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Seasonal changes in proteolytic activity and content of calpains in striated muscles of the longtailed ground squirrel Spermophilus undulatus were studied by casein zymography and Western blotting analysis. The results testify to hyperactivation of calpain proteases in the skeletal muscles of awakened animals during the 'winter' activity. The observed changes are discussed in the context of adaptation of skeletal muscles of long-tailed ground squirrels to hibernation. [ABSTRACT FROM AUTHOR]

Enteric co-innervation is a peculiar innervation pattern of striated esophageal musculature. Both anatomical and functional data on enteric co-innervation related to various transmitters have been collected in different species, although its function remains enigmatic. However, it is unclear whether catecholaminergic components are involved in such a co-innervation. Thus, we examined to identify catecholaminergic neuronal elements and clarify their relationship to other innervation components in the esophagus, using immunohistochemistry with antibodies against tyrosine hydroxylase (TH), vesicular acetylcholine transporter (VAChT), choline acetyltransferase (ChAT) and protein gene product 9.5 (PGP 9.5), α-bungarotoxin (α-BT) and PCR with primers for amplification of cDNA encoding TH and dopamine-β-hydroxylase (DBH). TH-positive nerve fibers were abundant throughout the myenteric plexus and localized on about 14 % of α-BT-labelled motor endplates differing from VAChT-positive vagal nerve terminals. TH-positive perikarya represented a subpopulation of only about 2.8 % of all PGP 9.5-positive myenteric neurons. Analysis of mRNA showed both TH and DBH transcripts in the mouse esophagus. As ChAT-positive neurons in the compact formation of the nucleus ambiguus were negative for TH, the TH-positive nerve varicosities on motor endplates are presumably of enteric origin, although a sympathetic origin cannot be excluded. In the medulla oblongata, the cholinergic ambiguus neurons were densely supplied with TH-positive varicosities. Thus, catecholamines may modulate vagal motor innervation of esophageal-striated muscles not only at the peripheral level via enteric co-innervation but also at the central level via projections to the nucleus ambiguus. As Parkinson's disease, with a loss of central dopaminergic neurons, also affects the enteric nervous system and dysphagia is prevalent in patients with this disease, investigation of intrinsic catecholamines in the esophagus may be worthwhile to understand such a symptom. [ABSTRACT FROM AUTHOR]

The striated muscle activator of Rho signaling (STARS) protein and members of its downstream signaling pathway, including myocardin-related transcription factor-A (MRTF-A) and SRF, are increased in response to prolonged resistance exercise training but also following a single bout of endurance cycling. The aim of the present study was to measure and compare the regulation of STARS, MRTF-A and SRF mRNA and protein following 10 weeks of endurance training (ET) versus resistance training (RT), as well as before and following a single bout of endurance (EE) versus resistance exercise (RE). Following prolonged training, STARS, MRTF-A and SRF mRNA levels were all increased by similar magnitude, irrespective of training type. In the training-habituated state, STARS mRNA increased following a single-bout RE when measured 2.5 and 5 h post-exercise and had returned to resting level by 22 h following exercise. MRTF-A and SRF mRNA levels were decreased by 2.5, 5, and 22 h following a single bout of RE and EE exercise when compared to their respective basal levels, with no significant difference seen between the groups at any of the time points. No changes in protein levels were observed following the two modes of exercise training or a single bout of exercise. This study demonstrates that the stress signals elicited by ET and RT result in a comparable regulation of members of the STARS pathway. In contrast, a single bout of EE and RE, performed in the trained state, elicit different responses. These observations suggest that in the trained state, the acute regulation of the STARS pathway following EE or RE may be responsible for exercise-specific muscle adaptations. [ABSTRACT FROM AUTHOR]

Following the onset of maturation, female athletes have a significantly higher risk for anterior cruciate ligament (ACL) injury compared with male athletes. While multiple sex differences in lower-extremity neuromuscular control and biomechanics have been identified as potential risk factors for ACL injury in females, the majority of these studies have focused specifically on the knee joint. However, increasing evidence in the literature indicates that lumbo-pelvic (core) control may have a large effect on knee-joint control and injury risk. This review examines the published evidence on the contributions of the trunk and hip to knee-joint control. Specifically, the sex differences in potential proximal controllers of the knee as risk factors for ACL injury are identified and discussed. Sex differences in trunk and hip biomechanics have been identified in all planes of motion (sagittal, coronal and transverse). Essentially, female athletes show greater lateral trunk displacement, altered trunk and hip ulexion angles, greater ranges of trunk motion, and increased hip adduction and internal rotation during sport manoeuvres, compared with their male counterparts. These differences may increase the risk of ACL injury among female athletes. Prevention programmes targeted towards trunk and hip neuromuscular control may decrease the risk for ACL injuries. [ABSTRACT FROM AUTHOR]

im: To investigate the effects of a neonatal low-protein diet on the morphology of myotubes in culture and the expression of key proteins that regulate myogenesis in young and adult rats. Methods: Male Wistar rats ( n = 18) were suckled by mothers fed diets containing 17% protein (controls, C) or 8% protein (undernourished, UN). All rats were fed a normal protein diet after weaning. Muscles were removed from the legs of 42-, 60- and 90-day-old rats. Muscle cells were cultured to assess cell number, morphology and the expression of major proteins involved in myogenesis (Pax7, cadherins, β1 integrin, IL-4Rα and myogenin) by western blotting. IL-4 levels in culture supernatants were measured by ELISA. Results: Offspring from mothers fed a low-protein diet showed a lower body weight gain. Cell number and myotube expansion were reduced in cultured muscle cells from UN, but the expression of myogenic marker proteins was unaltered. Conclusions: Dietary restriction during lactation had no impact on the synthesis of myogenic marker proteins, and myocyte differentiation occurred normally in the muscles of offspring aged 42, 60 or 90 days. Nevertheless, the number and morphology of the myotubes are altered. [ABSTRACT FROM AUTHOR]

While the industrialized world adopts a largely sedentary lifestyle, ultra- marathon running races have become increasingly popular in the last few years in many countries. The ability to run long distances is also considered to have played a role in human evolution. This makes the issue of ultra-long distance physiology important. In the ability to run multiples of 10km (up to 1000km in one stage), fatigue resistance is critical. Fatigue is generally defined as strength loss (i.e. a decrease in maximal voluntary contraction [MVC]), which is known to be dependent on the type of exercise. Critical task variables include the intensity and duration of the activity, both of which are very specific to ultra-endurance sports. They also include the muscle groups involved and the type of muscle contraction, two variables that depend on the sport under consideration. The first part of this article focuses on the central and peripheral causes of the alterations to neuromuscular function that occur in ultra-marathon running. Neuromuscular function evaluation requires measurements of MVCs and maximal electrical/magnetic stimulations; these provide an insight into the factors in the CNS and the muscles implicated in fatigue. However, such measurements do not necessarily predict how muscle function may influence ultra-endurance running and whether this has an effect on speed regulation during a real competition (i.e. when pacing strategies are involved). In other words, the nature of the relationship between fatigue as measured using maximal contractions/stimulation and submaximal performance limitation/regulation is questionable. To investigate this issue, we are suggesting a holistic model in the second part of this article. This model can be applied to all endurance activities, but is specifically adapted to ultra-endurance running: the flush model. This model has the following four components: (i) the ball-cock (or buoy), which can be compared with the rate of perceived exertion, and can increase or decrease based on (ii) the filling rate and (iii) the water evacuated through the waste pipe, and (iv) a security reserve that allows the subject to prevent physiological damage. We are suggesting that central regulation is not only based on afferent signals arising from the muscles and penpheral organs, but is also dependent on peripheral fatigue and spinal/supraspinal inhibition (or disfacilitation) since these alterations imply a higher central drive for a given power output. This holistic model also explains how environmental conditions, sleep deprivation/mental fatigue, pain-killers or psychostimulants, cognitive or nutritional strategies may affect ultra-running performance. [ABSTRACT FROM AUTHOR]

Some 12 years ago, a polymorphism of the angiotensin I-converting enzyme (ACE) gene became the first genetic element shown to impact substantially on human physical performance. The renin-angiotensin system (RAS) exists not just as an endocrine regulator, but also within local tissue and cells, where it serves a variety of functions. Functional genetic polymorphic variants have been identified for most components of RAS, of which the best known and studied is a polymorphism of the ACE gene. The ACE insertion/deletion (I/D) polymorphism has been associated with improvements in performance and exercise duration in a variety of populations. The I allele has been consistently demonstrated to be associated with endurance- orientated events, notably, in triathlons. Meanwhile, the D allele is associated with strength- and power-orientated performance, and has been found in significant excess among elite swimmers. Exceptions to these associations do exist, and are discussed. In theory, associations with ACE genotype may be due to functional variants in nearby loci, and/or related genetic polymorphism such as the angiotensin receptor, growth hormone and bradykinin genes. Studies of growth hormone gene variants have not shown significant associations with performance in studies involving both triathletes and military recruits. The angiotensin type-1 receptor has two functional polymorphisms that have not been shown to be associated with performance, although studies of hypoxic ascent have yielded conflicting results. ACE genotype influences bradykinin levels, and a common gene variant in the bradykinin 2 receptor exists. The high kinin activity haplotye has been associated with increased endurance performance at an Olympic level, and similar results of metabolic efficiency have been demonstrated in triathletes. Whilst the ACE genotype is associated with overall performance ability, at a single organ level, the ACE genotype and related polymorphism have significant associations. In cardiac muscle, ACE genotype has associations with left ventricular mass changes in response to stimulus, in both the health and diseased states. The D allele is associated with an exaggerated response to training, and the I allele with the lowest cardiac growth response. In light of the I-allele association with endurance performance, it seems likely that other regulatory mechanisms exist. Similarly in skeletal muscle, the D allele is associated with greater strength gains in response to training, in both healthy individuals and chronic disease states. As in overall performance, those genetic polymorphisms related to the ACE genotype, such as the bradykinin 2 gene, also influence skeletal muscle strength. Finally, the ACE genotype may influence metabolic efficiency, and elite mountaineers have demonstrated an excess of I alleles and I/I genotype frequency in comparison to controls. Interestingly, this was not seen in amateur climbers. Corroboratory evidence exists among high-altitude settlements in both South America and India, where the I allele exists in greater frequency in those who migrated from the lowlands. Unfortunately, if the ACE genotype does influence metabolic efficiency, associations with peak maximal oxygen consumption have yet to be rigorously demonstrated. The ACE genotype is an important but single factor in the determinant of sporting phenotype. Much of the mechanisms underlying this remain unexplored despite 12 years of research. [ABSTRACT FROM AUTHOR]

Strength training (ST) has long been considered a promising intervention for reversing the loss of muscle function and the deterioration of muscle structure associated with advanced age but, until recently, the evidence was insufficient to support its role in the prevention or treatment of disease. In recent decades, there has been a long list of quality reviews examining the effects of ST on functional abilities and a few on risk factors for specific diseases, but none have provided a comprehensive assessment of ST as an intervention for a broad range of diseases. This review provides an overview of research addressing the effectiveness of ST as an intervention for the prevention or treatment of the adverse consequences of (i) aging muscle; (ii) the metabolic syndrome (MetS) and its components, i.e. insulin resistance, abdominal obesity, hyperlipidaemia and hypertension; (iii) fibromyalgia; (iv) rheumatoid arthritis; and (v) Alzheimer's disease. Collectively, these studies indicate that ST may serve as an effective countermeasure to some of the adverse consequences of the MetS, fibromyalgia and rheumatoid arthritis. Evidence in support of the hypothesis that ST reduces insulin resistance or improves insulin action comes both from indirect biomarkers, such as glycosylated haemoglobin (HbAlc), and insulin responses to oral glucose tolerance tests, as well as from more direct procedures such as hyperglycaemic and hyperinsulinaemic-euglycaemic clamp techniques. The evidence for the use of ST as a countermeasure of abdominal obesity is less convincing. Although some reports show statistically significant reductions in visceral fat, it is unclear if the magnitude of these changes are physiologically meaningful and if they are independent of dietary influences. The efficacy of ST as an intervention for reducing dyslipidaemia is at best inconsistent, particularly when compared with other pharmacological and non-pharmacological interventions, such as aerobic exercise training. However, there is more consistent evidence for the effectiveness of ST in reducing triglyceride levels. This finding could have clinical significance, given that elevated triglyceride is one of the five criterion measures for the diagnosis of the MetS. Small to moderate reductions in resting and exercise blood pressure have been reported with some indication that this effect may be genotype dependent. ST improves or reverses some of the adverse effects of fibromyalgia and rheumatoid arthritis, particularly pain, inflammation, muscle weakness and fatigue. Investigations are needed to determine how these effects compare with those elicited from aerobic exercise training and/or standard treatments. There is no evidence that ST can reverse any of the major biological or behavioural outcomes of Alzheimer's disease, but there is evidence that the prevalence of this disease is inversely associated with muscle mass and strength. Some indicators of cognitive function may also improve with ST. Thus, ST is an effective countermeasure for some of the adverse effects experienced by patients of many chronic diseases, as discussed in this review. [ABSTRACT FROM AUTHOR]

Recent publications by Emeritus Professor Roy Shephard propose that a "small group of investigators who have argued repeatedly (over the past 13 years) for a 'Central Governor'," should now either "Put up or shut up." Failing this, their 'hypothesis' should be 'consigned to the bottom draw for future reference'; but Professor Shephard's arguments are contradictory. Thus, in different sections of his article, Professor Shephard explains: why there is no need for a brain to regulate exercise performance; why there is no proof that the brain regulates exercise performance; and why the brain's proven role in the regulation of exercise performance is already so well established that additional comment and research is unnecessary. Hence, "The higher centres of an endurance athlete … call forth an initial effort … at a level where a minimal accumulation of lactate in the peripheral muscles is sensed." Furthermore, "a variety of standard texts have illustrated the many mutually redundant feedback loops (to the nervous system) that limit exercise." Yet, the figure from Professor Shephard's 1982 textbook does not contain any links between the nervous system, "many mutually redundant feedback loops" and skeletal muscle. This disproves his contradictory claims that although there is neither any need for, nor any proof of, any role of the brain in the regulation of exercise performance, the physiological mechanisms for this (non-existent) control were already well established in 1982. In contrast, the Central Governor Model (CGM) developed by our "small group … in a single laboratory" after 1998, provides a simple and unique explanation of how 'redundant feedback loops' can assist in the regulation of exercise behaviour. In this rebuttal to his article, I identify (i) the numerous contradictions included in Professor Shephard's argument; (ii) the real meaning of the facts that he presents; (iii) the importance of the evidence that he ignores; and (iv) the different philosophies of how science should be conducted according to either the Kuhnian or the Popperian philosophies of scientific discovery. My conclusion is that the dominance of an authoritarian Kuhnian philosophy, which refuses to admit genuine error or "the need to alter one's course of belief or action," explains why there is little appetite in the exercise sciences for the acceptance of genuinely novel ideas such as the CGM. Furthermore, to advance the case for the CGM, I now include evidence from more than 30 studies, which, in my opinion, can only be interpreted according to a model of exercise regulation where the CNS, acting in an anticipatory manner, regulates the exercise behaviour by altering skeletal muscle recruitment, specifically to ensure that homeostasis is maintained during exercise. Since few, if any, of those studies can be explained by the 'brainless' A.V. Hill Cardiovascular Model on which Professor Shephard bases his arguments, I argue that it is now the appropriate time to retire that model. Perhaps this will bring to an end the charade that holds either (i) that the brain plays no part in the regulation of exercise performance; or, conversely, (ii) that the role of the brain is already so well defined that further research by other scientists is unnecessary. However, this cannot occur in a discipline that is dominated by an authoritarian Kuhnian philosophy. [ABSTRACT FROM AUTHOR]

The aim of this review is to highlight two emerging concepts for the elite athlete using the resistance-training model: (i) the short-term effects of testosterone (T) and cortisol (C) on the neuromuscular system; and (ii) the dose-response training role of these endogenous hormones. Exogenous evidence confirms that T and C can regulate long-term changes in muscle growth and performance, especially with resistance training. This evidence also confirms that changes in T or C concentrations can moderate or support neuromuscular performance through various short-term mechanisms (e.g. second messengers, lipid/protein pathways, neuronal activity, behaviour, cognition, motor-system function, muscle properties and energy metabolism). The possibility of dual T and C effects on the neuromuscular system offers a new paradigm for understanding resistance-training performance and adaptations. Endogenous evidence supports the short-term T and C effects on human performance. Several factors (e.g. workout design, nutrition, genetics, training status and type) can acutely modify T and/or C concentrations and thereby potentially influence resistance-training performance and the adaptive outcomes. This novel short-term pathway appears to be more prominent in athletes (vs non-athletes), possibly due to the training of the neuromuscular and endocrine systems. However, the exact contribution of these endogenous hormones to the training process is still unclear. Research also confirms a dose-response training role for basal changes in endogenous T and C, again, especially for elite athletes. Although full proof within the physiological range is lacking, this athlete model reconciles a proposed permissive role for endogenous hormones in untrained individuals. It is also clear that the steroid receptors (cell bound) mediate target tissue effects by adapting to exercise and training, but the response patterns of the membrane-bound receptors remain highly speculative. This information provides a new perspective for examining, interpreting and utilizing T and C within the elite sporting environment. For example, individual hormonal data may be used to better prescribe resistance exercise and training programmes or to assess the trainability of elite athletes. Possible strategies for acutely modifying the hormonal milieu and, thereafter, the performance/training outcomes were also identified (see above). The limitations and challenges associated with the analysis and interpretation of hormonal research in sport (e.g. procedural issues, analytical methods, research design) were another discussion point. Finally, this review highlights the need for more experimental research on humans, in particular athletes, to specifically address the concept of dual steroid effects on the neuromuscular system. [ABSTRACT FROM AUTHOR]

This series of reviews focuses on the most important neuromuscular function in many sport performances, the ability to generate maximal muscular power. Part 1 focuses on the factors that affect maximal power production, while part 2, which will follow in a forthcoming edition of Sports Medicine, explores the practical application of these findings by reviewing the scientific literature relevant to the development of training programmes that-most effectively enhance maximal power production. The ability of the neuromuscular system to generate maximal power is affected by a range of interrelated factors. Maximal muscular power is defined and limited by the force-velocity relationship and affected by the length-tension relationship. The ability to generate maximal power is influenced by the type of muscle action involved and, in particular, the time available to develop force, storage and utilization of elastic energy, interactions of contractile and elastic elements, potentiation of contractile and elastic filaments as well as stretch reflexes. Furthermore, maximal power production is influenced by morphological factors including fibre type contribution to whole muscle area, muscle architectural features and tendon properties as well as neural factors including motor unit recruitment, firing frequency, synchronization and intermuscular coordination. In addition, acute changes in the muscle environment (i.e. alterations resulting from fatigue, changes in hormone milieu and muscle temperature) impact the ability to generate maximal power. Resistance training has been shown to impact each of these neuromuscular factors in quite specific ways. Therefore, an understanding of the biological basis of maximal power production is essential for developing training programmes that effectively enhance maximal power production in the human. [ABSTRACT FROM AUTHOR]

Testosterone is one of the most potent naturally secreted androgenic-anabolic hormones, and its biological effects include promotion of muscle growth. In muscle, testosterone stimulates protein synthesis (anabolic effect) and inhibits protein degradation (anti-catabolic effect); combined, these effects account for the promotion of muscle hypertrophy by testosterone. These physiological signals from testosterone are modulated through the interaction of testosterone with the intracellular androgen receptor (AR). Testosterone is important for the desired adaptations to resistance exercise and training; in fact, testosterone is considered the major promoter of muscle growth and subsequent increase in muscle strength in response to resistance training in men. The acute endocrine response to a bout of heavy resistance exercise generally includes increased secretion of various catabolic (breakdown-related) and anabolic (growth-related) hormones including testosterone. The response of testosterone and AR to resistance exercise is largely determined by upper regulatory elements including the acute exercise programme variable domains, sex and age. In general, testosterone concentration is elevated directly following heavy resistance exercise in men. Findings on the testosterone response in women are equivocal with both increases and no changes observed in response to a bout of heavy resistance exercise. Age also significantly affects circulating testosterone concentrations. Until puberty, children do not experience an acute increase in testosterone from a bout of resistance exercise; after puberty some acute increases in testosterone from resistance exercise can be found in boys but not in girls. Aging beyond 35-40 years is associated with a 1-3% decline per year in circulating testosterone concentration in men; this decline eventually results in the condition known as andropause. Similarly, aging results in a reduced acute testosterone response to resistance exercise in men. In women, circulating testosterone concentration also gradually declines until menopause, after which a drastic reduction is found. In summary, testosterone is an important modulator of muscle mass in both men and women and acute increases in testosterone can be induced by resistance exercise. In general, the variables within the acute programme variable domains must be selected such that the resistance exercise session contains high volume and metabolic demand in order to induce an acute testosterone response. [ABSTRACT FROM AUTHOR]

Bone density and bone mass are commonly regarded as the essential parameters to describe fracture risk in osteology. Because fractures primarily depend on bone strength and secondarily on bone mass and density, bone strength should be the main parameter to describe fracture risk. The quantitative description of bone strength has the prerequisite that bone geometry is assessed despite bone density. Thus, volumetric osteodensitometric methods should be preferred, which enable the physician to evaluate parameters primarily associated with bone modeling or remodeling. Modeling describes the adaptation of bone geometry to applied muscular forces in contrast to remodeling representing bone turnover. The adaptation of bone geometry to muscle forces led to the term functional muscle-bone unit, which enables the physician to differentiate between primary and secondary bone diseases. Primary bone diseases are characterized by a defective adaptation of bone to muscle forces in contrast to secondary bone diseases, which are primary diseases of the neuromuscular system. Because muscle forces are essential in the feedback loop of bone adaptation to forces (mechanostat), the assessment of muscle function has become an essential part of osteologic diagnostics in pediatrics. Dynamometric and mechanographic methods have been introduced to properly characterize kinetic aspects of muscle function in children and adolescents. Therefore, emphasis should be put on the assessment of muscle function despite the evaluation of osteodensitometric parameters in pediatric osteology. [ABSTRACT FROM AUTHOR]

Plyometric training (PLY) is a very popular form of physical conditioning of healthy individuals that has been extensively studied over the last 3 decades. In this article, we critically review the available literature related to lower-body PLY and its effects on human neural and musculoskeletal systems, athletic performance and injury prevention. We also considered studies that combined lower-body PLY with other popular training modalities, as well as studies that applied PLY on non-rigid surfaces. The available evidence suggests that PLY, either alone or in combination with other typical training modalities, elicits numerous positive changes in the neural and musculoskeletal systems, muscle function and athletic performance of healthy individuals. Specifically, the studies have shown that long-term PLY (i.e. 3-5 sessions a week for 5-12 months) represents an effective training method for enhancing bone mass in prepubertal/early pubertal children, young women and premenopausal women. Furthermore, short-term PLY (i.e. 2-3 sessions a week for 6-15 weeks) can change the stiffness of various elastic components of the muscle-tendon complex of plantar flexors in both athletes and non-athletes. Short-term PLY also improves the lower-extremity strength, power and stretch-shortening cycle (SSC) muscle function in healthy individuals. These adaptive changes in neuromuscular function are likely the result of (i) an increased neural drive to the agonist muscles; (ii) changes in the muscle activation strategies (i.e. improved intermuscular coordination); (iii) changes in the mechanical characteristics of the muscle-tendon complex of plantar flexors; (iv) changes in muscle size and/or architecture; and (v) changes in single-fibre mechanics. Our results also show that PLY, either alone or in combination with other training modalities, has the potential to (i) enhance a wide range of athletic performance (i.e. jumping, sprinting, agility and endurance performance) in children and young adults of both sexes; and (ii) to reduce the risk of lower-extremity injuries in female athletes. Finally, available evidence suggests that short-term PLY on non-rigid surfaces (i.e. aquatic- or sand-based PLY) could elicit similar increases in jumping and sprinting performance as traditional PLY, but with substantially less muscle soreness. Although many issues related to PLY remain to be resolved, the results of this review allow us to recommend the use of PLY as a safe and effective training modality for improving lower-extremity muscle function and functional performance of healthy individuals. For performance enhancement and injury prevention in competitive sports, we recommend an implementation of PLY into a well designed, sport-specific physical conditioning programme. [ABSTRACT FROM AUTHOR]

ADP is generally accepted as a key regulator of oxygen consumption both in isolated mitochondria and in permeabilized fibers from skeletal muscle. The present study explored inorganic phosphate in a similar regulatory role. Saponin permeabilized fibers and isolated mitochondria from type-I and type-II muscle from male Wistar rats were prepared. Respiration was measured while the medium P(i) concentration was gradually increased. The apparent K(m) values for P(i) were 607 +/- 17 microM and 405 +/- 15 microM (P < 0.0001) for type-I and type-II fibers, respectively. For isolated mitochondria the values were significantly lower than type-1 permeabilized fibers, 338 +/- 130 microM and 235 +/- 30 microM (P < 0.05), but not different with respect to fiber type. The reason for this difference in K(m) values in the permeabilized muscle is unknown, but a similar pattern has been observed for K(m) of ADP. Our data indicate that phosphate may play a role in regulation of oxygen consumption in vitro and in vivo. [ABSTRACT FROM AUTHOR]