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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

Authors

  • Akash Sinha,

    1. Department of Paediatric Endocrinology, Great North Children's Hospital, Newcastle-upon-Tyne, UK
    2. Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, UK
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  • Kieren G. Hollingsworth,

    1. Newcastle Magnetic Resonance Centre, Institute of Cellular Medicine, Newcastle University, Newcastle-upon-Tyne, UK
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  • Steve Ball,

    1. Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, UK
    2. Department of Endocrinology, Royal Victoria Infirmary, Newcastle-upon-Tyne, UK
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  • Tim Cheetham

    Corresponding author
    1. Department of Paediatric Endocrinology, Great North Children's Hospital, Newcastle-upon-Tyne, UK
    2. Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, UK
    • Correspondence: Tim Cheetham, Department of Paediatric Endocrinology, Great North Children's Hospital, Newcastle-upon-Tyne, NE1 4LP, UK. Tel.: 00(44) 191 2829562;

      E-mail: tim.cheetham@nuth.nhs.uk

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Summary

Context

Growth hormone–deficient (GHD) adults often report impaired quality of life (QoL) – 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 QoL 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 (τ1/2PCr) and proton handling using spectroscopy. Fasting biochemical analyses and anthropometric measurement were obtained. All patients completed the QoL-AGHDA and physical activity assessment (IPAQ) questionnaires.

Results

Untreated and treated GHD adults complained of significantly increased fatigue and an impaired QoL (= 0·002) when compared to healthy controls. There was no difference in maximal mitochondrial function (= 0·53) nor pH recovery (= 0·38) of skeletal muscle between the three groups. Untreated GHD patients had significantly lower IGF-1 than both treated GHD and healthy volunteers (< 0·001), but there was no association between τ1/2PCr and serum IGF-1 (r = −0·13, = 0·32).

Conclusions

The impaired QoL 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 QoL in GHD may have a significant central rather than peripheral (skeletal muscle) component.

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