Aerobic Endurance Training Does Not Protect Bone Against Poorly Controlled Type 1 Diabetes in Young Adult Rats.

Streptozotocin (STZ)-induced type 1 diabetes mellitus (T1DM) decreases trabecular bone volume and bone strength in rodents. The current study investigated the potential protective effects of aerobic endurance training (AET) on bone in STZ-induced T1DM young adult rats. Sixty-four 8-week-old male Sprague-Dawley rats were randomly divided into 4 groups of 16: control non-T1DM sedentary (CS) and exercised (CX), T1DM sedentary (DS) and exercised (DX). Blood glucose was maintained at 9-15 mmol/L using subcutaneously implanted insulin pellets (Linplant, Linshin Canada, Inc.). AET was performed at ~75-85% VO2max for 1 h/day, 5 day/week for 10 weeks. Areal and volumetric bone mineral density (aBMD and vBMD; excised femur) were measured using dual-energy X-ray absorptiometry (DXA; QDR 4500A) and micro computed tomography (µCT; Aloka). Bone strength was tested using a 3-point bending test (Instron 5544 Load Frame). Two-way ANOVA was used to test for T1DM and exercise differences followed by Tukey's HSD tests for interaction effects; significance was set at P < 0.05. T1DM had lower body weight (18.0%), aBMD (8.6%), cortical vBMD (1.6%), trabecular vBMD (2.1%), maximum load at break (22.2%), and increased elastic modulus (11.3%) vs. control (P < 0.001). Exercise in T1DM further decreased body weight (4.7%) vs. sedentary (P = 0.043) and maximum extension during the bending test that demonstrated DX was increased (7.3%) vs. CX (P = 0.033). There were no other beneficial effects of exercise on bone. These results suggest that 10 weeks of AET in rats do not have protective effects on bone in the short term and that T1DM rats have compromised bone health.

Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific.

The dynamic adjustment and amplitude of the endothelium-dependent vasorelaxation of the carotid, aorta, iliac, and femoral vessels were measured in response to acute low- (LI) or high-intensity (HI) endurance exercise. Vasorelaxation to 10(-4) M ACh was evaluated in 10 control, 10 LI, and 10 HI rats. Two-millimeter sections of carotid, aorta, iliac, and femoral arteries were mounted onto a myography system. Vasorelaxation responses were modeled as a monoexponential function. The overall τ (control, 10.5 ± 6.0 s; LI, 10.4 ± 5.7 s; HI, 11.0 ± 6.9 s) and time-to-steady-state (control, 47.6 ± 24.0 s; LI, 46.2 ± 22.8 s; HI, 49.1 ± 28.3 s) was similar in LI, HI, and control (P > 0.05). The overall (average of four vessel-type) % vasorelaxation was larger in LI (73 ± 16%) and HI (73 ± 16%) than in control (66 ± 19%) (P < 0.05). The overall rate of vasorelaxation was greater in LI (1.9 ± 0.9%·s(-1)) and HI (1.9 ± 1.1%·s(-1)) compared with control (1.6 ± 0.7%·s(-1)) (P < 0.05). The vessel-specific responses (average response for the three conditions) showed that carotid displayed a slower adjustment (τ, 18.9 ± 4.4 s; time-to-steady-state, 80.4 ± 18.4 s) compared with the aorta (τ, 10.3 ± 3.8 s; time-to-steady-state, 46.3 ± 15.2 s), the iliac (τ, 6.3 ± 2.1 s; time-to-steady-state, 30.3 ± 9.0 s), and the femoral (τ, 6.0 ± 1.9 s; time-to-steady-state, 29.3 ± 8.4 s). The % vasorelaxation was larger in the carotid (82 ± 14%) than in the aorta (67 ± 16%), iliac (61 ± 13%), and femoral (71 ± 19%) (P > 0.05). The rate of vasorelaxation was carotid (1.1 ± 0.2%·s(-1)), aorta (1.5 ± 0.4%·s(-1)), iliac (2.2 ± 0.8%·s(-1)), and femoral (2.6 ± 1.0%·s(-1)). In conclusion, an acute bout of endurance exercise increased vascular responsiveness. The dynamic and percent adjustments were vessel-specific with vessel function likely determining the response.

hsp70 mRNA temporal localization in rat skeletal myofibers and blood vessels post-exercise.

Rapid transcription of the survival transcript, inducible heat shock protein 70 (hsp70), is critical for mounting cytoprotection against severe cellular stress, like elevated temperature. Previous investigations have demonstrated that exercise-induced expression of Hsp70 protein occurs in a fiber-specific pattern; however, the activation pattern of hsp70 mRNA expression remains unclear in skeletal muscle. Consequentially, the temporal localization of hsp70 mRNA was characterized via in situ hybridization (ISH) experiments examining fast-muscle, white vastus: 1, 3, 10, and 24 h after a single bout of intense treadmill running (1 h, 30 m/min, 6% grade) in rats. The role that the physiologic temperature stress associated with exercise (raising core body temperature to 40.0°C for 15 min (HS-40.0°C)) might play in inducing hsp70 mRNA expression was also explored. In skeletal muscle myofibers (SkM), hsp70 mRNA ISH signal was observed to be concentrated in a punctate manner that was associated with nuclei post-exercise. HS-40°C treatment produced minimal detectable hsp70 mRNA ISH signal in SkM. In large intermyofibrillar blood vessels (BV), peak hsp70 mRNA signal, distributed throughout the vessel wall, was observed 1 h post-exercise. In BV, no differences in hsp70 mRNA signal were observed between HS-40°C and EX-1 h. Results indicate that the majority of hsp70 mRNA is retained in a perinuclear localization in SkM post-exercise. They further suggest a muscle-type specific time course for peak hsp70 mRNA expression. This investigation suggests that the physiologic rise in core temperature associated with exercise per se is not the key stimulus responsible for inducing hsp70 mRNA transcription in SkM.