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Biomedical subjects

M Sanjak

Publications and source records attributed to M Sanjak.

12 recordsLinked to original sources
PubMed2004

Dissociation between mechanical and myoelectrical manifestation of muscle fatigue in amyotrophic lateral sclerosis.

Motor fatigue, during 30 seconds of maximum voluntary isometric contraction (MVIC) was simultaneously evaluated by the decline in mechanical force output, and from the compression in the power spectrum obtained from surface electromyogram (sEMG). Measurements were performed in patients diagnosed with amyotrophic lateral sclerosis (ALS) and normal control (NC) in two muscle groups, elbow flexors (EF) and ankle dorsiflexors (DF). The decline in force output, as a manifestation of mechanical fatigue, was digitally calculated online by partitioning the force versus time curve to determine the percent of MVIC reduction over a 30 sec period and was expressed as force fatigue index (FFI). The compression in the sEMG power spectrum, as a manifestation of myoelectrical fatigue, was tracked by calculating the median frequency shift (MFS) from the first 5 sec to the last 5 sec of the 30 sec MVIC using digital Fast Fourier Transformation. In ALS patients, the significantly higher reduction in mechanical force output during the 30 sec MVIC (higher FFI) was accompanied with significantly less compression in the sEMG power spectrum (less MFS) as compared to NC (P < or =0.005) in the two muscle groups. This dissociation between the mechanical and myoelectrical manifestation of muscle fatigue in ALS indicates that a reduction in muscle fiber conduction velocity (MFCV) may be a contributing peripheral factor in the pathogenesis of muscle fatigue in ALS. Alterations in motor unit functionality, especially in type II fast motor unit muscle fibers, and structural damage in denervated muscle fibers may contribute to the lower MFCV during motor fatigue in ALS patients.

Adult↗
PubMed2001

Quantitative assessment of motor fatigue in amyotrophic lateral sclerosis.

Motor fatigue is a common complaint in patients with amyotrophic lateral sclerosis (ALS), but is often excluded, unlike weakness, from the clinical assessment of these patients. This could be due to the complexity and often painful assessment techniques of this motor deficit. This study examines the feasibility of quantitative assessment of motor fatigue by modifying presently available force measurements. The relationship between weakness and fatigue in ALS patients was also examined. Fifty-four ALS patients and 39 normal control subjects performed 30 s of sustained maximal voluntary isometric contraction (MVIC) of elbow flexors (EF), knee extensors (NE), and ankle dorsiflexors (DF), using a computerized force measurement system and standardized testing procedures. Fatigue index (FI) was digitally calculated, from the force-time curve, as the percentage of MVIC unable to be sustained over the 30-s period. Fatigue was greater in ALS patients than in normal control (mean=23% vs. 15%) in all muscles including muscles that were not clearly weak. Weakness and fatigue were poorly correlated in ALS patients and may be independent measures of the pathogeneses of ALS.

Amyotrophic Lateral Sclerosis↗
PubMed1999

Quantitative assessment of motor fatigue and strength in MS.

OBJECTIVE: To determine the test-retest reliability of strength and fatigue measurements in patients with MS and in healthy control subjects, and to examine associations among motor fatigue, strength, and ambulatory impairment in MS patients. BACKGROUND: Motor fatigue, defined as the loss of the maximal capacity to generate force during exercise, and weakness are common in patients with MS. METHOD: Twenty ambulatory MS patients and 20 age- and sex-matched healthy control subjects participated in the study. Test-retest reliability was assessed in two identical testing sessions, separated by 3 to 5 days. Maximal voluntary isometric strength was determined by fixed myometry of seven muscle groups on each side. Motor fatigue was assessed using three exercise protocols: sustained maximal contractions (static fatigue), repetitive maximal contractions, and walking as far as 500 m. Four analysis models for static fatigue were examined for their test-retest reliability and their ability to discriminate between normal fatigue and pathologic fatigue from MS. RESULTS: Test-retest reliability in MS patients was excellent for isometric strength and very good for static fatigue. Test-retest reliability was lower for exercise protocols that involved repetitive contractions or ambulation. Compared with healthy control subjects, MS patients were weak in lower extremity muscles, but upper extremity strength was relatively preserved. Fatigue was greater in MS patients, even in muscles that were not clearly weak. There were no significant associations between strength and fatigue in any of the muscles tested. A fatigue analysis model based on the area under the force-versus-time curve gave the best combination of reliability and sensitivity to detect differences between MS patients and healthy control subjects. CONCLUSIONS: Strength and motor fatigue can be measured reliably in patients with MS. MS patients experience more fatigue than healthy control subjects during sustained contractions, repetitive contractions, and ambulation. Motor fatigue appears to be distinct from weakness because the degree of fatigue was not associated with the degree of weakness in individual muscles. Quantitative assessment of strength and fatigue may be useful to monitor changes in motor function over time in MS patients.

Adult↗
PubMed1997

Guidelines for the use and performance of quantitative outcome measures in ALS clinical trials.

ALS is a motor neuron disease defined as a progressive, neurological disorder, resulting from variable and combined degeneration of upper and lower motor neurons. The heterogeneity of clinical involvement early in the course of the disease makes it difficult to diagnose, as well as to identify one unique outcome measure to quantify neurological changes in the course of the disease. Since clinical evidence of upper and lower motor neuron degeneration must exist in four anatomical regions (bulbar, cervical, thoracic, and lumbosacral), outcome measures should assess these regions. The WFN Airline House recommendations specify the purpose, properties, and the preferred parameters which serve as outcome measures in ALS clinical trials. The purpose of this document is to serve as a review of these outcome measures in terms of their advantages, disadvantages, sensitivity, reliability, and other characteristics, as well as their proper performance in ALS clinical trials. Generally these outcome measures are allocated to four areas: respiratory function, muscle strength, general function, and bulbar function. Our review leads us to believe that respiratory function and strength provide the most useful information, both for research and clinical purposes, and are essential as outcome measures. Inclusion of bulbar and general function parameters in trial design may increase the possibility of identifying a beneficial effect of therapeutic intervention. It is essential to note that the guidelines and recommendations put forth are intended to provide initial evaluation and critique of the proper employment and performance of these outcome measures in ALS clinical trials, based on the available literature and our experience.

Amyotrophic Lateral Sclerosis↗
PubMed1996

CD8 and CD4 T cell-mediated polymyositis complicating the HTLV-1 associated myelopathy. Quantitative evaluation of corticosteroid treatment.

INTRODUCTION: Inflammatory myopathy is a treatable cause of worsening in the spectrum of neurological conditions that may develop during the course of HTLV-1 infection. MATERIAL AND METHODS: To investigate the cause of subacute worsening in the strength of a 46-y-old black male with HTLV-1 associated myelopathy we performed electrodiagnostic examination and a muscle biopsy which was studied with histochemistry, immunocytochemistry and electron microscopy. Serial measurements of isometric muscle strength were performed during the course of corticosteroid treatment. RESULTS: The muscle biopsy showed evidence of denervation atrophy and prominent inflammatory changes with autoaggressive features. Lymphocyte typing showed a predominance of CD8+ T cells. The patient had sustained, marked improvement in strength, especially of the upper extremities, with oral, high single-dose, alternate-day prednisone therapy. CONCLUSION: A muscle biopsy should be considered in all patients with HTLV-1 associated weakness, especially when electromyography indicates possible coexisting primary muscle involvement and/or serum creatine kinase levels are elevated. HTLV-1-associated polymyositis can be successfully treated with corticosteroids.

Anti-Inflammatory Agents↗
PubMed1987

Endurance training does not affect diaphragm mitochondrial respiration.

We sought to determine if chronic endurance training would increase mitochondrial respiration or protein content in rat diaphragm muscle. To this end, 20 male Wistar rats were randomly assigned to control (C) or an 8-week endurance training (T) group, n = 10 per group. At the end of T, VO2 max was 13% greater in T (83.3 vs 73.8 ml X kg-1 X min-1) and peak max power output was 32% greater (2.63 vs 1.98 kg X m X min-1). Mitochondrial specific activities of pyruvate-malate and cytochrome oxidase (expressed per mg mitochondrial protein) in both plantaris and diaphragm were similar in C and T rats, as were ADP/O and respiratory control ratios. When expressed per gram wet weight, whole muscle homogenate oxygen uptake (pyruvate + malate) and cytochrome oxidase activity increased 36 and 23%, respectively (P less than 0.05) in plantaris from T rats but did not change in diaphragm. Control oxidative capacity and mitochondrial protein content in the diaphragm were ca. 2-fold those in control plantaris. Plantaris mitochondrial protein content increased ca. 50% with T while the diaphragm was unaffected. We conclude that: plantaris muscle oxidative capacity adapts to training by increasing mitochondrial protein content, since there was no evidence for functional improvement of existing mitochondria, and in the face of a substantial training effect in whole animal and plantaris, the T stimulus was not sufficient to induce mitochondrial protein changes in the diaphragm. This finding is the result of either a 'pre-adaptation' secondary to the diaphragm's high chronic activity, or a sub-threshold increase in diaphragm recruitment during the exercise conditions studied.

Alcohol Oxidoreductases↗
PubMed1987

Physiologic and metabolic response to progressive and prolonged exercise in amyotrophic lateral sclerosis.

Physical work capacity in 35 ALS patients and 6 untrained controls was evaluated during progressive bicycle ergometry. In the ALS patients, maximum oxygen consumption (VO2max) and work capacity (Wmax) drop in relation to the decrease in ALS functional score. However, the oxygen cost (ml O2/kpm) of submaximal exercise was significantly increased. Prolonged submaximal exercise tests in six ALS patients and six matched untrained controls indicated that the exercise-induced increase in plasma free fatty acids, beta-hydroxybutyrate, esterified carnitine, and muscle esterified carnitine was significantly retarded in ALS patients.

3-Hydroxybutyric Acid↗
PubMed1987

Role of muscular exercise in amyotrophic lateral sclerosis.

The general, systemic, and specific neuromuscular adaptation to physical exercise and training in healthy individuals is reviewed with application to individuals with neuromuscular disease in general and ALS in particular. A pilot study utilizing patients with ALS suggests the cardiopulmonary response to acute exercise is similar to normal individuals. However, a case study of a training response suggests the success of neuromuscular adaptation will be dependent upon the degree of motor neuron involvement.

Adult↗
PubMed1986

Carnitine metabolism during prolonged exercise and recovery in humans.

Lennon et al. (J. Appl. Physiol. 55: 489-495, 1983) have recently reported a large loss of muscle total carnitine (TC) after 40 min of moderate exercise. These authors have also suggested that elevations in plasma esterified carnitine (EC) were due to the release of these carnitine esters from muscle during exercise. After 10 male subjects underwent 90 min of cycle egometry we found no alteration in muscle TC from preexercise values. Plasma EC progressively increased above resting values during exercise and remained elevated above rest at 0.75 and 1.5 h into recovery. Elevations of plasma EC were largely due to a decrement in free carnitine (FC) in both conditions. Immediately postexercise the urinary fractional reabsorbsion of EC and FC were similar to that at rest. These results suggest that a net loss of TC from exercising muscle does not occur. As in other conditions marked by falling insulin concentrations, elevations in plasma EC could result from an exchange of carnitine with the hepatic carnitine pool.

3-Hydroxybutyric Acid↗