Muscle Contractile Performance Research Articles

Territorial and mating success of dragonflies that vary in muscle power output and presence of gregarine gut parasites

Competition for mating territories in libellulid dragonflies involves aerial contests that require high levels of exertion and locomotor performance. Here we test the hypothesis that success of male Libellula pulchella dragonflies in territoriality and mating is affected by muscle contractile performance, and we examine how gregarine gut parasites affect muscle performance, energy reserves and territorial behaviour of their hosts. At a pond where gregarine parasites are rare, long-term territorial and mating success of males showed a significant positive association with muscle power output. At a nearby pond that had a much higher incidence and intensity of gregarine parasitism, there was no relationship between muscle performance and short-term territorial success. Instead, males assorted themselves into aggressive territory holders and submissive satellites, with the large majority of territory holders having no parasites and nearly all of the satellites parasitized. Unparasitized males showed a tight positive relationship between muscle power and fat content, which suggests that they use a known phenotypic adjustment in muscle contractile performance to allow the energy consumption rate of the flight muscles to match the rate at which energy can be mobilized from storage pools. Parasitized dragonflies showed a small decrease in average fat content and a marked change in the relationship between fat content and muscle power output. The apparent loss of the ability to match muscle contractility to the size of the energy storage pool in parasitized dragonflies suggests that gregarines may have systemic effects on signalling pathways and energy homeostasis. By indirectly choosing males that had successfully competed for territories, females consistently mated with physiologically or immunologically superior males despite large between-pond differences in male behaviour and the incidence and intensity of parasitic infection.

The effects of protease supplementation on skeletal muscle function and DOMS following downhill running

Protease supplementation has been shown to attenuate soft tissue injury resulting from intense exercise. The aim of this study was to evaluate the effects of protease supplementation on muscle soreness and contractile performance after downhill running. Ten matched pairs of male participants ran at a −10% grade for 30 min at 80% of their predicted maximal heart rate. The participants consumed two protease tablets (325 mg pancreatic enzymes, 75 mg trypsin, 50 mg papain, 50 mg bromelain, 10 mg amylase, 10 mg lipase, 10 mg lysozyme, 2 mg chymotrypisn) or a placebo four times a day beginning 1 day before exercise and lasting a total of 4 days. The participants were evaluated for perceived muscle soreness of the front and back of the dominant leg, pressure pain threshold by dolorimetry of the anterior medial, anterior lateral, posterior medial and posterior lateral quadrants of the thigh, and knee extension/flexion torque and power. The experimental group demonstrated superior recovery of contractile function and diminished effects of delayed-onset muscle soreness after downhill running when compared with the placebo group. Our results indicate that protease supplementation may attenuate muscle soreness after downhill running. Protease supplementation may also facilitate muscle healing and allow for faster restoration of contractile function after intense exercise.

Blood flow and muscle metabolism: a focus on insulin action.

The vascular system controls the delivery of nutrients and hormones to muscle, and a number of hormones may act to regulate muscle metabolism and contractile performance by modulating blood flow to and within muscle. This review examines evidence that insulin has major hemodynamic effects to influence muscle metabolism. Whole body, isolated hindlimb perfusion studies and experiments with cell cultures suggest that the hemodynamic effects of insulin emanate from the vasculature itself and involve nitric oxide-dependent vasodilation at large and small vessels with the purpose of increasing access for insulin and nutrients to the interstitium and muscle cells. Recently developed techniques for detecting changes in microvascular flow, specifically capillary recruitment in muscle, indicate this to be a key site for early insulin action at physiological levels in rats and humans. In the absence of increases in bulk flow to muscle, insulin may act to switch flow from nonnutritive to the nutritive route. In addition, there is accumulating evidence to suggest that insulin resistance of muscle in vivo in terms of impaired glucose uptake could be partly due to impaired insulin-mediated capillary recruitment. Exercise training improves insulin-mediated capillary recruitment and glucose uptake by muscle.

The Influences of L(+)-Lactate and pH on Contractile Performance in Rabbit Glycerinated Skeletal Muscle

To know whether L(+)-lactate directly induces the decrease in muscle contractile performance, several parameters of cross-bridge function were measured at various concentrations of lactate and pH in glycerinated rabbit psoas and soleus muscles at three different temperatures (5, 20, 28 degrees C). At all pHs studied (pH 7.0, 6.5, 6.0, and 5.5), isometric tension, unloaded velocity of shortening, and stiffness of a fiber during active and resting state in the presence of 50 mM lactate were not virtually different from those in the absence of lactate, but pH had remarkable effects on these parameters. The active stiffness decreased only slightly, and the small resting stiffness appeared at low pH; they were not affected by the presence of lactate. The present results indicate that the lactate anions may not have marked influence on the interaction between actin and myosin, and the concomitant change in pH with the production of lactate may remarkably affect it, as far as they were examined under the existing conditions of the experimental solutions.

Postactivation potentiation: role in human performance.

Postactivation potentiation (PAP) is the transient increase in muscle contractile performance after previous contractile activity. This review describes the features and mechanism of PAP, assesses its potential role in endurance and strength/speed performance, considers strategies for exploiting PAP, and outlines how PAP might be affected by training.

COMPARISON OF PROTEASE AND NSAID SUPPLEMENTATION ON MUSCLE SORENESS AND CONTRACTILE PERFORMANCE FOLLOWING ECCENTRIC CONTRACTIONS

Both protease and non-steroidal anti-inflammatory drug (NSAID) supplementation have been shown to attenuate the effects of delayed onset muscle soreness (DOMS) resulting from intense exercise. PURPOSE: To evaluate the effects of protease and NSAID supplementation on muscle soreness and contractile performance following downhill running (DHR). METHODS: Preliminary results were examined on data collected from male participants who ran at a - 10% grade for 30 min at 80% predicted maximum heart rate. Subjects consumed either 2 protease tablets (PRO) (325 mg pancreatic enzymes, 75 mg trypsin, 50 mg papain, 50 mg bromelain, 10 mg amylase, 10 mg lipase, 10 mg lysozyme), 1000 mg of acetaminophen (NSAID) or a placebo (PLAC) four times a day for four days (from 24 H pre-DHR to 72 H post-DHR). Supplementation was administered in randomized, double-blind fashion. Subjects were evaluated for perceived muscle soreness (MS) of the front and back of the dominant thigh and on the back of the shank of the same leg, pressure pain threshold (PPT) by dolorimetry of 4 locations on the thigh (the anterior medial, anterior lateral, posterior medial, and posterior lateral quadrants) and 3 locations on the shank (tibialis anterior and lateral and medial gastrocnemius), peak knee extension (KE)/flexion (KF) and plantar/dorsi-flexion torque and power at 3 speeds (90°/s, 180°/s, and 300°/s) immediately prior to DHR, 24 post-DHR, 48 H post-DHR, and 72 H post-DHR. RESULTS: PPT for the posterior aspects of the thigh was reduced at 24 and 48 H after DHR. PPT was lower in the back and front of the right leg in PLAC and NSAID as compared to PRO 24 and 48 H after DHR. KE torque and power at 90°/s and 180°/s was superior among the PRO compared to the PLAC and NSAID at 24 H, 48 H and 72 H after DHR. CONCLUSION: The results of this investigation indicate that protease supplementation may attenuate muscle soreness and facilitate the restoration of muscle function following downhill running. A potential explanation for these findings may lie within the action of protease to minimize inflammation and accelerate muscle healing. Supported by Enzymatic Therapy, Green Bay WI

Alternative splicing, muscle contraction and intraspecific variation: associations between troponin T transcripts, Ca2+ sensitivity and the force and power output of dragonfly flight muscles during oscillatory contraction

SUMMARYThe flight muscles of Libellula pulchella dragonflies contain a mixture of six alternatively spliced transcripts of a single troponin T (TnT) gene. Here, we examine how intraspecific variation in the relative abundance of different TnT transcripts affects the Ca2+ sensitivity of skinned muscle fibers and the performance of intact muscles during work-loop contraction regimes that approximate in vivo conditions during flight. The relative abundance of one TnT transcript, or the pooled relative abundance of two TnT transcripts, showed a positive correlation with a 10-fold range of variation in Ca2+ sensitivity of skinned fibers (r2=0.77, P<0.0001) and a threefold range in peak specific force (r2=0.74, P<0.0001), specific work per cycle (r2=0.54; P<0.0001) and maximum specific power output (r2=0.48, P=0.0005) of intact muscle. Using these results to reanalyze previously published data for wing kinematics during free flight, we show that the relative abundances of these particular transcripts are also positively correlated with wingbeat frequency and amplitude. TnT variation alone may be responsible for these effects, or TnT variation may be a marker for changes in a suite of co-regulated molecules. Dragonflies from two ponds separated by 16 km differed significantly in both TnT transcript composition and muscle contractile performance, and within each population there are two distinct morphs that showed different maturational trajectories of TnT transcript composition and muscle contractility. Thus, there is broad intraspecific variability and a high degree of population structure for contractile performance phenotypes, TnT ribotypes and ontogenetic patterns involving these traits that affect locomotor performance.

EFFECTS OF PROTEASE SUPPLEMENTATION ON MUSCLE SORENESS AND CONTRACTILE PERFORMANCE FOLLOWING DOWNHILL RUNNING

Protease supplementation has been shown to attenuate soft tissue injury resulting from intense exercise. The purpose of this investigation was to evaluate the effects of protease supplementation on muscle soreness and contractile performance following downhill running (DHR). Preliminary results were examined on data collected from five matched pairs of male participants who ran at a −10% grade for 30 min at 80% predicted maximum heart rate. Subjects consumed two protease tablets (PRO) (325 mg pancreatic enzymes, 75 mg trypisn, 50 mg papain, 50 mg bromelain, 10 mg amylase, 10 mg lipase, 10 mg lysozyme) or a placebo (PLAC) four times a day for four days (from 24 H pre-DHR to 72 H post-DHR). Supplementation was administered in randomized, double-blind fashion. Subjects were evaluated for perceived muscle soreness (MS) of the front and back of the dominant leg, pressure pain threshold (PPT) by dolorimetry of 4 locations on the thigh (the anterior medial, anterior lateral, posterior medial, and posterior lateral quadrants), peak knee extension (KE)/flexion (KF) torque and power at 3 speeds (90 deg/s, 180 deg/s, and 300 deg/s), and shuttle run time (SRT) immediately prior to DHR, 24 post-DHR, 48 H post-DHR, and 72 H post-DHR. PPT for the posterior aspects of the thigh was reduced at 24 and 48 H after DHR. PPT was lower in the back of the right leg in PLAC as compared to PRO 24 H after DHR. KE torque and power at 90 deg/s was superior among the PRO compared to the PLAC after 48 H. KE torque at 300 deg/s was superior among the PRO at 24 H, 48 H and 72 H after DHR. No differences in SRT were observed between the groups at any time. The results of this investigation indicate that protease supplementation may attenuate muscle soreness following downhill running. Protease supplementation may also facilitate muscle healing and allow for the restoration of contractile function following intense exercise.

RELATIONSHIP BETWEEN MUSCLE SORENESS AND CONTRACTILE PERFORMANCE FOLLOWING DOWNHILL RUNNING

Downhill running has consistently been shown to result in increased muscle soreness and damage; however, its effects on contractile performance are less clear. The purpose of this investigation was to examine the relationship between muscle soreness and contractile performance following downhill running (DHR). Ten male subjects (age = 23 ± 1 years, height = 1.81 ± 0.02m, weight = 87.5 ± 3.1kg) ran at a −10% grade for 30 min at 80% predicted maximum heart rate. Subjects were evaluated for perceived muscle soreness (MS) of the front and back of the dominant leg, pressure pain threshold (PPT) by dolorimetry of 4 locations on the thigh (the anterior medial, anterior lateral, posterior medial, and posterior lateral quadrants), peak knee extension (KE)/flexion (KF) torque and power at 3 speeds (90°/s, 180°/s, and 300°/s), and shuttle run time (SRT) immediately prior to DHR and 24 post-DHR. All variables were negatively affected as a result of DHR. Correlation analyses indicated that the relative change in PPT in the anterior lateral quadrant was negatively related to knee extension torque at 90°/s (r = −0.76, p = 0.01) and knee flexion torque at 180°/s (r = −0.67, p = 0.04). Furthermore, increases in shuttle run time (SRT) were related to declines in PPT in the anterior medial (r = 0.69, p = 0.02), posterior medial (r = 0.64, p = 0.04), and posterior lateral (r = 0.63, p = 0.05) quadrants. In comparison, changes in perceived MS were not correlated with any measure of contractile function. These results suggest that changes in PPT may be more effective at predicting changes in contractile performance due to muscle damage than perceived MS.

Variability in the size, composition, and function of insect flight muscles.

In order to fly, insects require flight muscles that constitute at least 12 to 16% of their total mass, and flight performance increases as this percentage increases. However, flight muscles are energetically and materially expensive to build and maintain, and investment in flight muscles constrains other aspects of function, particularly female fecundity. This review examines ways in which insects vary the size of their flight muscles, and how variation in the relative size and composition of flight muscles affects flight performance. Sources of variability in flight muscle size and composition include genetic differences within and between species, individual phenotypic responses to environmental stimuli, and maturational changes that occur before and during the adult stage. Insects have evolved a wide variety of ways to adjust flight muscle size and contractile performance in order to meet demands imposed by variation in life history and ecology.

Heat shock does not attenuate low-frequency fatigue

Whole-body hyperthermia or heat shock confers protection to myocardial contractility against reperfusion-induced injury. The purpose of this study was to determine whether heat shock could provide similar protection to skeletal muscle contractility against low-frequency fatigue. Male Sprague-Dawley rats (6 rats/group) were heat shocked at 41.5°C for 15 min either 24 h or 4 days prior to fatiguing stimulation to compare the contractile responses of the plantaris muscle with those of a nonheated group. Both 24 h and 4 days after heat shock, the 72-kDa heat shock protein (HSP72) was elevated above control levels. There were no differences between the heat-shocked and non-heat-shocked animals in measures of contractility prior to fatiguing contractions or in resistance to fatigue. Heat-shock preconditioning did not lead to improved postfatigue force recovery above control responses and, in fact, delayed the recovery of force. This study does not support the use of heat-shock therapy to improve skeletal muscle contractile performance under fatiguing conditions.Key words: heat shock proteins, rat, skeletal muscle, contractile properties, HSP72.

Heat shock does not attenuate low-frequency fatigue.

Whole-body hyperthermia or heat shock confers protection to myocardial contractility against reperfusion-induced injury. The purpose of this study was to determine whether heat shock could provide similar protection to skeletal muscle contractility against low-frequency fatigue. Male Sprague-Dawley rats (6 rats/group) were heat shocked at 41.5 degrees C for 15 min either 24 h or 4 days prior to fatiguing stimulation to compare the contractile responses of the plantaris muscle with those of a nonheated group. Both 24 h and 4 days after heat shock, the 72-kDa heat shock protein (HSP72) was elevated above control levels. There were no differences between the heat-shocked and non-heat-shocked animals in measures of contractility prior to fatiguing contractions or in resistance to fatigue. Heat-shock preconditioning did not lead to improved postfatigue force recovery above control responses and, in fact, delayed the recovery of force. This study does not support the use of heat-shock therapy to improve skeletal muscle contractile performance under fatiguing conditions.

Functional analyses of troponin T mutations that cause hypertrophic cardiomyopathy: insights into disease pathogenesis and troponin function.

Mutations in a number of cardiac sarcomeric protein genes cause hypertrophic cardiomyopathy (HCM). Previous findings indicate that HCM-causing mutations associated with a truncated cardiac troponin T (TnT) and missense mutations in the beta-myosin heavy chain share abnormalities in common, acting as dominant negative alleles that impair contractile performance. In contrast, Lin et al. [Lin, D., Bobkova, A., Homsher, E. & Tobacman, L. S. (1996) J. Clin. Invest. 97, 2842-2848] characterized a TnT point mutation (Ile79Asn) and concluded that it might lead to hypercontractility and, thus, potentially a different mechanism for HCM pathogenesis. In this study, three HCM-causing cardiac TnT mutations (Ile79Asn, Arg92Gln, and DeltaGlu160) were studied in a myotube expression system. Functional studies of wild-type and mutant transfected myotubes revealed that all three mutants decreased the calcium sensitivity of force production and that the two missense mutations (Ile79Asn and Arg92Gln) increased the unloaded shortening velocity nearly 2-fold. The data demonstrate that TnT can alter the rate of myosin cross-bridge detachment, and thus the troponin complex plays a greater role in modulating muscle contractile performance than was recognized previously. Furthermore, these data suggest that these TnT mutations may cause disease via an increased energetic load on the heart. This would represent a second paradigm for HCM pathogenesis.

Distinguishing metabolic heat from condensation heat during muscle recovery.

When a thermopile is used to measure the heat production of isolated muscle, the muscle is surrounded by gas saturated with water vapour, initially in equilibrium with the muscle. After contraction, the osmolarity of the muscle is raised so that it is no longer in equilibrium with the gas around it, and condensation will occur. When artificial muscles of known osmolarity were placed on a thermopile surrounded by gas in equilibrium with a solution of lower osmolarity, their temperature was found to be raised (by 102.7 mK osmol-1 l). This temperature increase was greatly reduced by covering the artificial muscle with a Teflon film. Experiments on living muscle from the dogfish Scyliorhinus canicula showed that muscle temperature was higher 2 min after a series of 20 twitches at 3 Hz if the muscle was not covered by Teflon than if it was covered. The Teflon covering did not diminish the muscle's contractile performance. We conclude that the condensation of water does contribute to the heat measured during the recovery period, but that when the muscle is covered by Teflon film condensation heat can largely be prevented so that only genuine metabolic recovery heat is produced.

ATP-sensitive K+ channel blocker glibenclamide and diaphragm fatigue during normoxia and hypoxia.

The role of ATP-sensitive K+ channels in skeletal muscle contractile performance is controversial: blockers of these channels have been found to not alter, accelerate, or attenuate fatigue. The present study reexamined whether glibenclamide affects contractile performance during repetitive contraction. Experiments systematically assessed the effects of stimulation paradigm, temperature, and presence of hypoxia and in addition compared intertrain with intratrain fatigue. Adult rat diaphragm muscle strips were studied in vitro. At 37 degrees C and normoxia, glibenclamide did not significantly affect any measure of fatigue during continuous 5- or 100-Hz or intermittent 20-Hz stimulation but progressively prolonged relaxation time during 20-Hz stimulation. At 20 degrees C and normoxia, neither force nor relaxation rate was affected significantly by glibenclamide during 20-Hz stimulation. At 37 degrees C and hypoxia, glibenclamide did not significantly affect fatigue at 5-Hz or intertrain fatigue during 20-Hz stimulation but reduced intratrain fatigue and prolonged relaxation time during 20-Hz stimulation. These findings indicate that, although ATP-sensitive K+ channels may be activated during repetitive contraction, their activation has only a modest effect on the rate of fatigue development.

Respiratory muscle dysfunction in sepsis.

It became evident in the past 12 years that venitlatory muscle contractile performance is significantly impaired during the course of septic shock. In animal models of septic shock, depression of ventilatory muscle contractile performance has been shown to cause hypercapneic ventilatory failure and respiratory arrest. Failure of ventilatory muscle contractility in septic shock has never been attributed to a single factor, but two groups of factors are likely to be involved: (a) increased ventilatory muscle metabolic demands due to augmentation of ventilation, hypoxemia and increased pulmonary impedance; and (b) specific cellular, metabolic, immune and hemodynamic defects which interfere with several processes necessary for normal force generation. These defects are mediated by complex interactions between several local and systematic mediator such a bacterial endotoxin, proinflammatory cytokines, prostaglandins, platelet activating factor, reactive oxygen species and nitric oxide. This is a summary of how these interactions are likely to interfere with ventilatory muscle contractile performance in septic shock with particular emphasis on the newly described role of nitric oxide.

This Month in the Journal

This Month in the Journal

Vascular and endocrine control of muscle metabolism.

Important differences exist between perfused and incubated (or perifused) skeletal muscle preparations with regard to their metabolism and control. A growing body of evidence suggests that the differences may be due to the role played by the vascular system. In the constant-flow perfused rat hindlimb preparation, a group of vasoconstrictors has been identified that enhance muscle metabolism and aerobic contractility. Another group of vasoconstrictors decrease muscle metabolism and aerobic contractility even though perfusate flow remains constant. All effects of both groups of vasoconstrictors are opposed by vasodilators. Because none of the vasoconstrictor effects is evident when isolated muscles are incubated or perifused, involvement of an active vascular system is indicated. Although some hormones may act directly on muscle by purely endocrine effects, a vascular component of their actions is now emerging. Mechanisms to account for vascular control of perfused skeletal muscle metabolism may involve 1) functional vascular shunts where the proportion of flow processed by these is regulated by site-specific vasomodulators, 2) a direct response to a change in the rate of supply of nutrients and removal of products, and 3) a signal substance released by vascular tissue in association with vasoconstriction that interacts with surrounding skeletal muscle cells. Impaired control at the level of the vascular system may have implications for long-term access of nutrients and hormones and therefore the control of skeletal muscle metabolism and contractile performance.

Morphologic and Functional Alterations in Aging Rat Muscle

To understand better the causes of reduced contractile force in aging skeletal muscle, we performed a physiologic and morphologic analysis of plantaris muscle in old rats. The peak twitch tension (Fmax) and rates of force development and relaxation were significantly lower in old (24 months old) rats than in young (six month old) rats. In teased muscle fiber preparations, there was a 5% reduction in the mean number of fibers in the aging plantaris muscle. Histologically, a net loss of fibers occurred only in the muscle belly. Histochemically, fewer Type I fibers were seen in the belly and proximal regions, whereas distally fewer Type IIa fibers were seen. The loss of Types I and IIa oxidative fibers suggested a conservation of fast-twitch Type IIb fibers in a fast-twitch muscle. The relatively small loss of muscle fibers does not explain the large decline in muscle contractile performance which, despite established doctrine, was independent of muscle mass, fiber number or size, or number of fast-twitch fibers. The reduced force production in aging rat muscle appears to be due to a defect in excitation, contraction performance or metabolic activity, rather than a purely anatomical abnormality of muscle.

Cardiac muscle function following chronic dietary potassium depletion in the rabbit

The aim was to investigate a possible defect in cardiac muscle contractile performance following chronic K+ depletion. Cardiac muscle force development, membrane potential, and action potential configuration were measured in isolated superfused right ventricular papillary muscles or trabeculae from control or K+ depleted NZW rabbits. The effects of adrenaline, strophanthidin, and changes in external [Ca2+] and [K+] were investigated. Experiments were performed on 50 adult NZW rabbits, average weight 2.3 kg, which were fed either a control diet (n = 25), or a K+ deficient diet (n = 25) for 25 d. There was a significant reduction in contractile force in preparations from the K+ depleted group compared to those from control animals. This was associated with an increased positive inotropic response to low [K+], but an apparent reduction in response to adrenaline. There was no significant difference between groups as to the effect of strophanthidin. It is suggested that the reduction in response to adrenaline reflects a down regulation in beta receptor density, due to an increased level of circulating catecholamines, and that the defect in myocardial function is a result of adaptive changes to Ca2+ handling mechanisms within the cell.