The objectives of this study were to (1) quantify experimentally in vivo changes in pennation angle, fibre length and muscle thickness in the triceps surae complex in man in response to changes in ankle position and isometric plantarflexion moment and (2) compare changes in the above muscle architectural characteristics occurring in the transition from rest to a given isometric plantarflexion intensity with the estimations of a planimetric muscle model assuming constant thickness and straight muscle fibres. The gastrocnemius medialis (GM), gastrocnemius lateralis (GL) and soleus (SOL) muscles of six males were scanned with ultrasonography at different sites along and across the muscle belly at rest and during maximum voluntary contraction (MVC) trials at ankle angles of −15 deg (dorsiflexed direction), 0 deg (neutral position), +15 deg (plantarflexed direction) and +30 deg. Additional images were taken at 80, 60, 40 and 20 % of MVC at an ankle angle of 0 deg. In all three muscles and all scanned sites, as ankle angle increased from −15 to +30 deg, pennation increased (by 6–12 deg, 39–67 %, P < 0.01 at rest and 9–16 deg, 29–43 %, P < 0.01 during MVC) and fibre length decreased (by 15–28 mm, 32–34 %, P < 0.01 at rest and 8–10 mm, 27–30 %, P < 0.05 during MVC). Thickness in GL and SOL increased during MVC compared with rest (by 5–7 mm, 36–47 %, P < 0.01 in GL and 6–7 mm, 38–47 %, P < 0.01 in SOL) while thickness of GM did not differ (P > 0.05) between rest and MVC. At any given ankle angle the model underestimated changes in GL and SOL occurring in the transition from rest to MVC in pennation angle (by 9–12 deg, 24–38 %, P < 0.01 in GL and 9–14 deg, 25–28 %, P < 0.01 in SOL) and fibre length (by 6–15 mm, 22–39 %, P < 0.01 in GL and 6–8 mm, 23–24 %, P < 0.01 in SOL). The findings of the study indicate that the mechanical output of muscle as estimated by the model used may be unrealistic due to errors in estimating the changes in muscle architecture during contraction compared with rest.
The effect of changing muscle temperature on performance of short term dynamic exercise in man was studied. Four subjects performed 20 s maximal sprint efforts at a constant pedalling rate of 95 crank rev.min-1 on an isokinetic cycle ergometer under four temperature conditions: from rest at room temperature; and following 45 min of leg immersion in water baths at 44; 18; and 12 degrees C. Muscle temperature (Tm) at 3 cm depth was respectively 36.6, 39.3, 31.9 and 29.0 degrees C. After warming the legs in a 44 degrees C water bath there was an increase of approximately 11% in maximal peak force and power (PPmax) compared with normal rest while cooling the legs in 18 and 12 degrees C water baths resulted in reductions of approximately 12% and 21% respectively. Associated with an increased maximal peak power at higher Tm was an increased rate of fatigue. Two subjects performed isokinetic cycling at three different pedalling rates (54, 95 and 140 rev.min-1) demonstrating that the magnitude of the temperature effect was velocity dependent: At the slowest pedalling rate the effect of warming the muscle was to increase PPmax by approximately 2% per degree C but at the highest speed this increased to approximately 10% per degree C.
The purpose of the present study was to examine the effect of a plantarflexor maximum voluntary contraction (MVC) on Achilles tendon moment arm length. Sagittal magnetic resonance (MR) images of the right ankle were taken in six subjects both at rest and during a plantarflexor MVC in the supine position at a knee angle of 90 deg and at ankle angles of ‐30 deg (dorsiflexed direction), ‐15 deg, 0 deg (neutral ankle position), +15 deg (plantarflexed direction), +30 deg and +45 deg. A system of mechanical stops, support triangles and velcro straps was used to secure the subject in the above positions. Location of a moving centre of rotation was calculated for ankle rotations from ‐30 to 0 deg, ‐15 to +15 deg, 0 to +30 deg and +15 to +45 deg. All instant centres of rotation were calculated both at rest and during MVC. Achilles tendon moment arms were measured at ankle angles of ‐15, 0, +15 and +30 deg. At any given ankle angle, Achilles tendon moment arm length during MVC increased by 1‐1.5 cm (22‐27 %, P < 0.01) compared with rest. This was attributed to a displacement of both Achilles tendon by 0.6‐1.1 cm (P < 0.01) and all instant centres of rotation by about 0.3 cm (P < 0.05) away from their corresponding resting positions. The findings of this study have important implications for estimating loads in the musculoskeletal system. Substantially unrealistic Achilles tendon forces and moments generated around the ankle joint during a plantarflexor MVC would be calculated using resting Achilles tendon moment arm measurements.
Selected contractile properties and fatigability of the quadriceps muscle were studied in seven spinal cord–injured (SCI) and 13 able‐bodied control (control) individuals. The SCI muscles demonstrated faster rates of contraction and relaxation than did control muscles and extremely large force oscillation amplitudes in the 10‐Hz signal (65 ± 22% in SCI versus 23 ± 8% in controls). In addition, force loss and slowing of relaxation following repeated fatiguing contractions were greater in SCI compared with controls. The faster contractile properties and greater fatigability of the SCI muscles are in agreement with a characteristic predominance of fast glycolytic muscle fibers. Unexpectedly, the SCI muscles exhibited a force–frequency relationship shifted to the left, most likely as the result of relatively large twitch amplitudes. The results indicate that the contractile properties of large human locomotory muscles can be characterized using the approach described and that the transformation to faster properties consequent upon changes in contractile protein expression following SCI can be assessed. These measurements may be useful to optimize stimulation characteristics for functional electrical stimulation and to monitor training effects induced by electrical stimulation during rehabilitation of paralyzed muscles. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 1249–1256, 1999.
In this study, we estimated the specific tensions of soleus (Sol) and tibialis anterior (TA) muscles in six men. Joint moments were measured during maximum voluntary contraction (MVC) and during electrical stimulation. Moment arm lengths and muscle volumes were measured using magnetic resonance imaging, and pennation angles and fascicular lengths were measured using ultrasonography. Tendon and muscle forces were modeled. Two approaches were followed to estimate specific tension. First, muscle moments during electrical stimulation and moment arm lengths, fascicular lengths, and pennation angles during MVC were used (data set A). Then, MVC moments, moment arm lengths at rest, and cadaveric fascicular lengths and pennation angles were used (data set B). The use of data set B yielded the unrealistic specific tension estimates of 104 kN/m(2) in Sol and 658 kN/m(2) in TA. The use of data set A, however, yielded values of 150 and 155 kN/m(2) in Sol and TA, respectively, which agree with in vitro results from fiber type I-predominant muscles. In fact, both Sol and TA are such muscles. Our study demonstrates the feasibility of accurate in vivo estimates of human muscle intrinsic strength.
Force exerted and power generated were measured during short-term exercise performed on a bicycle ergometer that had been modified by the addition of an electric motor driving the cranks at a chosen constant velocity. Five subjects made a series of 20-s maximum efforts at different crank velocities (range 23--171 rev/min). The forces exerted were continuously monitored with strain gauges bonded to the cranks. Peak force was exerted at approximately 90 degrees past top dead center in each revolution. During the 20-s effort peak force declined from the maximum level (PFmax) attained near the start of exercise, the rate of decline being velocity dependent. PFmax was found to be inversely and linearly related to crank velocity and when standardized for upper leg muscle (plus bone) volume (ULV) was given by PFmax (kgf/l ULV) = 27.51--0.125 crank velocity (rev/min). Integration of the force records with pedal velocity enabled power output to be calculated. Maximum power output was a parabolic function of crank velocity, the apex of the relationship indicating that the velocity for greatest power output was 110 rev/min. At this velocity our subjects achieved a maximum mean power output, averaged over a complete revolution, of 840 +/- 153 W (85 +/- 5 W/l ULV). This was compared with the calculated value for maximum mechanical power output from aerobic sources, which was 272 +/- 49 W (30 +/- 1 W/l ULV).
The effects of single isovelocity shortening contractions on force production of the electrically stimulated human adductor pollicis muscle were investigated in seven healthy male subjects. Redeveloped isometric force immediately following isovelocity shortening was always depressed compared with the isometric force recorded at the same muscle length but without preceding shortening. The maximal isometric force deficit (FD) was (mean ± s.e.m.) 37 ± 2 % after 38 deg of shortening at 6.1 deg s−1. The FD was positively correlated with angular displacement (r2 > 0.98) and decreased with increasing velocity of the shortening step. Stimulation at 20 Hz instead of 50 Hz reduced absolute force levels during the contractions to about 73 % and the FD was decreased to a similar extent. Eighty‐nine per cent of the velocity‐related variation in the FD could be explained by the absolute force levels during shortening. FD was largely abolished by allowing the muscle to relax briefly (approximately 200 ms), a time probably too short for significant metabolic recovery. At all but the highest velocities there was a linear decline in force during the latter part of the isovelocity shortening phase, suggesting that the mechanisms underlying FD were active during shortening. Our results show that shortening‐induced force deficit is a significant feature of human muscle working in situ and is proportional to the work done by the muscle‐tendon complex. This finding has important implications for experimental studies of force‐velocity relationships in the intact human.
1. A slow component to pulmonary oxygen uptake (V02) is reported during prolonged high power exercise performed at constant power output at, or above, approximately 60 % of the maximal oxygen uptake. The magnitude of the slow component is reported to be associated with the intensity of exercise and to be largely accounted for by an increased V0, across the exercising legs.2. On the assumption that the control mechanism responsible for the increased V02 is intensity dependent we hypothesized that it should also be apparent in multi-stage incremental exercise tests with the result that the V102-power output relationship would be curvilinear.3. We further hypothesized that the change in the 102-power output relationship could be related to the hierarchical recruitment of different muscle fibre types with a lower mechanical efficiency. 4. Six subjects each performed five incremental exercise tests, at pedalling rates of 40, 60, 80, 100 and 120 rev min-1, over which range we expected to vary the proportional contribution of different fibre types to the power output. Pulmonary V02 was determined continuously and arterialized capillary blood was sampled and analysed for blood lactate concentration ([lactate]b). 5. Below the level at which a sustained increase in [lactate]b was observed pulmonary V02 showed a linear relationship with power output; at high power outputs, however, there was an additional increase in V02 above that expected from the extrapolation of that linear relationship, leading to a positive curvilinear V02-power output relationship.6. No systematic effect on the magnitude or onset of the 'extra' VO2 was found in relation to pedalling rate, which suggests that it is recruitment in any simple way.
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