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Hans Degens

Researcher at Manchester Metropolitan University

Publications -  273
Citations -  9922

Hans Degens is an academic researcher from Manchester Metropolitan University. The author has contributed to research in topics: Skeletal muscle & Muscle hypertrophy. The author has an hindex of 47, co-authored 254 publications receiving 8144 citations. Previous affiliations of Hans Degens include University of Liverpool & Maastricht University.

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Physical activity in older age: perspectives for healthy ageing and frailty.

TL;DR: The physiological rationale for physical activity, risks of adverse events, societal and psychological factors are discussed with a view to inform public health initiatives for the relatively healthy older person as well as those with physical frailty.
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Sarcopenia: Aging-Related Loss of Muscle Mass and Function.

TL;DR: This review focuses on the aging-related structural changes and mechanisms at cellular and subcellular levels underlying changes in the individual motor unit: specifically, the perikaryon of the α-motoneuron, its neuromuscular junction(s), and the muscle fibers that it innervates.
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The acute effect of stretching on the passive stiffness of the human gastrocnemius muscle tendon unit.

TL;DR: Passive stretching was commonly used to increase limb range of movement prior to athletic performance but it is unclear which component of the muscle–tendon unit (MTU) is affected by this procedure but post‐conditioning this was not the case suggesting that at least part of the change in muscle with conditioning stretches was due to altered properties of connective tissue.
Journal Article

Reporting whole-body vibration intervention studies: recommendations of the International Society of Musculoskeletal and Neuronal Interactions.

TL;DR: Experts in the field of WBV invited to provide suggestions on how the intervention should be described in such reports on how to improve the quality of reports about WBV treatment studies.
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Diaphragm Dysfunction in Chronic Obstructive Pulmonary Disease

TL;DR: The data suggest that enhanced diaphragm protein degradation through the ubiquitin-proteasome pathway plays a role in loss of contractile protein and, consequently, failure of the diphragm to generate force in COPD.