title: Whole-body vibration can reduce calciuria induced by high protein intakes and may counteract bone resorption: A preliminary study.
abstract: Excess protein intake can adversely affect the bone via an increase in calcium excretion, while suitable mechanical loading promotes osteogenesis. We therefore investigated whether vibration exposure could alleviate the bone mineral losses associated with a metabolic acidosis. Ten healthy individuals aged 22 - 29 years (median = 25) underwent three 5-day study periods while monitoring their dietary intake. The study consisted of recording the participants' usual dietary intake for 5 consecutive days. Participants were then randomly divided into two groups, one of which received a protein supplement (2 g x kg(-1) body mass x day(-1); n = 5) and the other whole-body low-magnitude (3.5 g), low-frequency (30 Hz) mechanical vibration (WBV) delivered through a specially designed vibrating plate for 10 min each day (n = 5). Finally, for the third treatment period, all participants consumed the protein supplement added to their normal diet and were exposed to WBV exercise for 10 min per day. Daily urine samples were collected throughout the experimental periods to determine the excretion of calcium, phosphate, titratable acid, urea, and C-telopeptide. As expected, when the participants underwent the high protein intake, there was an increase in urinary excretion rates of calcium (P < 0.001), phosphate (P < 0.003), urea (P < 0.001), titratable acid (P < 0.001), and C-telopeptide (P < 0.05) compared with baseline values. However, high protein intake coupled with vibration stimulation resulted in a significant reduction in urinary calcium (P = 0.006), phosphate excretion (P = 0.021), and C-telopeptide (P < 0.05) compared with protein intake alone, but did not affect titratable acid and urea output. The participants showed no effect of WBV exercise alone on urinary excretion of calcium, phosphate, urea, titratable acid, or C-telopeptide. The results indicate that vibration stimulation can moderate the increase in bone resorption and reduction in bone formation caused by a metabolic acidosis.
authors.affiliation: Olympic Medical Institute, Northwick Park Hospital, Harrow, UK. Marco.Cardinale@boa.org.uk
authors.forename: M
authors.initials: M
authors.lastname: Cardinale
authors.forename: J
authors.initials: J
authors.lastname: Leiper
authors.forename: P
authors.initials: P
authors.lastname: Farajian
authors.forename: M
authors.initials: M
authors.lastname: Heer
mesh_terms: D000138:Acidosis / Q000503:physiopathology*; D000143:Acids / Q000652:urine; D000328:Adult; D001862:Bone Resorption / Q000503:physiopathology / Q000517:prevention & control*; D002118:Calcium / Q000652:urine*; D024042:Collagen Type I / Q000652:urine; D004044:Dietary Proteins / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D008297:Male; D010455:Peptides / Q000652:urine; D010710:Phosphates / Q000652:urine; D014508:Urea / Q000652:urine; D014732:Vibration
chemical_list: D000143:Acids; D024042:Collagen Type I; D004044:Dietary Proteins; D010455:Peptides; D010710:Phosphates; C052929:collagen type I trimeric cross-linked peptide; D014508:Urea; D002118:Calcium