Osteoporosis and low bone mass are one of the major public health problems affecting elderly subjects (Kelley et al., 2000). Several pharmacological treatments have been used in preventing or attenuating osteoporosis, notably alendronate sodium, risedronate sodium, zoledronic acid, and selective estrogen receptor modulators, such as raloxifene (Cavanagh et al., 2005). There has also been interest in anabolic agents such as parathyroid hormone (PTH), vitamin D and calcium (Cavanagh et al., 2005) recently. Exercise has been recommended as a nonpharmacological approach for maximizing bone mineral density during the younger years (Snow-Harter and Marcus, 1991). Measurement of bone biochemical markers can also provide a practical way for early detection of the exercise response on bone cells. Serum bone alkaline phosphatase (B-ALP) and serum osteocalcin were used to reflect newly synthesized bone (Price et al., 1980; Garnero and Delmas, 1993). Maimoun et al., (2006) reported a significant rise (10 and 12%) in both biochemical markers to 50-min cycling tests performed at 15% above the ventilatory threshold. This observation likely indicates an immediate anabolic effect of exercise on bone tissue. Parathyroid hormone (PTH) which is the major regulator of bone metabolism functions to maintain the calcium-ion concentration of the extracellular fluids within physiological limits (Arnaud et al., 1967). PTH is also a primary determinant of intracellular calcium homeostasis (Rasmussen, 1968). The principal target organs for PTH are the kidney (increasing proximal tubular resorption of calcium, phosphate excretion and 1,25 dihydroxyvitamin D formation) and the skeleton. An indirect effect, increasing intestinal calcium absorption, is mediated by the increase in 1,25 dihydroxyvitamin D formation in the kidney (Poole and Reeve, 2005).
Posted on: Sat, 05 Oct 2013 21:18:14 +0000
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