Thomas J O'Leary1, Neil P Walsh2, Anna Casey1, Rachel M Izard3, Jonathan C Y Tang4, William D Fraser, Julie P Greeves. 1. Army Health and Performance Research, Army Headquarters, Andover, UNITED KINGDOM. 2. Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, UNITED KINGDOM. 3. Department of Occupational Medicine, HQ Army Recruiting and Initial Training Command, Upavon, UNITED KINGDOM. 4. Norwich Medical School, University of East Anglia, Norwich, UNITED KINGDOM.
Abstract
PURPOSE: This study aimed to investigate the effect of supplementary energy on bone formation and resorption during arduous military training in energy deficit. METHODS: Thirty male soldiers completed an 8-wk military combat course (mean ± SD, age = 25 ± 3 yr, height = 1.78 ± 0.05 m, body mass = 80.9 ± 7.7 kg). Participants received either the habitual diet (control group, n = 15) or an additional 5.1 MJ·d-1 to eliminate the energy deficit (supplemented group, n = 15). Circulating markers of bone formation and resorption, and reproductive, thyroid, and metabolic status, were measured at baseline and weeks 6 and 8 of training. RESULTS: Bone-specific alkaline phosphatase decreased in controls (-4.4 ± 1.9 μg·L-1) and increased in the supplemented group (16.0 ± 6.6 μg·L-1), between baseline and week 8 (P < 0.001). Procollagen type 1 N-terminal propeptide increased between baseline and week 6 for both groups (5.6 ± 8.1 μg·L-1, P = 0.005). Beta carboxy-terminal cross-linking telopeptide of type 1 collagen decreased between baseline and week 8 for both groups (-0.16 ± 0.20 μg·L-1, P < 0.001). Prolactin increased from baseline to week 8 for the supplemented group (148 ± 151 IU·L-1, P = 0.041). The increase in adiponectin from baseline to week 8 was higher in controls (4.3 ± 1.8 mg·L-1, P < 0.001) than that in the supplemented group (1.4 ± 1.0 mg·L-1, P < 0.001). Insulin-like growth factor binding protein-3 was lower at week 8 than baseline for controls (-461 ± 395 ng·mL-1, P < 0.001). CONCLUSION: The increase in bone-specific alkaline phosphatase, a marker of bone formation, with supplementation supports a role of energy in osteoblastic activity; the implications for skeletal adaptation and stress fracture risk are unclear. The mechanism is likely through protecting markers of metabolic, but not reproductive or thyroid, function.
PURPOSE: This study aimed to investigate the effect of supplementary energy on bone formation and resorption during arduous military training in energy deficit. METHODS: Thirty male soldiers completed an 8-wk military combat course (mean ± SD, age = 25 ± 3 yr, height = 1.78 ± 0.05 m, body mass = 80.9 ± 7.7 kg). Participants received either the habitual diet (control group, n = 15) or an additional 5.1 MJ·d-1 to eliminate the energy deficit (supplemented group, n = 15). Circulating markers of bone formation and resorption, and reproductive, thyroid, and metabolic status, were measured at baseline and weeks 6 and 8 of training. RESULTS: Bone-specific alkaline phosphatase decreased in controls (-4.4 ± 1.9 μg·L-1) and increased in the supplemented group (16.0 ± 6.6 μg·L-1), between baseline and week 8 (P < 0.001). Procollagen type 1 N-terminal propeptide increased between baseline and week 6 for both groups (5.6 ± 8.1 μg·L-1, P = 0.005). Beta carboxy-terminal cross-linking telopeptide of type 1 collagen decreased between baseline and week 8 for both groups (-0.16 ± 0.20 μg·L-1, P < 0.001). Prolactin increased from baseline to week 8 for the supplemented group (148 ± 151 IU·L-1, P = 0.041). The increase in adiponectin from baseline to week 8 was higher in controls (4.3 ± 1.8 mg·L-1, P < 0.001) than that in the supplemented group (1.4 ± 1.0 mg·L-1, P < 0.001). Insulin-like growth factor binding protein-3 was lower at week 8 than baseline for controls (-461 ± 395 ng·mL-1, P < 0.001). CONCLUSION: The increase in bone-specific alkaline phosphatase, a marker of bone formation, with supplementation supports a role of energy in osteoblastic activity; the implications for skeletal adaptation and stress fracture risk are unclear. The mechanism is likely through protecting markers of metabolic, but not reproductive or thyroid, function.
Authors: Shaun Chapman; Henry C Chung; Alex J Rawcliffe; Rachel Izard; Lee Smith; Justin D Roberts Journal: Nutrients Date: 2021-04-23 Impact factor: 5.717