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Kristian Vissing

Publications and source records attributed to Kristian Vissing.

3 recordsLinked to original sources

Sex differences in hormone-sensitive lipase expression, activity, and phosphorylation in skeletal muscle at rest and during exercise.

Women have been shown to use more intramuscular triacylglycerol (IMTG) during exercise than men. To investigate whether this could be due to sex-specific regulation of hormone-sensitive lipase (HSL) and to use sex comparison as a model to gain further insight into HSL regulation, nine women and eight men performed bicycle exercise (90 min, 60% Vo(2peak)), and skeletal muscle HSL expression, phosphorylation, and activity were determined. Supporting previous findings, basal IMTG content (P < 0.001) and net IMTG decrease during exercise (P < 0.01) were higher in women than in men and correlated significantly (r = 0.72, P = 0.001). Muscle HSL mRNA (80%, P = 0.11) and protein content (50%, P < 0.05) were higher in women than in men. HSL total activity increased during exercise (47%, P < 0.05) but did not differ between sexes. Accordingly, HSL specific activity (HSL activity per HSL protein content) increased during exercise (62%, P < 0.05) and was generally higher in men than in women (82%, P < 0.05). A similar pattern was observed for HSL Ser(659) phosphorylation, suggesting a role in regulation of HSL activity. Likewise, plasma epinephrine increased during exercise (P < 0.05) and was higher in men than in women during the end of the exercise bout (P < 0.05). We conclude that, although HSL expression and Ser(659) phosphorylation in skeletal muscle during exercise is sex specific, total muscle HSL activity measured in vitro was similar between sexes. The higher basal IMTG content in women compared with men is therefore the best candidate to explain the higher IMTG net hydrolysis during exercise in women.

Adult↗

Gene expression of myogenic factors and phenotype-specific markers in electrically stimulated muscle of paraplegics.

The transcription factors myogenin and MyoD have been suggested to be involved in maintaining slow and fast muscle-fiber phenotypes, respectively, in rodents. Whether this is also the case in human muscle is unknown. To test this, 4 wk of chronic, low-frequency electrical stimulation training of the tibialis anterior muscle of paraplegic subjects were used to evoke a fast-to-slow transformation in muscle phenotype. It was hypothesized that this would result from an upregulation of myogenin and a downregulation of MyoD. The training evoked the expected mRNA increase for slow fiber-specific markers myosin heavy chain I and 3-hydroxyacyl-CoA dehydrogenase A, whereas an mRNA decrease was seen for fast fiber-specific markers myosin heavy chain IIx and glycerol phosphate dehydrogenase. Although the slow fiber-specific markers citrate synthase and muscle fatty acid binding protein did not display a significant increase in mRNA, they did tend to increase. As hypothesized, myogenin mRNA was upregulated. However, contrary to the hypothesis, MyoD mRNA also increased, although later than myogenin. The mRNA levels of the other myogenic regulatory factor family members, myogenic factor 5 and myogenic regulatory factor 4, and the myocyte enhancer factor (MEF) family members, MEF-2A and MEF-2C, did not change. The results indicate that myogenin is indeed involved in the regulation of the slow oxidative phenotype in human skeletal muscle fibers, whereas MyoD appears to have a more complex regulatory function.

Adaptation, Physiological↗

Are exercise-induced genes induced by exercise?

Numerous human in vivo studies on skeletal muscle gene expression have investigated the effects of given interventions. These have been founded on the assumption that presampling can be regarded as a representative control for postintervention sampling. However, many genes are responsive to the metabolic status, which varies during the day, so that observed differences in gene expression between the pre- and post-sample may therefore be a result of the daily variations rather than an intervention. Furthermore, the sampling itself can cause a local stress response, which may also influence the expression of some genes in later samples from the same localized area. To test this, we performed a short-term human endurance exercise study in which muscle biopsies were obtained from healthy untrained individuals (n=14) before and in the hours after exercise to measure the expression of mRNA for previously reported exercise-related genes (e.g., PPARgamma coactivator-1alpha (PGC-1alpha), pyruvate dehydrogenase kinase 4 (PDK4), MyoD, p21, (heat shock protein 72 (HSP72), lipoprotein lipase (LPL), citrate synthase (CS), and glucose transporter 4 (GLUT4)). To test for changes unrelated to exercise, one half of the subjects did not exercise. As suspected, several presumed exercise-induced genes were induced even without the exercise. Our data demonstrate that presampling is not always a representative control for postintervention sampling, illustrating that use of presampling can cause erroneous interpretations of the underlying induction signals.

Adult↗