Marie-Christine Thibault

Human skeletal muscle fiber type alteration with high-intensity intermittent training

SummaryThe response of muscle fiber type proportions and fiber areas to 15 weeks of strenuous high-intensity intermittent training was investigated in twenty-four carefully ascertained sedentary (14 women and 10 men) and 10 control (4 women and 6 men) subjects. The supervised training program consisted mainly of series of supramaximal exercise lasting 15 s to 90 s on a cycle ergometer. Proportions of muscle fiber type and areas of the fibers were determined from a biopsy of the vastus lateralis before and after the training program. No significant change was observed for any of the histochemical charactertics in the control group. Training significantly increased the proportion of type I and decreased type IIb fibers, the proportion of type IIa remained unchanged. Areas of type I and IIb fibers increased significantly with training. These results suggest that high-intensity intermittent training in humans may alter the proportion of type I and the area of type I and IIb fibers and in consequence that fiber type composition in human vastus lateralis muscle is not determined solely by genetic factors.

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

SummaryThe 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 90 s. 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 90 s 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.

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.

Inheritance of Human Muscle Enzyme Adaptation to Isokinetic Strength Training

Five monozygotic twin pairs were submitted to a 10-week isokinetic strength training program and biochemical characteristics measured before and after training to determine the role of heredity in skeletal muscle adaptation, while 5 unrelated sedentary subjects served as control group. Experimental subjects performed twice 3 series of 5 bilateral reciprocal alternating knee flexions and extensions at a velocity of 90 degrees/s 5 times per week. Before and after the training period, for each subject, the peak muscular torque output was measured at the same velocity and the vastus lateralis muscle was biopsied for biochemical determinations. No significant change was observed in the control group. Training increased peak muscular torque output by 24%. The activities of hexokinase, malate dehydrogenase and 3-hydroxyacyl CoA dehydrogenase also increased significantly by 28, 26 and 38%, respectively. Interindividual variations in the response of these variables to training were noted but these were shown to be independent of the genotype. No overall effect of training was observed for oxoglutarate dehydrogenase activity (OGDH). However, changes were seen in individual pairs of twins and these were in opposite directions in some pairs compared to others, thus explaining the absence of a general training effect. Significant intrapair resemblance in the training response was present for OGDH (r = 0.76), indicating that the sensitivity to isokinetic strength training for OGDH was highly variable, not random and probably genetically determined.

Absence of charge variants in human skeletal muscle enzymes of the glycolytic pathway

SummaryPhenotypes of various glycolytic enzymes were determined in muscle biopsies. The results suggest that genetic effects on maximal enzyme activities may be associated with regulatory elements of the appropriate genes.

Lack of genetic polymorphism in human skeletal muscle enzymes of the tricarboxylic acid cycle

SummarySkeletal muscle mitochondrial forms of the tricarboxylic acid cycle enzymes were examined for genetic variance. The methods used revealed no genetic variants.