Chronic and Acute Neural Adaptations to Strength Training

Abstract

Adaptations to strength training are usually divided in two broad categories: morphological (peripheral) and neural (central) adaptations. The purpose of this thesis was to investigate the chronic neural adaptations in response to various strength training interventions (Paper I-III), and the acute neural adjustments that occur after heavy resistance exercise (Paper IV and V). Improved understanding of the mechanisms should allow better prescription of exercise to athletic, clinical, and the general population.

The principal measurement techniques employed to assess neural changes were surface electromyogram (EMG) activity and evoked spinal reflexes, namely H-reflex and V-wave responses. Paper I investigated whether maximal functional multiple-joint leg press training could induce neural adaptations to the plantar flexor muscles in a single-joint contraction task. In accordance with the hypothesis, significant “carry-over” effects of neural drive and muscle strength were observed. Paper II assessed the effects of unilateral, maximal strength training on neural adaptations of the untrained contralateral limb. It is extensively documented that “cross-education” of muscle strength occurs, but the mechanisms require further inspection. In agreement with the hypothesis, the findings reinforced the concept that enhanced neural drive to the contralateral agonist muscles is the underlying mechanism for cross-education of strength. Paper III investigated the effects of lower limb strength training on neural drive to the muscle in multiple sclerosis (MS) patients. MS-patients are not able to fully activate motor units (recruitment and/or firing frequency) in the lower limbs, and therefore suffer from reduced leg strength compared to healthy individuals. Conversely, strength training induces opposite neural effects, but has never been assessed in this population. Neural drive and muscle strength was enhanced in response to strength training with no negative interactions, in accordance with the hypothesis.

Central neural fatigue occurs after resistive exercise. In paper IV it was investigated whether caffeine supplementation could enhance the recovery of efferent neural drive after maximal fatiguing contractions. Contrary to our hypothesis, caffeine did not influence neural recovery and thus did not affect muscle strength. However, this study established a significant relationship between the two measures of efferent neural drive, namely EMG activity and Vwave responses. In contrast to muscle fatigue - the most obvious effect of contractile history, paper V investigated post-activation potentiation (PAP) which is a transient enhancement of power/strength performance after heavy muscle work. This study established the time-courses of the muscular and neural mechanisms proposed being responsible for PAP. Opposite to our hypothesis, strength/power performance was not enhanced at the arbitrarily chosen timepoint.

Collectively, increased EMG activity and V-wave responses after strength training demonstrated adaptive changes in the central nervous system leading to increased muscle strength. H-reflex responses remained unchanged in response to the heavy strength training, indicating that adaptations of this pathway were not underlying the present strength gains. Transient changes in the central nervous activation of muscle was observed after acute resistance exercise, although no effects of caffeine were observed, nor were there any evidence of PAP despite the occurrence of the proposed underlying mechanisms.