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Terminal H-reflex Measurements in Mice
Published on: June 16, 2022
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Temperature affects maximum H-reflex amplitude but not homosynaptic postactivation depression.
Sébastien Racinais1, Andrew G Cresswell
1Aspetar, Qatar Orthopaedic and Sports Medicine Hospital Doha, Qatar.
Physiological Reports
|December 5, 2013
Summary
Hyperthermia significantly reduces Hoffman reflex (H-reflex) amplitude, impacting Ia-afferent spinal pathway transmission. Elevated core temperature affects neuromuscular transmission but not postactivation depression.
Area of Science:
- Neuroscience
- Exercise Physiology
- Human Physiology
Background:
- The Ia-afferent spinal pathway plays a crucial role in proprioception and motor control.
- Understanding how physiological changes like hyperthermia affect neural pathways is vital for performance and safety.
Purpose of the Study:
- To investigate the impact of hyperthermia on the transmission efficacy of the Ia-afferent spinal pathway.
- To determine if elevated core temperature influences the Hoffman reflex (H-reflex) and associated neuromuscular parameters.
Main Methods:
- 14 volunteers underwent H-reflex and M-wave recruitment, along with postactivation depression (HPAD) recovery, at controlled ambient temperatures yielding core temperatures of ~37.3°C (CON) and ~39.0°C (HOT).
- Electromyographic responses from soleus (SOL) and medial gastrocnemius (MG) muscles were recorded following tibial nerve stimulation.
- Paired pulse frequencies ranged from 0.07 to 10 Hz.
Main Results:
- Maximal H-reflex amplitude occurred at similar stimulation intensities in both CON and HOT conditions.
- H-reflex amplitude was significantly decreased in the HOT condition compared to CON, both in absolute terms and when normalized to the M-wave.
- Elevated core temperature did not significantly affect the HPAD recovery curve in either muscle.
Conclusions:
- Hyperthermia can impair neuromuscular transmission at the neuromuscular junction and/or muscle membrane.
- The efficacy of Ia-afferent spinal pathway transmission is reduced by hyperthermia, but this effect is not mediated by increased homosynaptic postactivation depression.
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