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Mechanisms in Aerobic Endurance Training

This is an excerpt from Advanced Neuromuscular Exercise Physiology-2nd Edition by Phillip Gardiner.

Training of the Monosynaptic Reflex

Monkeys (which were studied in the classic research), rats, and humans can be trained to either increase or decrease the amplitude of the monosynaptic stretch reflex response. This finding is the result of experimentation by Wolpaw and colleagues since the early 1980s. The original series of experiments involved conditioning monkeys to either decrease or increase amplitude of the spinal stretch reflex, measured with indwelling EMG electrodes, resulting from a sudden extension torque applied to the elbow during a background of extension. Conditioning occurred with up to 6,000 trials per day, with a juice reward for success. Their results demonstrated that monkeys were capable of gradually doubling or halving the stretch reflex amplitude within 80 d (figure 7.6). The investigators also demonstrated that hardwired changes in spinal cord circuitry resulted from this behavioral conditioning. For example, these investigators found that changes in the amplitude of H-reflexes were apparent when measurements were taken with the animal anesthetized and for up to 3 d following removal of supraspinal influences by spinalization (Wolpaw and Lee 1989). They also ascertained that at least a portion of the adaptation may involve changes in intrinsic motoneuron properties. For example, in monkeys trained to decrease the amplitude of their triceps surae H-reflex, motoneurons had a more positive firing threshold and thus needed more depolarization to reach that threshold (Carp and Wolpaw 1994). The authors proposed that this change may be caused by a positive shift in the voltage for sodium channel activation in the involved motoneurons that is due to a change in activation of intraneuronal PKC (Halter, Carp, and Wolpaw 1995). The spinal changes produced by conditioning to upregulate and downregulate the amplitude of the H-reflex are not mirror images, since the latter (but not the former) is accompanied by changes detectable at the single-motoneuron level (Carp and Wolpaw 1995). Thus, these adaptive responses most likely include adaptations at several levels: motoneuron, afferent–motoneuron synapse, and interneuron.

This work has continued, with demonstrations of the benefits of this operant conditioning of the H-reflex to correct locomotor deficits resulting from nervous system trauma. For example, in rats with a compromised stance and gait asymmetry due to a lesion of the lateral column, upconditioning of the H-reflex improved stance and gait (Chen et al. 2006). In individuals with spinal cord injuries that suffer from spasticity that interferes with normal locomotion, downregulation of the H-reflex improves locomotor ability (Chen et al. 2014; Thompson et al. 2019; Thompson and Wolpaw 2021). The latter research is quite exciting, in that the operant conditioning was applied dynamically (not under static limb conditions, as in the original studies), at a specific phase of the locomotor cycle, thus demonstrating the success of targeting parts of movements that cause deficits. What are the implications for endurance training? This phenomenon of up- and downconditioning of the H-reflex obviously impacts locomotion in individuals with various kinds of locomotor deficits and may be at work during exercise training of nonimpaired individuals to fine-tune locomotor function, both during the training period, when muscles are adapting and changing their properties, and acutely during fatiguing exercise, when optimal locomotor function is crucial to performance success.

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Key Point

As first shown in monkeys, then rats and humans, the amplitude of the monosynaptic spinal stretch reflex can be changed to a larger or smaller response voluntarily, through operant conditioning. The long-term changes are most likely due to structural changes to this synapse. This phenomenon is now used clinically to enhance the stretch reflex in cases where injury has caused a gait deficit, and to downregulate the amplitude of this reflex in cases where hyperreflexia may hinder normal locomotor function.

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