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At least 1,099 records · Page 61Linked to original sources
PubMed2003

The relative position of EDL muscle affects the length of sarcomeres within muscle fibers: experimental results and finite-element modeling.

BACKGROUND: Effects of extramuscular connective tissues on muscle force (experimentally measured) and lengths of sarcomeres (modeled) were investigated in rat. It was hypothesized that changes of muscle-relative position affect the distribution of lengths of sarcomeres within muscle fibers. METHOD OF APPROACH: The position of extensor digitorum longus muscle (EDL) relative to intact extramuscular connective tissues of the anterior crural compartment was manipulated without changing its muscle-tendon complex length. RESULTS: Significant effects of EDL muscle relative position on proximal and distal EDL forces were found, indicating changes of extramuscular myofascial force transmission. EDL isometric force exerted at its proximal and distal tendons differed significantly. Finite-element modeling showed that the distribution of lengths of sarcomeres is altered by changes of muscle-relative position. CONCLUSIONS: It is concluded that forces exerted on a muscle via extramuscular myofascial pathways augment distributions of lengths of sarcomeres within that muscle.

Animals↗
PubMed1992

Both muscle-specific and ubiquitous nuclear factors are required for muscle-specific expression of the myosin heavy-chain beta gene in cultured cells.

Expression of the myosin heavy-chain beta gene is controlled by multiple cis-acting regulatory elements in the 5' flanking region; two of these, referred to as A (-276 to -263) and B (-207 to -180), are essential for conferring muscle-specific activation on homologous and heterologous promoters. Here we report on the identification of nuclear protein factors that specifically bind to these two elements. By using the A element as a probe, as well as nuclear extracts from muscle cells, we found two protein-DNA complexes that displayed distinct bands in a gel mobility shift assay but had identical methylation interference patterns. One complex was present mainly in nuclear extracts from undifferentiated muscle and nonmuscle cells, whereas the other was observed mainly in nuclear extracts from differentiated muscle cells. Thus, the muscle-specific complex formation with the A element appears to be involved in determining tissue-specific expression. Furthermore, competition analysis demonstrated that the A-element-binding factors also bind to the muscle-CAT motif in the cardiac troponin T gene. By using the B element as a probe, we saw similar patterns of gel-shifted bands and methylation interference in nonmuscle and muscle nuclear extracts. In addition, both elements A and B were found to be necessary for tissue-specific expression, suggesting that the muscle-specific activation of the myosin heavy-chain beta gene may require interaction between a muscle-specific and a ubiquitous protein-DNA complex.

Animals↗
PubMed1998

Muscle-specific splicing of a heterologous exon mediated by a single muscle-specific splicing enhancer from the cardiac troponin T gene.

The chicken cardiac troponin T (cTNT) gene contains a single 30-nucleotide alternative exon that is included in embryonic striated muscle and skipped in the adult. Transient-transfection analysis of cTNT minigenes in muscle and fibroblast cell cultures previously identified four muscle-specific splicing enhancers (MSEs) that promote exon inclusion specifically in embryonic striated muscle cultures. Three MSEs located in the intron downstream from the alternative exon were sufficient for muscle-specific exon inclusion. In the present study, the boundaries of these MSEs were defined by scanning mutagenesis, allowing analysis of individual elements in gain-of-function experiments. Concatamers of MSE2 were necessary and sufficient to promote muscle-specific inclusion of a heterologous exon, indicating that it is a target for muscle-specific regulation. Sequences present in MSE2 are also found in MSE4, suggesting that these two MSEs act in a similar manner. MSE3 appears to be different from MSE2 and MSE4 yet is able to functionally replace both of these elements, demonstrating functional redundancy of elements that are likely to bind different factors. MSE2 and MSE4 each contain a novel sequence motif that is found adjacent to a number of alternative exons that undergo regulated splicing in striated muscle, suggesting a common role for this element in muscle-specific regulation.

Animals↗
PubMed2003

Androgen therapy improves muscle mass and strength but not muscle quality: results from two studies.

The relationship of strength to muscle area was used to assess change in muscle quality after anabolic interventions. Study 1: asymptomatic human immunodeficiency virus-positive men (39 +/- 9 yr) were randomized to nandrolone (600 mg/wk) +/- resistance training (RT). Study 2: older healthy men (72 +/- 5 yr) were randomized to oxandrolone (20 mg/day) or placebo. Maximum voluntary strength was determined by the 1-repetition maximum (1-RM) method for leg press, flexion and extension, and cross-sectional area of leg muscles by MRI. From study week 0 to study week 12, muscle quality was unchanged with nandrolone, oxandrolone, or oxandrolone placebo, respectively, for total thigh muscles (1.23 +/- 0.012 vs. 1.27 +/- 0.29 kg/cm2; 9.0 +/- 1.1 vs. 8.9 +/- 1.2 N/cm2; 8.9 +/- 1.2 vs. 8.9 +/- 1.9 N/cm2) and hamstrings (0.41 +/- 0.08 vs. 0.43 +/- 0.07 kg/cm2; 0.90 +/- 0.14 vs. 0.95 +/- 0.016 N/cm2; 0.94 +/- 0.23 vs. 0.93 +/- 0.21 N/cm2). Lower-extremity 1-RM strength increased several times greater with RT+nandrolone (51-63% increases) than with nandrolone alone (4.7-16%), despite similar increases in muscle area; therefore, muscle quality increased from 1.13 +/- 0.17 to 1.51 +/- 0.18 kg/cm2 (+36 +/- 19%; P < 0.001) for total thigh muscle, 0.37 +/- 0.10 to 0.53 +/- 0.08 kg/cm2 (+49 +/- 39%; P < 0.001) for hamstrings, and 0.73 +/- 0.19 to 1.07 +/- 0.16 kg/cm2 (+55 +/- 36%; P < 0.001) for quadriceps. Thus androgen therapy alone did not improve muscle quality, but the addition of RT to nandrolone produced substantive improvements.

Aged↗
PubMed1997

Latency of muscle chemoreflex to vascular occlusion of active muscle during dynamic exercise.

When oxygen delivery to active muscle is too low for the ongoing rate of metabolism, metabolites accumulate and activate a muscle chemoreflex that raises arterial pressure. During static muscular contractions, the latency of the onset of increments in sympathetic activity attributed to the muscle chemoreflex is long (1-2 min). This long latency might be caused by slow accumulation of metabolites attributable to low rates of metabolism. Because shortening contractions at a given force per unit time have a much higher energy cost than do static contractions, the muscle chemoreflex should have a much shorter latency during dynamic exercise than during static contractions, and the latency should shorten further with rising exercise intensity. To test these ideas, the latency to the onset of the rise in arterial pressure induced by the muscle chemoreflex following vascular occlusion of active muscle was measured in four dogs exercising on a treadmill. During steady-state exercise of mild to moderate intensity, pressor responses to muscle ischemia were elicited by rapid, complete occlusion of the terminal aorta; this procedure mimics the blockage of muscle blood flow that occurs normally during static contractions. There was a statistically significant effect of exercise intensity on latency (P < 0.001). The latency was 23.5 +/- 4.5, 16.4 +/- 5.6, and 10.1 +/- 2.3 s (means +/- SE) at 3.2 km/h 0% grade, 6.5 km/h 0% grade, and 6.5 km/h 10% grade, respectively. Also, the rate of rise of arterial pressure during chemoreflex activation increased progressively with rising exercise intensity from 0.8 +/- 0.2 mmHg/s during exercise at 3.2 km/h 0% grade to 2.0 +/- 0.5 mmHg/s during exercise at 6.5 km/h 10% grade. Thus the latency of the muscle chemoreflex in response to vascular occlusion during mild dynamic exercise is shorter than has been reported during static contractions of moderate intensity.

Animals↗
PubMed1999

Muscle metaboreflex improves O2 delivery to ischemic active skeletal muscle.

Ischemia of active skeletal muscle elicits a powerful pressor response, termed the muscle metaboreflex. We recently reported that the muscle metaboreflex pressor response acts to partially restore blood flow to the ischemic active skeletal muscle. However, because this reflex is activated by reductions in O2 delivery rather than blood flow per se, gain of the muscle metaboreflex as analyzed on the basis of blood flow alone may underestimate its true strength if this reflex also acts to increase arterial O2 content. In conscious dogs chronically instrumented to measure systemic arterial pressure, cardiac output, and hindlimb blood flow, we activated the muscle metaboreflex via graded, partial reductions in hindlimb blood flow during mild (3.2 km/h) and moderate (6.4 km/h, 10% grade) workloads. At rest, during free-flow exercise, and with metaboreflex activation, we analyzed arterial blood samples for Hb concentration and O2 content and compared muscle metaboreflex gain calculations based on the ability to partially restore flow with those based on the ability to partially restore O2 delivery (blood flow x arterial O2 content). During both mild and moderate exercise, metaboreflex activation caused significant increases in arterial Hb concentration and O2 content. Metaboreflex gain quantified on the ability to partially restore O2 delivery was significantly greater than that based on restoration of blood flow during both mild and moderate workloads (0.52 +/- 0.10 vs. 0.39 +/- 0.08, P < 0.05, and 0.61 +/- 0. 05 vs. 0.46 +/- 0.04, P < 0.05, respectively). We conclude that the muscle metaboreflex acts to increase both arterial O2 content and blood flow to ischemic muscle such that when combined, O2 delivery is substantially increased and metaboreflex gain is greater when analyzed with a more integrative approach.

Animals↗
PubMed2003

Arm-cranking muscle power and arm isometric muscle strength are independent predictors of all-cause mortality in men.

Poor muscle strength is associated with mortality, presumably due to low muscle mass. Notably, muscle power declines more rapidly than muscle strength with increasing age, which may be related to more complex central nervous system movement control. We examined arm-cranking power against four workloads and isometric strength measured in the upper extremities of 993 men longitudinally tested over a 25-yr period. Muscle mass was estimated by using 24-h creatinine excretion; physical activity was assessed by self-reported questionnaire. Muscle power and strength were modeled by time by using mixed-effects models, which developed regression equations for each individual. The first derivative of these equations estimated rate of change in strength or power at each evaluation. Survival analyses, using the counting method, examined the impact of strength, power, and their rates of change on all-cause mortality while adjusting for age. Arm-cranking power [relative risk (rr) = 0.984 per 100 kg.m.min(-1), P < 0.001] was a stronger predictor of mortality than was arm strength (rr = 0.986 per 10 kg, P = not significant), whereas rate of power change (rr = 0.989 per 100 kg.min(-1).yr(-1)) and rate of arm strength change (rr = 0.888 per 10 kg/yr) were risks independent of the power or strength levels. The impacts of power and strength were partially independent of muscle mass and physical activity. The risk of mortality was similar across the four power workloads (rr = 0.93-0.96 per 100 kg.m.min(-1)), whereas the lowest load generated less than one-half the power as the higher loads. Arm-cranking power is a risk factor for mortality, independent of muscle strength, physical activity, and muscle mass. The impact is found with loads that do not generate maximal power, suggesting an important role for motor coordination and speed of movement.

Adult↗
PubMed2005

Muscle size and strength are increased following walk training with restricted venous blood flow from the leg muscle, Kaatsu-walk training.

Previous studies have shown that low-intensity resistance training with restricted muscular venous blood flow (Kaatsu) causes muscle hypertrophy and strength gain. To investigate the effects of daily physical activity combined with Kaatsu, we examined the acute and chronic effects of walk training with and without Kaatsu on MRI-measured muscle size and maximum dynamic (one repetition maximum) and isometric strength, along with blood hormonal parameters. Nine men performed Kaatsu-walk training, and nine men performed walk training alone (control-walk). Training was conducted two times a day, 6 days/wk, for 3 wk using five sets of 2-min bouts (treadmill speed at 50 m/min), with a 1-min rest between bouts. Mean oxygen uptake during Kaatsu-walk and control-walk exercise was 19.5 (SD 3.6) and 17.2 % (SD 3.1) of treadmill-determined maximum oxygen uptake, respectively. Serum growth hormone was elevated (P < 0.01) after acute Kaatsu-walk exercise but not in control-walk exercise. MRI-measured thigh muscle cross-sectional area and muscle volume increased by 4-7%, and one repetition maximum and maximum isometric strength increased by 8-10% in the Kaatsu-walk group. There was no change in muscle size and dynamic and isometric strength in the control-walk group. Indicators of muscle damage (creatine kinase and myoglobin) and resting anabolic hormones did not change in both groups. The results suggest that the combination of leg muscle blood flow restriction with slow-walk training induces muscle hypertrophy and strength gain, despite the minimal level of exercise intensity. Kaatsu-walk training may be a potentially useful method for promoting muscle hypertrophy, covering a wide range of the population, including the frail and elderly.

Adult↗
PubMed1984

Absence of somatotopic projection of muscle afferents onto motoneurons of same muscle.

During weak voluntary contractions, muscle afferents from a restricted region of the tibialis anterior of humans were activated with mechanical or electrical stimuli while electromyographic recordings (EMG) were made from pairs of motor units. One motor unit of a pair was located in the region of muscle from which the afferents arose; the other was at least 10 cm distal. The territories of the motor units of each pair did not overlap. All motor units were of low threshold, recruited at less than 5% of maximal voluntary strength. Direct recordings of muscle afferent activity, using a microelectrode in the nerve fascicle innervating the tibialis anterior, showed that taps delivered to the muscle belly activated submaximally a discrete population of receptors, restricted to the site of the taps. The spread of the disturbance set up by the taps or by vibration at 100 Hz applied to the muscle belly was measured with an accelerometer and was also found to be restricted to the site of application of the vibrator tip. With each of 12 pairs of motor units, vibration at 100 Hz was applied to the muscle near the motor unit of higher threshold for recruitment in a voluntary contraction. The vibration produced detectable reflex effects but did not alter recruitment order within any pair of motor units. During voluntary contractions involving 10 pairs of motor units, taps were applied to the muscle belly near each motor unit of a pair. The taps produced, at short latency, an increase in the probability of discharge of each motor unit. This change in probability is related to a composite excitatory postsynaptic potential (EPSP) caused by dynamically responding mechanoreceptors near the tap site and is generated through monosynaptic/oligosynaptic pathways. Taps near one motor unit of a pair did not selectively or preferentially affect the discharge of that motoneuron. During a voluntary contraction of tibialis anterior, electrical stimuli just below threshold for efferent axons, and so probably above threshold for afferent axons, were delivered singly and in brief trains through a microelectrode in a nerve fascicle innervating that muscle. Such stimulation had no detectable effect on the discharge pattern of four pairs of motor units. These findings suggest that the feedback from a few receptors in the muscle has a negligible effect on the motoneuron pool, in comparison with the total excitatory drive present during a voluntary contraction.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Papillary muscle perfusion pattern. A hypothesis for ischemic papillary muscle dysfunction.

BACKGROUND: The pathogenesis of posterior papillary muscle dysfunction is poorly understood. We hypothesized that papillary muscle perfusion pattern may explain the higher prevalence of posterior papillary muscle dysfunction after myocardial infarction. METHODS AND RESULTS: Twenty patients were monitored by transesophageal echocardiography during coronary surgery. Superselective coronary graft injections of 0.2 to 0.5 mL of sonicated albumin microbubbles were performed to assess graft patency and papillary muscle perfusion. Thirty-five graft injections were analyzed: 13 in the right coronary artery, 15 in an obtuse marginal branch, 1 in the left anterior descending coronary artery, and 6 in the first diagonal branch. The posterior papillary muscle was opacified in 16 patients, 11 from the right coronary artery and 5 from one obtuse marginal branch. In 10 of 16 patients (63%), the papillary muscle was perfused by one vessel, while in 6 of 16 (37%), it was perfused by two vessels. The anterior papillary muscle was opacified in 14 patients. Ten patients (71%) had double-vessel and 4 (29%) had single-vessel supply. In the subgroup of 10 patients with old inferior myocardial infarction, mitral regurgitation was present only among those 6 with single rather than double blood supply (P < .05). CONCLUSIONS: Myocardial infarction may cause papillary muscle dysfunction when the blood supply is provided by one rather than two vessels, as is more frequently the case with the posterior rather than the anterior papillary muscle.

Adult↗
PubMed1997

The integrin very late antigen-4 is expressed in human smooth muscle cell. Involvement of alpha 4 and vascular cell adhesion molecule-1 during smooth muscle cell differentiation.

Vascular cell adhesion molecule-1 (VCAM-1) and its counterreceptor, the integrin very late antigen-4 (VLA-4), have recently been identified in smooth muscle cells during intimal thickening in humans and in newly forming vessels during ontogeny in mice, respectively. We examined the coexpression of VCAM-1 and the alpha 4 integrin subunit in human smooth muscle cells. The expression of VCAM-1 and alpha 4 subunit were studied during development of the aorta. In the 10-week-old human fetal aorta, VCAM-1 and alpha 4 were strongly expressed in smooth muscle cells. Their expression was dramatically reduced within the 24th week of gestation and disappeared in the adult aortic media. However, smooth muscle cells from intimal atherosclerotic thickening of adult aorta reexpressed both VCAM-1 and alpha 4. In a culture model mimicking smooth muscle differentiation, VCAM-1 mRNA and protein and alpha 4 integrin protein were coexpressed with smooth muscle-specific variants of cytoskeletal and contractile proteins, smooth muscle myosin heavy chain, caldesmon heavy chain, and desmin. Treatment with antibodies against VCAM-1 or alpha 4 integrin subunit interfered with the mRNA induction of smooth muscle-specific markers of differentiation. These results in vitro, associated with the transitory expression of VCAM-1 and VLA-4 during vascular ontogeny and the atherosclerosis process, point to a possible role of VCAM-1 and VLA-4 in the induction of smooth muscle differentiation.

Adult↗
PubMed1999

Molecular cloning and characterization of the intermediate-conductance Ca(2+)-activated K(+) channel in vascular smooth muscle: relationship between K(Ca) channel diversity and smooth muscle cell function.

Recent evidence suggests that functional diversity of vascular smooth muscle is produced in part by a differential expression of ion channels. The aim of the present study was to examine the role of Ca(2+)-activated K(+) channels (K(Ca) channels) in the expression of smooth muscle cell functional phenotype. We found that smooth muscle cells exhibiting a contractile function express predominantly large-conductance ( approximately 200 pS) K(Ca) (BK) channels. In contrast, proliferative smooth muscle cells express predominantly K(Ca) channels exhibiting a much smaller conductance ( approximately 32 pS). These channels are blocked by low concentrations of charybdotoxin (10 nmol/L) but, unlike BK channels, are insensitive to iberiotoxin (100 nmol/L). To determine the molecular identity of this K(+) channel, we cloned a 1.9-kb cDNA from an immature-phenotype smooth muscle cell cDNA library. The cDNA contains an open reading frame for a 425 amino acid protein exhibiting sequence homology to other K(Ca) channels, in particular with mIK1 and hIK1. Expression in oocytes gives rise to a K(+)-selective channel exhibiting intermediate-conductance (37 pS at -60 mV) and potent activation by Ca(2+) (K(d) 120 nmol/L). Thus, we have cloned and characterized the vascular smooth muscle intermediate-conductance K(Ca) channel (SMIK), which is markedly upregulated in proliferating smooth muscle cells. The differential expression of these K(Ca) channels in functionally distinct smooth muscle cell types suggests that K(Ca) channels play a role in defining the physiological properties of vascular smooth muscle.

Amino Acid Sequence↗
PubMed2002

Respiratory and limb muscle weakness induced by tumor necrosis factor-alpha: involvement of muscle myofilaments.

The respiratory and limb skeletal muscles become weakened in sepsis, congestive heart failure, and other inflammatory diseases. A potential mediator of muscle weakness is tumor necrosis factor (TNF)-alpha, a cytokine that can stimulate muscle wasting and also can induce contractile dysfunction without overt catabolism. This study addressed the latter process. Murine diaphragm and limb muscle (flexor digitorum brevis [FDB]) preparations were used to determine the relative sensitivities of these muscles to TNF-alpha. Intact muscle fibers were isolated from FDB and microinjected with indo-1 to measure changes in sarcoplasmic calcium regulation. We found that TNF-alpha depressed tetanic force of the diaphragm and FDB to comparable degrees across a range of stimulus frequencies. In isolated muscle fibers, TNF-alpha decreased tetanic force without altering tetanic calcium transients or resting calcium levels. We conclude that (1) TNF-alpha compromises contractile function of diaphragm and limb muscle similarly, and (2) TNF-alpha decreases force by blunting the response of muscle myofilaments to calcium activation.

Actin Cytoskeleton↗
PubMedDate not supplied

Preseason hamstring muscle weakness associated with hamstring muscle injury in Australian footballers.

Hamstring muscle strain is the most prevalent injury in Australian Rules Football, accounting for 16% of playing time missed as a result of injury. Thirty-seven professional footballers from an Australian Football League team had preseason measurements of hamstring and quadriceps muscle concentric peak torque at 60, 180, and 300 deg/sec measured on a Cybex 340 dynamometer. Players were studied prospectively throughout the 1995 season. During that time, six players sustained clinically diagnosed hamstring muscle injuries that caused them to miss match-playing time. The injured hamstring muscles were all weaker than in the opposite leg in absolute values and hamstring-to-quadriceps muscle ratios. According to our t-test results, hamstring muscle injury was significantly associated with a low hamstring-to-quadriceps muscle peak torque ratio at 60 deg/sec on the injured side and a low hamstring muscle side-to-side peak torque ratio at 60 deg/sec. Flexibility (as measured by the sit-and-reach test) did not correlate with injury. Discriminant-function analysis using the two significant ratio variables resulted in a canonical correlation with injury of 0.4594 and correctly classified legs into injury groups with 77.4% success. These results indicate that preseason isokinetic testing of professional Australian Rules footballers can identify players at risk of developing hamstring muscle strains.

Adult↗
PubMed2005

Expression of eight distinct MHC isoforms in bovine striated muscles: evidence for MHC-2B presence only in extraocular muscles.

This study aimed to analyse the expression of myosin heavy chain (MHC) isoforms in bovine muscles, with particular attention to the MHC-2B gene. Diaphragm, longissimus dorsi, masseter, several laryngeal muscles and two extraocular muscles (rectus lateralis and retractor bulbi) were sampled in adult male Bos taurus (age 18-24 months, mass 400-500 kg) and analysed by RT-PCR, gel electrophoresis and immunohistochemistry. Transcripts and proteins corresponding to eight MHC isoforms were identified: MHC-alpha and MHC-beta/slow (or MHC-1), two developmental isoforms (MHC-embryonic and MHC-neonatal), three adult fast isoforms (MHC-2A, MHC-2X and MHC-2B) and the extraocular isoform MHC-Eo. All eight MHC isoforms were found to be co-expressed in extrinsic eye muscles, retractor bulbi and rectus lateralis, four (beta/slow, 2A, 2X, neonatal) in laryngeal muscles, three (beta/slow, 2A and 2X) in trunk and limb muscles and two (beta/slow and alpha) in masseter. The expression of MHC-2B and MHC-Eo was restricted to extraocular muscles. Developmental MHC isoforms (neonatal and embryonic) were only found in specialized muscles in the larynx and in the eye. MHC-alpha was only found in extraocular and masseter muscle. Single fibres dissected from masseter, diaphragm and longissimus were classified into five groups (expressing, respectively, beta/slow, alpha, slow and 2A, 2A and 2X) on the basis of MHC isoform electrophoretical separation, and their contractile properties [maximum shortening velocity (v(0)) and isometric tension (P(0))] were determined. v(0) increased progressively from slow to fast 2A and fast 2X, whereas hybrid 1-2A fibres and fibres containing MHC-alpha were intermediate between slow and fast 2A.

Analysis of Variance↗
PubMed1992

The influence of temperature on muscle function in the fast swimming scup. I. Shortening velocity and muscle recruitment during swimming.

In this study, electromyography showed that scup can swim to a maximum speed of 80 cm s-1 with their red muscle whereas previous results showed that carp can swim to only 45 cm s-1. Our aim was to evaluate the adaptations that enable scup to swim nearly twice as fast as carp. Although we anticipated that, at their respective maximum speeds, the red muscle of scup would be shortening at twice the velocity (V) of carp muscle, we found that the values of V were the same (2.04 muscle lengths s-1). At any given swimming speed, V was higher in carp than in scup because carp had a larger sarcomere length excursion and higher tail-beat frequency. The smaller sarcomere excursion in scup is primarily associated with using a less undulatory style of swimming (i.e. with a smaller backbone curvature). This less undulatory style of swimming may be an important adaptation that not only reduces V but may also reduce drag. At their respective maximum speeds, however, the 28% lower sarcomere length excursion in scup is balanced by a 26% higher tail-beat frequency, giving an equal V to that of carp. Although the scup in this study were somewhat longer than the carp in the previous one (19.7 vs 13.4 cm), we believe that many of the observed differences are species-related rather than size-related. We also found that scup swam in a kinematically similar fashion at 10 degrees C and 20 degrees C. However, at 10 degrees C, the scup could swim to only 54 cm s-1 before recruiting their white muscle whereas, at 20 degrees C, they could swim to 80 cm s-1. The difference in speed of initial white muscle recruitment, as well as information on muscle mechanics, suggests that the scup compress their recruitment order into a narrow speed range at low temperatures, thereby recruiting more muscle fibres. Quantitative analysis of red muscle electromyograms in this paper supports this hypothesis.

Animals↗
PubMed1992

The influence of temperature on muscle function in the fast swimming scup. II. The mechanics of red muscle.

To understand better how scup can swim twice as fast as carp with its red muscle, we measured the mechanical properties of red muscle bundles in scup. The values of the mean maximum velocity of shortening (Vmax) at 10 degrees C (3.32 muscle lengths s-1) and at 20 degrees C (5.55 muscle lengths s-1; Q10 = 1.69) were nearly the same as those in carp. Isometric force, however, was approximately 50% greater (183 kN m-2; Q10 = 1.08). The maximal power generation was correspondingly about 50% greater in scup than in carp (71 W kg-1 at 10 degrees C and 134 W kg-1 at 20 degrees C; Q10 = 1.88). The larger power output of its muscle may be important in the faster swimming of the scup. In addition, the fact that scup use a less undulatory style of swimming means that, when they are swimming twice as fast, their red muscle shortens at the same velocity (V) and with the same V/Vmax (0.37, i.e. where maximum power is generated) as that of carp. The importance of V/Vmax is further shown by the comparison of scup swimming at different temperatures. The 1.69-fold higher Vmax at 20 degrees C than at 10 degrees C enables scup to swim with a 1.67-fold faster V at 20 degrees C. Thus, at both 10 degrees C and 20 degrees C, red muscle is used only over the same narrow range of V/Vmax (0.17-0.37), where experiments on isolated muscle suggest that power and efficiency are maximal. Therefore, V/Vmax appears to be an important design constraint that limits the range of velocities over which muscle is used in vivo, both at different temperatures and in fast- and slow-locomoting species.

Animals↗
PubMed1997

Why do tuna maintain elevated slow muscle temperatures? Power output of muscle isolated from endothermic and ectothermic fish.

It has been hypothesised that regional endothermy has evolved in the muscle of some tunas to enhance the locomotory performance of the fish by increasing muscle power output. Using the work loop technique, we have determined the relationship between cycle frequency and power output, over a range of temperatures, in isolated bundles of slow muscle fibres from the endothermic yellowfin tuna (Thunnus albacares) and its ectothermic relative the bonito (Sarda chiliensis). Power output in all preparations was highly temperature-dependent. A counter-current heat exchanger which could maintain a 10 degrees C temperature differential would typically double maximum muscle power output and the frequency at which maximum power is generated (fopt). The deep slow muscle of the tuna was able to operate at higher temperatures than slow muscle from the bonito, but was more sensitive to temperature change than more superficially located slow fibres from both tuna and bonito. This suggests that it has undergone some evolutionary specialisation for operation at higher, but relatively stable, temperatures. fopt of slow muscle was higher than the tailbeat frequency of undisturbed cruising tuna and, together with the high intrinsic power output of the slow muscle mass, suggests that cruising fish have a substantial slow muscle power reserve. This reserve should be sufficient to power significantly higher sustainable swimming speeds, presumably at lower energetic cost than if intrinsically less efficient fast fibres were recruited.

Animals↗