyopathy and cardiomyopathy, we analyzed the sequence heterogeneity of the skeletal muscle mitochondrial DNA from a patient with Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes (MELAS). A mtDNA segment of 347 bp amplified from the total DNA was cloned into a vector. Analysis of 60 independent clones (20,800 bp in total) revealed the 3243 A-->G transition in all the sequenced clones and additional nucleotide substitutions at 5 sites in 10 clones. The frequency of mutant clones (10/60) in the MELAS patient was significantly higher [chi2 = 10.909, P < 0.05] than that in an age-matched skeletal muscle control (0/60) as well as in a normal placenta (2/60). These results support our hypothesis that secondary somatic mtDNA mutations can be initiated by the 3243 A-->G mutation and that the accumulation of somatic mutation in individuals with deleterious inherited mitochondrial genotype can contribute to the progressive mitochondrial dysfunction in MELAS.

Adult↗

PubMed1985

[Lipid peroxidation and the functioning of the Ca pump of the sarcoplasmic reticulum of skeletal muscle in hypercholesterolemia].

During prolonged hypercholesterolemia (HCh), there was a reduction in the efficacy of Ca-pump function of the sarcoplasmic reticulum (SR) of rabbit skeletal muscles, an increase in cholesterol content, and intensification of lipid peroxidation in SR membranes. Supplementation of the cholesterol-rich diet with alpha-tocopherol effectively prevented dysfunction of the SR Ca-pump and reduced the enhanced LPO level in SR membranes without having any effect on cholesterol content in blood serum and SR membranes. The increase in the LPO level seems likely to be primarily responsible for abnormalities in the SR Ca-pump during HCh.

Animals↗

PubMed1994

Spectrum analysis of diaphragmatic global electromyograms in cattle, with special regard to appropriate strategy for detection of fatigue.

Although the respiratory tract of healthy and diseased cattle has been intensively studied during the past few years, only a few attempts to detect dysfunctions of bovine inspiratory muscles have been reported. Such technique would be useful in assessing the possibility of inspiratory muscle fatigue in the context of ventilatory failure. Fatigue in skeletal muscle is associated with characteristic changes in the electromyographic power spectrum. Power spectral analysis was therefore applied to cattle diaphragmatic electromyograms (EMGdi) to precisely determine the exact influence of motion and ECG artifacts, describe its basic frequency content, and extract a spectral index capable of providing an accurate warning of fatigue. The EMGdi was recorded via intramuscularly placed fishhook electrodes in 5 healthy young bulls during resting and stimulated respiration. The EMGdi and EGC signals were analyzed by use of power spectral density analysis after band-pass filtering (20 to 1,800 Hz). The EMGdi spectrum was concentrated in the band width 20 to 530 Hz. Electrode motion artifacts were absent, and it was always possible to find an electrode pair giving ECG-free EMGdi. Of the 12 power and frequency values used to quantitate the spectrum, the most stable was the centroid frequency. It was reproducible within and between calves and was only minimally altered by changing inspiratory load.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗