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Biomedical subjects

M C Thibault

Publications and source records attributed to M C Thibault.

At least 19 recordsLinked to original sources
PubMed1998

The interrater reliability of force measurements using a modified sphygmomanometer in elderly subjects.

BACKGROUND AND PURPOSE: Physical therapists working with elderly people require an instrument that provides reliable force measurements and can be used in a clinical setting. The modified sphygmomanometer has been identified as potentially fulfilling these requirements, yet there is an absence of research on the reliability of measurements taken with this instrument on elderly patients. This study was undertaken to investigate the interrater reliability of force measurements, in a group of elderly subjects, using a modified sphygmomanometer. SUBJECTS: Thirty-six hospitalized subjects (mean age=75.28 years, SD=9.43, range=62-95) participated in the study. METHODS: With the modified sphygmomanometer, 3 examiners evaluated the isometric force of the elbow extensors and hip extensors using a break test and a make test, respectively. RESULTS: Intraclass correlation coefficients (2,1) reflecting reliability were .87 for the elbow extensors and .65 for the hip extensors. The estimation of the components of variance for hip extensors revealed that these results were due in part to the raters but that random error contributed to a much larger extent. CONCLUSION AND DISCUSSION: The modified sphygmomanometer appears to be practical to use, and the high correlations found in this study for the elbow extensors suggest that reliable measurements can be obtained with this instrument. Further research is needed, however, to specify the manner in which the modified sphygmomanometer can be used when assessing different muscle groups.

Aged↗
PubMed1994

The myotonin-protein kinase phosphorylates tyrosine residues in normal human skeletal muscle.

As a first approach to study the cellular events involved in myotonic dystrophy, we have produced a polyclonal antibody against a peptide sequence of the predicted gene product. This antibody specifically recognizes a 54 kDa protein in human skeletal muscle. This protein phosphorylates a co-polymer Glu/Tyr but not Myelin Basic Protein. This indicates that the myotonin-protein kinase has a tyrosine kinase activity in human skeletal muscle. This is the first demonstration of the kinase activity of the myotonin-protein kinase.

Amino Acid Sequence↗
PubMed1993

Mitochondrial DNA sequence polymorphism, VO2max, and response to endurance training.

Mitochondrial DNA sequence variation was determined in 46 sedentary young adult males who took part in ergocycle endurance training programs in two laboratories to assess whether mitochondrial DNA variants were associated with individual differences in maximal oxygen uptake (VO2max) and its response to training. VO2max was obtained from a progressive ergocycle test to exhaustion. White blood cell mitochondrial DNA was characterized with the restriction fragment length polymorphism (RFLP) technique using 22 restriction enzymes and human mitochondrial DNA as a probe for hybridization. Multiple mitochondrial DNA variants were detected with 15 of the enzymes. Some subjects exhibited many RFLPs, while others showed no variation. These RFLPs (morphs) were generated by base substitutions located in gene regions coding for mitochondrial proteins as well as in the noncoding regions. Carriers of three mitochondrial DNA morphs, two in the subunit 5 of the NADH dehydrogenase gene and one in the tRNA for threonine, had a VO2max (ml.kg-1.min-1) in the untrained state significantly higher than noncarriers, while carriers of one mitochondrial DNA morph in subunit 2 of NADH dehydrogenase had a lower initial VO2max. Endurance training increased VO2max by a mean of 0.5 l of O2, with individual differences ranging from gains of 0.06 to 1.03. After adjustment for training site and initial VO2max, a lower response was observed for three carriers of a variant in subunit 5 of the NADH dehydrogenase detected with HincII (mean gain of 0.28 l; P < 0.05). These results suggest that sequence variation in mitochondrial DNA may contribute to individual difference in VO2max and its response to training.

Adolescent↗
PubMed1991

Mitochondrial DNA sequence polymorphism, VO2max, and response to endurance training.

Mitochondrial DNA sequence variation was determined in 46 sedentary young adult males who took part in ergocycle endurance training programs in two laboratories to assess whether mitochondrial DNA variants were associated with individual differences in maximal oxygen uptake (VO2max) and its response to training. VO2max was obtained from a progressive ergocycle test to exhaustion. White blood cell mitochondrial DNA was characterized with the restriction fragment length polymorphism (RFLP) technique using 22 restriction enzymes and human mitochondrial DNA as a probe for hybridization. Multiple mitochondrial DNA variants were detected with 15 of the enzymes. Some subjects exhibited many RFLPs, while others showed no variation. These RFLPs (morphs) were generated by base substitutions located in gene regions coding for mitochondrial proteins as well as in the noncoding regions. Carriers of three mitochondrial DNA morphs, two in the subunit 5 of the NADH dehydrogenase gene and one in the tRNA for threonine, had a VO2max (ml.kg-1.min-1) in the untrained state significantly higher than noncarriers, while carriers of one mitochondrial DNA morph in subunit 2 of NADH dehydrogenase had a lower initial VO2max. Endurance training increased VO2max by a mean of 0.51 of O2, with individual differences ranging from gains of 0.06 to 1.03. After adjustment for training site and initial VO2max, a lower response was observed for three carriers of a variant in subunit 5 of the NADH dehydrogenase detected with HincII (mean gain of 0.28 I; P less than 0.05). These results suggest that sequence variation in mitochondrial DNA may contribute to individual difference in VO2max and its response to training.

Adolescent↗
PubMed1991

Detection of linkage disequilibrium between the myotonic dystrophy locus and a new polymorphic DNA marker.

We have examined the linkage of two new polymorphic DNA markers (D19S62 and D19S63) and a previously unreported polymorphism with an existing DNA marker (ERCC1) to the myotonic dystrophy (DM) locus. In addition, we have used pulsed-field gel electrophoresis to obtain a fine-structure map of this region. The detection of linkage disequilibrium between DM and one of these markers (D19S63) is the first demonstration of this phenomenon in a heterogeneous DM population. The results suggest that at least 58% of DM patients in the British population, as well as those in a French-Canadian subpopulation, are descended from the same ancestral DM mutation. We discuss the implications of this finding in terms of strategies for cloning the DM gene, for a possible role in modification of risk for prenatal and presymptomatic testing, and we speculate on the origin and number of existing mutations which may result in a DM phenotype.

Chromosomes, Human, Pair 19↗
PubMed1990

Tight linkage of creatine kinase (CKMM) to myotonic dystrophy on chromosome 19.

The myotonic dystrophy (DM) gene is localized to the proximal long arm of chromosome 19. There have been reports of tight linkage to a number of chromosome 19 markers, including APOC2 and creatine kinase muscle type (CKMM), but they did not establish orientation of the 2 markers to DM. We screened several large multi-generational DM families for linkage to a series of chromosome 19 markers including CKMM. CKMM is tightly linked to DM in these data with z(theta) = 28.41; theta = 0.01. Analysis of cross-over data indicates CKMM is on the same side and closer to DM than APOC2. Thus, CKMM is a useful probe for carrier detection studies in presymptomatic individuals as well as for prenatal diagnosis.

Chromosome Mapping↗
PubMed1989

Hypertriglyceridemia and lower LDL cholesterol concentration in relation to apolipoprotein E phenotypes in myotonic dystrophy.

Plasma lipid, lipoprotein levels and apolipoprotein apo E phenotypes were determined in 70 patients with myotonic dystrophy (MyD) and 81 controls. Marked differences were noticed in the apo E phenotype frequencies between the two groups. Plasma triglycerides and VLDL cholesterol were higher in MyD than controls, but only the latter was related to differences in the apo E phenotypes between two groups. Accordingly, the ratio of VLDL cholesterol/plasma triglycerides was increased significantly in MyD, suggesting accumulation of intermediary density particles due to lower affinity of E2 containing lipoproteins for lipoprotein cell receptors. The LDL cholesterol concentration was lower in MyD than controls and was related to differences in the apo E phenotype frequencies between the two groups. These results indicate increased removal of LDL particles in the apo E2 phenotypes, perhaps due to upregulation of LDL (B, E) receptor activity. Plasma cholesterol and HDL cholesterol concentrations were similar in both groups. Another feature of the study was lower levels of plasma cholesterol, triglycerides, VLDL and LDL cholesterol in the homozygous E4:E4 phenotype. These results suggest increased clearance rate of both VLDL and LDL particles and support the concept that apo E4-containing lipoproteins have higher in vivo affinity for ape E and/or B, E receptors.

Adolescent↗
PubMed1989

Myotonic dystrophy: linkage with apolipoprotein E and estimation of the gene carrier status with genetic markers.

The genes for myotonic dystrophy (MD) and for apolipoprotein E (ApoE) belong to a chromosome 19 synthenic group of markers. A familial linkage analysis between MD and ApoE was performed using the J Ott LIPED program (IBM PC/XT, April 1984) to estimate the genetic distance between these 2 genes. Of a total of 136 individuals in 11 MD families, 81 were confirmed to be affected by the disease and 41 were asymptomatic. ApoE phenotypes were determined in 115 of these 122 individuals. No recombinant was observed out of 74 meioses which were informatives for both MD and the ApoE isoproteins. A global maximal lod score Z of 19.00 was obtained at the recombination fraction theta = 0. The upper theta value at the confidence interval corresponding to the peak lod score (Z max) - 1 was 0.03. This suggests that the loci for MD and ApoE are at a distance of 0 to 0.03 Morgan. Since ApoE and apolipoprotein C2 (ApoC2) have been shown by others to be about 40 kb apart, our data are therefore consistent with the distance estimate of 0.02 Morgan reported between MD and ApoC2. The D19S19 (LDR152) polymorphic DNA sequence is also tightly linked to MD on chromosome 19. The segregation of ApoE isoproteins and of ApoC2 and D19S19 DNA polymorphism was utilized for evaluating the probability for individuals at risk of inheriting the disease gene in MD families. Data are presented on 3 families to emphasize the usefulness of genetic markers to estimate the MD gene carrier status of asymptomatic individuals and also for those presenting a partial syndrome. The limitations of such approach are also discussed.

Apolipoproteins E↗
PubMed1989

Mitochondrial DNA polymorphism detected with the restriction enzymes BstNI and BclI in a French Canadian population.

The enzymes BstNI and BclI were used to detect various human mitochondrial DNA RFLPs in a sample of 104 unrelated French Canadians. These sequence variations were found in total white blood cell DNA probed with whole human mitochondrial DNA. With BstNI, 6 mitochondrial DNA restriction patterns (morphs) were identified. BstNI morphs 2-6 each differ from morph 1 by one single distinct restriction site gain or loss on the mitochondrial DNA molecule. Although BstNI morph 1 was found in most of the subjects (80%), each other morph was observed at a frequency of at least 3%. With the enzyme BclI, 4 different morphs were detected. Morphs 2-4 also result from different single restriction site alteration as compared with BclI morph 1. The morph 1 was clearly the most frequent (95%) while morphs 3 and 4 were present in only 1% of the subjects. These data indicate that the enzyme BstNI and, to a much lesser extent, the enzyme BclI detect mitochondrial DNA polymorphism in Caucasians. They are therefore of interest for population genetics studies.

Canada↗
PubMed1989

Muscle genetic variants and relationship with performance and trainability.

Samples were obtained in a maximum of 295 males and females from the vastus lateralis muscle and proteins fractionated by thin-layer isoelectric focusing. Muscle creatine kinase (CKM) and adenylate kinase (myokinase) (AK1M) were studied for the presence of variants. Six individuals exhibited a CKM variant described here for the first time, for a frequency of the variant gene of 1%. For AK1M, 21 individuals were heterozygotes for an inherited variant protein, an allele frequency of 3.5%. CKM (N = 5) and AK1M (N = 18) variant individuals were paired with control subjects who had the common CKM or AK1M muscle phenotype and compared for several performance indicators. There was no significant difference between the CKM and AK1M common and variant phenotypes for any of the performance measurements. However, the CKM variant subjects tended to be more effective than controls in a 90-min performance test (by about 22%) and had less percent decline over 60 s in force generation (by about 26%). In a subsequent experiment, a few variant subjects could be compared to controls in terms of response to exercise training. Although trends were observed, the CKM and AK1M variant subjects had a response to training generally comparable to that of the nonvariant individuals. While human variation in performance and trainability cannot be accounted for by the genetic polymorphism of the two kinase enzymes, the trends in the data suggest that allelic variation at these two gene loci may be of some functional significance.

Adenylate Kinase↗
PubMed1988

Isokinetic strength training protocols: do they induce skeletal muscle fiber hypertrophy?

Sedentary subjects were submitted to repeated concentric isokinetic strength training protocols separated by a 50-day detraining period. Peak torque output of the quadriceps muscle group increased by 54% after the first ten-week training protocol. No significant changes in mean skeletal muscle fiber area were observed while a significant increase in percent fiber type and percent fiber area was noticed for type IIa fibers. The activities of the enzymes hexokinase, malate dehydrogenase, 3-hydroxyacyl CoA dehydrogenase, and oxoglutarate dehydrogenase were also increased significantly. Fifty days without training induced a significant decline in peak torque output. All the enzymes that responded to the first training protocol maintained their elevated activities over the detraining period except for the enzyme oxoglutarate dehydrogenase. A second training protocol administered to the same subjects following the 50-day inactivity period did not result in any significant increase in maximum torque output and fiber area. It is concluded that the isokinetic strength training protocol used can increase the functional capacity of skeletal muscle, but this effect does not appear to be related to skeletal muscle fiber hypertrophy.

Adult↗
PubMed1987

Effects of two high-intensity intermittent training programs interspaced by detraining on human skeletal muscle and performance.

The purpose of this study was to investigate the effects of repeated high-intensity intermittent training programs interspaced by detraining on human skeletal muscle and performances. First, nineteen subjects were submitted to a 15-week cycle ergometer training program which involved both continuous and high-intensity interval work patterns. Among these 19 subjects, six participated in a second 15-week training program after 7 weeks of detraining. Subjects were tested before and after each training program for maximal aerobic power and maximal short-term ergocycle performances of 10 and 90s. Muscle biopsy from the vastus lateralis before and after both training programs served for the determination of creatine kinase (CK), hexokinase, phosphofructokinase (PFK), lactate dehydrogenase (LDH), malate dehydrogenase, 3-hydroxyacyl-CoA dehydrogenase (HADH) and oxoglutarate dehydrogenase (OGDH) activities. The first training program induced significant increases in all performances and enzyme activities but not in CK. Seven weeks of detraining provoked significant decreases in maximal aerobic power and maximal 90s ergocycle performance. While the interruption of training had no effect on glycolytic enzyme markers (PFK and LDH), oxidative enzyme activities (HADH and OGDH) declined. These results suggest that a fairly long interruption in training has negligeable effects on glycolytic enzymes while a persistent training stimulus is required to maintain high oxidative enzyme levels in human skeletal muscle. The degree of adaptation observed after the second training program confirms that the magnitude of the adaptive response to exercise-training is limited.

Adult↗
PubMed1987

Role of trophic factors in muscle differentiation.

Muscle genes are developmentally regulated. In vivo, the differential expression of muscle structural genes during myogenesis is controlled in complex ways by extrinsic factors and by a pre-determined genetic program. Terminal differentiation, which is achieved when differentiated myoblasts fuse to form multi-nucleated myotubes, appears mainly regulated by intrinsic factors. Environmental components, on the other hand, play a significant role in the developmental regulation of genes during the course of muscle fiber maturation. In culture, the differential expression of muscle genes is assumed to be solely controlled by intrinsic genetic factors, in the sense that, once precursors cease to proliferate and are committed to become myoblasts, they inevitably progress through terminal differentiation, whatever the environment. The system lacks the necessary elements to proceed towards fiber maturation. Consequently, muscle culture models have, until recently, been limited in studies dealing with the roles played both by genetic and environmental factors in the regulation of muscle gene expression. The accumulating data, however, suggest that under given culture conditions, it is becoming possible to make cells mature beyond embryonic stages and express specific phenotypes in response to extrinsic factors. This paper reviews some of the progress in the development of culture systems which will be useful in studies of muscle plasticity.

Animals↗
PubMed1986

Inheritance of human skeletal muscle and anaerobic capacity adaptation to high-intensity intermittent training.

The role of heredity in the response of maximal anaerobic capacities and skeletal muscle histochemical and biochemical characteristics to a 15-week cycle ergometer training program involving both continuous and interval work patterns was investigated in 14 pairs of monozygotic twins. The training program consisted mainly of series of ergocycle supramaximal exercises lasting from 15 s to 90 s and performed 4 and 5 times a week. The subjects were submitted to 10 s and 90 s all-out ergocycle tests to estimate maximal anaerobic alactacid (AAC) and lactacid (ALC) capacities, respectively. Muscle fiber types and creatine kinase (CK), hexokinase (HK), phosphofructokinase (PFK), lactate dehydrogenase (LDH), malate dehydrogenase (MDH), 3-hydroxyacyl CoA dehydrogenase (HADH), and oxoglutarate dehydrogenase (OGDH) activities were determined in a biopsy from the vastus lateralis. Training increased AAC, ALC, fiber type I proportion, MDH, HADH, and OGDH (P less than 0.05) and decreased fiber type IIb proportion and the PFK/OGDH ratio. No significant change was observed for CK, HK, PFK, and LDH. Large interindividual differences in the response to training were observed for all variables. However, intraclass correlations indicated that the extent of the response of ALC and CK, HK, LDH, MDH, and OGDH activities and of the PFK/OGDH activity ratio to training were significantly similar within pairs of twins. Although the role of heredity appeared absent for the changes in fiber type proportions and in anaerobic alactacid capacity, the present results suggest that the response of anaerobic lactacid capacity and most enzyme activities to high-intensity intermittent training is significantly determined by the genotype.

Adaptation, Physiological↗