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Impaired quality of life in growth hormone–deficient adults is independent of the altered skeletal muscle oxidative metabolism found in conditions with peripheral fatigue
Author(s) -
Sinha Akash,
Hollingsworth Kieren G.,
Ball Steve,
Cheetham Tim
Publication year - 2014
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.12252
Subject(s) - medicine , skeletal muscle , endocrinology , oxidative phosphorylation , biology , biochemistry
Summary Context Growth hormone–deficient ( GHD ) adults often report impaired quality of life ( Q o L ) – with fatigue, a key element. This deficit can improve following GH replacement. The basis of this response is unclear. Perturbations in skeletal muscle metabolism have been demonstrated in several conditions in which fatigue is a prominent symptom. We wished to define the role of skeletal muscle metabolism in the impaired Q o L observed in patients with GHD . Objective To compare in vivo skeletal muscle mitochondrial oxidative phosphorylation using phosphorus‐31 magnetic resonance spectroscopy in matched untreated GHD adults, treated GHD adults and healthy volunteers. Design Twenty‐two untreated GHD adults, 23 treated GHD adults and 20 healthy volunteers were recruited at a regional centre. All patients underwent assessment of muscle mitochondrial function (τ 1/2 PC r) and proton handling using spectroscopy. Fasting biochemical analyses and anthropometric measurement were obtained. All patients completed the Q o L ‐ AGHDA and physical activity assessment ( IPAQ ) questionnaires. Results Untreated and treated GHD adults complained of significantly increased fatigue and an impaired Q o L ( P = 0·002) when compared to healthy controls. There was no difference in maximal mitochondrial function ( P = 0·53) nor pH recovery ( P = 0·38) of skeletal muscle between the three groups. Untreated GHD patients had significantly lower IGF ‐1 than both treated GHD and healthy volunteers ( P < 0·001), but there was no association between τ 1/2 PC r and serum IGF ‐1 ( r = −0·13, P = 0·32). Conclusions The impaired Q o L seen in GHD adults is not associated with the skeletal muscle spectroscopic ‘footprint’ of altered mitochondrial oxidative function, anaerobic glycolysis or proton clearance that are a feature of several conditions in which fatigue is a prominent feature. These data suggest that the pathophysiology of fatigue and impaired Q o L in GHD may have a significant central rather than peripheral (skeletal muscle) component.