The maximal rate of rise in muscle force [rate of force development (RFD)] has important functional consequences as it determines the force that can be generated in the early phase of muscle contraction (0-200 ms). The present study examined the effect of resistance training on contractile RFD and efferent motor outflow ("neural drive") during maximal muscle contraction. Contractile RFD (slope of force-time curve), impulse (time-integrated force), electromyography (EMG) signal amplitude (mean average voltage), and rate of EMG rise (slope of EMG-time curve) were determined (1-kHz sampling rate) during maximal isometric muscle contraction (quadriceps femoris) in 15 male subjects before and after 14 wk of heavy-resistance strength training (38 sessions). Maximal isometric muscle strength [maximal voluntary contraction (MVC)] increased from 291.1 +/- 9.8 to 339.0 +/- 10.2 N. m after training. Contractile RFD determined within time intervals of 30, 50, 100, and 200 ms relative to onset of contraction increased from 1,601 +/- 117 to 2,020 +/- 119 (P < 0.05), 1,802 +/- 121 to 2,201 +/- 106 (P < 0.01), 1,543 +/- 83 to 1,806 +/- 69 (P < 0.01), and 1,141 +/- 45 to 1,363 +/- 44 N. m. s(-1) (P < 0.01), respectively. Corresponding increases were observed in contractile impulse (P < 0.01-0.05). When normalized relative to MVC, contractile RFD increased 15% after training (at zero to one-sixth MVC; P < 0.05). Furthermore, muscle EMG increased (P < 0.01-0.05) 22-143% (mean average voltage) and 41-106% (rate of EMG rise) in the early contraction phase (0-200 ms). In conclusion, increases in explosive muscle strength (contractile RFD and impulse) were observed after heavy-resistance strength training. These findings could be explained by an enhanced neural drive, as evidenced by marked increases in EMG signal amplitude and rate of EMG rise in the early phase of muscle contraction.

The evaluation of rate of force development during rapid contractions has recently become quite popular for characterising explosive strength of athletes, elderly individuals and patients. The main aims of this narrative review are to describe the neuromuscular determinants of rate of force development and to discuss various methodological considerations inherent to its evaluation for research and clinical purposes. Rate of force development (1) seems to be mainly determined by the capacity to produce maximal voluntary activation in the early phase of an explosive contraction (first 50–75 ms), particularly as a result of increased motor unit discharge rate; (2) can be improved by both explosive-type and heavy-resistance strength training in different subject populations, mainly through an improvement in rapid muscle activation; (3) is quite difficult to evaluate in a valid and reliable way. Therefore, we provide evidence-based practical recommendations for rational quantification of rate of force development in both laboratory and clinical settings.

Combined V-wave and Hoffmann (H) reflex measurements were performed during maximal muscle contraction to examine the neural adaptation mechanisms induced by resistance training. The H-reflex can be used to assess the excitability of spinal alpha-motoneurons, while also reflecting transmission efficiency (i.e., presynaptic inhibition) in Ia afferent synapses. Furthermore, the V-wave reflects the overall magnitude of efferent motor output from the alpha-motoneuron pool because of activation from descending central pathways. Fourteen male subjects participated in 14 wk of resistance training that involved heavy weight-lifting exercises for the muscles of the leg. Evoked V-wave, H-reflex, and maximal M-wave (M(max)) responses were recorded before and after training in the soleus muscle during maximal isometric ramp contractions. Maximal isometric, concentric, and eccentric muscle strength was measured by use of isokinetic dynamometry. V-wave amplitude increased approximately 50% with training (P < 0.01) from 3.19 +/- 0.43 to 4.86 +/- 0.43 mV, or from 0.308 +/- 0.048 to 0.478 +/- 0.034 when expressed relative to M(max) (+/- SE). H-reflex amplitude increased approximately 20% (P < 0.05) from 5.37 +/- 0.41 to 6.24 +/- 0.49 mV, or from 0.514 +/- 0.032 to 0.609 +/- 0.025 when normalized to M(max). In contrast, resting H-reflex amplitude remained unchanged with training (0.503 +/- 0.059 vs. 0.499 +/- 0.063). Likewise, no change occurred in M(max) (10.78 +/- 0.86 vs. 10.21 +/- 0.66 mV). Maximal muscle strength increased 23-30% (P < 0.05). In conclusion, increases in evoked V-wave and H-reflex responses were observed during maximal muscle contraction after resistance training. Collectively, the present data suggest that the increase in motoneuronal output induced by resistance training may comprise both supraspinal and spinal adaptation mechanisms (i.e., increased central motor drive, elevated motoneuron excitability, reduced presynaptic inhibition).

In human pennate muscle, changes in anatomical cross‐sectional area (CSA) or volume caused by training or inactivity may not necessarily reflect the change in physiological CSA, and thereby in maximal contractile force, since a simultaneous change in muscle fibre pennation angle could also occur. Eleven male subjects undertook 14 weeks of heavy‐resistance strength training of the lower limb muscles. Before and after training anatomical CSA and volume of the human quadriceps femoris muscle were assessed by use of magnetic resonance imaging (MRI), muscle fibre pennation angle (θp) was measured in the vastus lateralis (VL) by use of ultrasonography, and muscle fibre CSA (CSAfibre) was obtained by needle biopsy sampling in VL. Anatomical muscle CSA and volume increased with training from 77.5 ± 3.0 to 85.0 ± 2.7 cm2 and 1676 ± 63 to 1841 ± 57 cm3, respectively (±s.e.m.). Furthermore, VL pennation angle increased from 8.0 ± 0.4 to 10.7 ± 0.6 deg and CSAfibre increased from 3754 ± 271 to 4238 ± 202 μm2. Isometric quadriceps strength increased from 282.6 ± 11.7 to 327.0 ± 12.4 N m. A positive relationship was observed between θp and quadriceps volume prior to training (r = 0.622). Multifactor regression analysis revealed a stronger relationship when θp and CSAfibre were combined (R= 0.728). Post‐training increases in CSAfibre were related to the increase in quadriceps volume (r = 0.749). Myosin heavy chain (MHC) isoform distribution (type I and II) remained unaltered with training. VL muscle fibre pennation angle was observed to increase in response to resistance training. This allowed single muscle fibre CSA and maximal contractile strength to increase more (+16 %) than anatomical muscle CSA and volume (+10 %). Collectively, the present data suggest that the morphology, architecture and contractile capacity of human pennate muscle are interrelated, in vivo. This interaction seems to include the specific adaptation responses evoked by intensive resistance training.

'Explosive' muscle strength or contractile rate of force development (RFD) is a term to describe the ability to rapidly develop muscular force, and can be measured as the slope of the torque-time curve obtained during isometric conditions. Previously, conflicting results have been reported regarding the relationship between contractile RFD and various physiological parameters. One reason for this discrepancy may be that RFD in various time intervals from the onset of contraction is affected by different physiological parameters. The aim of the present study was to investigate the relationship between voluntary contractile RFD in time intervals of 0-10, 0-20, ..., 0-250 ms from the onset of contraction and two main parameters: (1) voluntary maximal muscle strength and (2) electrically evoked muscle twitch contractile properties. The main finding was that voluntary RFD became increasingly more dependent on MVC and less dependent on muscle twitch contractile properties as time from the onset of contraction increased. At time intervals later than 90 ms from the onset of contraction maximal muscle strength could account for 52-81% of the variance in voluntary RFD. In the very early time interval (<40 ms from the onset of contraction) voluntary RFD was moderately correlated to the twitch contractile properties of the muscle and was to a less extent related to MVC. The present results suggest that explosive movements with different time spans are influenced by different physiological parameters. This may have important practical implications when designing resistance training programs for specific sports.

The present investigation measured the load‐displacement and stress‐strain characteristics of the proximal and distal human triceps surae aponeurosis and tendon in vivo during graded voluntary 10 s isometric plantarflexion efforts in five subjects. During the contractions synchronous real‐time ultrasonography of aponeurosis displacement, electromyography of the gastrocnemius, soleus and dorsiflexor muscles, and joint angular rotation were obtained. Tendon cross‐sectional area and moment arm were obtained from magnetic resonance (MR) images. Force and electromyography data from dorsiflexion efforts were used to examine the effect of coactivation. Tendon force was calculated from the joint moments and tendon moment arm, and stress was obtained by dividing force by cross‐sectional area. Aponeurosis and tendon strain were obtained from the displacements normalised to tendon length. Tendon force was 3171 ± 201 N, which corresponded to 2.6 % less than the estimated force when coactivation was accounted for (3255 ± 206 N). Aponeurosis displacement (13.9‐ 12.9 mm) decreased 30 % (9.6‐10.7 mm) when accounting for joint angular rotation (3.6 deg). Coactivation and angular rotation‐corrected stiffness yielded a quadratic relationship, R2= 0.98± 0.01, which was similar for the proximal (467 N mm−1) and distal (494 N mm−1) aponeurosis and tendon. Maximal strain and stress were 4.4‐5.6 % and 41.6 ± 3.9 MPa, respectively, which resulted in a Young's modulus of 1048‐1474 MPa. The mechanical properties of the human triceps surae aponeurosis and tendon in vivo were for the first time examined. The stiffness and Young's modulus exceeded those previously reported for the tibialis anterior tendon in vivo, but were similar to those obtained for various isolated mammalian and human tendons.

A randomized-controlled single-blind trial was conducted to investigate the clinical, structural and functional effects of peritendinous corticosteroid injections (CORT), eccentric decline squat training (ECC) and heavy slow resistance training (HSR) in patellar tendinopathy. Thirty-nine male patients were randomized to CORT, ECC or HSR for 12 weeks. We assessed function and symptoms (VISA-p questionnaire), tendon pain during activity (VAS), treatment satisfaction, tendon swelling, tendon vascularization, tendon mechanical properties and collagen crosslink properties. Assessments were made at 0 weeks, 12 weeks and at follow-up (half-year). All groups improved in VISA-p and VAS from 0 to 12 weeks (Po0.05). VISA-p and VAS improvements were maintained at follow-up in ECC and HSR but deteriorated in CORT (Po0.05). In CORT and HSR, tendon swelling decreased ( À 13 AE 9% and À 12 AE 13%, Po0.05) and so did vascularization ( À 52 AE 49% and À 45 AE 23%, Po0.01) at 12 weeks. Tendon mechanical properties were similar in healthy and injured tendons and were unaffected by treatment. HSR yielded an elevated collagen network turnover. At the half-year follow-up, treatment satisfaction differed between groups, with HSR being most satisfied. Conclusively, CORT has good short-term but poor long-term clinical effects, in patellar tendinopathy. HSR has good short-and long-term clinical effects accompanied by pathology improvement and increased collagen turnover.

Aging is characterized by loss of spinal motor neurons (MNs) due to apoptosis, reduced insulin-like growth factor I signaling, elevated amounts of circulating cytokines, and increased cell oxidative stress. The age-related loss of spinal MNs is paralleled by a reduction in muscle fiber number and size (sarcopenia), resulting in impaired mechanical muscle performance that in turn leads to a reduced functional capacity during everyday tasks. Concurrently, maximum muscle strength, power, and rate of force development are decreased with aging, even in highly trained master athletes. The impairment in muscle mechanical function is accompanied and partly caused by an age-related loss in neuromuscular function that comprise changes in maximal MN firing frequency, agonist muscle activation, antagonist muscle coactivation, force steadiness, and spinal inhibitory circuitry. Strength training appears to elicit effective countermeasures in elderly individuals even at a very old age (480 years) by evoking muscle hypertrophy along with substantial changes in neuromuscular function, respectively. Notably, the training-induced changes in muscle mass and nervous system function leads to an improved functional capacity during activities of daily living.