S. P. Magnusson

Role of the nervous system in sarcopenia and muscle atrophy with aging: strength training as a countermeasure

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 (>80 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.

A mechanism for altered flexibility in human skeletal muscle.

1. We investigated the effect of a long‐term stretching regimen on the tissue properties and stretch tolerance of human skeletal muscle. 2. Resistance to stretch was measured as torque (in N m) offered by the hamstring muscle group during passive knee extension while electromyographic (EMG) activity, knee joint angle and velocity were continuously monitored during a standardized stretch manoeuvre. Seven healthy subjects were tested before and after a 3 week training period using two separate protocols. Protocol 1 consisted of a slow stretch at 0.087 rad s‐1 to a predetermined angle followed by a 90 s holding phase. Subjects were brought to the same angle before and after the training period. Protocol 2 was a similar stretch, but continued to the point of pain. 3. During protocol 1 the torque rose during the stretch and then declined during the holding phase. EMG activity was small and did not change significantly during the protocol. No significant differences in stiffness, energy and peak torque about the knee joint were seen as a result of the training. During protocol 2 the angle to which the knee could be extended was significantly increased as a result of the training. This was accompanied by a comparable increase in peak torque and energy. EMG activity was small and not affected by training. 4. It is concluded that reflex EMG activity does not limit the range of movement during slow stretches and that the increased range of motion achieved from training is a consequence of increased stretch tolerance on the part of the subject rather than a change in the mechanical or viscoelastic properties of the muscle.

Passive properties of human skeletal muscle during stretch maneuvers

Despite limited scientific knowledge, stretching of human skeletal muscle to improve flexibility is a widespread practice among althletes. This article reviews recent findings regarding passive properties of the hamstring muscle group during stretch based on a model that was developed which could synchronously and continuously measure passive hamstring resistance and electromyographic activity, while the velocity and angle of stretch was controlled. Resistance to stretch was defined as passive torque (Nm) offered by the hamstring muscle group during passive knee extension using an isokinetic dynamometer with a modified thigh pad. To simulate a clinical static stretch, the knee was passively extended to a pre‐determined final position (0.0875 rad/s, dynamic phase) where it remained stationary for 90s (static phase). Alternatively, the knee was extended to the point of discomfort (stretch tolerance). From the torque‐angle curve of the dynamic phase of the static stretch, and in the stretch tolerance protocol, passive energy and stiffness were calculated. Torque decline in the static phase was considered to represent viscoelastis stress relaxation. Using the model, studies were conducted which demonstrated that a single static stretch resulted in a 30% viscoelastic stress relaxation. With repeated stretches muscle stiffness declined, but returned to baseline values within 1 h. Long‐term stretching (3 weeks) increased joint range of motion as a result of a change in stretch tolerance rather than in the passive properties. Strength training resulted in increased muscle stiffness, which was unaffected by daily stretching. The effectiveness of different stretching tecniques was attributed to a change in strech tolerance rather than passive properties. Inflexible and older subjects have increased muscle stiffness, but a lower stretch tolerance compared to subjects with normal flexiblity and younger subjects, respectively. Although far from all questions regarding the passive properties of humans skeletal muscle have been answered in these studies, the measurement technique permited skeletal muscle.

Load-displacement properties of the human triceps surae aponeurosis and tendon in runners and non-runners

The load‐displacement and stress–strain characteristics of the human triceps surae tendon and aponeurosis, in vivo, was examined during graded maximal voluntary plantarflexion efforts in runners who trained 80 km/ week or more and age‐matched non‐runners. Synchronous real‐time ultrasonography of triceps surae tendon and aponeurosis displacement, electromyography of the gastrocnemius, soleus and dorsiflexor muscles, and joint angular rotation were obtained. Tendon cross‐sectional area and ankle joint moment arm were obtained from magnetic resonance imaging. Tensile tendon force was calculated from the joint moments and tendon moment arm and stress was obtained by dividing force by cross‐sectional area. Strain was obtained from the displacements normalized to tendon length. Antagonist coactivation and small amounts of ankle joint rotation significantly affected tensile tendon force and aponeurosis and tendon displacement, respectively (P < 0.01). Plantarflexion moment was similar in runners (138 ± 27 Nm, mean ± SEM) and non‐runners (142 ± 17 Nm). Tendon moment arm was alike in non‐runner (58.3 ± 0.2 mm) and runners (55.1 ± 0.1 mm). Similarly, there was no difference in tendon tensile force between runners (2633 ± 465 N) and non‐runners (2556 ± 401 N). The cross‐sectional area of the Achilles tendon was larger in runners (95 ± 3 mm2) than non‐runners (73 ± 3 mm2) (P < 0.01). The load‐deformation data yielded similar stiffness (runners 306 ± 61 N/mm, non‐runners 319 ± 42 N/mm). The maximal strain and stress was 4.9 ± 0.8% and 38.2 ± 9.8 MPa in non‐runners and 4.1 ± 0.8% and 26.3 ± 5.1 MPa in runners. The larger tendon cross‐sectional area in trained runners suggests that chronic exposure to repetitive loading has resulted in a tissue adaptation.

The effect of supervised rehabilitation on strength, postural sway, position sense and re‐injury risk after acute ankle ligament sprain

The effect of an early rehabilitation program, including postural training, on ankle joint function after an ankle ligament sprain was investigated prospectively. Ninety‐two subjects, matched for age, sex, and level of sports activity, were randomized to a control or training group. All subject received the same standard information regarding early ankle mobilization. In addition, the training group participated in supervised physical therapy rehabilitation (1 h. twice weekly) with emphasis on balance training. Postural sway, position sense and isometric ankle strength were measured 6 weeks and 4 months after the injury, and at 12 months re‐injury data were obtained. In the training group, there was a significant difference between the injured and uninjured side for plantar flexion (P<0.01), eversion (P<0.01) and inversion (P<0.05), but not for dorsiflexion at 6 weeks. In the control group, there was a significant difference between the injured and uninjured side for plantar flexion (P<0.01), eversion (P<0.01), inversion (P<0.01), and dorsiflexion (P<0.05) at 6 weeks. Postural sway, but not position sense, differed between the injured and uninjured side in both groups (P<0.01) at 6 weeks. The side‐to‐side percent differences were similar in both groups for all variables (P>0.05) at 6 weeks, and there were no side‐to‐side differences at 4 months in either group. In the control group, 11/38 (29%) suffered a re‐injury. while this number was only 2/29 (7%)) in the training group (P<0.05). These data showed that an ankle injury resulted in reduced ankle strength and postural control at 6 weeks, but that these variables had normalized at 4 months, independent of the supervised rehabilitation. However, the findings also demonstrated that supervised rehabilitation may reduce the number of re‐injuries, and therefore may play a role in injury prevention.

Region specific patellar tendon hypertrophy in humans following resistance training

Aim:  To examine if cross‐sectional area (CSA) differs along the length of the human patellar tendon (PT), and if there is PT hypertrophy in response to resistance training.

Antagonist muscle coactivation during isokinetic knee extension

The aim of the present study was to quantify the amount of antagonist coactivation and the resultant moment of force generated by the hamstring muscles during maximal quadriceps contraction in slow isokinetic knee extension. The net joint moment at the knee joint and electromyographic (EMG) signals of the vastus medialis, vastus lateralis, rectus femoris muscles (quadriceps) and the biceps femoris caput longum and semitendinosus muscles (hamstrings) were obtained in 16 male subjects during maximal isokinetic knee joint extension (KinCom, ROM 90–10°, 30° · s−1). Two types of extension were performed: [1] maximal concentric quadriceps contractions and [2] maximal eccentric hamstring contractions. Hamstring antagonist EMG in [1] were converted into antagonist moment based on the EMG‐moment relationships determined in [2] and vice versa. Since antagonist muscle coactivation was present in both [1] and [2] a set of related equations was constructed to yield the moment/EMG relationships for the hamstring and quadriceps muscles, respectively. The equations were solved separately for every 0.05° knee joint angle in the 90–10° range of excursion (0°=full extension) ensuring that the specificity of muscle length and internal muscle lever arms were incorporated into the moment/EMG relationships established. Substantial hamstring coactivation was observed during quadriceps agonist contraction. This resulted in a constant level of antagonist hamstring moment of about 30 Nm throughout the range of motion. In the range of 30–10° from full knee extension this antagonist hamstring moment corresponded to 30–75% of the measured knee extensor moment. The level of antagonist coactivation was 3‐fold higher for the lateral (Bfcl) compared to medial (ST) hamstring muscles. The amount of EMG crosstalk between agonist–antagonist muscle pairs was negligible (RXY2<0.02–0.06). The present data show that substantial antagonist coactivation of the hamstring muscles may be present during slow isokinetic knee extension. In consequence substantial antagonist flexor moments are generated. The antagonist hamstring moments potentially counteract the anterior tibial shear and excessive internal tibial rotation induced by the contractile forces of the quadriceps near full knee extension. In doing so the hamstring coactivation is suggested to assist the mechanical and neurosensory functions of the anterior cruciate ligament (ACL).

Eccentric rehabilitation exercise increases peritendinous type I collagen synthesis in humans with Achilles tendinosis

It has been shown that 12 weeks of eccentric heavy resistance training can reduce pain in runners suffering from chronic Achilles tendinosis, but the mechanism behind the effectiveness of this treatment is unknown. The present study investigates the local effect of an eccentric training regime on elite soccer players suffering from chronic Achilles tendinosis on the turnover of the peritendinous connective tissue.

Effects of aging on human skeletal muscle after immobilization and retraining

Inactivity is a recognized compounding factor in sarcopenia and muscle weakness in old age. However, while the negative effects of unloading on skeletal muscle in young individuals are well elucidated, only little is known about the consequence of immobilization and the regenerative capacity in elderly individuals. Thus the aim of this study was to examine the effect of aging on changes in muscle contractile properties, specific force, and muscle mass characteristics in 9 old (61-74 yr) and 11 young men (21-27 yr) after 2 wk of immobilization and 4 wk of retraining. Both young and old experienced decreases in maximal muscle strength, resting twitch peak torque and twitch rate of force development, quadriceps muscle volume, pennation angle, and specific force after 2 wk of immobilization (P < 0.05). The decline in quadriceps volume and pennation angle was smaller in old compared with young (P < 0.05). In contrast, only old men experienced a decrease in quadriceps activation. After retraining, both young and old regained their initial muscle strength, but old had smaller gains in quadriceps volume compared with young, and pennation angle increased in young only (P < 0.05). The present study is the first to demonstrate that aging alters the neuromuscular response to short-term disuse and recovery in humans. Notably, immobilization had a greater impact on neuronal motor function in old individuals, while young individuals were more affected at the muscle level. In addition, old individuals showed an attenuated response to retraining after immobilization compared with young individuals.

Corticosteroid injections, eccentric decline squat training and heavy slow resistance training in patellar tendinopathy.

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 (P<0.05). VISA‐p and VAS improvements were maintained at follow‐up in ECC and HSR but deteriorated in CORT (P<0.05). In CORT and HSR, tendon swelling decreased (−13±9% and −12±13%, P<0.05) and so did vascularization (−52±49% and −45±23%, P<0.01) 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.