Strength
Narrative Review
2007
The adaptations to strength training: Morphological and neurological contributions to increased strength
By Jonathan P. Folland and Alun G. Williams
Sports Medicine, 37(2), pp. 145-168
<h2>Abstract</h2>
<p>This review examines the morphological and neurological contributions to strength gains following resistance training. Strength development is a multifaceted process mediated by both structural changes within muscle tissue and functional adaptations within the nervous system. Neurological adaptations — including increased <a href="/terms/motor-unit/" class="term-link" data-slug="motor-unit" title="motor unit">motor unit</a> recruitment, elevated discharge rates, reduced antagonist coactivation, and enhanced inter-muscular coordination — account for the disproportionate strength gains observed in the early phases of training (typically weeks 1 through 4), often preceding any measurable <a href="/terms/muscle-hypertrophy/" class="term-link" data-slug="muscle-hypertrophy" title="hypertrophy">hypertrophy</a>. As training progresses beyond this initial period, morphological adaptations — including myofibrillar protein accretion, increases in <a href="/terms/muscle-fiber/" class="term-link" data-slug="muscle-fiber" title="muscle fiber">muscle fiber</a> <a href="/terms/cross-sectional-area/" class="term-link" data-slug="cross-sectional-area" title="cross-sectional area">cross-sectional area</a>, and changes in architectural pennation angle — assume increasing prominence and become the dominant driver of long-term strength improvement. This review synthesizes the mechanistic evidence underpinning both adaptive pathways, evaluates methods used to quantify their respective contributions, and discusses their integration in producing the strength gains observed across training timescales. A comprehensive understanding of these dual adaptation mechanisms is critical for practitioners seeking to design evidence-based programs that optimize strength development across diverse populations and training phases [1].</p>
<h2>Introduction</h2>
<p>Resistance training consistently produces substantial improvements in voluntary muscular strength, with gains ranging from 25% to over 100% reported in controlled studies depending on training duration, intensity, and population characteristics [1]. Despite decades of research, a complete mechanistic account of how resistance training translates into strength gains remains an active area of inquiry. The two principal categories of adaptation — neurological and morphological — interact dynamically across the training timeline, and their relative contributions shift as an individual progresses from novice to advanced training status.</p>
<p>Early observations that strength improvements significantly outpace measurable <a href="/terms/muscle-hypertrophy/" class="term-link" data-slug="muscle-hypertrophy" title="muscle hypertrophy">muscle hypertrophy</a>, particularly in the first weeks of a training program, led researchers to hypothesize that neural mechanisms must play a critical initial role [2]. This "neural hypothesis" of early strength gain has since been substantiated by electromyographic, twitch interpolation, and imaging studies demonstrating that untrained individuals operate at a fraction of their theoretical maximal <a href="/terms/motor-unit/" class="term-link" data-slug="motor-unit" title="motor unit">motor unit</a> activation capacity. Resistance training rapidly improves the nervous system's ability to more fully activate the available muscular apparatus, resulting in strength gains that precede and are independent of tissue-level changes.</p>
<p>Concurrently, morphological adaptations — primarily increases in myofibrillar protein content and <a href="/terms/muscle-fiber/" class="term-link" data-slug="muscle-fiber" title="muscle fiber">muscle fiber</a> hypertrophy — emerge as the sustained driver of strength beyond the initial training period. The mechanical relationship between <a href="/terms/cross-sectional-area/" class="term-link" data-slug="cross-sectional-area" title="muscle CSA">muscle CSA</a> and force production capacity (the so-called "size principle" applied at the tissue level) means that larger muscles are intrinsically capable of generating greater force, assuming neural drive is adequate [3].</p>
<p>Understanding the temporal sequencing and relative magnitudes of these two adaptive streams is not merely of academic interest. It has direct implications for program design, <a href="/terms/periodization/" class="term-link" data-slug="periodization" title="periodization">periodization</a> strategy, and the interpretation of training responses in both clinical and athletic settings. This review synthesizes the current evidence base with respect to both neural and morphological mechanisms.</p>
<h2>Neural Adaptations</h2>
<h3><a href="/terms/motor-unit/" class="term-link" data-slug="motor-unit" title="Motor Unit">Motor Unit</a> Recruitment and Firing Rate</h3>
<p>Voluntary force production depends upon the recruitment of motor units — the functional neuromuscular pairing of an alpha motor neuron and the muscle fibers it innervates. Force regulation is achieved through two primary mechanisms: the spatial summation of recruited motor units and the temporal summation achieved by modulating motor unit discharge rates. Both parameters are amenable to training-induced modification [1].</p>
<p>Resistance training increases the number and size of motor units activated at a given submaximal force level, enabling greater force production from the same neural command. Concurrently, trained individuals demonstrate higher motor unit discharge rates — a phenomenon sometimes described as rate coding — which increases the mechanical force produced by each active fiber through greater tetanic fusion. Studies using intramuscular <a href="/terms/electromyography/" class="term-link" data-slug="electromyography" title="EMG">EMG</a> have demonstrated that trained individuals achieve higher peak motor unit firing rates during maximal contractions compared to untrained controls [2].</p>
<h3>Antagonist Coactivation and Coordination</h3>
<p>During voluntary contractions, antagonist muscle groups — those opposing the prime movers — are simultaneously activated, partly through protective reflex mechanisms. This coactivation imposes a mechanical braking force that reduces net force output. Resistance training reduces antagonist coactivation, enabling more of the agonist's force to be expressed as net external force. This adaptation is particularly pronounced in multi-joint exercises where coordination between muscle groups is complex [3].</p>
<p>Inter-muscular coordination improvements also contribute to strength gains in compound movements. As the nervous system learns the specific motor pattern demanded by an exercise, the temporal sequencing and relative magnitudes of agonist, synergist, and stabilizer activation become more precisely tuned. This "motor learning" component explains why exercise-specific strength gains often exceed those measured using different assessment methods, and underscores the importance of specificity in training [1].</p>
<h3>Cortical and Spinal Mechanisms</h3>
<p>Evidence from transcranial magnetic stimulation and H-reflex studies suggests that adaptations occur at multiple levels of the neural axis, including supraspinal (cortical and subcortical) sites and spinal interneuronal networks. Changes in corticospinal excitability, enhanced descending drive, and reduced inhibitory interneuron activity collectively contribute to the improved voluntary activation capacity that characterizes strength-trained individuals [2].</p>
<h2>Morphological Adaptations</h2>
<h3><a href="/terms/muscle-fiber/" class="term-link" data-slug="muscle-fiber" title="Muscle Fiber">Muscle Fiber</a> <a href="/terms/muscle-hypertrophy/" class="term-link" data-slug="muscle-hypertrophy" title="Hypertrophy">Hypertrophy</a></h3>
<p>The most extensively studied morphological adaptation to resistance training is the increase in muscle fiber <a href="/terms/cross-sectional-area/" class="term-link" data-slug="cross-sectional-area" title="cross-sectional area">cross-sectional area</a> — a process driven by the net accumulation of contractile proteins, specifically actin and myosin, within the myofibrillar compartment. <a href="/terms/mechanical-tension/" class="term-link" data-slug="mechanical-tension" title="Mechanical tension">Mechanical tension</a> applied to muscle fibers during resistance exercise activates a cascade of intracellular signaling events, most prominently through the <a href="/terms/mtor/" class="term-link" data-slug="mtor" title="mechanistic target of rapamycin">mechanistic target of rapamycin</a> complex 1 (mTORC1) pathway, which promotes ribosomal biogenesis and <a href="/terms/muscle-protein-synthesis/" class="term-link" data-slug="muscle-protein-synthesis" title="protein synthesis">protein synthesis</a> [1].</p>
<p>Both Type I (slow-twitch, oxidative) and Type II (fast-twitch, glycolytic) muscle fibers exhibit hypertrophic responses to resistance training, though Type II fibers tend to demonstrate a greater absolute magnitude of cross-sectional area increase, owing partly to their larger baseline size and greater contractile protein content. The composition of fiber type hypertrophy is influenced by training variables including load, repetition range, and <a href="/terms/inter-set-rest-interval/" class="term-link" data-slug="inter-set-rest-interval" title="rest interval">rest interval</a> duration [2].</p>
<h3><a href="/terms/satellite-cells/" class="term-link" data-slug="satellite-cells" title="Satellite Cells">Satellite Cells</a> and <a href="/terms/myonuclei/" class="term-link" data-slug="myonuclei" title="Myonuclear Domain">Myonuclear Domain</a></h3>
<p>Skeletal muscle fibers are post-mitotic, meaning they cannot divide to generate new fibers under normal conditions. Fiber growth is therefore dependent upon the activation and proliferation of satellite cells — muscle stem cells residing beneath the basal lamina of mature fibers. Upon mechanical or metabolic stimulation, satellite cells undergo asymmetric division, with daughter cells differentiating and fusing into existing fibers, contributing new myonuclei. This expansion of the myonuclear pool supports the increased protein synthesis demand of a growing fiber within the framework of the myonuclear domain theory [3].</p>
<h3>Architectural Changes</h3>
<p>Beyond fiber hypertrophy, resistance training induces changes in muscle architecture, specifically fascicle length and pennation angle. Pennation angle — the angle at which muscle fascicles attach relative to the line of force production — increases with hypertrophy, allowing more fibers to pack into the same anatomical cross-section and thereby increasing physiological cross-sectional area (PCSA), which more directly determines maximum force production capacity than anatomical CSA. Fascicle length changes are exercise-specific, with longer-duration eccentric training particularly effective at promoting fascicle lengthening [1,2].</p>
<h2>Integration of Neural and Morphological Factors</h2>
<h3>Temporal Sequencing of Adaptations</h3>
<p>The integration of neural and morphological adaptive mechanisms follows a characteristic temporal pattern. In the first 2 to 4 weeks of a resistance training program, strength gains typically proceed at a rate that substantially exceeds any measurable change in muscle size, a pattern that can only be explained by rapid neural reorganization. <a href="/terms/cross-sectional-area/" class="term-link" data-slug="cross-sectional-area" title="Cross-sectional area">Cross-sectional area</a> measurements via imaging modalities typically do not reveal statistically significant <a href="/terms/muscle-hypertrophy/" class="term-link" data-slug="muscle-hypertrophy" title="hypertrophy">hypertrophy</a> until 6 to 8 weeks of consistent training in most populations [1].</p>
<p>As training continues beyond this initial phase, the rate of neural adaptation begins to plateau as the nervous system approaches an improved but limited optimal activation state. Simultaneously, the slow but cumulative accumulation of contractile proteins within muscle fibers begins to manifest as measurable hypertrophy. By the 8- to 12-week mark, morphological adaptations contribute increasingly to continued strength improvements, a shift that becomes even more pronounced across months to years of sustained training [2].</p>
<h3>Practical <a href="/terms/periodization/" class="term-link" data-slug="periodization" title="Periodization">Periodization</a> Implications</h3>
<p>This dual-mechanism model has direct implications for periodization design. Phases of training emphasizing heavy loads and lower repetitions (1-5RM) are particularly effective at eliciting further neural adaptations in experienced trainees, potentially by demanding high-threshold <a href="/terms/motor-unit/" class="term-link" data-slug="motor-unit" title="motor unit">motor unit</a> recruitment and pushing discharge rate adaptations toward their ceiling. Conversely, moderate-load, higher-repetition protocols (6-20RM) provide a more potent stimulus for myofibrillar <a href="/terms/muscle-protein-synthesis/" class="term-link" data-slug="muscle-protein-synthesis" title="protein synthesis">protein synthesis</a> and satellite cell activation [3].</p>
<p>A comprehensive periodization strategy that systematically alternates between these training emphases — commonly formalized as block periodization with accumulation, transmutation, and realization phases — can theoretically optimize both neural and morphological contributions to long-term strength development.</p>
<h3>Limitations and Future Directions</h3>
<p>Current methods for partitioning the relative contributions of neural versus morphological factors to strength gains are imperfect. Twitch interpolation, <a href="/terms/electromyography/" class="term-link" data-slug="electromyography" title="surface EMG">surface EMG</a>, and voluntary activation measures provide indirect estimates of neural drive but cannot fully account for intramuscular coordination, reflex contributions, or series elastic element compliance. Future research employing high-density EMG, advanced imaging, and longitudinal study designs will refine our understanding of how these mechanisms interact across diverse training contexts and populations [1].</p>