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Graham P. Holloway

Researcher at University of Guelph

Publications -  156
Citations -  6066

Graham P. Holloway is an academic researcher from University of Guelph. The author has contributed to research in topics: Skeletal muscle & Mitochondrion. The author has an hindex of 39, co-authored 142 publications receiving 5167 citations. Previous affiliations of Graham P. Holloway include Medical University of Białystok & Maastricht University.

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Repeated transient mRNA bursts precede increases in transcriptional and mitochondrial proteins during training in human skeletal muscle

TL;DR: The training‐induced increases in transcriptional and mitochondrial proteins appear to result from the cumulative effects of transient bursts in their mRNAs, and training-induced mitochondrial biogenesis appears to involve re‐modelling in addition to increased mitochondrial content.
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AMPK regulation of fatty acid metabolism and mitochondrial biogenesis: implications for obesity.

TL;DR: The current paradigms regarding the influence of AMPK in regulating skeletal muscle fatty acid metabolism and mitochondrial biogenesis at rest and during exercise are discussed, and the potential implications in the development of insulin resistance are highlighted.
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One Week of Bed Rest Leads to Substantial Muscle Atrophy and Induces Whole-Body Insulin Resistance in the Absence of Skeletal Muscle Lipid Accumulation

TL;DR: 1 week of bed rest substantially reduces skeletal muscle mass and lowers whole-body insulin sensitivity, without affecting mechanisms implicated in high-fat diet–induced insulin resistance.
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Fatty acid transport across the cell membrane: Regulation by fatty acid transporters

TL;DR: Current understanding of the mechanism of transmembrane fatty acid transport, and the function of fatty acid transporters in healthy cardiac and skeletal muscle, and in insulin resistance/type-2 diabetes are reviewed.
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Modest PGC-1α Overexpression in Muscle in Vivo Is Sufficient to Increase Insulin Sensitivity and Palmitate Oxidation in Subsarcolemmal, Not Intermyofibrillar, Mitochondria

TL;DR: In skeletal muscle in vivo, a modest PGC-1α overexpression up-regulated selected plasmalemmal and mitochondrial fuel-handling proteins, increased SS (not IMF) mitochondrial fatty acid oxidation, and improved insulin sensitivity.