Study design: Review article on bone metabolism and therapeutic approach on bone loss in patients with spinal cord injury (SCI). Objective: The first part aims to describe the process of bone demineralization and its effects on bone mass in patients with SCI. The second part describes and discusses the therapeutic approaches to limiting the alteration in bone metabolism related to neurological lesions. Setting: Propara Rehabilitation Center, Montpellier, France. Results: During the first 24 months postinjury, demineralization occurs exclusively in the sublesional areas and predominantly in weight-bearing skeletal sites such as the distal femur and proximal tibia, both of which are trabecular-rich sites. Reduced bone mass, in association with a modified bone matrix property and composition, is very likely at the origin of pathological fractures after minor trauma to which these patients are frequently exposed. Since these fractures may be asymptomatic yet may lead to complications, preventing and managing 'neurological osteoporosis' remains a considerable challenge. Two main approaches are considered: the first consists in applying a mechanical stimulus to the bone tissue by standing, orthotically aided walking or functional electrical stimulation (FES). The second uses medications, particularly antiresorptive drugs such as calcitonin or diphosphonates. Conclusion: To develop well-adapted treatments, a more precise understanding of bone loss etiology is needed. The current rehabilitation programs are based on the idea that the bone physiological changes observed in patients with SCI are due to immobility, but results indicate that alterations inherent to neurological damage may play an even greater role in inducing osteoporosis.
We investigated whether the spontaneous transition between walking and running during moving with increasing speed corresponds to the speed at which walking becomes less economical than running. Seven active male subjects [mean age, 23.7 (SEM 0.7) years, mean maximal oxygen uptake (VO2max), 57.5 (SEM 3.3) ml.kg-1.min-1, mean ventilatory threshold (VTh), 37.5 (SEM3) ml.kg-1.min-1] participated in this study. Each subject performed four exercise tests separated by 1-week intervals: test 1, VO2max and VTh were determined; test 2, the speed at which the transition between walking and running spontaneously occurs (ST) during increasing speed (increases of 0.5 km.h-1 every 4 min from 5 km.h-1) was determined; test 3, the subjects were constrained to walk for 4 min at ST, at ST +/- 0.5 km.h-1 and at ST +/- 1 km.h-1; and test 4, the subjects were constrained to run for 4 min at ST, at ST +/- 0.5 km.h-1 and at ST +/- 1 km.h-1. During exercise oxygen uptake (VO2), heart rate (HR), ventilation (VE), ventilatory equivalents for oxygen and carbon dioxide (VE/VO2, VE/VCO2), respiratory exchange ratio (R), stride length (SL), and stride frequency (SF) were measured.(ABSTRACT TRUNCATED AT 250 WORDS)
This study analyzed the temporal and regional variations in bone loss and explored bone cell activities via biochemical markers during an extended follow-up in patients with spinal cord injury (SCI). In parallel, the possible role of the osteoprotegerin (OPG)/RANKL system in disuse osteoporosis was investigated. Seven male patients with acute and complete SCI (31.3 +/- 9.5 years) and 12 able-bodied (AB) men (26.9 +/- 4.2 years) participated in the study. Measurements were performed 16, 24, 36, 48, and 71 weeks after injury. At week 16, marked calcium homeostasis disturbance and a concomitant increase in bone resorption markers were observed, reflecting an intense bone degradation process. Resorption activity decreased continuously with time. Contrasting with the great rise in the resorption markers, the bone formation markers showed little variation. During the period of investigation, a loss in bone mineral density (BMD) was demonstrated for the total body (-4.3%), pelvis (-15.7%) and lower limbs (-15.2%), whereas BMD did not change at the lumbar spine, upper limbs, or skull. At all stages, SCI patients had lower serum RANKL levels and higher serum OPG levels than did AB controls, but no significant variation with time was observed for either cytokine. These findings suggest that bone resorption persisted long after SCI and specifically affected BMD at sublesional sites. The marked modification of serum OPG/RANKL levels in SCI patients suggests that this system is affected, in disuse osteoporosis. However, the precise biologic role of the OPG/RANKL system in the bone tissue of SCI patients has yet to be determined.
Sports characterized by little or moderate weight bearing or impact have a low osteogenic effect. However, the action of such sports on bone turnover remains unclear. The objective of this study was to determine the effect on bone remodelling of physical activities that induce moderate external loading on the skeleton. Thirty-eight male athletes aged 18-39 years (cyclists, n = 11; swimmers, n = 13; triathletes, n = 14) and 10 age-matched sedentary controls aged 22-35 years participated in the study. The study combined measurement of bone mineral density by dual-energy X-ray absorptiometry and bone turnover assessment from specific biochemical markers: serum bone-specific alkaline phosphatase, osteocalcin, urinary type I collagen C-telopeptide and calcium. Compared with the controls and swimmers, adjusted bone mineral density was higher (P < 0.05) in triathletes at the total proximal femur and lower limbs. No differences in bone mineral density were found between cyclists, swimmers and controls. Compared with controls, osteocalcin was higher (P < 0.05) in triathletes and swimmers and urinary type I collagen C-telopeptide was higher in swimmers only. Serum bone-specific alkaline phosphatase was lower (P < 0.05) in cyclists than in all other groups. In conclusion, an osteogenic effect was found only in triathletes, mainly at bone sites under high mechanical stress. Bone turnover differed in athletes compared with controls, suggesting that bone turnover may be sport-practice dependent. Despite some encouraging observations, it was not possible to show that changes in the bone remodelling process were sport-discipline dependent.
The aim of this study was to validate an incremental field test performed by wheelchair dependent (WD) athletes. Nine male paraplegic subjects (mean age: 28.9±4.2 years) performed an incremental field test (FT) and a comparable laboratory test (LT) with their own usual wheelchairs. Both tests started with an initial speed of 4 km.hr -I and increased by increments of 1 km.hr -I every minute until volitional exhaustion. The FT was an adapted Leger and Boucher test (ALBT) and was conducted on a 400 m tartan field marked-off every 50 m with pylons. Ventilatory data were collected every 15 s using a portable telemetric system (Cosmed K2, JFB International, Italy). The LT was performed on an adapted treadmill (Sopur, Germany) and ventilatory data were collected every minute using a breath-by-breath automated system (CPX, Medical Graphics, MN, USA). The LT and the FT were not significantly different for duration (8 min 50 ± 1 min 24 vs 9 min 55 ± 29 s), percentage of maximal heart rate (HR, 86.2±3.9 vs 89.7±5.3%), maximal minute ventilation (VE, 101.6±28.5 vs 96.8±28.2 l.min -I ), and peak oxygen uptake (Vo2 peak, 39.7+7.3 vs 36.1 +5.8 m1.kg -l .min -l ) assessed with the CPX and the K2, respectively. We concluded that the FT proposed in the present study is a valid test for direct V02 peak assessment in wheelchair athletes using a portable V02 telemetric system. Nonetheless, the Leger and Mercier model equation did not accurately predict V02 max and further investigation is needed to determine a valid V02 max prediction equation for these subjects during the FT.
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