Decrease In Force-generating Capacity Research Articles

Changes in Motor Coordination Induced by Local Fatigue during a Sprint Cycling Task.

This study investigated how muscle coordination is adjusted in response to a decrease in the force-generating capacity of one muscle group during a sprint cycling task. Fifteen participants were tested during a sprint before and after a fatigue electromyostimulation protocol was conducted on the quadriceps of one leg. Motor coordination was assessed by measuring myoelectrical activity, pedal force, and joint power. The decrease in force-generating capacity of the quadriceps (-28.0% ± 6.8%) resulted in a decrease in positive knee extension power during the pedaling task (-34.4 ± 30.6 W; P = 0.001). The activity of the main nonfatigued synergist and antagonist muscles (triceps surae, gluteus maximus and hamstrings) of the ipsilateral leg decreased, leading to a decrease in joint power at the hip (-30.1 ± 37.8 W; P = 0.008) and ankle (-20.8 ± 18.7 W; P = 0.001). However, both the net power around the knee and the ability to effectively orientate the pedal force were maintained during the extension by reducing the coactivation and the associated negative power produced by the hamstrings. Adaptations also occurred in flexion phases in both legs, exhibiting an increased power (+17.9 ± 28.3 [P = 0.004] and +19.5 ± 21.9 W [P = 0.026]), associated with an improvement in mechanical effectiveness. These results demonstrate that the nervous system readily adapts coordination in response to peripheral fatigue by (i) decreasing the activation of adjacent nonfatigued muscles to maintain an effective pedal force orientation (despite reducing pedal power) and (ii) increasing the neural drive to muscles involved in the flexion phases such that the decrease in total pedal power is limited.

Impact of vaginal parity and aging on the architectural design of pelvic floor muscles

Vaginal delivery and aging are key risk factors for pelvic floor muscle dysfunction, which is a critical component of pelvic floor disorders. However, alterations in the pelvic floor muscle intrinsic structure that lead to muscle dysfunction because of childbirth and aging remain elusive. The purpose of this study was to determine the impact ofvaginal deliveries and aging on human cadaveric pelvic floor muscle architecture, which is the strongest predictor of active muscle function. Coccygeus, iliococcygeus, and pubovisceralis were obtained from younger donors who were ≤51 years old, vaginally nulliparous (n= 5) and vaginally parous (n= 6) and older donors who were >51 years old, vaginally nulliparous (n= 6) and vaginally parous (n= 6), all of whom had no history of pelvic floor disorders. Architectural parameters, which are predictive of muscle's excursion and force-generating capacity, were determined with the use of validated methods. Intramuscular collagen content was quantified by hydroxyproline assay. Main effects of parity and aging and the interactions were determined with the use of 2-way analysis of variance, with Tukey's post-hoc testing and a significance level of .05. The mean age of younger and older donors differed by approximately 40 years (P= .001) but was similar between nulliparous and parous donors within each age group (P > .9). The median parity was 2 (range, 1-3) in younger and older vaginally parous groups (P= .7). The main impact of parity was increased fiber length in the more proximal coccygeus (P= .03) and iliococcygeus (P= .04). Aging changes manifested as decreased physiologic cross-sectional area across all pelvic floor muscles (P < .05), which substantially exceeded the age-related decline in muscle mass. The physiologic cross-sectional area was lower in younger vaginally parous, compared with younger vaginally nulliparous, pelvic floor muscles; however, the differences did not reach statistical significance. Pelvic floor muscle collagen content was not altered by parity but increased dramatically with aging (P < .05). Increased fiber length in more proximal pelvic floor muscles likely represents an adaptive response to the chronically increased load placed on these muscles by the displaced apical structures, presumably as a consequence of vaginal delivery. In younger specimens, a consistent trend towards decrease in force-generating capacity of all pelvic floor muscles in the parous group suggests a potential mechanism for clinically identified pelvic floor muscle weakness in vaginally parous women. The substantial decrease in predicted muscle force production and fibrosis with aging represent likely mechanisms for the pelvic floor muscle dysfunction in older women.

A computational model of neural activation, force generation and intracellular bioenergetics during muscle fatigue

Muscle fatigue, an acute decrease in force‐generating capacity in response to repeated or prolonged activation, is a process whose mechanisms are difficult to discern due to the complicated nature of in vivo voluntary muscle force development. Computational modeling has been used to gain insight into the mechanisms of similarly complicated systems. The neuromuscular response to repeated voluntary activation is an attractive target for this approach. Here, we present a comprehensive model of neuromuscular activation, torque generation, bioenergetics and fatigue that provides a theoretical framework by which hypotheses related to the mechanisms of fatigue might be tested. A series of modular components were formulated, each representing a component of neuromuscular function. Multiple simulations were run to confirm accurate contractile and metabolic predictions when compared with in vivo data. A simulation that emulated a contraction protocol in the literature was run to evaluate the ability of the model to predict fatigue. Overall, the model predicted intracellular metabolic responses similar to in vivo data. Fatigue predicted by the model was within 6.6% of the reference data‐set from the literature, validating this model as a powerful tool for investigating the mechanisms of fatigue in voluntary isometric contractions.

Endotoxemia does not limit energy supply in exercising rat skeletal muscle

Although depletion in high-energy phosphorylated compounds and mitochondrial impairment have been reported in septic skeletal muscle at rest, their impact on energy metabolism has not been documented during exercise. In this study we aimed to investigate strictly gastrocnemius muscle function non-invasively, using magnetic resonance techniques in endotoxemic rats. Endotoxemia was induced by injecting animals intraperitoneally at t(0) and t(0) + 24 h with Klebsiella pneumoniae lipopolysaccharides (at 3 mg kg(-1)). Investigations were performed at t(0) + 48 h during a transcutaneous electrical stimulation protocol consisting of 5.7 min of repeated isometric contractions at a frequency of 3.3 HZ. Endotoxin treatment produced a depletion in basal phosphocreatine content and a pronounced reduction in oxidative adenosine triphosphate (ATP) synthesis capacity, whereas the resting ATP concentration remained unchanged. During the stimulation period, endotoxemia caused a decrease in force-generating capacity that was fully accounted for by the loss of muscle mass. It further induced an acceleration of glycolytic ATP production and an increased accumulation of adenosine diphosphate (ADP, an important mitochondrial regulator) that allowed a near-normal rate of oxidative ATP synthesis. Finally, endotoxemia did not affect the total rate of ATP production or the ATP cost of contraction throughout the whole stimulation period. These data demonstrate that, in an acute septic phase, metabolic alterations in resting muscle do not impact energy supply in exercising muscle, likely as a result of adaptive mechanisms.

Comparison Between Animal and Human Studies of Skeletal Muscle Adaptation to Chronic Stimulation

Functional electrical stimulation (FES) has recently emerged as a clinical tool for treatment of neuromuscular disorders. Chronic muscle stimulation, however, has long been used by basic scientists studying the details of the muscular adaptation process. Biochemical, morphological, and functional changes occur in skeletal muscle secondary to chronic stimulation. Chronic stimulation (12-24 hours per day for six weeks) results in a well-defined progression of changes in which a "fast" muscle becomes a typical "slow" muscle with a large decrease in force-generating capacity. On the other hand, clinical studies of FES have demonstrated muscle strengthening following treatment. An attempt is made to reconcile the results obtained in the two fields.

Glucose uptake in rat soleus: effect of acute unloading and subsequent reloading

The effect of acutely reduced weight bearing (unloading) on the in vitro uptake of 2-[1,2-3H]deoxy-D-glucose was studied in the soleus muscle by tail casting and suspending rats. After just 4 h, the uptake of 2-deoxy-D-glucose fell (-19%, P less than 0.01) and declined further after an additional 20 h of unloading. This diminution at 24 h was associated with slower oxidation of [14C]glucose and incorporation of [14C]glucose into glycogen. Unlike after 1 day, at 3 days of unloading basal uptake of 2-deoxy-D-glucose did not differ from control. Reloading of the soleus after 1 or 3 days of unloading increased uptake of 2-deoxy-D-glucose above control and returned it to normal within 6 h and 4 days, respectively. These effects of unloading and recovery were caused by local changes in the soleus, because the extensor digitorum longus from the same hindlimbs did not display any alterations in uptake of 2-deoxy-D-glucose or metabolism of glucose. This study demonstrates that alterations in contractile activity, brought about by unloading or recovery from unloading, can influence the regulation of glucose transport in the soleus.

Force-length dependence of arterial lamellar, smooth muscle, and myofilament orientations.

Force generation by contractile elements of arterial tissue can be affected by alterations in their alignment with shortening. The orientation and morphometry of smooth muscle (SM) myofilaments, medial lamellae, and elastic laminae were examined as a function of length in intact swine carotid arteries or strips. Intimal-medial tissue strips were fixed during isometric contractions at lengths (L) defined with respect to the optimal length for force generation (Lo). The average orientation of SM cells in two perpendicular planes remained parallel to the long axis of the tissue at all lengths, but the absolute value of angular deviations increased with shortening. Tissue lengthening was associated with decreased folding of the elastic laminae. This decrease in waviness was quantified by a stretch index (SI). Ultrastructural observations indicated that the myofilament absolute angular deviation was greater than that for the cellular alignment. For arteries fixed in situ while constricted, SI was least in the periintimal laminae and increased in the peripheral laminae. The average decrease in force-generating capacity on shortening from Lo to 0.6 Lo attributed to increasing SM and myofilament angular deviations was calculated to be 7%.