Statistical Methods for Health Care Research

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.

Increased rate of force development and neural drive of human skeletal muscle following resistance training

OBJECTIVE: to examine the clinical evidence reporting the prevalence of sarcopenia and the effect of nutrition and exercise interventions from studies using the consensus definition of sarcopenia proposed by the European Working Group on Sarcopenia in Older People (EWGSOP).METHODS: PubMed and Dialog databases were searched (January 2000-October 2013) using pre-defined search terms. Prevalence studies and intervention studies investigating muscle mass plus strength or function outcome measures using the EWGSOP definition of sarcopenia, in well-defined populations of adults aged ≥50 years were selected.RESULTS: prevalence of sarcopenia was, with regional and age-related variations, 1-29% in community-dwelling populations, 14-33% in long-term care populations and 10% in the only acute hospital-care population examined. Moderate quality evidence suggests that exercise interventions improve muscle strength and physical performance. The results of nutrition interventions are equivocal due to the low number of studies and heterogeneous study design. Essential amino acid (EAA) supplements, including ∼2.5 g of leucine, and β-hydroxy β-methylbutyric acid (HMB) supplements, show some effects in improving muscle mass and function parameters. Protein supplements have not shown consistent benefits on muscle mass and function.CONCLUSION: prevalence of sarcopenia is substantial in most geriatric settings. Well-designed, standardised studies evaluating exercise or nutrition interventions are needed before treatment guidelines can be developed. Physicians should screen for sarcopenia in both community and geriatric settings, with diagnosis based on muscle mass and function. Supervised resistance exercise is recommended for individuals with sarcopenia. EAA (with leucine) and HMB may improve muscle outcomes.

/pdf/prevalence-of-and-interventions-for-sarcopenia-in-ageing-1i4ujsqpcg.pdf

Prevalence of and interventions for sarcopenia in ageing adults: a systematic review. Report of the International Sarcopenia Initiative (EWGSOP and IWGS)

The extracellular matrix (ECM), and especially the connective tissue with its collagen, links tissues of the body together and plays an important role in the force transmission and tissue structure maintenance especially in tendons, ligaments, bone, and muscle. The ECM turnover is influenced by physical activity, and both collagen synthesis and degrading metalloprotease enzymes increase with mechanical loading. Both transcription and posttranslational modifications, as well as local and systemic release of growth factors, are enhanced following exercise. For tendons, metabolic activity, circulatory responses, and collagen turnover are demonstrated to be more pronounced in humans than hitherto thought. Conversely, inactivity markedly decreases collagen turnover in both tendon and muscle. Chronic loading in the form of physical training leads both to increased collagen turnover as well as, dependent on the type of collagen in question, some degree of net collagen synthesis. These changes will modify the mechanical properties and the viscoelastic characteristics of the tissue, decrease its stress, and likely make it more load resistant. Cross-linking in connective tissue involves an intimate, enzymatical interplay between collagen synthesis and ECM proteoglycan components during growth and maturation and influences the collagen-derived functional properties of the tissue. With aging, glycation contributes to additional cross-linking which modifies tissue stiffness. Physiological signaling pathways from mechanical loading to changes in ECM most likely involve feedback signaling that results in rapid alterations in the mechanical properties of the ECM. In developing skeletal muscle, an important interplay between muscle cells and the ECM is present, and some evidence from adult human muscle suggests common signaling pathways to stimulate contractile and ECM components. Unaccostumed overloading responses suggest an important role of ECM in the adaptation of myofibrillar structures in adult muscle. Development of overuse injury in tendons involve morphological and biochemical changes including altered collagen typing and fibril size, hypervascularization zones, accumulation of nociceptive substances, and impaired collagen degradation activity. Counteracting these phenomena requires adjusted loading rather than absence of loading in the form of immobilization. Full understanding of these physiological processes will provide the physiological basis for understanding of tissue overloading and injury seen in both tendons and muscle with repetitive work and leisure time physical activity.

Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading

High-resistance strength training (HRST) is one of the most widely practiced forms of physical activity, which is used to enhance athletic performance, augment musculo-skeletal health and alter body aesthetics. Chronic exposure to this type of activity produces marked increases in muscular strength, which are attributed to a range of neurological and morphological adaptations. This review assesses the evidence for these adaptations, their interplay and contribution to enhanced strength and the methodologies employed. The primary morphological adaptations involve an increase in the cross-sectional area of the whole muscle and individual muscle fibres, which is due to an increase in myofibrillar size and number. Satellite cells are activated in the very early stages of training; their proliferation and later fusion with existing fibres appears to be intimately involved in the hypertrophy response. Other possible morphological adaptations include hyperplasia, changes in fibre type, muscle architecture, myofilament density and the structure of connective tissue and tendons. Indirect evidence for neurological adaptations, which encompasses learning and coordination, comes from the specificity of the training adaptation, transfer of unilateral training to the contralateral limb and imagined contractions. The apparent rise in whole-muscle specific tension has been primarily used as evidence for neurological adaptations; however, morphological factors (e.g. preferential hypertrophy of type 2 fibres, increased angle of fibre pennation, increase in radiological density) are also likely to contribute to this phenomenon. Changes in inter-muscular coordination appear critical. Adaptations in agonist muscle activation, as assessed by electromyography, tetanic stimulation and the twitch interpolation technique, suggest small, but significant increases. Enhanced firing frequency and spinal reflexes most likely explain this improvement, although there is contrary evidence suggesting no change in cortical or corticospinal excitability. The gains in strength with HRST are undoubtedly due to a wide combination of neurological and morphological factors. Whilst the neurological factors may make their greatest contribution during the early stages of a training programme, hypertrophic processes also commence at the onset of training.

http://performancetrainingsystems.net/Resources/Adaptations_to_Strength_Training.pdf

The adaptations to strength training : morphological and neurological contributions to increased strength.

1. 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. 2. 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 (theta(p)) was measured in the vastus lateralis (VL) by use of ultrasonography, and muscle fibre CSA (CSA(fibre)) was obtained by needle biopsy sampling in VL. 3. Anatomical muscle CSA and volume increased with training from 77.5 +/- 3.0 to 85.0 +/- 2.7 cm(2) and 1676 +/- 63 to 1841 +/- 57 cm(3), respectively (+/- S.E.M.). Furthermore, VL pennation angle increased from 8.0 +/- 0.4 to 10.7 +/- 0.6 deg and CSA(fibre) increased from 3754 +/- 271 to 4238 +/- 202 microm (2). Isometric quadriceps strength increased from 282.6 +/- 11.7 to 327.0 +/- 12.4 N m. 4. A positive relationship was observed between theta(p) and quadriceps volume prior to training (r = 0.622). Multifactor regression analysis revealed a stronger relationship when theta(p) and CSA(fibre) were combined (R = 0.728). Post-training increases in CSA(fibre) were related to the increase in quadriceps volume (r = 0.749). 5. Myosin heavy chain (MHC) isoform distribution (type I and II) remained unaltered with training. 6. 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 %). 7. 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.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1469-7793.2001.t01-1-00613.x

A mechanism for increased contractile strength of human pennate muscle in response to strength training: changes in muscle architecture.

Contractile force is transmitted to the skeleton through tendons and aponeuroses, and, although it is appreciated that the mechanocharacteristics of these tissues play an important role for movement performance with respect to energy storage, the association between tendon mechanical properties and the contractile muscle output during high-force movement tasks remains elusive. The purpose of the study was to investigate the relation between the mechanical properties of the connective tissue and muscle performance in maximal isometric and dynamic muscle actions. Sixteen trained men participated in the study. The mechanical properties of the vastus lateralis tendon-aponeurosis complex were assessed by ultrasonography. Maximal isometric knee extensor force and rate of torque development (RTD) were determined. Dynamic performance was assessed by maximal squat jumps and countermovement jumps on a force plate. From the vertical ground reaction force, maximal jump height, jump power, and force-/velocity-related determinants of jump performance were obtained. RTD was positively related to the stiffness of the tendinous structures (r = 0.55, P < 0.05), indicating that tendon mechanical properties may account for up to 30% of the variance in RTD. A correlation was observed between stiffness and maximal jump height in squat jumps and countermovement jumps (r = 0.64, P < 0.05 and r = 0.55, P < 0.05). Power, force, and velocity parameters obtained during the jumps were significantly correlated to tendon stiffness. These data indicate that muscle output in high-force isometric and dynamic muscle actions is positively related to the stiffness of the tendinous structures, possibly by means of a more effective force transmission from the contractile elements to the bone.

Muscle performance during maximal isometric and dynamic contractions is influenced by the stiffness of the tendinous structures

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.







The force from muscle contraction is transferred to bone via tendons to produce joint movement. Tendons are, however, not inextensible, but have non-linear spring-like characteristics, which allows for a dynamic mechanical interaction between the muscle and tendon (Griffiths & Selesnick, 1998; Lieber et al. 2000). During locomotion the tendon is stretched and energy is stored which is subsequently converted into kinetic energy upon release (Alexander & Vernon, 1975; Ker et al. 1988).

Although it has been recognised that tendon properties contribute to the complex interaction of the central nervous system, muscle-tendon unit and bony structures to produce joint movement, there is scarce information on human tendon behaviour in vivo. Moreover, investigations of human tendon behaviour have largely been limited to biomechanical testing of isolated cadaver tissue specimens (Rack & Ross, 1984; Goldstein et al. 1987; Loren & Lieber, 1995; McGough et al. 1996), or invasive in vivo methods (Amis et al. 1987; Fellows & Rack, 1987). Therefore, the recent advance of using real-time ultrasonography to non-invasively determine fascicle movement during muscle contraction has provided a method for studying human aponeurosis and tendon tissue behaviour during isometric muscle contraction in vivo (Fukashiro et al. 1995a; Ito et al. 1998).

Thus far, the mechanical properties of the tibialis anterior in the leg have been examined using ultrasonography during voluntary (Ito et al. 1998) and electrically induced (Maganaris & Paul, 1999) contractions, with considerably different results with respect to both tendon force and deformation. The dissimilarities may in part be explained by the different methodologies. In this context, it should be noted that previous studies (Ito et al. 1998; Maganaris & Paul, 1999) have not accounted for the potential error in tendon displacement due to joint angular rotation, or the tendon load attributed to coactivation of the antagonist muscles during the isometric contraction.

Since the aponeurosis of the triceps surae complex and Achilles’ tendon is subject to appreciable stresses during human locomotion, the in vivo study of their mechanical properties is of considerable interest and relevant to loading history and ageing. Furthermore, the Achilles’ tendon is frequently associated with various pathologies related to loading history (Kannus et al. 1997), including complete tendon ruptures (Kannus & Jozsa, 1991). While several studies have estimated Achilles’ tendon force during various activities (Scott & Winter, 1990; Fukashiro et al. 1995b; Finni et al. 1998; Giddings et al. 2000) aponeurosis deformation of the triceps surae has thus far not been measured. Therefore, the purpose of the present investigation was to (1) measure the load- displacement and stress-strain characteristics of the human triceps surae aponeurosis and tendon in vivo, during graded maximal voluntary plantarflexion efforts and (2) examine whether the Load–displacement characteristics of the proximal and distal aponeurosis differed.

Load‐displacement properties of the human triceps surae aponeurosis in vivo

Tendons are designed to withstand considerable loads. Mechanical loading of tendon tissue results in upregulation of collagen expression and increased synthesis of collagen protein, the extent of which is probably regulated by the strain experienced by the resident fibroblasts (tenocytes). This increase in collagen formation peaks around 24 h after exercise and remains elevated for about 3 days. The degradation of collagen proteins also rises after exercise, but seems to peak earlier than the synthesis. Despite the ability of tendons to adapt to loading, repetitive use often results in injuries, such as tendinopathy, which is characterized by pain during activity, localized tenderness upon palpation, swelling and impaired performance. Tendon histological changes include reduced numbers and rounding of fibroblasts, increased content of proteoglycans, glycosaminoglycans and water, hypervascularization and disorganized collagen fibrils. At the molecular level, the levels of messenger RNA for type I and III collagens, proteoglycans, angiogenic factors, stress and regenerative proteins and proteolytic enzymes are increased. Tendon microrupture and material fatigue have been suggested as possible injury mechanisms, thus implying that one or more 'weak links' are present in the structure. Understanding how tendon tissue adapts to mechanical loading will help to unravel the pathogenesis of tendinopathy.

The pathogenesis of tendinopathy: balancing the response to loading

Tendon properties contribute to the complex interaction of the central nervous system, muscle-tendon unit and bony structures to produce joint movement. Until recently limited information on human tendon behaviour in vivo was available; however, novel methodological advancements have enabled new insights to be gained in this area. The present review summarizes the progress made with respect to human tendon and aponeurosis function in vivo, and how tendons adapt to ageing, loading and unloading conditions. During low tensile loading or with passive lengthening not only the muscle is elongated, but also the tendon undergoes significant length changes, which may have implications for reflex responses. During active loading, the length change of the tendon far exceeds that of the aponeurosis, indicating that the aponeurosis may more effectively transfer force onto the tendon, which lengthens and stores elastic energy subsequently released during unloading, in a spring-like manner. In fact, data recently obtained in vivo confirm that, during walking, the human Achilles tendon provides elastic strain energy that can decrease the energy cost of locomotion. Also, new experimental evidence shows that, contrary to earlier beliefs, the metabolic activity in human tendon is remarkably high and this affords the tendon the ability to adapt to changing demands. With ageing and disuse there is a reduction in tendon stiffness, which can be mitigated with resistance exercises. Such adaptations seem advantageous for maintaining movement rapidity, reducing tendon stress and risk of injury, and possibly, for enabling muscles to operate closer to the optimum region of the length-tension relationship.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2007.139105

S. Peter Magnusson

Papers

A mechanism for increased contractile strength of human pennate muscle in response to strength training: changes in muscle architecture.

Muscle performance during maximal isometric and dynamic contractions is influenced by the stiffness of the tendinous structures

Load‐displacement properties of the human triceps surae aponeurosis in vivo

The pathogenesis of tendinopathy: balancing the response to loading

Human tendon behaviour and adaptation, in vivo.