Simulation-based biomechanical assessment of unpowered exoskeletons for running

Due to the complexity and high degrees of freedom, the detailed assessment of human biomechanics is necessary for the design and optimization of an effective exoskeleton. In this paper, we present full kinematics, dynamics, and biomechanics assessment of unpowered exoskeleton augmentation for human running gait. To do so, the considered case study is the assistive torque profile of I-RUN. Our approach is using some extensive data-driven OpenSim simulation results employing a generic lower limb model with 92-muscles and 29-DOF. In the simulation, it is observed that exoskeleton augmentation leads to $$4.62\%$$ 4.62 % metabolic rate reduction for the stiffness coefficient of $$\alpha ^*=0.6$$ α ∗ = 0.6 . Moreover, this optimum stiffness coefficient minimizes the biological hip moment by $$26\%$$ 26 % . The optimum stiffness coefficient ($$\alpha ^*=0.6$$ α ∗ = 0.6 ) also reduces the average force of four major hip muscles, i.e., Psoas, Gluteus Maximus, Rectus Femoris, and Semimembranosus. The effect of assistive torque profile on the muscles’ fatigue is also studied. Interestingly, it is observed that at $$\alpha ^{\#}=0.8$$ α # = 0.8 , both all 92 lower limb muscles’ fatigue and two hip major mono-articular muscles’ fatigue have the maximum reduction. This result re-confirm our hypothesis that ”reducing the forces of two antagonistic mono-articular muscles is sufficient for involved muscles’ total fatigue reduction.” Finally, the relation between the amount of metabolic rate reduction and kinematics of hip joint is examined carefully where for the first time, we present a reliable kinematic index for prediction of the metabolic rate reduction by I-RUN augmentation. This index not only explains individual differences in metabolic rate reduction but also provides a quantitative measure for training the subjects to maximize their benefits from I-RUN.

A Kinematic Index for Estimation of Metabolic Rate Reduction in Running with I-RUN

ABSTRACTIn this paper, we target multiple goals related to our passive running assistive device, called I-RUN. The major goals are: (1) finding the main reason behind individual differences in benefiting from our assistive device at the muscles level, (2) devising a simple measure for on-line I-RUN stiffness tuning, and creating a lab-free simple kinematic measure for (3) estimating metabolic rate reduction as well as (4) training subjects to maximize their benefit from I-RUN. Our approach is using some extensive data-driven OpenSim simulation results employing a generic lower limb model with 92-muscles and 29-DOF.It is observed that there is a significant relation between the hip joints kinematic and changes in the metabolic rate in the presence of I-RUN. Accordingly, a simple kinematic index is devised to estimate metabolic rate reduction. This index not only explains individual differences in metabolic rate reduction but also provides a quantitative measure for training subjects to maximize their benefits from I-RUN.The simulation results also re-confirm our hypothesis that “reducing the forces of two antagonistic mono-articular muscles is sufficient for involved muscles’ total effort reduction”. Consequently, we introduce a two-muscles EMG-based metric for the on-line tuning of I-RUN.

Anesthetic Effects on Cerebral Metabolic Rate Predict Histologic Outcome from Near-complete Forebrain Ischemia in the Rat

Background Although reduction of cerebral metabolic rate is thought to contribute to anesthetic neuroprotection, histologic evidence to support this concept has not been provided. In this study, histologic outcome was evaluated in rats subjected to different durations of severe forebrain ischemia while anesthetized with volatile anesthetics that have substantially different effects on cerebral metabolic rate. Methods Normothermic rats that underwent fasting were anesthetized with 0.75 minimum alveolar concentration (MAC) isoflurane-60% nitrous oxide (N2O) or 0.75 MAC halothane-60% N2O. Ischemia was induced with use of a combination of bilateral carotid occlusion and controlled hypotension. Rats in the isoflurane group were subjected to 6.5 min or 8.0 min ischemia, whereas the halothane group received 6.5 min ischemia. Histologic damage was assessed 4 days later. Results With 6.5 min ischemia, mean +/- SD, hippocampal CA1 percent of dead (% dead) neurons was reduced with isoflurane-N2O (45 +/- 18) versus halothane-N2O (60 +/- 23, P = 0. 023). Eight minutes of ischemia increased % dead neurons in the isoflurane-N2O group (60 +/- 17, P = 0.017). There was no difference between the isoflurane 8.0-min and halothane 6.5-min groups (P = 0. 935). A similar pattern was observed in hippocampal CA4 and the neocortex. Striatal damage was not affected by anesthetic or ischemic duration. Conclusions At 6.5 min ischemia, isoflurane provided improved outcome versus halothane. Previous research has shown that 0.75 MAC isoflurane-N2O increases the time to onset of ischemic depolarization by 1.5 min and reduces cerebral metabolic rate by 42% versus 0.75 MAC halothane-N2O. In the current study, when the duration of ischemia was increased by 1.5 min in the isoflurane-N2O group, histologic outcome became similar to that in halothane-N2O-anesthetized rats. These results provide evidence that cerebral metabolic rate reduction has an advantageous effect on outcome from severe brain ischemia, but also suggest that such benefit is likely to be small.

Thermal relations of metabolic rate reduction in a hibernating marsupial

We tested whether the reduction of metabolic rate (MR) in hibernating Cercartetus nanus (Marsupialia, 36 g) is better explained by the reduction of body temperature (Tb), the differential (ΔT) between Tb and air temperature (Ta), or thermal conductance (C). Above the critical Ta during torpor (Ttc) of 4.8 ± 0.7°C, where the Tb was not regulated, the steady-state MR was an exponential function of Tb( r 2 = 0.92), and the overall Q10 was 3.3. However, larger Q10 values were observed at high Tb values during torpor, particularly within the thermoneutral zone (Q10 = 9.5), whereas low Q10 values were observed below Tb 20°C (Q10 = 1.9). The ΔT did not change over Ta 5–20°C, although MR fell, and therefore the two variables were not correlated. Below the Ttc, Tb was regulated at 6.1 ± 1.0°C and MR increased proportionally to ΔT. Our study suggests that MR in torpid C. nanus is largely determined by temperature effects and metabolic inhibition. In contrast, ΔT explains MR only below the Ttc and C appears to affect MR only indirectly via changes of Tb, suggesting that ΔT and C play only a secondary role in MR reduction during hibernation.