Henriette Pilegaard

TL;DR: It is demonstrated that exercise induces a dramatic transient increase in PGC‐1α transcription and mRNA content in human skeletal muscle, consistent with its role as a transcriptional coactivator, and suggest that PGC•1α may coordinate the activation of metabolic genes in human muscle in response to exercise.

TL;DR: In this paper, the brain contributed 70-80% of circulating BDNF, while that contribution decreased following 1 h of recovery following 1.5 hours of exercise, and the importance of the cortex and hippocampus as a source for BDNF becomes even more prominent in response to exercise.

TL;DR: Low levels of BDNF accompany impaired glucose metabolism, and may be a pathogenetic factor involved not only in dementia and depression, but also in type 2 diabetes, potentially explaining the clustering of these conditions in epidemiological studies.

TL;DR: It is demonstrated that exercise induces transient increases in transcription of metabolic genes in human skeletal muscle, and the findings suggest that the cumulative effects of transient rises in transcription during recovery from consecutive bouts of exercise may represent the underlying kinetic basis for the cellular adaptations associated with exercise training.

TL;DR: The data demonstrate that exercise activates transcription of the IL‐6 gene in working skeletal muscle, a response that is dramatically enhanced when glycogen levels are low, and support the hypothesis that IL‐ 6 may be produced by contracting myofibers when glycogens levels become critically low as a means of signaling the liver to increase glucose production.