scholarly journals Maximal muscular power: lessons from sprint cycling

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Jamie Douglas ◽  
Angus Ross ◽  
James C. Martin
Keyword(s):  
Power Loss ◽  
Power Production ◽  
Maximum Force ◽  
Muscular Power ◽  
Shortening Velocity ◽  
Relaxation Kinetics ◽  
Power Frequency ◽  
Force Velocity ◽  
Sprint Cycling ◽  
Frequency Relationship

AbstractMaximal muscular power production is of fundamental importance to human functional capacity and feats of performance. Here, we present a synthesis of literature pertaining to physiological systems that limit maximal muscular power during cyclic actions characteristic of locomotor behaviours, and how they adapt to training. Maximal, cyclic muscular power is known to be the main determinant of sprint cycling performance, and therefore we present this synthesis in the context of sprint cycling. Cyclical power is interactively constrained by force-velocity properties (i.e. maximum force and maximum shortening velocity), activation-relaxation kinetics and muscle coordination across the continuum of cycle frequencies, with the relative influence of each factor being frequency dependent. Muscle cross-sectional area and fibre composition appear to be the most prominent properties influencing maximal muscular power and the power-frequency relationship. Due to the role of muscle fibre composition in determining maximum shortening velocity and activation-relaxation kinetics, it remains unclear how improvable these properties are with training. Increases in maximal muscular power may therefore arise primarily from improvements in maximum force production and neuromuscular coordination via appropriate training. Because maximal efforts may need to be sustained for ~15-60 s within sprint cycling competition, the ability to attenuate fatigue-related power loss is also critical to performance. Within this context, the fatigued state is characterised by impairments in force-velocity properties and activation-relaxation kinetics. A suppression and leftward shift of the power-frequency relationship is subsequently observed. It is not clear if rates of power loss can be improved with training, even in the presence adaptations associated with fatigue-resistance. Increasing maximum power may be most efficacious for improving sustained power during brief maximal efforts, although the inclusion of sprint interval training likely remains beneficial. Therefore, evidence from sprint cycling indicates that brief maximal muscular power production under cyclical conditions can be readily improved via appropriate training, with direct implications for sprint cycling as well as other athletic and health-related pursuits.

Optimal shortening velocity (V/Vmax) of skeletal muscle during cyclical contractions: length-force effects and velocity-dependent activation and deactivation.

1998 ◽  
Vol 201 (10) ◽  
pp. 1527-1540 ◽  
Author(s):  
G N Askew ◽  
R L Marsh
Keyword(s):  
Power Output ◽  
Power Production ◽  
Cycle Duration ◽  
Shortening Velocity ◽  
Wide Range ◽  
Velocity Relationship ◽  
Strain Trajectory ◽  
Force Velocity ◽  
Net Power Output ◽  
Force Relationship

The force-velocity relationship has frequently been used to predict the shortening velocity that muscles should use to generate maximal net power output. Such predictions ignore other well-characterized intrinsic properties of the muscle, such as the length-force relationship and the kinetics of activation and deactivation (relaxation). We examined the effects of relative shortening velocity on the maximum net power output (over the entire cycle) of mouse soleus muscle, using sawtooth strain trajectories over a range of cycle frequencies. The strain trajectory was varied such that the proportion of the cycle spent shortening was 25, 50 or 75 % of the total cycle duration. A peak isotonic power output of 167 W kg-1 was obtained at a relative shortening velocity (V/Vmax) of 0.22. Over the range of cyclical contractions studied, the optimal V/Vmax for power production ranged almost fourfold from 0.075 to 0.30, with a maximum net power output of 94 W kg-1. The net power output increased as the proportion of the cycle spent shortening increased. Under conditions where the strain amplitude was high (i.e. low cycle frequencies and strain trajectories where the proportion of time spent shortening was greater than that spent lengthening), the effects of the length-force relationship reduced the optimal V/Vmax below that predicted from the force-velocity curve. At high cycle frequencies and also for strain trajectories with brief shortening periods, higher rates of activation and deactivation with increased strain rate shifted the optimal V/Vmax above that predicted from the force-velocity relationship. Thus, the force-velocity relationship alone does not accurately predict the optimal V/Vmax for maximum power production in muscles that operate over a wide range of conditions (e.g. red muscle of fish). The change in the rates of activation and deactivation with increasing velocity of stretch and shortening, respectively, made it difficult to model force accurately on the basis of the force-velocity and length-force relationships and isometric activation and deactivation kinetics. The discrepancies between the modelled and measured forces were largest at high cycle frequencies.

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.

Induction of a fatigue-resistant phenotype in rabbit fast muscle by small daily amounts of stimulation

2001 ◽  
Vol 90 (5) ◽  
pp. 1909-1918 ◽  
Author(s):  
Ana Lopez-Guajardo ◽  
Hazel Sutherland ◽  
Jonathan C. Jarvis ◽  
Stanley Salmons
Keyword(s):  
Fatigue Resistance ◽  
Tibialis Anterior ◽  
Power Loss ◽  
Power Production ◽  
Fast Muscle ◽  
Clinical Use ◽  
Low Frequencies ◽  
Continuous Stimulation ◽  
Resistant Phenotype

We have shown that fatigue resistance can be induced in rabbit tibialis anterior (TA) muscles without excessive power loss by continuous stimulation at low frequencies, such as 5 Hz, and that the same result is obtained by delivering a 10-Hz pattern in equal on/ offperiods. Here we ask whether the same phenotype could be produced with daily amounts of stimulation that would be more appropriate for clinical use. We stimulated rabbit TA muscles for 6 wk, alternating fixed 30-min on periods of stimulation at 10 Hz with off periods of different duration. All patterns transformed fast-glycolytic fibers into fast-oxidative fibers. The muscles had fatigue-resistant properties but retained a higher contractile speed and power production than muscles transformed completely to the slow-oxidative type. We conclude that in the rabbit as little as one 30-min period of stimulation in 24 h can result in a substantial increase in the resistance of the muscle to fatigue.

scholarly journals Power fatigue of the rat diaphragm muscle

2000 ◽  
Vol 89 (6) ◽  
pp. 2215-2219 ◽  
Author(s):  
Bill T. Ameredes ◽  
Wen-Zhi Zhan ◽  
Y. S. Prakash ◽  
Rene Vandenboom ◽  
Gary C. Sieck
Keyword(s):  
Diaphragm Muscle ◽  
Fiber Types ◽  
Rat Diaphragm ◽  
Shortening Velocity ◽  
Reduction In Force ◽  
Novel Technique ◽  
Velocity Relationship ◽  
Stimulus Train ◽  
Force Velocity

We hypothesized that decrements in maximum power output (W˙max) of the rat diaphragm (Dia) muscle with repetitive activation are due to a disproportionate reduction in force (force fatigue) compared with a slowing of shortening velocity (velocity fatigue). Segments of midcostal Dia muscle were mounted in vitro (26°C) and stimulated directly at 75 Hz in 400-ms-duration trains repeated each second (duty cycle = 0.4) for 120 s. A novel technique was used to monitor instantaneous reductions in maximum specific force (Po) andW˙max during fatigue. During each stimulus train, activation was isometric for the initial 360 ms during which Po was measured; the muscle was then allowed to shorten at a constant velocity (30% V max) for the final 40 ms, and W˙max was determined. Compared with initial values, after 120 s of repetitive activation, Po andW˙max decreased by 75 and 73%, respectively. Maximum shortening velocity was measured in two ways: by extrapolation of the force-velocity relationship ( V max) and using the slack test [maximum unloaded shortening velocity ( V o)]. After 120 s of repetitive activation, V max slowed by 44%, whereas V o slowed by 22%. Thus the decrease inW˙max with repetitive activation was dominated by force fatigue, with velocity fatigue playing a secondary role. On the basis of a greater slowing of V max vs. V o, we also conclude that force and power fatigue cannot be attributed simply to the total inactivation of the most fatigable fiber types.

Force-velocity relationship of expiratory muscles in normal subjects

1982 ◽  
Vol 52 (4) ◽  
pp. 930-938 ◽  
Author(s):  
Y. Kikuchi ◽  
H. Sasaki ◽  
K. Sekizawa ◽  
K. Aihara ◽  
T. Takishima
Keyword(s):  
Respiratory Muscles ◽  
Normal Subjects ◽  
Contractile Element ◽  
Shortening Velocity ◽  
Mean Values ◽  
Significant Difference ◽  
Velocity Relationship ◽  
Force Velocity ◽  
Expiratory Muscles ◽  
Relationship Of

We examined the force-velocity relationship of the respiratory muscles in normal subjects under nearly isotonic conditions, taking into consideration the pleural pressure (Ppl) changes during maximum forced expirations (MFE). We used an electromagnetic valve (EMV) to select the Ppl value at the onset of mouth flow; and both a pressure reservoir and a variable resistance to control the Ppl changes after the opening of the EMV during MFE. To simulate isotonic conditions and to obtain the shortening velocity of the contractile element (CE), we mathematically corrected the velocity of the series elastic component (SEC), using a modified version of Hill's equation. Although the maximum tension at total lung capacity (TLC) [1,156 +/- 215 (SD) g/cm] was larger than that at functional residual capacity (FRC) (782 +/- 97 g/cm) there was no significant difference in the maximum shortening velocity, 3.4 +/- 1.0 and 3.2 +/- 0.8 circumference/s at TLC and FRC, respectively. The mean values of k (slope) for the SEC at TLC and FRC were 19 +/- 4 and 18 +/- 5 circumference-1, respectively, and they were not significantly different. We concluded that the force-velocity relationship of the expiratory muscles exhibited the same mechanical properties as that of the other skeletal muscles.

Instantaneous force-velocity-length relations in isolated dog heart

1977 ◽  
Vol 232 (3) ◽  
pp. H241-H249 ◽  
Author(s):  
K. T. Weber ◽  
J. S. Janicki
Keyword(s):  
Fiber Length ◽  
Initial Period ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Steady State Response ◽  
Shortening Velocity ◽  
Contractile State ◽  
State Response ◽  
Force Velocity ◽  
Isolated Dog Heart

The mechanics of left ventricular contraction were investigated in terms of instantaneous mural force, mid-wall circumferential fiber shortening velocity (dL/dt), and fiber length (L) in seven servo-regulated hearts. The steady-state response of series of variably preloaded or afterloaded allasotonic contractions were utilized. Norepinephrine (0.55-1.38 mug/min) or propranolol (0.07-0.14 mg/min) were given to alter inotropic background. For any given contractile state and initial L, maximum dL/dt was not attained instantly but after a finite time of ejection (39 ms +/- 0.2 SE; range, 24-60) and from a lesser length (92% +/- 0.5 SE; range, 83-99) than present at end diastole. Beyond this initial period instantaneous dL/dt was dependent on both instantaneous force and length while independent of time after contraction and initial L. Instantaneous dL/dt also varied with contractile state, e.g., dL/dt was less after propranolol and greater after norepinephrine. Peak dL/dt for all conditions was a function of the extent of shortening (r = 0.90). Thus, the trajectory describing instantaneous force, velocity, and length provides a useful description of both the mechanical behavior and contractile state of the ventricular myocardium.

Effects of microtubule disruption on force, velocity, stiffness and [Ca2+]i in porcine coronary arteries

2000 ◽  
Vol 279 (5) ◽  
pp. H2493-H2501 ◽  
Author(s):  
Richard J. Paul ◽  
Peggy Sue Bowman ◽  
Michael S. Kolodney
Keyword(s):  
Smooth Muscle ◽  
Coronary Arteries ◽  
Isometric Force ◽  
Shortening Velocity ◽  
Cultured Fibroblasts ◽  
Microtubule Disruption ◽  
Highly Sensitive ◽  
Artery Stiffness ◽  
Force Velocity ◽  
Microtubule Stabilizer

Force generated by smooth muscle cells is believed to result from the interaction of actin and myosin filaments and is regulated through phosphorylation of the myosin regulatory light chain (LC20). The role of other cytoskeleton filaments, such as microtubules and intermediate filaments, in determining the mechanical output of smooth muscle is unclear. In cultured fibroblasts, microtubule disruption results in large increases in force similar to contractions associated with LC20 phosphorylation (15). One hypothesis, the “tensegrity” or “push-pull” model, attributes this increase in force to the disruption of microtubules functioning as rigid struts to resist force generated by actin-myosin interaction (9). In porcine coronary arteries, the disruption of microtubules by nocodazole (11 μM) also elicited moderate but significant increases in isometric force (10–40% of a KCl contracture), which could be blocked or reversed by taxol (a microtubule stabilizer). We tested whether this nocodazole-induced force was accompanied by changes in coronary artery stiffness or unloaded shortening velocity, parameters likely to be highly sensitive to microtubule resistance elements. Few changes were seen, ruling out push-pull mechanisms for the increase in force by nocodazole. In contrast, the intracellular calcium concentration, measured by fura 2 in the intact artery, was increased by nocodazole in parallel with force, and this was inhibited and/or reversed by taxol. Our results indicate that microtubules do not significantly contribute to vascular smooth muscle mechanical characteristics but, importantly, may play a role in modulation of Ca2+ signal transduction.

Effect of airway inflammation on smooth muscle shortening and contractility in guinea pig trachealis

1993 ◽  
Vol 265 (6) ◽  
pp. L549-L554 ◽  
Author(s):  
R. W. Mitchell ◽  
I. M. Ndukwu ◽  
K. Arbetter ◽  
J. Solway ◽  
A. R. Leff
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Neurogenic Inflammation ◽  
Isometric Force ◽  
Electrical Field Stimulation ◽  
Shortening Velocity ◽  
Lever System ◽  
Force Velocity

We studied the effect of either 1) immunogenic inflammation caused by aerosolized ovalbumin or 2) neurogenic inflammation caused by aerosolized capsaicin in vivo on guinea pig tracheal smooth muscle (TSM) contractility in vitro. Force-velocity relationships were determined for nine epithelium-intact TSM strips from ovalbumin-sensitized (OAS) vs. seven sham-sensitized controls and TSM strips for seven animals treated with capsaicin aerosol (Cap-Aer) vs. eight sham controls. Muscle strips were tethered to an electromagnetic lever system, which allowed isotonic shortening when load clamps [from 0 to maximal isometric force (Po)] were applied at specific times after onset of contraction. Contractions were elicited by supramaximal electrical field stimulation (60 Hz, 10-s duration, 18 V). Optimal length for each muscle was determined during equilibration. Maximal shortening velocity (Vmax) was increased in TSM from OAS (1.72 +/- 0.46 mm/s) compared with sham-sensitized animals (0.90 +/- 0.15 mm/s, P < 0.05); Vmax for TSM from Cap-Aer (0.88 +/- 0.11 mm/s) was not different from control TSM (1.13 +/- 0.08 mm/s, P = NS). Similarly, maximal shortening (delta max) was augmented in TSM from OAS (1.01 +/- 0.15 mm) compared with sham-sensitized animals (0.72 +/- 0.14 mm, P < 0.05); delta max for TSM from Cap-Aer animals (0.65 +/- 0.11 mm) was not different from saline aerosol controls (0.71 +/- 0.15 mm, P = NS). We demonstrate Vmax and delta max are augmented in TSM after ovalbumin sensitization; in contrast, neurogenic inflammation caused by capsaicin has no effect on isolated TSM contractility in vitro. These data suggest that airway hyperresponsiveness in vivo that occurs in association with immunogenic or neurogenic inflammation may result from different effects of these types of inflammation on airway smooth muscle.

Response of slow and fast muscle to hypothyroidism: maximal shortening velocity and myosin isoforms

1992 ◽  
Vol 263 (1) ◽  
pp. C86-C94 ◽  
Author(s):  
V. J. Caiozzo ◽  
R. E. Herrick ◽  
K. M. Baldwin
Keyword(s):  
Skeletal Muscles ◽  
Relative Content ◽  
Type I ◽  
Myosin Isoforms ◽  
Velocity Data ◽  
Sprague Dawley ◽  
Shortening Velocity ◽  
Sprague Dawley Rats ◽  
Force Velocity ◽  
Fast Twitch

This study examined both the shortening velocity and myosin isoform distribution of slow- (soleus) and fast-twitch (plantaris) skeletal muscles under hypothyroid conditions. Adult female Sprague-Dawley rats were randomly assigned to one of two groups: control (n = 7) or hypothyroid (n = 7). In both muscles, the relative contents of native slow myosin (SM) and type I myosin heavy chain (MHC) increased in response to the hypothyroid treatment. The effects were such that the hypothyroid soleus muscle expressed only the native SM and type I MHC isoforms while repressing native intermediate myosin and type IIA MHC. In the plantaris, the relative content of native SM and type I MHC isoforms increased from 5 to 13% and from 4 to 10% of the total myosin pool, respectively. Maximal shortening velocity of the soleus and plantaris as measured by the slack test decreased by 32 and 19%, respectively, in response to hypothyroidism. In contrast, maximal shortening velocity as estimated by force-velocity data decreased only in the soleus (-19%). No significant change was observed for the plantaris.

Aminophylline increases submaximum power but not intrinsic velocity of shortening of frog muscle

1992 ◽  
Vol 73 (1) ◽  
pp. 71-74 ◽  
Author(s):  
B. M. Block ◽  
S. R. Barry ◽  
J. A. Faulkner
Keyword(s):  
Skeletal Muscles ◽  
Isometric Force ◽  
Frog Muscle ◽  
Measured Parameter ◽  
Shortening Velocity ◽  
Force Development ◽  
Velocity Of Shortening ◽  
Force Velocity ◽  
Maximum Isometric Force ◽  
Frequency Of Stimulation

We hypothesized that methylxanthines, such as aminophylline, increase the power developed by submaximally activated frog skeletal muscles by increasing the force developed at any given velocity of shortening. Frog semitendinosus muscles were excised and tested at 20 degrees C in oxygenated control and aminophylline Ringer solutions. Force-velocity relationships were determined and power was calculated from muscles stimulated at frequencies of 80 and 300 Hz. The 300-Hz frequency of stimulation produced a maximum rate of force development. In 50 and 500 microM aminophylline, twitch force increased by 25 +/- 12 and 75 +/- 13%, respectively. Aminophylline did not affect maximum isometric force generation or the shortening velocity at any relative load. At 80-Hz stimulation and in the presence of 500 microM aminophylline, power increased by an average of 11% at 10 of 14 relative loads. At maximum frequencies of stimulation, aminophylline had no effect on any measured parameter. We conclude that aminophylline increases the power developed by submaximally activated frog muscles through an increase in the force generated particularly at the lower velocities of shortening.

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