Maximal Force Development Research Articles

Comparison of Supervised versus Self-Administered Stretching on Bench Press Maximal Strength and Force Development.

While there is reported superior effectiveness with supervised training, it usually requires specialized exercise facilities and instructors. It is reported in the literature that high-volume stretching improves pectoralis muscles strength under supervised conditions while practical relevance is discussed. Therefore, the study objective was to compare the effects of volume equated, supervised- and self-administered home-based stretching on strength performance. Sixty-three recreational participants were equally assigned to either a supervised static stretching, home-based stretching, or control group. The effects of 15 min pectoralis stretching, 4 days per week for 8 weeks, were assessed on dynamic and isometric bench press strength and force development. While there was a large magnitude maximal strength increase (p < 0.001-0.023, ƞ2 = 0.118-0.351), force development remained unaffected. Dynamic maximal strength in both groups demonstrated large magnitude increases compared to the control group (p < 0.001-0.001, d = 1.227-0.905). No differences between the intervention group for maximal strength (p = 0.518-0.821, d = 0.101-0.322) could be detected. The results could potentially be attributed to stretch-induced tension (mechanical overload) with subsequent anabolic adaptations, and alternative explanatory approaches are discussed. Nevertheless, home-based stretching seems a practical alternative to supervised training with potential meaningful applications in different settings.

Strain rate of stretch affects crossbridge detachment during relaxation of intact cardiac trabeculae.

Mechanical Control of Relaxation refers to the dependence of myocardial relaxation on the strain rate just prior to relaxation, but the mechanisms of enhanced relaxation are not well characterized. This study aimed to characterize how crossbridge kinetics varied with strain rate and time-to-stretch as the myocardium relaxed in early diastole. Ramp-stretches of varying rates (amplitude = 1% muscle length) were applied to intact rat cardiac trabeculae following a load-clamp at 50% of the maximal developed twitch force, which provides a first-order estimate of ejection and coupling to an afterload. The resultant stress-response was calculated as the difference between the time-dependent stress profile between load-clamped twitches with and without a ramp-stretch. The stress-response exhibited features of the step-stretch response of activated, permeabilized myocardium, such as distortion-dependent peak stress, rapid force decay related to crossbridge detachment, and stress recovery related to crossbridge recruitment. The peak stress was strain rate dependent, but the minimum stress and the time-to-minimum stress values were not. The initial rapid change in the stress-response indicates enhanced crossbridge detachment at higher strain rates during relaxation in intact cardiac trabeculae. Physiologic considerations, such as time-varying calcium, are discussed as potential limitations to fitting these data with traditional distortion-recruitment models of crossbridge activity.

N-terminal truncated cardiac troponin I enhances Frank-Starling response by increasing myofilament sensitivity to resting tension.

Cardiac troponin I (cTnI) of higher vertebrates has evolved with an N-terminal extension, of which deletion via restrictive proteolysis occurs as a compensatory adaptation in chronic heart failure to increase ventricular relaxation and stroke volume. Here, we demonstrate in a transgenic mouse model expressing solely N-terminal truncated cTnI (cTnI-ND) in the heart with deletion of the endogenous cTnI gene. Functional studies using ex vivo working hearts showed an extended Frank-Starling response to preload with reduced left ventricular end diastolic pressure. The enhanced Frank-Starling response effectively increases systolic ventricular pressure development and stroke volume. A novel finding is that cTnI-ND increases left ventricular relaxation velocity and stroke volume without increasing the end diastolic volume. Consistently, the optimal resting sarcomere length (SL) for maximum force development in cTnI-ND cardiac muscle was not different from wild-type (WT) control. Despite the removal of the protein kinase A (PKA) phosphorylation sites in cTnI, β-adrenergic stimulation remains effective on augmenting the enhanced Frank-Starling response of cTnI-ND hearts. Force-pCa relationship studies using skinned preparations found that while cTnI-ND cardiac muscle shows a resting SL-resting tension relationship similar to WT control, cTnI-ND significantly increases myofibril Ca2+ sensitivity to resting tension. The results demonstrate that restrictive N-terminal deletion of cTnI enhances Frank-Starling response by increasing myofilament sensitivity to resting tension rather than directly depending on SL. This novel function of cTnI regulation suggests a myofilament approach to utilizing Frank-Starling mechanism for the treatment of heart failure, especially diastolic failure where ventricular filling is limited.

Force requirement profiles for swing to strength hold elements on still rings in men´s artistic gymnastics

ABSTRACT Swing to strength hold elements are important for a top ranking on still rings, require a high level of upper body strength of the gymnasts and have not yet been scientifically investigated. Therefore, the aim of this study was to determine force requirement profiles for these elements using a dynamometric measuring system. Two force sensors attached to the cables of each ring and synchronised with video recorded the forces exerted by the gymnast. For eight swing to strength hold elements (Uprise backward to support scale straddled, Uprise backward to swallow, Uprise backward to cross, Honma to cross, Uprise backward to support scale, Kip to cross, Back kip to swallow and Uprise backward to inverted cross), the variables maximal force (Fmax), minimal force (Fmin), time over Fhold (t1–3), rate of maximal force development (RFD) and impulse (p) were analysed. Honma to cross shows the highest force requirements (Median: Fmax = 120.4% BW, Fmin = 109.8% BW, t1–3 = 882 ms, RFD = 143.93% BW/s, p = 9.85% BWs) whereas back kip to swallow shows the least (Fmax = 102.3% BW, RFD = 34.99% BW/s and p = 0.84% BW/s). The biomechanical demand profiles can be used to provide feedback to coaches and gymnasts. In future research, they should be extended with kinematic and electromyographic data.

Collagen and Vitamin C Supplementation Increases Lower Limb Rate of Force Development.

Exercise and vitamin C-enriched collagen supplementation increase collagen synthesis, potentially increasing matrix density, stiffness, and force transfer. To determine whether vitamin C-enriched collagen (hydrolyzed collagen [HC] + C) supplementation improves rate of force development (RFD) alongside a strength training program. Using a double-blinded parallel design, over 3weeks, healthy male athletes (n = 50, 18-25years) were randomly assigned to the intervention (HC + C; 20g HC + 50mg vitamin C) or placebo (20g maltodextrin). Supplements were ingested daily 60min prior to training. Athletes completed the same targeted maximal muscle power training program. Maximal isometric squats, countermovement jumps, and squat jumps were performed on a force plate at the same time each testing day (baseline, Tests 1, 2, and 3) to measure RFD and maximal force development. Mixed-model analysis of variance compared performance variables across the study timeline, whereasttests were used to compare the change between baseline and Test 3. Over 3weeks, maximal RFD in the HC + C group returned to baseline, whereas the placebo group remained depressed (p = .18). While both groups showed a decrease in RFD through Test 2, only the treatment group recovered RFD to baseline by Test 3 (p = .036). In the HC + C group, change in countermovement jumps eccentric deceleration impulse (p = .008) and eccentric deceleration RFD (p = .04) wasimproved. A strong trend was observed for lower limb stiffness assessed in the countermovement jumps (p = .08). No difference was observed in maximal force or squat jump parameters. The HC + C supplementation improved RFD in the squat and countermovement jump alongside training.

The air-breathing Alaska blackfish (Dallia pectoralis) remodels ventricular Ca2+ cycling with chronic hypoxic submergence to maintain ventricular contractility.

The Alaska blackfish (Dallia pectoralis) is a facultative air-breather endemic to northern latitudes where it remains active in winter under ice cover in cold hypoxic waters. To understand the changes in cellular Ca2+ cycling that allow the heart to function in cold hypoxic water, we acclimated Alaska blackfish to cold (5 °C) normoxia or cold hypoxia (2.1–4.2 kPa; no air access) for 5–8 weeks. We then assessed the impact of the acclimation conditions on intracellular Ca2+ transients (Δ[Ca2+]i) of isolated ventricular myocytes and contractile performance of isometrically-contracting ventricular strips. Measurements were obtained at various contractile frequencies (0.2–0.6 Hz) in normoxia, during acute exposure to hypoxia, and reoxygenation at 5 °C. The results show that hypoxia-acclimated Alaska blackfish compensate against the depressive effects of hypoxia on excitation-contraction coupling by remodelling cellular Δ[Ca2+]i to maintain ventricular contractility. When measured at 0.2 Hz in normoxia, hypoxia-acclimated ventricular myocytes had a 3.8-fold larger Δ[Ca2+]i peak amplitude with a 4.1-fold faster rate of rise, compared to normoxia-acclimated ventricular myocytes. At the tissue level, maximal developed force was 2.1-fold greater in preparations from hypoxia-acclimated animals. However, maximal attainable contraction frequencies in hypoxia were lower in hypoxia-acclimated myocytes and strips than preparations from normoxic animals. Moreover, the inability of hypoxia-acclimated ventricular myocytes and strips to contract at high frequency persisted upon reoxygenation. Overall, the findings indicate that hypoxia alters aspects of Alaska blackfish cardiac myocyte Ca2+ cycling, and that there may be consequences for heart rate elevation during hypoxia, which may impact cardiac output in vivo.

Exercise training induces benign right ventricular hypertrophy along with functional improvement and without pathological processes or arrhythmogenicity in a rodent model of athletes heart

Abstract Introduction Regular sport activity leads to the adaptation of cardiac structure and function, the so-called athlete's heart. Research projects over the last years have focused on exercise-induced adaptation of the right ventricle (RV), because the disproportionate load on the RV - when compared with the left ventricle - might lead to pathological consequences, such as myocardial interstital fibrosis or chamber dilation. Purpose We aimed at investigating comprehensively RV alterations induced by regular aerobic exercise training in a rat model of athlete's heart. Methods Young, adult rats were divided into control (Co) and exercised (Ex) groups (n=12–12). Exercised rats underwent a 12-week-long swim training program. In vivo electrophysiological study and in vitro cellular force assessments on isolated cardiomyocytes were carried out to investigate electrical and functional RV alterations, respectively. Molecular biological (qRT-PCR, Western-blot) and histological investigations were applied to reveal underlying mechanisms. Results Exercise training was associated with increased RV cardiomyocyte diameter (12.5±0.1 μm Co vs. 13.8±0.2 μm Ex, p&amp;lt;0.05), that was associated with hyperphosphorylation of protein kinase B (Akt). RV cardiomyocytes from exercised animals showed improved calcium sensitivity and increased maximal force development, that was associated with hypophosphorylation of troponin I. We found increased length of repolarization as reflected by prolonged QT interval and ventricular effective refracter period (VERP: 44.0±1.6 ms Co vs. 52.8±2.1 ms Ex, p&amp;lt;0.05) along with decreased gene expression of potassium channels (Kcnd2, Kcnj2). We could not induce ventricular arrhythmia by programmed stimulation. Picrosirius staining did not reveal fibrosis, that was associated with unchanged protein expression of connective tissue growth factor (CTGF) and gene expression of profibrotic markers (such as TGF-β). Gene expression of apoptotic markers (Bax, Bcl-2) and fetal gene program (such as β-MHC) did not differ between groups. Conclusions According to our data, regular swim training induced RV hypertrophy, that was associated with functional improvement (improved calcium sensitivity and maximal force), hypophosphorylation of troponin I and prolonged repolarization without characteristic pathological alterations or arrhythmogenicity of RV myocardial tissue. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Research, Development and Innovation Office of Hungary

Indirect evidence that anoxia exposure and cold acclimation alter transarcolemmal Ca2+ flux in the cardiac pacemaker, right atrium and ventricle of the red-eared slider turtle (Trachemys scripta)

We indirectly assessed if altered transarcolemmal Ca2+ flux accompanies the decreased cardiac activity displayed by Trachemys scripta with anoxia exposure and cold acclimation. Turtles were first acclimated to 21 °C or 5 °C and held under normoxic (21N; 5N) or anoxic conditions (21A; 5A). We then compared the response of intrinsic heart rate (fH) and maximal developed force of spontaneously contracting right atria (Fmax,RA), and maximal developed force of isometrically-contracting ventricular strips (Fmax,V), to Ni2+ (0.1–10 mM), which respectively blocks T-type Ca2+ channels, L-type Ca2+ channels and the Na+-Ca2+-exchanger at the low, intermediate and high concentrations employed. Dose-response curves were established in simulated in vivo normoxic (Sim Norm) or simulated in vivo anoxic extracellular conditions (Sim Anx; 21A and 5A preparations). Ni2+ decreased intrinsic fH, Fmax,RA and Fmax,V of 21N tissues in a concentration-dependent manner, but the responses were blunted in 21A tissues in Sim Norm. Similarly, dose-response curves for Fmax,RA and Fmax,V of 5N tissues were right-shifted, whereas anoxia exposure at 5 °C did not further alter the responses. The influence of Sim Anx was acclimation temperature-, cardiac chamber- and contractile parameter-dependent. Combined, the findings suggest that: (1) reduced transarcolemmal Ca2+ flux in the cardiac pacemaker is a potential mechanism underlying the slowed intrinsic fH of anoxic turtles at 21 °C, but not 5 °C, (2) a downregulation of transarcolemmal Ca2+ flux may aid cardiac anoxia survival at 21 °C and prime the turtle myocardium for winter anoxia and (3) confirm that altered extracellular conditions with anoxia exposure can modify turtle cardiac transarcolemmal Ca2+ flux.

Reduced preload increases Mechanical Control (strain-rate dependence) of Relaxation by modifying myosin kinetics

Rapid myocardial relaxation is essential in maintaining cardiac output, and impaired relaxation is an early indicator of diastolic dysfunction. While the biochemical modifiers of relaxation are well known to include calcium handling, thin filament activation, and myosin kinetics, biophysical and biomechanical modifiers can also alter relaxation. We have previously shown that the relaxation rate is increased by an increasing strain rate, not a reduction in afterload. The slope of the relaxation rate to strain rate relationship defines Mechanical Control of Relaxation (MCR). To investigate MCR further, we performed in vitro experiments and computational modeling of preload-adjustment using intact rat cardiac trabeculae. Trabeculae studies are often performed using isometric (fixed-end) muscles at optimal length (Lo, length producing maximal developed force). We determined that reducing muscle length from Lo increased MCR by 20%, meaning that reducing preload could substantially increase the sensitivity of the relaxation rate to the strain rate. We subsequently used computational modeling to predict mechanisms that might underlie this preload-dependence. Computational modeling was not able to fully replicate experimental data, but suggested that thin-filament properties are not sufficient to explain preload-dependence of MCR because the model required the thin-filament to become more activated at reduced preloads. The models suggested that myosin kinetics may underlie the increase in MCR at reduced preload, an effect that can be enhanced by force-dependence. Relaxation can be modified and enhanced by reduced preload. Computational modeling implicates myosin-based targets for treatment of diastolic dysfunction, but further model refinements are needed to fully replicate experimental data.

Strength training restores force-generating capacity in patients with schizophrenia.

Patients with schizophrenia spectrum disorders have impaired skeletal muscle force-generating capacity (FGC) of the lower extremities, that is, one repetition maximum (1RM) and rapid force development, and poor functional performance. We therefore investigated whether 12weeks of maximal strength training (MST) could (a) restore FGC and functional performance to the level of healthy references, (b) increase patient activation and quality of life, and (c) explore associations between symptom severity, defined daily dose of medication, illness duration, level of patient activation, and improvements in FGC and functional performance. Forty-eight outpatients were randomized to a training group (TG) or control group (CG). TG performed leg press MST 2day/week at~90% 1RM. The CG received two introductory training sessions and encouragement to train independently. Leg press 1RM, rapid force development, a battery of functional performance tests, Patient Activation Measure-13, and 36-Item Short Form Health Survey were tested. Healthy references performed baseline tests of FGC and functional performance. Thirty-six patients completed the study (TG: 17, CG: 19). TG improved 1RM (28%) and rapid force development (20%, both P<.01) to a level similar to healthy references, while no change was apparent in the CG. TG's improvement in rapid force development was negatively associated with defined daily dose of medication (r=-0.5, P=.05). Both TG and CG improved 30-second sit-to-stand test performance (P<.05) which was associated with improved rapid force development (r=0.6, P<.05). In conclusion, 12weeks of MST restored patients' lower extremity FGC to a level similar to healthy references and improved 30-second sit-to-stand test performance.

In Vitro Assessment of Cardiac Function Using Skinned Cardiomyocytes.

In this article, we describe the steps required to isolate a single permeabilized ("skinned") cardiomyocyte and attach it to a force-measuring apparatus and a motor to perform functional studies. These studies will allow measurement of cardiomyocyte stiffness (passive force) and its activation with different calcium (Ca2+)-containing solutions to determine, amongst others: maximum force development, myofilament Ca2+-sensitivity (pCa50), cooperativity (nHill) and the rate of force redevelopment (ktr). This method also enables determination of the effects of drugs acting directly on myofilaments and of the expression of exogenous recombinant proteins on both active and passive properties of cardiomyocytes. Clinically, skinned cardiomyocyte studies highlight the pathophysiology of many myocardial diseases and allow in vitro assessment of the impact of therapeutic interventions targeting the myofilaments. Altogether, this technique enables the clarification of cardiac pathophysiology by investigating correlations between in vitro and in vivo parameters in animal models and human tissue obtained during open heart or transplant surgery.

INDICATORS OF NEUROMUSCULAR FATIGUE IN LEG PRESS EXERCISE IN MEN AND WOMEN

ABSTRACT Introduction Muscle fatigue is characterized by reduced ability to produce maximum strength or power, and may differ between men and women. Changes in velocity of movement during exercise, and in the ability to produce strength after exercise, may help when comparing fatigue in men and women. Objective To analyze the differences between men and women in relation to number of repetitions, kinetics, kinematics and isometric force-time curve performance, and their respective muscle activation in horizontal leg press exercises. Methods Fifteen men and fifteen women underwent isometric force-time curve (Cf-t) and electromyographic (EMG) assessments before and after performing horizontal leg press exercises. The exercises were performed in three sets until voluntary exhaustion, at 70% maximal repetition. During the exercises, kinetic and kinematic variables were obtained by means of two force transducers, a linear position potentiometer and accelerometer adapted for the horizontal leg press and synchronized by a signal conditioning plate. Results The mean propulsive velocity significantly reduced between the first and last repetition of each series, with a similar reduction for men (-12.4 to -29.2%) and women (-29.2 to -35.6%). The same pattern was observed for the other kinetic and kinematic variables. The maximum voluntary contraction and peak force development rate also decreased for both men (-15.1 ± 8.7% and -26.9 ± 21.2%, respectively) and women (-13.9 ± 10.4% and -28.2 ± 11.5%, respectively). Conclusion Based on the different variables used to quantify the effect of fatigue during and after horizontal leg press exercises, the research found practically no differences between men and women. Level of evidence II; Comparative prospective study.

Regulation of Myofilament Contractile Function in Human Donor and Failing Hearts.

Heart failure (HF) often includes changes in myocardial contractile function. This study addressed the myofibrillar basis for contractile dysfunction in failing human myocardium. Regulation of contractile properties was measured in cardiac myocyte preparations isolated from frozen, left ventricular mid-wall biopsies of donor (n = 7) and failing human hearts (n = 8). Permeabilized cardiac myocyte preparations were attached between a force transducer and a position motor, and both the Ca2+ dependence and sarcomere length (SL) dependence of force, rate of force, loaded shortening, and power output were measured at 15 ± 1°C. The myocyte preparation size was similar between groups (donor: length 148 ± 10 μm, width 21 ± 2 μm, n = 13; HF: length 131 ± 9 μm, width 23 ± 1 μm, n = 16). The maximal Ca2+-activated isometric force was also similar between groups (donor: 47 ± 4 kN⋅m–2; HF: 44 ± 5 kN⋅m–2), which implicates that previously reported force declines in multi-cellular preparations reflect, at least in part, tissue remodeling. Maximal force development rates were also similar between groups (donor: ktr = 0.60 ± 0.05 s–1; HF: ktr = 0.55 ± 0.04 s–1), and both groups exhibited similar Ca2+ activation dependence of ktr values. Human cardiac myocyte preparations exhibited a Ca2+ activation dependence of loaded shortening and power output. The peak power output normalized to isometric force (PNPO) decreased by ∼12% from maximal Ca2+ to half-maximal Ca2+ activations in both groups. Interestingly, the SL dependence of PNPO was diminished in failing myocyte preparations. During sub-maximal Ca2+ activation, a reduction in SL from ∼2.25 to ∼1.95 μm caused a ∼26% decline in PNPO in donor myocytes but only an ∼11% change in failing myocytes. These results suggest that altered length-dependent regulation of myofilament function impairs ventricular performance in failing human hearts.

Preparation of athletes in cyclic sports taking into account the functional state of the external respiratory system and cardiovascular system

The purpose of the study is to investigate the preparation of athletes in cyclic sports, taking into account the functional state of the external respiratory system and cardiovascular system (on the example of academic rowing). Material and methods. The study involved 13 athletes aged 19-22 years old. Athletes went for academic rowing in the Dnipropetrovsk region. A control and experimental group of 6 and 7 people were created, respectively. At the beginning of the experiment, there were no significant differences in fitness, physical development, and functional status between groups (p&gt; 0.05). All study participants gave written consent to participate in the study. The studies were carried out at the specialized school of the Olympic reserve in rowing of the Dnepropetrovsk regional organization of the sports society "Ukraine", the regional school of higher sportsmanship. Medical and biological testing was conducted at the scientific laboratory of the Pridneprovsk State Academy of Physical Culture and Sports. Results . The dynamics of the indicators of the functional status of light weight rowers in rowing academic after using the experimental method was shown. It has been determined that under the influence of the experimental methods the cardiovascular system parameters underwent positive changes. These are the indices of variation range, vegetative rhythm index, pressure index, PWC170 test, maximal oxygen consumption, cardiovascular system response to exercise, recovery period. The introduced technique had a positive effect on the performance of athletes. In the experimental method, it was proposed to change the load in the complexes of exercises for the development of strength, maximum force, strength and speed endurance. The proposed technique of improving physical fitness was reflected in the formation of the plan of the annual training cycle. In accordance with the tasks of the period and mesocycles, exercises aimed at developing the leading qualities of light weight rowers were included. Conclusions. The analysis of the literature on the problem of research and generalization of the training of athletes in cyclic sports at the stage of preparation for higher achievements has revealed problematic issues. On the example of academic rowing these questions relate to the peculiarities of improving the process of physical preparation of rowers with light body weight, the peculiarities of functional state, the study of indicators of their physical and functional fitness. The dynamics of the functional state of the external respiratory system and cardiovascular system of athletes in cyclic sports (on the example of academic rowing) has been investigated. Some positive changes in the results of the vegetative index of the rhythm of the athletes were revealed. These indicators have approximated the value of the autonomic balance of athletes in the direction of parasympathetic regulation. There is a tendency to decrease the index of pressure. There was a decrease in heart rate, an increase in the maximum oxygen consumption and the level of physical performance.

Cycling Cross-Bridges Contribute to Thin Filament Activation in Human Slow-Twitch Fibers.

It has been shown that not only calcium but also strong binding myosin heads contribute to thin filament activation in isometrically contracting animal fast-twitch and cardiac muscle preparations. This behavior has not been studied in human muscle fibers or animal slow-twitch fibers. Human slow-twitch fibers are interesting since they contain the same myosin heavy chain isoform as the human heart. To explore myosin-induced activation of the thin filament in isometrically contracting human slow-twitch fibers, the endogenous troponin complex was exchanged for a well-characterized fast-twitch skeletal troponin complex labeled with the fluorescent dye N-((2-(Iodoacetoxy)ethyl)-N-methyl)amino-7-nitrobenz-2-oxa-1,3-diazole (fsTn-IANBD). The exchange was ≈70% complete (n = 8). The relative contributions of calcium and strong binding cross-bridges to thin filament activation were dissected by increasing the concentration of calcium from relaxing (pCa 7.5) to saturating levels (pCa 4.5) before and after incubating the exchanged fibers in the myosin inhibitor para-aminoblebbistatin (AmBleb). At pCa 4.5, the relative contributions of calcium and strong binding cross-bridges to thin filament activation were ≈69 and ≈31%, respectively. Additionally, switching from isometric to isotonic contraction at pCa 4.5 revealed that strong binding cross-bridges contributed ≈29% to thin filament activation (i.e., virtually the same magnitude obtained with AmBleb). Thus, we showed through two different approaches that lowering the number of strong binding cross-bridges, at saturating calcium, significantly reduced the activation of the thin filament in human slow-twitch fibers. The contribution of myosin to activation resembled that which was previously reported in rat cardiac and rabbit fast-twitch muscle preparations. This method could be applied to slow-twitch human fibers obtained from the soleus muscle of cardiomyopathy patients. Such studies could lead to a better understanding of the effect of point mutations of the cardiac myosin head on the regulation of muscle contraction and could lead to better management by pharmacological approaches.

Ankle and knee extensor muscle effort during locomotion in young and older athletes: Implications for understanding age-related locomotor decline

Age-related reduction in muscle force generation capacity is similarly evident across different lower limb muscle groups, yet decline in locomotor performance with age has been shown to depend primarily on reduced ankle extensor muscle function. To better understand why ageing has the largest detrimental effect on ankle joint function during locomotion, we examined maximal ankle and knee extensor force development during a two-leg hopping test in older and young men, and used these forces as a reference to calculate relative operating efforts for the knee and ankle extensors as participants walked, ran and sprinted. We found that, across locomotion modes in both age groups, ankle extensors operated at a greater relative effort compared to knee extensors; however, slightly less pronounced differences between ankle and knee extensor muscle efforts were present among older men, mainly due to a reduction in the ankle extensor force generation during locomotion modes. We consider these findings as evidence that reduced ankle push-off function in older age is driven by a tendency to keep ankle extensor effort during locomotion lower than it would otherwise be, which, in turn, may be an important self-optimisation strategy to prevent locomotor-induced fatigue of ankle extensor muscles.

Concurrent Resistance Training Enhances Performance in Competitive Distance Runners: A Review and Programming Implementation

ABSTRACT Concurrent training, defined as resistance training sessions programmed alongside endurance training sessions during the same cycle, is a tool that highly trained runners can use to augment performance. A review of the current literature explains how resistance training focused on increasing maximal force development and power output can improve running economy, a key performance indicator for endurance running. This review explains the current concepts in concurrent training for competitive distance runners, discusses misconceptions related to concurrent training, and offers practical implementation examples for coaches, athletes, and strength and conditioning practitioners working with this special population.

Contractile performance of the Alaska blackfish (Dallia pectoralis) ventricle: Assessment of the effects of temperature, pacing frequency, the role of the sarcoplasmic reticulum in contraction and adrenergic stimulation

The air-breathing Alaska blackfish (Dallia pectoralis) experiences aquatic hypoxia, but restricted air-access in winter due to ice-cover. To lend insight into its overwintering strategy, we examined the effects of thermal acclimation (15 °C vs. 5 °C), acute temperature change (to 10 °C), increased pacing frequency, inhibition of sarcoplasmic reticulum (SR) Ca2+ release and uptake and adrenaline (1000 nmol l−1) on the contractile performance of isometrically-contracting, electrically-paced ventricular strips. At routine pacing frequencies, maximal developed force (Fmax) was equivalent at 5 °C (2.1 ± 0.2 mN mm−2) and 15 °C (2.2 ± 0.3 mN mm−2), whereas contraction durations were 2.2- to 2.4-times longer and contraction rates 2.4- to 3.5-times slower at 5 °C. Maximum contraction frequency was reduced by decreased temperature, being 0.91 ± 0.04 Hz at 15 °C, 0.35 ± 0.02 Hz at 5 °C and equivalent between acclimation groups at 10 °C (~0.8 Hz). 15 °C and 5 °C strips were insensitive to SR inhibition at routine stimulation frequencies, but SR function supported high contraction rates at 10 °C and 15 °C. Adrenaline shortened T0.5R and increased relaxation rate by 18–40% at 15 °C, whereas at 5 °C, adrenaline augmented Fmax by 15–25%, in addition to increasing contraction kinetics by 22–82% and decreasing contraction duration by 20%. Overall, the results reveal that ventricular contractility is suppressed in cold-acclimated Alaska blackfish largely by acute and perhaps direct effects of decreased temperature, which effectively preconditions the tissue for low energy supply during winter hypoxia. Additionally, the level of cardiac performance associated with maintained activity in winter is supported by enhanced inotropic responsiveness to adrenaline at 5 °C.

Nitric oxide dependent delay in post‐fatigue contractile recovery in isolated fast‐twitch muscle: The role of the S‐nitrosoglutathione reductase

During fatiguing contractions, skeletal muscle fibers produce nitric oxide (NO) (and possibly S‐nitrosoglutathione (GSNO)) due to the activation of calcium‐calmodulin dependent NO‐synthases (NOS). Myofibers contain GSNO reductase (GSNOR), an enzyme that consumes GSNO, thereby controlling intracellular protein S‐nitrosylation. The present investigation tested the hypothesis that GSNOR scavenges the GSNO produced during repetitive contractions to protect contractile and calcium handling proteins from being S‐nitrosylated. To test this hypothesis, the effects of acute inhibition of GSNOR (GSNORi; SPL‐334, 10 μM) on contractility during and after fatiguing contractions in fast‐twitch muscle were examined. Extensor digitorum longus (EDL) muscles from both hindlimbs of mice (C57BL6/J; 8–9 weeks old) were dissected and placed in an experimental chamber for ex‐vivo isometric force measurements during electrical stimulation. For each mouse, one EDL was treated with the GSNORi, or L‐NMMA (L‐N‐monomethyl Arginine, a NOS inhibitor; 400 μM), or both, while the other EDL served as an untreated control. Muscles were repetitively stimulated at increasing frequencies until force was decreased to 30% of initial force. Contractile recovery from fatigue was determined at submaximal and maximal frequencies of stimulation for 120 min post‐fatigue. The treatment with either GSNORi or L‐NMMA did not change maximal or submaximal force development. Acute GSNORi incubation significantly decreased the force development during fatiguing contractions (~30% less force) compared to untreated muscles. During muscle recovery from fatigue in the untreated control muscle, force developed at low frequencies of stimulation was ~80% of pre‐fatigue values after 120 min of recovery. However, when GSNORi was present during fatigue and during recovery post‐fatigue, the force developed at submaximal and maximal frequencies of stimulation were both significantly impaired compared to control (to 55–70% of pre‐fatigue values after 120 min, P&lt;0.05 vs control). The NO‐dependent effects of GSNORi incubation on post‐fatigue recovery were tested when L‐NMMA was present to block NO production. L‐NMMA completely abolished the delayed contractile recovery detected with GSNORi. These data suggest that fatiguing contractions increase NO production thereby enhancing the intracellular amounts of GSNO, which can negatively affect muscle recovery post‐fatigue when GSNOR is inhibited. These results indicate that GSNOR activity has an important role in protecting contractile function during stimulation patterns that lead to muscle fatigue.Support or Funding InformationNIH (AR069577), CNPq (Universal)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Impact of heat therapy on body composition and skeletal muscle function in a model of peripheral artery disease

IntroductionPatients with symptomatic peripheral artery disease (PAD) have a profound limitation in exercise performance that is partly caused by ischemia‐related skeletal muscle abnormalities, including reduced muscle mass and strength. Current medical therapy for the exercise limitation in PAD is limited. We recently reported that exposure to leg heat therapy (HT) causes a marked increase in leg blood flow in patients with PAD. In this study, we used a model of diet‐induced obesity and peripheral arterial insufficiency to examine the effects of repeated treatment with HT on body composition and skeletal contractile function.MethodsMale 32‐week‐old C57Bl/6 mice were fed 60% high‐fat diet for 10 weeks. At 42 weeks of age, the animals underwent bilateral ligation of the femoral artery to induce hindlimb ischemia. After two weeks of recovery, the animals were randomly assigned to receive HT or a control intervention. Heat therapy was applied by placing the animal in a flat bottom restrainer and immersing the lower half of the body in a glass container filled with water at 39°C (n=7) for 30 min daily over 3 consecutive weeks. Animals assigned to the control group (n=8) were also restrained, but were placed in an empty container. Rectal temperature was measured before and during exposure to a single session of HT or the control intervention (n=3/group). Body composition was assessed prior to the onset of the treatment and then once a week throughout the intervention. Forty‐eight hours following the last treatment session, the animals were anesthetized and the soleus and extensor digitorum longus (EDL) muscles were harvested for the assessment of contractile function.ResultsRectal temperature increased during acute exposure to HT from a baseline of 35.1±0.4°C to 38.3±0.2°C. In the control group, rectal temperature remained at baseline levels throughout the treatment session (35.4±0.3°C). At baseline, fat mass (Control: 17.2±0.7 g vs. 16.0±0.8 g, p=0.51) and lean mass (Control: 28.4 g vs. HT: 28.4 g, p=0.7) were not different between groups. However, fat mass was significantly lower in the group exposed to HT at week 2 (Control: 19.6 g vs. HT: 14.72 g, p=0.03) and week 3 (Control: 20.32 g vs. HT: 14.54 g, p=0.01), while there was no difference between groups in lean mass throughout the intervention period (p&gt;0.05). Muscle mass relative to body mass was significantly higher in animals exposed to HT as compared to the control group in the EDL muscle (Control: 0.33±0.01 mg/g vs. HT: 0.38±0.01 mg/g, p=0.003). Maximal absolute force of the EDL muscle was also higher in animals treated with HT when compared to the control group (Control: 488.5±12.4 mN, HT: 529.5±14.5 mN, p=0.05). There were no differences between groups in relative muscle mass and maximal force development of the soleus muscle (p&gt;0.05).ConclusionThese findings indicate that repeated exposure to HT has positive effects on body composition and improves skeletal muscle function in a mouse model of diet‐induced obesity and PAD. This new therapeutic tool might be a practical alternative for PAD patients with restricted locomotion and multiple comorbidities, including diabetes and obesity.Support or Funding InformationFunding: Ralph W. and Grace M. Showalter Research Trust AwardThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.