ABSTRACT
Renal autoregulation is impaired in early (1 wk) diabetes mellitus (DM) induced by streptozotocin, but effective in established DM (4 wk). Furthermore nitric oxide synthesis (NOS) inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) significantly improved autoregulation in early DM but not in established DM. We hypothesized that autoregulation is transiently impaired in early DM because of increased NO availability in the kidney. Because of the conflicting evidence available for a role of NO in DM, we tested the hypothesis that DM reduces autoregulation effectiveness by reducing the spatial similarity of autoregulation. Male Long-Evans rats were divided into control (CON) and diabetic (DM; streptozotocin) groups and followed for either 1 wk (CON1, n = 6; DM1, n = 5) or 4 wk (CON4, n = 7; DM4, n = 7). At the end of the experiment, dynamic autoregulation was assessed in isoflurane-anesthetized rats by whole kidney RBF during baseline, NOS1 inhibition, and nonselective NOS inhibition. Kidney surface perfusion, monitored with laser speckle contrast imaging, was used to assess spatial heterogeneity of autoregulation. Autoregulation was significantly impaired in DM1 rats and not impaired in DM4 rats. L-NAME caused strong renal vasoconstriction in all rats, but did not significantly affect autoregulation dynamics. Autoregulation was more spatially heterogeneous in DM1, but not DM4. Therefore, our results, which are consistent with transient impairment of autoregulation in DM, argue against the hypothesis that this impairment is NO-dependent, and suggest that spatial properties of autoregulation may also contribute to reduced autoregulatory effectiveness in DM1.
Subject(s)
Diabetes Mellitus, Experimental/complications , Homeostasis/physiology , Kidney/physiology , Animals , Blood Glucose , Body Weight , Gene Expression Regulation, Enzymologic , Male , Nitric Oxide Synthase Type I/antagonists & inhibitors , Nitric Oxide Synthase Type I/genetics , Nitric Oxide Synthase Type I/metabolism , Rats , Rats, Long-Evans , Time FactorsABSTRACT
Tendons are elastic structures that connect muscle to the skeletal system and transmit force relative to the amount of stretch they experience. The mechanical properties of human tendons are difficult to measure non-invasively, so generic values are often assumed in musculoskeletal models to represent all subjects. We aimed to determine the in vivo mechanical properties of the human Achilles tendon by calculating tendon stiffness and resting length in 10 male and 10 female trained cyclists. B-mode ultrasound coupled with motion capture was used to track the tendon lengths for the medial and lateral gastrocnemii concurrently with ankle torque measurements during ramped isometric contractions. Achilles tendon stiffness was calculated as the slope of the linear portion of the force-length curve, and this was extrapolated to zero force to yield the tendon resting length. Average Achilles tendon stiffness was 201.8 ± 5.9 N mm(-1). There was no difference in Achilles tendon stiffness or maximum isometric force between males and females, however tendon stiffness varied between individuals. The resting lengths of the MG and LG tendon were 0.209 ± 0.002 m and 0.222 ± 0.002 m respectively, and regression models determined that shank length was the best predictor of resting tendon length. Our results indicate that Achilles tendon stiffness varies with muscle strength and not sex. The variability in Achilles tendon stiffness between subjects support the need for experimentally measured subject-specific tendon properties as input parameters to improve the accuracy of musculoskeletal models.
