J J Steventon1, J Collett2, H Furby3, K Hamana4, C Foster5, P O'Callaghan6, A Dennis7, R Armstrong8, A H Németh8, A E Rosser9, K Murphy10, L Quinn11, M Busse12, H Dawes13. 1. School of Physics and Astronomy, Cardiff University, UK; NMHRI, School of Medicine, Cardiff University, UK; CUBRIC, School of Psychology, Cardiff University, UK. Electronic address: steventonjj@cardiff.ac.uk. 2. Centre for Movement, Occupation and Rehabilitation Sciences, OxINMAHR, Oxford Brookes University, Oxford, UK; Faculty of Health and Life Sciences, Oxford Brookes University, Oxford, UK. 3. NMHRI, School of Medicine, Cardiff University, UK; CUBRIC, School of Psychology, Cardiff University, UK. 4. School of Healthcare Sciences, Cardiff University, UK. 5. CUBRIC, School of Psychology, Cardiff University, UK. 6. Cardiology Department, University Hospital of Wales, Cardiff, UK. 7. FMRIB Centre, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, OX3 9DU, UK. 8. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. 9. IPMCN, School of Medicine, Cardiff University, UK. 10. School of Physics and Astronomy, Cardiff University, UK; CUBRIC, School of Psychology, Cardiff University, UK. 11. Department of Biobehavioral Sciences, Teachers College, Columbia University, USA. 12. Centre for Trials Research, Cardiff University, UK. 13. Centre for Movement, Occupation and Rehabilitation Sciences, OxINMAHR, Oxford Brookes University, Oxford, UK; Department of Clinical Neurology, University of Oxford, Oxford, UK.
Abstract
BACKGROUND: Limited data suggests that an altered metabolic and cardiorespiratory exercise response may affect exercise performance in individuals with Huntington's disease (HD). There is no clear exploration of the response in individuals at different stages of the disease or in relation to genetic markers. This study aimed to examine the exercise response and recovery of HD participants, and the relationship to genetic and clinical markers. METHOD: HD gene-positive participants (n = 31; 9 pre-manifest; 22 manifest HD) and a healthy control group (n = 29) performed an incremental exercise test until exhaustion. Performance, cardiorespiratory, metabolic and perceptual responses to exercise were determined from a maximal cycle ergometer test throughout the exercise test and during a recovery period. RESULTS: During sub-maximal exercise, metabolic (lactate levels, oxygen uptake) and cardiorespiratory markers (heart rate) were elevated in HD participants compared to controls. Lactate elevation was specific to pre-manifest HD participants. Work capacity was reduced in both pre-manifest and manifest HD participants with tests terminated with no difference in metabolic, perceptual or cardiorespiratory markers. Submaximal oxygen uptake was correlated with motor score, whilst peak measures were unrelated to genetic or clinical markers. Heart rate recovery was attenuated in pre-manifest and manifest HD participants. CONCLUSIONS: Our findings confirm metabolic and cardiorespiratory deficits reduce exercise performance and affect recovery from an early stage in HD, with submaximal deficits related to phenotypic expression. Exercise capacity appears to be limited by an altered movement economy, thus clinicians should consider an altered exercise response and recovery may affect prescription in HD.
BACKGROUND: Limited data suggests that an altered metabolic and cardiorespiratory exercise response may affect exercise performance in individuals with Huntington's disease (HD). There is no clear exploration of the response in individuals at different stages of the disease or in relation to genetic markers. This study aimed to examine the exercise response and recovery of HD participants, and the relationship to genetic and clinical markers. METHOD: HD gene-positive participants (n = 31; 9 pre-manifest; 22 manifest HD) and a healthy control group (n = 29) performed an incremental exercise test until exhaustion. Performance, cardiorespiratory, metabolic and perceptual responses to exercise were determined from a maximal cycle ergometer test throughout the exercise test and during a recovery period. RESULTS: During sub-maximal exercise, metabolic (lactate levels, oxygen uptake) and cardiorespiratory markers (heart rate) were elevated in HD participants compared to controls. Lactate elevation was specific to pre-manifest HD participants. Work capacity was reduced in both pre-manifest and manifest HD participants with tests terminated with no difference in metabolic, perceptual or cardiorespiratory markers. Submaximal oxygen uptake was correlated with motor score, whilst peak measures were unrelated to genetic or clinical markers. Heart rate recovery was attenuated in pre-manifest and manifest HD participants. CONCLUSIONS: Our findings confirm metabolic and cardiorespiratory deficits reduce exercise performance and affect recovery from an early stage in HD, with submaximal deficits related to phenotypic expression. Exercise capacity appears to be limited by an altered movement economy, thus clinicians should consider an altered exercise response and recovery may affect prescription in HD.
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Authors: Jessica J Steventon; Hannah Furby; James Ralph; Peter O'Callaghan; Anne E Rosser; Richard G Wise; Monica Busse; Kevin Murphy Journal: Brain Commun Date: 2020-04-16