Power loss is greater in old men than young men during fast plantar flexion contractions

2010 ◽  
Vol 109 (5) ◽  
pp. 1441-1447 ◽  
Author(s):  
Brian H. Dalton ◽  
Geoffrey A. Power ◽  
Anthony A. Vandervoort ◽  
Charles L. Rice
Keyword(s):  
Peak Power ◽  
Contractile Function ◽  
Plantar Flexion ◽  
Constant Load ◽  
Triceps Surae ◽  
Voluntary Activation ◽  
Maximal Velocity ◽  
Shortening Velocity ◽  
Maximal Voluntary Isometric Contraction ◽  
Old Men

It is unclear during human aging whether healthy older adults (>70 yr old) experience greater, lesser, or the same fatigability compared with younger adults. The reported disparate findings may be related to the task-dependent nature of fatigue and the limited number of studies exploring nonisometric contractile function and aging. The purpose here was to determine the effects of fast shortening contractions on the fatigability of the triceps surae in 10 young (∼24 yr old) and 10 old (∼78 yr old) men using isometric and dynamic measures. Participants performed 50 maximal velocity-dependent plantar flexions at a constant load of 20% maximal voluntary isometric contraction (MVC). Isometric twitch properties and MVCs were tested at baseline and during and following the fatigue task. Voluntary activation was similar between the old and young (∼98%) and was unaltered with fatigue. The old had 26% lower ( P < 0.01) isometric MVC torque and 18% slower ( P < 0.01) maximal shortening velocity than the young. Hence, peak power was 38% lower in the old ( P < 0.01). At task termination, MVC torque was maintained in the old ( P = 0.15) but decreased by 21% in the young ( P < 0.01). Twitch half-relaxation time was lengthened in the old at task termination by 26% ( P < 0.01) but unchanged in the young ( P = 0.10). Peak power was reduced by 24% and 17% at task termination in the old and young, respectively ( P < 0.01). Despite a better maintenance in isometric MVC torque production, the weaker and slower contracting triceps surae of the old was more fatigable than the young during fast dynamic efforts with an unconstrained velocity.

Recovery of Motoneuron Output Is Delayed in Old Men Following High-Intensity Fatigue

2010 ◽  
Vol 103 (2) ◽  
pp. 977-985 ◽  
Author(s):  
Brian H. Dalton ◽  
Brad Harwood ◽  
Andrew W. Davidson ◽  
Charles L. Rice
Keyword(s):  
High Intensity ◽  
Contractile Function ◽  
Contractile Properties ◽  
Triceps Surae ◽  
Voluntary Activation ◽  
Task Failure ◽  
Contraction Duration ◽  
Age Related ◽  
Ageing Model ◽  
Old Men

Despite an age-related slowing in the contractile properties of the triceps surae, inherently low maximal motor unit firing rates (MUFRs) in the soleus are unchanged. Fatigue following high-intensity contractions is characterized by contractile slowing in conjunction with a reduction in MUFRs in young adults. Here we exploit the ageing model of the soleus to assess changes in neuromuscular function during fatigue and short-term recovery. We hypothesize that a high-intensity sustained contraction will cause minimal reductions in MUFRs in young and old subjects but that recovery of MUFRs will be delayed in aged subjects. We compared the effects of a high-intensity sustained task on the MUFRs of the soleus and triceps surae contractile properties in six young (∼24 yr) and six old (∼75 yr) men. Various measures of the contractile function of the triceps surae were tested during two to six sessions via maximal voluntary isometric contractions (MVCs) and tibial nerve stimulation. Populations of MUFR trains were recorded from the soleus during brief (∼7 s) MVCs, a high-intensity (75% MVC) sustained fatiguing task, and brief MVCs following task failure at 1, 2, 5, and 10 min. Old men had greater time to task failure than the young (∼138 and ∼100 s, respectively). Voluntary activation was near maximal (>99%) for all subjects but at task failure, decreased to ∼89% in both groups. Maximal MUFRs, for both groups, were reduced by ∼44% and twitch contraction duration slowed by ∼30% following task failure. Contraction duration recovered equally for both groups within 2 min, but maximal MUFRs did not recover until 5 min in the old compared with 1 min for the young. The surprising fatigue-induced reduction in MUFRs was similar for both groups, but despite a similar recovery of contractile properties for both, recovery of MUFRs was impaired in the old subjects.

scholarly journals Velocity of the muscle tendon unit is sex-dependent and not altered with acute static stretch

2018 ◽  
Vol 43 (3) ◽  
pp. 227-232 ◽  
Author(s):  
Carey L. Simpson ◽  
Rowan R. Smart ◽  
Dylan E.E. Melady ◽  
Jennifer M. Jakobi
Keyword(s):  
Plantar Flexion ◽  
Voluntary Contraction ◽  
Voluntary Activation ◽  
Plantar Flexors ◽  
Shortening Velocity ◽  
Static Stretch ◽  
Twitch Interpolation ◽  
Tendon Lengthening ◽  
The Individual ◽  
The Relationship

Contraction velocity of a muscle tendon unit (MTU) is dependent upon the interrelationship between fascicles shortening and the tendon lengthening. Altering the mechanical properties of these tissues through a perturbation such as static stretching slows force generation. Females, who have inherently greater compliance compared with males, have slower velocity of MTU components. The addition of a static stretch might further exacerbate this sex difference. The purpose of this study was to investigate the velocity of fascicle shortening and tendon lengthening in males and females during isometric maximal voluntary contraction (MVC) of the plantar flexors prior to and following an acute static stretch. The MTU was imaged with ultrasound and voluntary activation tested with twitch interpolation for the 5-s plantar flexion MVC, which proceeded and followed an acute stretch. For the 3-min stretch the ankle was passively rotated to maximal dorsi-flexion. The males were stronger (128.71 ± 7.88 Nm) than the females (89.92 ± 4.70 Nm) but voluntary activation did not differ. Tendon lengthening velocity (p = 0.001) and fascicle shortening velocity (p = 0.01) were faster in males than females. Tendon velocity was positively and significantly correlated with fascicle velocity, (r2 = 0.307, p = 0.02). Although sex was significant as a predictor (p = 0.05) time was not independently significant. Thus, stretch did not alter this relationship in either sex (p = 0.6). The velocity of the individual components of the MTU is slower in females when compared with males; however, acute stretch does not alter the relationship between these components in males or females.

scholarly journals Sex differences in central and peripheral fatigue induced by sustained isometric ankle plantar flexion

2021 ◽  
Author(s):  
Donguk Jo ◽  
Miriam Goubran ◽  
Martin Bilodeau
Keyword(s):  
Sex Differences ◽  
Plantar Flexion ◽  
Recovery Period ◽  
Isometric Exercise ◽  
Voluntary Contraction ◽  
Voluntary Activation ◽  
Peripheral Fatigue ◽  
Plantar Flexors ◽  
Maximal Voluntary Isometric Contraction ◽  
Males And Females

The main aim of this study was to determine sex differences in central and peripheral fatigue produced by a sustained isometric exercise of ankle plantar flexors in healthy young adults. Ten males and fourteen females performed a sustained isometric ankle exercise until task failure. Maximal voluntary isometric contraction torque (plantarflexion), voluntary activation level (using the twitch interpolation technique), and twitch contractile properties (twitch peak torque, twitch half relaxation time, and low frequency fatigue index) were measured before, immediately after, and throughout a recovery period (1, 2, 5, and 10 min) following the exercise protocol in order to characterize neuromuscular fatigue. Fatigue had a significant effect (p £ 0.05) on all dependent variables. Other than for the maximal voluntary contraction torque, where males showed a greater fatigue-related decrease than females, males and females showed generally similar changes with fatigue. Altogether, our findings indicate no major differences in central or peripheral fatigue mechanisms between males and females to explain a somewhat greater fatigability in males.

In vivo maximal fascicle-shortening velocity during plantar flexion in humans

2015 ◽  
Vol 119 (11) ◽  
pp. 1262-1271 ◽  
Author(s):  
Hugo Hauraix ◽  
Antoine Nordez ◽  
Gaël Guilhem ◽  
Giuseppe Rabita ◽  
Sylvain Dorel
Keyword(s):  
Angular Velocity ◽  
Fiber Type ◽  
Plantar Flexion ◽  
Load Condition ◽  
Ultrasound Images ◽  
Maximal Velocity ◽  
Shortening Velocity ◽  
Hill Model ◽  
Angular Velocities

Interindividual variability in performance of fast movements is commonly explained by a difference in maximal muscle-shortening velocity due to differences in the proportion of fast-twitch fibers. To provide a better understanding of the capacity to generate fast motion, this study aimed to 1) measure for the first time in vivo the maximal fascicle-shortening velocity of human muscle; 2) evaluate the relationship between angular velocity and fascicle-shortening velocity from low to maximal angular velocities; and 3) investigate the influence of musculo-articular features (moment arm, tendinous tissues stiffness, and muscle architecture) on maximal angular velocity. Ultrafast ultrasound images of the gastrocnemius medialis were obtained from 31 participants during maximal isokinetic and light-loaded plantar flexions. A strong linear relationship between fascicle-shortening velocity and angular velocity was reported for all subjects (mean R2 = 0.97). The maximal shortening velocity (VFmax) obtained during the no-load condition (NLc) ranged between 18.8 and 43.3 cm/s. VFmax values were very close to those of the maximal shortening velocity (Vmax), which was extrapolated from the F-V curve (the Hill model). Angular velocity reached during the NLc was significantly correlated with this VFmax ( r = 0.57; P < 0.001). This finding was in agreement with assumptions about the role of muscle fiber type, whereas interindividual comparisons clearly support the fact that other parameters may also contribute to performance during fast movements. Nevertheless, none of the biomechanical features considered in the present study were found to be directly related to the highest angular velocity, highlighting the complexity of the upstream mechanics that lead to maximal-velocity muscle contraction.

Triceps surae contractile properties and firing rates in the soleus of young and old men

2009 ◽  
Vol 107 (6) ◽  
pp. 1781-1788 ◽  
Author(s):  
Brian H. Dalton ◽  
Brad Harwood ◽  
Andrew W. Davidson ◽  
Charles L. Rice
Keyword(s):  
Contractile Properties ◽  
Triceps Surae ◽  
Maximal Voluntary Isometric Contraction ◽  
Firing Rates ◽  
Lower Limb Muscles ◽  
Contraction Duration ◽  
Age Related ◽  
Limb Muscles ◽  
Muscle Groups ◽  
Old Men

Mean maximal motor unit firing rates (MUFRs) of the human soleus are lower (5–20 Hz) than other limb muscles (20–50 Hz) during brief sustained contractions. With healthy adult aging, maximal MUFRs are 20–40% lower and twitch contractile speed of lower limb muscles are 10–40% slower compared with young adults. However, it is unknown whether the inherently low maximal MUFRs for the soleus are further reduced with aging in association with age-related slowing in contractile properties. The purpose of the present study was to compare the changes in triceps surae contractile properties and MUFRs of the soleus throughout a variety of contraction intensities in six old (∼75 yr old) and six young (∼24 yr old) men. Neuromuscular measures were collected from the soleus and triceps surae during repeated sessions (2–6 sessions). Populations of single MUFR trains were recorded from the soleus with tungsten microelectrodes during separate sustained 6- to 10-s isometric contractions of varying intensities [25%, 50%, 75%, and 100% maximal voluntary isometric contraction (MVC)]. The old men had weaker triceps surae strength (MVC; 35% lower) and slower contractile properties (contraction duration; 20% longer) than the young men. However, there was no difference in average MUFRs of the soleus at 75% and 100% MVC (∼14.5 Hz and ∼16.5 Hz, respectively). At 25% and 50% MVC, average rates were 10% and 20% lower in the old men compared with young, respectively. Despite a significant slowing in triceps surae contraction duration, there was no age-related change in MUFRs recorded at high contractile intensities in the soleus. Thus the relationship between the whole muscle contractile properties and MUFRs found in other muscle groups may not exist between the triceps surae and soleus and may be muscle dependent.

scholarly journals Neuronostatin inhibits cardiac contractile function via a protein kinase A- and JNK-dependent mechanism in murine hearts

2009 ◽  
Vol 297 (3) ◽  
pp. R682-R689 ◽  
Author(s):  
Yinan Hua ◽  
Heng Ma ◽  
Willis K. Samson ◽  
Jun Ren
Keyword(s):  
Contractile Function ◽  
Peptide Hormone ◽  
Left Ventricular ◽  
Maximal Velocity ◽  
Cardiac Contractile Function ◽  
Mechanical Responses ◽  
Cardiac Contractile ◽  
Short Term Exposure ◽  
The Impact ◽  
Dependent Mechanism

Neuronostatin, a newly identified peptide hormone sharing the same precursor with somatostatin, exerts multiple pharmacological effects in gastrointestinal tract, hypothalamus, and cerebellum. However, the cardiovascular effect of neuronostatin is unknown. The aim of this study was to elucidate the impact of neuronostatin on cardiac contractile function in murine hearts and isolated cardiomyocytes. Short-term exposure of neuronostatin depressed left ventricular developed pressure (LVDP), maximal velocity of pressure development (±dP/d t), and heart rate in Langendorff heart preparation. Consistently, neuronostatin inhibited peak shortening (PS) and maximal velocity of shortening/relengthening (±dL/d t) without affecting time-to-PS (TPS) and time-to-90% relengthening (TR90) in cardiomyocytes. The neuronostatin-elicited cardiomyocyte mechanical responses were mimicked by somatostatin, the other posttranslational product of preprosomatostatin. Furthermore, the neuronostatin-induced cardiomyocyte mechanical effects were ablated by the PKA inhibitor H89 (1 μM) and the Jun N-terminal kinase (JNK) inhibitor SP600125 (20 μM). The PKC inhibitor chelerythrine (1 μM) failed to alter neuronostatin-induced cardiomyocyte mechanical responses. To the contrary, chelerythrine, but not H89, abrogated somatostatin-induced cardiomyocyte contractile responses. Our results also showed enhanced c-fos and c-jun expression in response to neuronostatin exposure (0.5 to 2 h). Taken together, our data suggest that neuronostatin is a peptide hormone with overt cardiac depressant action. The neuronostatin-elicited cardiac contractile response appears to be mediated, at least in part, through a PKA- and/or JNK-dependent mechanism.

Reproducibility of velocity-dependent power: before and after lengthening contractions

2011 ◽  
Vol 36 (5) ◽  
pp. 626-633 ◽  
Author(s):  
Geoffrey A. Power ◽  
Brian H. Dalton ◽  
Charles L. Rice ◽  
Anthony A. Vandervoort
Keyword(s):  
Peak Power ◽  
High Reliability ◽  
Similar Amount ◽  
Shortening Velocity ◽  
Lengthening Contractions ◽  
Isokinetic Testing ◽  
Typical Error ◽  
Before And After ◽  
Absolute Reliability ◽  
Ankle Dorsiflexors

The determination of power using isokinetic testing has been shown to be highly reliable. However, isotonic and isokinetic testing involve specific mechanical constraints that likely necessitate different neuromuscular strategies. Therefore, the purpose here was to establish test–retest intrarater reliability (separated by 7 days) of loaded maximal shortening velocity and velocity-dependent power of the ankle dorsiflexors using the isotonic mode of the Biodex dynamometer (i) at baseline and (ii) throughout recovery following 150 high-intensity lengthening contractions. Intraclass correlation coefficients (ICC)2,1 with 95% CIs were used to determine relative reliability, whereas absolute reliability included typical error (TEM) and typical error expressed as a coefficient of variation (TEMCV). Twenty-four young men and women volunteered for the study. Maximal shortening velocity and power were determined with a fixed resistance set at 20% of maximal voluntary isometric contraction across 2 testing sessions separated by 7 days. ICCs were 0.93 and 0.98 for maximal shortening velocity and peak power, respectively. Following the lengthening contractions, ICCs indicated high reliability for maximal shortening velocity and peak power, 0.86 and 0.94, respectively, suggesting that a similar amount of fatigue was incurred on both days. Measures of absolute reliability for maximal shortening velocity and peak power also yielded high reliability. The isotonic mode is highly reliable when testing velocity-dependent power of the ankle dorsiflexors at baseline and following fatiguing lengthening contractions. The high reliability of this measure is encouraging and suggests that the isotonic mode can be used in various settings to track group changes before and after training and following fatigue and lengthening contractions.

Force-velocity and force-power properties of single muscle fibers from elite master runners and sedentary men

1996 ◽  
Vol 271 (2) ◽  
pp. C676-C683 ◽  
Author(s):  
J. J. Widrick ◽  
S. W. Trappe ◽  
D. L. Costill ◽  
R. H. Fitts
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Power Output ◽  
Peak Power ◽  
Isometric Force ◽  
Peak Force ◽  
Peak Power Output ◽  
Type I ◽  
Shortening Velocity ◽  
Force Velocity

Gastrocnemius muscle fiber bundles were obtained by needle biopsy from five middle-aged sedentary men (SED group) and six age-matched endurance-trained master runners (RUN group). A single chemically permeabilized fiber segment was mounted between a force transducer and a position motor, subjected to a series of isotonic contractions at maximal Ca2+ activation (15 degrees C), and subsequently run on a 5% polyacrylamide gel to determine myosin heavy chain composition. The Hill equation was fit to the data obtained for each individual fiber (r2 > or = 0.98). For the SED group, fiber force-velocity parameters varied (P < 0.05) with fiber myosin heavy chain expression as follows: peak force, no differences: peak tension (force/fiber cross-sectional area), type IIx > type IIa > type I; maximal shortening velocity (Vmax, defined as y-intercept of force-velocity relationship), type IIx = type IIa > type I; a/Pzero (where a is a constant with dimensions of force and Pzero is peak isometric force), type IIx > type IIa > type I. Consequently, type IIx fibers produced twice as much peak power as type IIa fibers, whereas type IIa fibers produced about five times more peak power than type I fibers. RUN type I and IIa fibers were smaller in diameter and produced less peak force than SED type I and IIa fibers. The absolute peak power output of RUN type I and IIa fibers was 13 and 27% less, respectively, than peak power of similarly typed SED fibers. However, type I and IIa Vmax and a/Pzero were not different between the SED and RUN groups, and RUN type I and IIa power deficits disappeared after power was normalized for differences in fiber diameter. Thus the reduced absolute peak power output of the type I and IIa fibers from the master runners was a result of the smaller diameter of these fibers and a corresponding reduction in their peak isometric force production. This impairment in absolute peak power production at the single fiber level may be in part responsible for the reduced in vivo power output previously observed for endurance-trained athletes.

scholarly journals The cross-bridge cycle and skeletal muscle fatigue

2008 ◽  
Vol 104 (2) ◽  
pp. 551-558 ◽  
Author(s):  
Robert H. Fitts
Keyword(s):  
Peak Power ◽  
Molecular Mechanisms ◽  
Fiber Type ◽  
Low Ph ◽  
Forward Rate ◽  
Maximal Velocity ◽  
Functional Changes ◽  
Cross Bridge ◽  
The Cross

The functional correlates of fatigue observed in both animals and humans during exercise include a decline in peak force (P0), maximal velocity, and peak power. Establishing the extent to which these deleterious functional changes result from direct effects on the myofilaments is facilitated through understanding the molecular mechanisms of the cross-bridge cycle. With actin-myosin binding, the cross-bridge transitions from a weakly bound low-force state to a strongly bound high-force state. Low pH reduces the number of high-force cross bridges in fast fibers, and the force per cross bridge in both fast and slow fibers. The former is thought to involve a direct inhibition of the forward rate constant for transition to the strong cross-bridge state. In contrast, inorganic phosphate (Pi) is thought to reduce P0 by accelerating the reversal of this step. Both H+ and Pi decrease myofibrillar Ca2+ sensitivity. This effect is particularly important as the amplitude of the Ca2+ transient falls with fatigue. The inhibitory effects of low pH and high Pi on P0 are reduced as temperature increases from 10 to 30°C. However, the H+-induced depression of peak power in the slow fiber type, and Pi inhibition of myofibrillar Ca2+ sensitivity in slow and fast fibers, are greater at high compared with low temperature. Thus the depressive effects of H+ and Pi at in vivo temperatures cannot easily be predicted from data collected below 25° C. In vitro, reactive oxygen species reduce myofibrillar Ca2+ sensitivity; however, the importance of this mechanism during in vivo exercise is unknown.

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