Swimming training potentiates the recovery of femoral neck strength in young diabetic rats under insulin therapy

Abstract

OBJECTIVE: To test whether swimming training benefits femoral neck strength in young diabetic rats under insulin therapy. METHODS: A total of 60 male Wistar rats (age: 40 days) were divided equally into the following six groups: control sedentary, control exercise, diabetic sedentary, diabetic exercise, diabetic sedentary plus insulin and diabetic exercise plus insulin. Diabetes was induced with a unique intraperitoneal injection (60 mg/kg body weight) of streptozotocin. Seven days after the injection and after 12 hours of fasting, the animals with blood glucose levels ≥300 mg/dL were considered diabetic. Seven days after the induction of diabetes, the animals in the exercise groups were subjected to progressive swimming training (final week: 90 min/day; 5 days/week; 5% load) for eight weeks. The animals in the insulin groups received a daily dose of insulin (2-4 U/day) for the same period. RESULTS: Severe streptozotocin-induced diabetes reduced the structural properties of the femoral neck (trabecular bone volume, trabecular thickness and collagen fiber content). The femoral neck mechanical properties (maximum load and tenacity) were also impaired in the diabetic rats. Insulin therapy partially reversed the damage induced by diabetes on the structural properties of the bone and mitigated the reductions in the mechanical properties of the bone. The combination of therapies further increased the femoral neck trabecular bone volume (∼30%), trabecular thickness (∼24%), collagen type I (∼19%) and type III (∼13%) fiber contents, maximum load (∼25%) and tenacity (∼14%). CONCLUSIONS: Eight weeks of swimming training potentiates the recovery of femoral neck strength in young rats with severe streptozotocin-induced diabetes under insulin therapy.

Swimming Training Does Not Affect the Recovery of Femoral Midshaft Structural and Mechanical Properties in Growing Diabetic Rats Treated with Insulin

“…The applied treatment with insulin enhanced the femoral midshaft tenacity in diabetic rats. As bone tenacity is determined primarily by the unmineralized matrix [ 26 ], it is conceivable that the observed insulin benefit to femoral tenacity is due to an increase in the femoral collagen content promoted by insulin in this model of experimental diabetes, as reported previously by our group [ 10 ].…”

“…Thus, it is conceivable that the diminished femoral area, BMC, BMD and cortical thickness resulted in reduced bone resistance to fracture in the diabetic rats. Although it was not measured in the present study, reduced collagen content has been reported in this model of severe diabetes [ 10 ]. Concerning the low tenacity observed in diabetic rats, it is possible that a reduction in the femoral collagen in these rats has contributed to such damage, since this measure relies on the unmineralized matrix [ 26 ].…”

“…One week after hyperglycemia, animals from DE, DEI and CE groups underwent the swimming training, as previously described [ 10 ]. In summary, the animals exercised 90 min/day, 5 days/week for 8 weeks.…”

“…Impaired bone quality in individuals with type 1 diabetes has been observed at an early age. For instance, young girls with type 1 diabetes [ 7 ], and growing female and male rats with streptozotocin (STZ)-induced diabetes exhibit abnormal bone structure (i.e., reduced bone mineral content-BMC and density-BMD) and strength (i.e., reduced resistance to fracture) [ 8 , 9 , 10 , 11 ]. It is noteworthy that type 1 diabetes damages bone health even at the early stages of life, and that bone fracture is elevated in diabetic people [ 3 ], which negatively affects life quality.…”

“…Physical exercise promotes benefits to bone health [ 14 ], as it counterbalances bone fragility because of its inherent osteogenic properties. Swimming training has been shown, by our group [ 10 ] and elsewhere [ 15 , 16 ], to enhance cancellous bone (i.e., femoral neck) structure and strength in young rats with type 1 diabetes; however, the low impact of swimming training, and, hence, its osteogenic properties are controversial [ 17 , 18 ]. Considering that cortical bone (i.e., femoral shaft) is less responsive than cancellous bone to the mechanical load imposed by exercise [ 19 ], we hypothesized that swimming training does not affect the cortical bone structural and mechanical properties in young rats with STZ-induced severe type 1 diabetes, even when associated with insulin treatment.…”