A computational model of torque generation: neural, contractile, metabolic and musculoskeletal components.
A computational model of torque generation: neural, contractile, metabolic and musculoskeletal components.
复制标题
DOI:
10.1371/journal.pone.0056013
复制
发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Kent-Braun JA
中科院分区:
文献类型:
--
作者:
Callahan DM;Umberger BR;Kent-Braun JA
The pathway of voluntary joint torque production includes motor neuron recruitment and rate-coding, sarcolemmal depolarization and calcium release by the sarcoplasmic reticulum, force generation by motor proteins within skeletal muscle, and force transmission by tendon across the joint. The direct source of energetic support for this process is ATP hydrolysis. It is possible to examine portions of this physiologic pathway using various in vivo and in vitro techniques, but an integrated view of the multiple processes that ultimately impact joint torque remains elusive. To address this gap, we present a comprehensive computational model of the combined neuromuscular and musculoskeletal systems that includes novel components related to intracellular bioenergetics function. Components representing excitatory drive, muscle activation, force generation, metabolic perturbations, and torque production during voluntary human ankle dorsiflexion were constructed, using a combination of experimentally-derived data and literature values. Simulation results were validated by comparison with torque and metabolic data obtained in vivo. The model successfully predicted peak and submaximal voluntary and electrically-elicited torque output, and accurately simulated the metabolic perturbations associated with voluntary contractions. This novel, comprehensive model could be used to better understand impact of global effectors such as age and disease on various components of the neuromuscular system, and ultimately, voluntary torque output.
登录
查看更多内容
DOI:
10.1083/jcb.3.5.631
发表时间:
1957-09-25
期刊:
The Journal of biophysical and biochemical cytology
影响因子:
--
作者:
HUXLEY HE
通讯作者:
HUXLEY HE
影响因子:
5.5
作者:
Debold, E. P.;Beck, S. E.;Warshaw, D. M.
通讯作者:
Warshaw, D. M.
影响因子:
2.4
作者:
HAWKINS, DA;HULL, ML
通讯作者:
HULL, ML
影响因子:
64.8
作者:
HANSON, J;HUXLEY, HE
通讯作者:
HUXLEY, HE
影响因子:
5.5
作者:
GUSTAFSSON, B;PINTER, MJ
通讯作者:
PINTER, MJ