Maria Papageorgiou1, Daniel Martin2, Hannah Colgan3, Simon Cooper4, Julie P Greeves5, Jonathan C Y Tang6, William D Fraser7, Kirsty J Elliott-Sale8, Craig Sale9. 1. Musculoskeletal Physiology Research Group, Sport, Health and Performance Enhancement Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, NG11 8NS, UK; Academic Diabetes, Endocrinology and Metabolism, Hull Medical School, University of Hull, Brocklehurst Building, Hull Royal Infirmary, Anlaby Road, Hull HU3 2RW, UK. Electronic address: M.Papageorgiou@hull.ac.uk. 2. Musculoskeletal Physiology Research Group, Sport, Health and Performance Enhancement Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, NG11 8NS, UK; School of Sport and Exercise Science, University of Lincoln, LN6 7TS, UK. Electronic address: DaMartin@lincoln.ac.uk. 3. Musculoskeletal Physiology Research Group, Sport, Health and Performance Enhancement Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, NG11 8NS, UK. Electronic address: Hannah.Colgan2011@my.ntu.ac.uk. 4. Musculoskeletal Physiology Research Group, Sport, Health and Performance Enhancement Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, NG11 8NS, UK. Electronic address: Simon.Cooper@ntu.ac.uk. 5. Army Personnel Research Capability, HQ Army, Monxton Road, Andover, Hampshire, SP11 8HT, UK. Electronic address: Julie.Greeves143@mod.uk. 6. Norwich Medical School, University of East Anglia, UK, Norfolk and Norwich University Hospital, Norfolk, NR4 7UQ, UK. Electronic address: Jonathan.Tang@uea.ac.uk. 7. Norwich Medical School, University of East Anglia, UK, Norfolk and Norwich University Hospital, Norfolk, NR4 7UQ, UK. Electronic address: W.Fraser@uea.ac.uk. 8. Musculoskeletal Physiology Research Group, Sport, Health and Performance Enhancement Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, NG11 8NS, UK. Electronic address: Kirsty.Elliottsale@ntu.ac.uk. 9. Musculoskeletal Physiology Research Group, Sport, Health and Performance Enhancement Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Campus, NG11 8NS, UK. Electronic address: Craig.Sale@ntu.ac.uk.
Abstract
PURPOSE: We aimed to explore the effects of low energy availability (EA)[15 kcal·kg lean body mass (LBM)-1·d-1] achieved by diet or exercise on bone turnover markers in active, eumenorrheic women. METHODS: By using a crossover design, ten eumenorrheic women (VO2 peak: 48.1 ± 3.3 ml·kg-1·min-1) completed all three, 3-day conditions in a randomised order: controlled EA (CON; 45 kcal·kgLBM-1·d-1), low EA through dietary energy restriction (D-RES; 15 kcal·kgLBM-1·d-1) and low EA through increasing exercise energy expenditure (E-RES; 15 kcal·kgLBM-1·d-1), during the follicular phase of three menstrual cycles. In CON, D-RES and E-RES, participants consumed diets providing 45, 15 and 45 kcal·kgLBM-1·d-1. In E-RES only, participants completed supervised running sessions (129 ± 10 min·d-1) at 70% of their VO2 peak that resulted in an exercise energy expenditure of 30 kcal·kg LBM-1·d-1. Blood samples were collected at baseline (BASE) and at the end of the 3-day period (D6) and analysed for bone turnover markers (β-CTX and P1NP), markers of calcium metabolism (PTH, albumin-adjusted Ca, Mg and PO4) and hormones (IGF-1, T3, insulin, leptin and 17β-oestradiol). RESULTS: In D-RES, P1NP concentrations at D6 decreased by 17% (BASE: 54.8 ± 12.7 μg·L-1, D6: 45.2 ± 9.3 μg·L-1, P < 0.001, d = 0.91) and were lower than D6 concentrations in CON (D6: 52.5 ± 11.9 μg·L-1, P = 0.001). P1NP did not change significantly in E-RES (BASE: 55.3 ± 14.4 μg·L-1, D6: 50.9 ± 15.8 μg·L-1, P = 0.14). β-CTX concentrations did not change following D-RES (BASE: 0.48 ± 0.18 μg·L-1, D6: 0.55 ± 0.17 μg·L-1) or E-RES (BASE: 0.47 ± 0.24 μg·L-1, D6: 0.49 ± 0.18 μg·L-1) (condition × time interaction effect, P = 0.17). There were no significant differences in P1NP (P = 0.25) or β-CTX (P = 0.13) responses between D-RES and E-RES. Both conditions resulted in reductions in IGF-1 (-13% and - 23% from BASE in D-RES and E-RES, both P < 0.01) and leptin (-59% and - 61% from BASE in D-RES and E-RES, both P < 0.001); T3 decreased in D-RES only (-15% from BASE, P = 0.002) and PO4 concentrations decreased in E-RES only (-9%, P = 0.03). CONCLUSIONS: Low EA achieved through dietary energy restriction resulted in a significant decrease in bone formation but no change in bone resorption, whereas low EA achieved through exercise energy expenditure did not significantly influence bone metabolism. Both low EA conditions elicited significant and similar changes in hormone concentrations. Crown
PURPOSE: We aimed to explore the effects of low energy availability (EA)[15 kcal·kg lean body mass (LBM)-1·d-1] achieved by diet or exercise on bone turnover markers in active, eumenorrheic women. METHODS: By using a crossover design, ten eumenorrheic women (VO2 peak: 48.1 ± 3.3 ml·kg-1·min-1) completed all three, 3-day conditions in a randomised order: controlled EA (CON; 45 kcal·kgLBM-1·d-1), low EA through dietary energy restriction (D-RES; 15 kcal·kgLBM-1·d-1) and low EA through increasing exercise energy expenditure (E-RES; 15 kcal·kgLBM-1·d-1), during the follicular phase of three menstrual cycles. In CON, D-RES and E-RES, participants consumed diets providing 45, 15 and 45 kcal·kgLBM-1·d-1. In E-RES only, participants completed supervised running sessions (129 ± 10 min·d-1) at 70% of their VO2 peak that resulted in an exercise energy expenditure of 30 kcal·kg LBM-1·d-1. Blood samples were collected at baseline (BASE) and at the end of the 3-day period (D6) and analysed for bone turnover markers (β-CTX and P1NP), markers of calcium metabolism (PTH, albumin-adjusted Ca, Mg and PO4) and hormones (IGF-1, T3, insulin, leptin and 17β-oestradiol). RESULTS: In D-RES, P1NP concentrations at D6 decreased by 17% (BASE: 54.8 ± 12.7 μg·L-1, D6: 45.2 ± 9.3 μg·L-1, P < 0.001, d = 0.91) and were lower than D6 concentrations in CON (D6: 52.5 ± 11.9 μg·L-1, P = 0.001). P1NP did not change significantly in E-RES (BASE: 55.3 ± 14.4 μg·L-1, D6: 50.9 ± 15.8 μg·L-1, P = 0.14). β-CTX concentrations did not change following D-RES (BASE: 0.48 ± 0.18 μg·L-1, D6: 0.55 ± 0.17 μg·L-1) or E-RES (BASE: 0.47 ± 0.24 μg·L-1, D6: 0.49 ± 0.18 μg·L-1) (condition × time interaction effect, P = 0.17). There were no significant differences in P1NP (P = 0.25) or β-CTX (P = 0.13) responses between D-RES and E-RES. Both conditions resulted in reductions in IGF-1 (-13% and - 23% from BASE in D-RES and E-RES, both P < 0.01) and leptin (-59% and - 61% from BASE in D-RES and E-RES, both P < 0.001); T3 decreased in D-RES only (-15% from BASE, P = 0.002) and PO4 concentrations decreased in E-RES only (-9%, P = 0.03). CONCLUSIONS: Low EA achieved through dietary energy restriction resulted in a significant decrease in bone formation but no change in bone resorption, whereas low EA achieved through exercise energy expenditure did not significantly influence bone metabolism. Both low EA conditions elicited significant and similar changes in hormone concentrations. Crown
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