Creatine supplementation affects sprint endurance in juvenile rainbow trout

Fingerling rainbow trout were supplemented with equal amounts of creatine (Cr) by two routes: dietary (12.5 mg Cr per g food); or intraperitoneal injection (0.5 mg Cr per g fish). Endurance in a fixed velocity sprint test (at a speed of 7 BL s(-1)), and resting levels of white muscle metabolites (total creatine [a measure of free creatine plus phosphocreatine (PCr), ATP, lactate and glycogen] were assessed following 7 days of supplementation and compared to controls. None of the treatments had a significant effect on growth, muscle total creatine, percent phosphorylation of creatine, ATP or lactate. However, resting muscle glycogen was elevated in creatine-supplemented fish. Higher muscle glycogen corresponded to significantly greater endurance in creatine-supplemented fish. Although fish do not actively transport additional creatine into the muscle, a mechanism whereby circulating creatine acts to enhance muscle glycogen is present. These results suggest that the improved endurance may be due to an insulin-dependent mechanism (similar to that elucidated in mammalian studies) that allows fish to supercompensate muscle glycogen stores, thus extending endurance through enhanced glycolytic flux.     

How important is endogenous muscle glycogen to fatigue in prolonged exercise?

Endogenous muscle glycogen represents a primary fuel source during large muscle group activity in the human. The depletion of this fuel source during submaximal exercise at intensities ranging between 60 and 85% of maximal aerobic power (Vo2max) is widely believed to be the cause of an inability to sustain exercise. Alterations of preexercise muscle glycogen reserves by dietary and exercise manipulations and changing the degree of dependency on endogenous glycogen during exercise by modifying the availability of other fuel sources have in general served to establish a close relationship between muscle glycogen and fatigue resistance. However, in spite of the evidence implicating glycogen depletion to fatigue, the mechanism remains elusive. The most popular theory is that glycogen is an essential substrate, the depletion of which results in a reduction in the rate of ATP regeneration and an inability to maintain energy supply to one or more of the processes involved in excitation and contraction in the muscle. As a consequence, the muscle is unable to translate the motor drive into an expected force and fatigue develops. However, there is little experimental evidence to support this theory. Most studies report no or only minimal changes in ATP concentration at fatigue with low glycogen and no further change in the by-products of ATP hydrolysis. These findings suggest that fatigue might be caused by other nonmetabolic factors. This review examines these other nonmetabolic factors and analyzes their potential role in fatigue during prolonged exercise with depletion of muscle glycogen reserves.     

Muscle fatigue in McArdle's disease studied by 31P-NMR: effect of glucose infusion

In muscle phosphorylase deficiency (McArdle's disease) there is an abnormally rapid fatigue during strenuous exercise. Increasing substrate availability to working muscle can improve exercise tolerance but the effect on muscle energy metabolism has not been studied. Using phosphorus-31 nuclear magnetic resonance (31P-NMR) we examined forearm muscle ATP, phosphocreatine (PCr), inorganic phosphate (Pi) and pH in a McArdle patient (MP) and two healthy subjects (HS) at rest and during intermittent maximal effort handgrip contractions under control conditions (CC) and during intravenous glucose infusion (GI). Under CC, MP gripped to impending forearm muscle contracture in 130 s with a marked decline in muscle PCr and a dramatic elevation in Pi. During GI, MP exercised easily for greater than 420 s at higher tensions and with attenuated PCr depletion and Pi accumulation. In HS, muscle PCr and Pi changed more modestly and were not affected by GI. In MP and HS, ATP changed little or not at all with exercise. The results suggest that alterations in the levels of muscle PCr and Pi but not ATP are involved in the muscle fatigue in McArdle's disease and the improved exercise performance during glucose infusion.     

Increased intramyocellular lipids but unaltered in vivo mitochondrial oxidative phosphorylation in skeletal muscle of adipose triglyceride lipase-deficient mice

Adipose triglyceride lipase (ATGL) is a lipolytic enzyme that is highly specific for triglyceride hydrolysis. The ATGL-knockout mouse (ATGL(-/-)) accumulates lipid droplets in various tissues, including skeletal muscle, and has poor maximal running velocity and endurance capacity. In this study, we tested whether abnormal lipid accumulation in skeletal muscle impairs mitochondrial oxidative phosphorylation, and hence, explains the poor muscle performance of ATGL(-/-) mice. In vivo 1H magnetic resonance spectroscopy of the tibialis anterior of ATGL(-/-) mice revealed that its intramyocellular lipid pool is approximately sixfold higher than in WT controls (P = 0.0007). In skeletal muscle of ATGL(-/-) mice, glycogen content was decreased by 30% (P < 0.05). In vivo 31P magnetic resonance spectra of resting muscles showed that WT and ATGL(-/-) mice have a similar energy status: [PCr], [P(i)], PCr/ATP ratio, PCr/P(i) ratio, and intracellular pH. Electrostimulated muscles from WT and ATGL(-/-) mice showed the same PCr depletion and pH reduction. Moreover, the monoexponential fitting of the PCr recovery curve yielded similar PCr recovery times (τPCr; 54.1 ± 6.1 s for the ATGL(-/-) and 58.1 ± 5.8 s for the WT), which means that overall muscular mitochondrial oxidative capacity was comparable between the genotypes. Despite similar in vivo mitochondrial oxidative capacities, the electrostimulated muscles from ATGL(-/-) mice displayed significantly lower force production and increased muscle relaxation time than the WT. These findings suggest that mechanisms other than mitochondrial dysfunction cause the impaired muscle performance of ATGL(-/-) mice.     

Skeletal muscle energy metabolism during prolonged, fatiguing exercise.

A depletion of phosphocreatine (PCr), fall in the total adenine nucleotide pool (TAN = ATP + ADP + AMP), and increase in TAN degradation products inosine 5'-monophosphate (IMP) and hypoxanthine are observed at fatigue during prolonged exercise at 70% maximal O(2) uptake in untrained subjects [J. Baldwin, R. J. Snow, M. F. Carey, and M. A. Febbraio. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R295-R300, 1999]. The present study aimed to examine whether these metabolic changes are also prevalent when exercise is performed below the blood lactate threshold (LT). Six healthy, untrained humans exercised on a cycle ergometer to voluntary exhaustion at an intensity equivalent to 93 +/- 3% of LT ( approximately 65% peak O(2) uptake). Muscle biopsy samples were obtained at rest, at 10 min of exercise, approximately 40 min before fatigue (F-40 =143 +/- 13 min), and at fatigue (F = 186 +/- 31 min). Glycogen concentration progressively declined (P < 0.01) to very low levels at fatigue (28 +/- 6 mmol glucosyl U/kg dry wt). Despite this, PCr content was not different when F-40 was compared with F and was only reduced by 40% when F was compared with rest (52. 8 +/- 3.7 vs. 87.8 +/- 2.0 mmol/kg dry wt; P < 0.01). In addition, TAN concentration was not reduced, IMP did not increase significantly throughout exercise, and hypoxanthine was not detected in any muscle samples. A significant correlation (r = 0.95; P < 0. 05) was observed between exercise time and glycogen use, indicating that glycogen availability is a limiting factor during prolonged exercise below LT. However, because TAN was not reduced, PCr was not depleted, and no correlation was observed between glycogen content and IMP when glycogen stores were compromised, fatigue may be related to processes other than those involved in muscle high-energy phosphagen metabolism.     

Metabolic recovery in herring larvae following strenuous activity

Larvae of spring spawning Clyde herring Clupea harengus L. were reared at 5 and 12° C. Metabolism following burst swimming was studied in 7-day-old larvae at their respective rearing temperatures. Escape responses were repeatedly elicited using tactile stimulation for a period of 3 min. Larval herring were hard to fatigue and still responded to tactile stimuli after 3 min. Whole larvae were freeze-quenched in liquid nitrogen, either immediately after exercise, or after periods of recovery of up to 24 h. Samples were freeze-dried and analysed for whole body creatine (Cr), phosphocreatine (PCr), ATP, ADP, AMP, lactate, glucose, and glycogen using high performance liquid chromatography and enzymatic methods. The exercise regime resulted in a marked decrease in PCr, ATP and glycogen concentrations and an increase in creatine, glucose and lactate concentrations whereas there was no significant change in either AMP or ADP concentrations. The extent of phosphagen hydrolysis (approx. 110 to 15μmol PCr g ⁻¹ dry body mass) and lactate accumulation (approx. 7 to 40 μmol lactate g⁻¹ dry body mass) over the exercise period was similar at the two temperatures, consistent with a relatively constant degree of effort. The rates of recovery of PCr and ATP were essentially the same at 5 and 12° C; returning to resting levels after approximately 30 min. Lactate and glycogen concentrations were restored 60 min after exercise at both temperatures. Maximum lactate clearance rates (1.2 μmol min ⁻¹ g ⁻¹ wet muscle mass) were an order of magnitude faster than reported for adult fish in the literature.     

The Recovery of Repeated-Sprint Exercise Is Associated with PCr Resynthesis,while Muscle pH and EMG Amplitude Remain Depressed

The physiological equivalents of power output maintenance and recovery during repeated-sprint exercise (RSE) remain to be fully elucidated. In an attempt to improve our understanding of the determinants of RSE performance we therefore aimed to determine its recovery following exhaustive exercise (which affected intramuscular and neural factors) concomitantly with those of intramuscular concentrations of adenosine triphosphate [ATP], phosphocreatine [PCr] and pH values and electromyography (EMG) activity (a proxy for net motor unit activity) changes. Eight young men performed 10, 6-s all-out sprints on a cycle ergometer, interspersed with 30 s of recovery, followed, after 6 min of passive recovery, by five 6-s sprints, again interspersed by 30 s of passive recovery. Biopsies of the vastus lateralis were obtained at rest, immediately after the first 10 sprints and after 6 min of recovery. EMG activity of the vastus lateralis was obtained from surface electrodes throughout exercise. Total work (TW), [ATP], [PCr], pH and EMG amplitude decreased significantly throughout the first ten sprints (P<0.05). After 6 min of recovery, TW during sprint 11 recovered to 86.3±7.7% of sprint 1. ATP and PCr were resynthesized to 92.6±6.0% and 85.3±10.3% of the resting value, respectively, but muscle pH and EMG amplitude remained depressed. PCr resynthesis was correlated with TW done in sprint 11 (r = 0.79, P<0.05) and TW done during sprints 11 to 15 (r = 0.67, P<0.05). There was a ∼2-fold greater decrease in the TW/EMG ratio in the last five sprints (sprint 11 to 15) than in the first five sprints (sprint 1 to 5) resulting in a disproportionate decrease in mechanical power (i.e., TW) in relation to EMG. Thus, we conclude that the inability to produce power output during repeated sprints is mostly mediated by intramuscular fatigue signals probably related with the control of PCr metabolism.     

A study of the swimming performance of the Crucian carp Carassius carassius (L.) in relation to the effects of exercise and recovery on biochemical changes in the myotomal muscles and liver

A study has been made of the maximum sustained swimming speed of Crucian carp Carassius carassius (L.) using a fixed velocity technique. The data obtained from swimming tests on 214 carp have been analysed using the method of probit analysis. The 50% fatigue level for 13–16 cm fish acclimated to 9.5±0.6°C has been estimated to be 3.35 lengths/sec. Biochemical measurements have been made on the red and white myotomal muscles and liver of fish subjected to both varying intensities of sustained swimming and short periods of vigorous swimming. Free creatine was found to increase only during high speed swimming in the white muscle. Elevated lactate concentrations occurred at both low and high sustained swimming speeds in the red superficial muscle but not during short periods of strenuous exercise. Glycogen depletion from the red musculature also only took place at the sustained swimming speeds investigated. The reverse situation was operative in the white muscle, significant glycogen depletion occurring only at the highest swimming speed studied. Lactate levels were only significantly different from non-exercised fish in the fish swimming at the higher velocities. The effects of periods of recovery following 200 min of sustained swimming were also investigated. White muscle lactate was at a higher level than non-exercise fish 5 h post-exercise, while both red muscle glycogen and lactate rapidly returned to pre-exercise concentrations. Biochemical measurements on the myotomal muscle types have been discussed in relation to the swimming performance of the fish and the division of labour between red and white fibres.     

Metabolic factors limiting performance in marathon runners

Each year in the past three decades has seen hundreds of thousands of runners register to run a major marathon. Of those who attempt to race over the marathon distance of 26 miles and 385 yards (42.195 kilometers), more than two-fifths experience severe and performance-limiting depletion of physiologic carbohydrate reserves (a phenomenon known as 'hitting the wall'), and thousands drop out before reaching the finish lines (approximately 1-2% of those who start). Analyses of endurance physiology have often either used coarse approximations to suggest that human glycogen reserves are insufficient to fuel a marathon (making 'hitting the wall' seem inevitable), or implied that maximal glycogen loading is required in order to complete a marathon without 'hitting the wall.' The present computational study demonstrates that the energetic constraints on endurance runners are more subtle, and depend on several physiologic variables including the muscle mass distribution, liver and muscle glycogen densities, and running speed (exercise intensity as a fraction of aerobic capacity) of individual runners, in personalized but nevertheless quantifiable and predictable ways. The analytic approach presented here is used to estimate the distance at which runners will exhaust their glycogen stores as a function of running intensity. In so doing it also provides a basis for guidelines ensuring the safety and optimizing the performance of endurance runners, both by setting personally appropriate paces and by prescribing midrace fueling requirements for avoiding 'the wall.' The present analysis also sheds physiologically principled light on important standards in marathon running that until now have remained empirically defined: The qualifying times for the Boston Marathon.     

Human muscle fatigue after glycogen depletion: a 31P magnetic resonance study.

To differentiate the effects of high energy phosphates, pH, and [H2PO4-] on skeletal muscle fatigue, intracellular acidosis during handgrip exercise was attenuated by prolonged submaximal exercise. Healthy human subjects (n = 6) performed 5-min bouts of maximal rhythmic handgrip (RHG) before (CONTROL) and after prolonged (60-min) handgrip exercise (ATTEN-EX) designed to attenuate lactic acidosis in active muscle by partially depleting muscle glycogen. Concentrations of free intracellular phosphocreatine ([PCr]), adenosine triphosphate ([ATP]), and orthophosphate ([P(i)]) and pH were measured by 31P nuclear magnetic resonance spectroscopy and used to calculate adenosine diphosphate [ADP], [H2PO4-], and [HPO4(2-)]. Handgrip force output was measured with a dynamometer, and fatigue was determined by loss of maximal contractile force. After ATTEN-EX, the normal exercise-induced muscle acidosis was reduced. At peak CONTROL RHG, pH fell to 6.3 +/- 0.1 (SE) and muscle fatigue was correlated with [PCr] (r = 0.83), [P(i)] (r = 0.82), and [H2PO4-] (r = 0.81); [ADP] was 22.0 +/- 5.7 mumol/kg. At peak RHG after ATTEN-EX, pH was 6.9 +/- 0.1 and [ADP] was 116.1 +/- 18.2 mumol/kg, although [PCr] and [P(i)] were not different from CONTROL RHG (P greater than 0.05). After ATTEN-EX, fatigue correlated most closely with [ADP] (r = 0.84). The data indicate that skeletal muscle fatigue 1) is multifactorial, 2) can occur without decreased pH or increased [H2PO4-], and 3) is correlated with [ADP] after exercise-induced glycogen depletion.     

The analysis of metabolites in rainbow trout white muscle: a comparison of different sampling and processing methods

We have investigated the effects of different sampling and processing methods on metabolite concentrations [glycogen (Gly), glucose (Glu), lactate (Lac), pyruvate (Pyr), ammonia (Amm), creatine phosphate (PCr), creatine (Cr), and adenosine triphosphate (ATP)] measured in white muscle of rainbow trout at rest and immediately after exhaustive exercise. When samples were taken from resting fish by rapid needle biopsy (without anaesthesia), direct freezing of the needles in liquid N₂ yielded lower Lac and Glu levels than if the muscle cores were quickly blown out into liquid N₂. However, killing of the fish by an overdose of MS-222 followed by freeze-clamping of excised muscle was superior to the biopsy method in preserving high levels of PCr and Gly (91 and 62% higher, respectively). In parallel, the MS-222 method also yielded lower levels of Amm (80%) and Lac (47%). Samples freeze-clamped by the MS-222 method were used to evaluate three methods of subsequent processing for enzymatic analysis of metabolites: classic glass homogenization (GH) in 8% perchloric acid (PCA) c. mortar and pestle (MP) pulverization or freeze-drying (FD) prior to PCA extraction. For all metabolites, GH and MP methods produced similar values. However, the FD technique yielded 20% higher PCr levels which represented over 80% phosphorylation of the total Cr pool at rest, the highest ever reported via enzymatic analysis. Glu was also higher by FD, bul Gly, Lac, and ATP were not affected. Indeed ATP was relatively stable throughout all sampling and processing procedures. MP, GH, MP&GH combination, and high speed motor driven grinding techniques all yielded similar Amm levels in resting muscle. However, tests demonstrated that even brief thawing of tissue greatly elevated Amm, while FD resulted in artificially low Amm values due to evaporative losses during lyophilization. Overall, muscle sampling by freeze-clamping on trout killed by MS-222 overdose, followed by FD prior to PCA extraction, appears to be the best combination for the measurement of all white muscle metabolites except Amm, for which MP or GH are preferable.     

Reduced volume but increased training intensity elevates muscle Na+-K+ pump alpha1-subunit and NHE1 expression as well as short-term work capacity in humans

The present study examined muscle adaptations and alterations in work capacity in endurance-trained runners after a change from endurance to sprint training. Fifteen runners were assigned to either a sprint training (ST, n = 8) or a control (CON, n = 7) group. ST replaced their normal training by 30-s sprint runs three to four times a week, whereas CON continued the endurance training (approximately 45 km/wk). After the 4-wk sprint period, the expression of the muscle Na+-K+ pump alpha1-subunit and Na+/H+-exchanger isoform 1 was 29 and 30% higher (P < 0.05), respectively. Furthermore, plasma K+ concentration was reduced (P < 0.05) during repeated intense running. In ST, performance in a 30-s sprint test, Yo-Yo intermittent recovery test, and two supramaximal exhaustive runs was improved (P < 0.05) by 7, 19, 27, and 19%, respectively, after the sprint training period, whereas pulmonary maximum oxygen uptake and 10-k time were unchanged. No changes in CON were observed. The present data suggest a role of the Na+-K+ pump in the control of K+ homeostasis and in the development of fatigue during repeated high-intensity exercise. Furthermore, performance during intense exercise can be improved and endurance performance maintained even with a reduction in training volume if the intensity of training is very high.     

Metabolic correlates of fatigue and of recovery from fatigue in single frog muscle fibers

Fatigue and recovery from fatigue were related to metabolism in single fibers of the frog semitendinosus muscle. The fibers were held at a sarcomere length of 2.3 microm in oxygenated Ringer solution at 15 degrees C and were stimulated for up to 150 s by a schedule of 10-s, 20-Hz tetanic trains that were interrupted by 1-s rest periods, after which they were rapidly frozen for biochemical analysis. Two kinds of fatigue were produced in relation to stimulus duration. A rapidly reversed fatigue occurred with stimulation for under 40 s and was evidenced by a decline in tetanic tension that could be overcome by 1 s of rest. A prolonged fatigue was caused by stimulation for 100-150 s. It was evidenced during stimulation by a fall in tetanic tension that could not be overcome by 1 s of rest, and after stimulation by a reduction, lasting for up to 82 min, in the peak tension of a 200-ms test tetanus. Fiber phosphocreatine (PCr) fell logarithmically in relation to stimulus duration, from a mean of 121 +/- 8 nmol/mg protein (SEM, n = 12) to 10% of this value after 150 s of stimulation. PCr returned to normal levels after 90-120 min of rest. Stimulation for 150 s did not significantly affect fiber glycogen and reduced fiber ATP by at most 15%. It is suggested that the prolonged fatigue caused by 100-150 s of tetanic stimulation was caused by long-lasting failure of excitation-contraction coupling, as it was not accompanied by depletion of energy stores in the form of ATP. One possibility is that H+ accumulated in fatigued fibers so as to interfere with the action of Ca2+ in the coupling process.     

水流速度对黑鲷和美国红鱼续航游泳能力及生理代谢的影响

为了确保黑鲷(Acanthopagrus schlegeli)和美国红鱼(Sciaenops ocellatus)在开放海域的养殖产量和鱼类养殖福利,在20℃下,对体长差异性不显著(P>0.05)的两种鱼进行续航游泳能力测试。首先,确定不同流速下的耐力游泳时间,然后选择耐力游泳时间为150min时的速度进行续航游泳实验。其中黑鲷和美国红鱼分别被迫以3.15和4.32 BL/s的恒定游泳速度,进行0、30min、60min、90min、120min和150min的测试,解剖鱼获得肌肉、血液和肝脏,测定样品在6个时间点的代谢物浓度,每个时间点保证3组有效数据。对0和150min的实验组对比,结果显示,两种鱼肝糖原、背肌乳酸和血糖浓度差异显著(P<0.05),肌肉糖原浓度差异不显著(P>0.05)。双变量相关分析显示,随着疲劳程度增加,肝糖原浓度下降,背肌乳酸和血糖上升。灰度关联分析和主成分分析显示,血糖和肝糖原浓度是影响疲劳的主要因素,但黑鲷相比美国红鱼,其浓度变化范围更大。综上:(1)美国红鱼比黑鲷拥有更强的游泳能力,而且黑鲷和美国红鱼不适合养殖在流速超过3.15和4....     

Effect of various doses of cocaine on endurance capacity in rats

To determine the effects of a variety of doses of cocaine on endurance capacity, rats were injected intraperitoneally with either 0.1, 0.5, 2.5, 12.5, or 20 mg/kg body wt 20 min before running to exhaustion at 26 m/min up a 10% grade. Animals given saline ran 116 +/- 9 (SE) min. At doses of 12.5 and 20 mg/kg, cocaine reduced endurance time significantly (34 and 74%, respectively). At rest the drug had no effect on liver or fast-twitch muscle glycogen but significantly reduced (20-40%) soleus glycogen at the two highest doses. However, at exhaustion, the quantity of glycogen depleted in the fast-twitch red and white vastus muscles was similar in all groups despite the reduced run times of the animals receiving a higher dose implying a greater rate of glycogenolysis due to cocaine. Blood lactate in the 20 mg/kg group (9.9 +/- 1.2 mM) at exhaustion was nearly twice that of the saline controls at exhaustion (5.1 +/- 0.6). Before exercise plasma norepinephrine (at doses of 2.5, 12.5 and 20 mg/kg) was higher than saline controls and remained higher (20 mg/kg groups) at exhaustion. We conclude that high doses of cocaine cause rapid muscle glycogen depletion and early fatigue. The mechanism by which cocaine causes these effects is not clear.     

狗在运动中的肌糖原消耗与无氧阈的关系

本实验测定了5条狗的无氧阈值,运动耐受时间、衰竭时的血乳酸浓度及运动中的肌糖原消耗量。结果如下:无氧阈值,1.与运动耐受时间呈正相关(r=0.947,P<0.02);2.与运动中肌糖原消耗量呈负相关(r=-0.959,P<0.01);3.与衰竭时的血乳酸浓度呈负相关(r=-0.942,P<0.02)。实验结果提示,无氧阈值是反映机体耐力的可靠指标。而运动中肌糖原消耗少,血乳酸积累程度轻,可能是无氧阈值之所以能够反映机体耐力的物质基础。     

Skeletal muscle metabolic and ionic adaptations during intense exercise following sprint training in humans.

The effects of sprint training on muscle metabolism and ion regulation during intense exercise remain controversial. We employed a rigorous methodological approach, contrasting these responses during exercise to exhaustion and during identical work before and after training. Seven untrained men undertook 7 wk of sprint training. Subjects cycled to exhaustion at 130% pretraining peak oxygen uptake before (PreExh) and after training (PostExh), as well as performing another posttraining test identical to PreExh (PostMatch). Biopsies were taken at rest and immediately postexercise. After training in PostMatch, muscle and plasma lactate (Lac(-)) and H(+) concentrations, anaerobic ATP production rate, glycogen and ATP degradation, IMP accumulation, and peak plasma K(+) and norepinephrine concentrations were reduced (P<0.05). In PostExh, time to exhaustion was 21% greater than PreExh (P<0.001); however, muscle Lac(-) accumulation was unchanged; muscle H(+) concentration, ATP degradation, IMP accumulation, and anaerobic ATP production rate were reduced; and plasma Lac(-), norepinephrine, and H(+) concentrations were higher (P<0.05). Sprint training resulted in reduced anaerobic ATP generation during intense exercise, suggesting that aerobic metabolism was enhanced, which may allow increased time to fatigue.     

Glycogen as a fuel: metabolic interaction between glycogen and ATP catabolism in oxygen-independent muscle contraction

The main role of muscular oxygen-independent glycolysis, starting from glycogen as the initial substrate, is the production of three ATP molecules from ADP and P_i per glucosyl moiety transformed into two lactate molecules. During this catabolic process not only there is no proton release, but one proton is consumed. Metabolic acidosis occurs because the three ATP molecules are immediately hydrolysed by myosin ATPase back to 3P_i and 3ADP, to sustain contraction. As a consequence of this ATP turnover, the ATP pool (~5?mmol?kg^?1 wet weight) should remain constant. However, a bulk of experimental evidence has clearly shown that depletion of the muscular ATP pool, and accumulation of ATP catabolites occur even during short sprint bouts. In the present article the interrelationship between glycogen and ATP catabolism in anaerobic contracting muscle is discussed. It is shown how myosin ATPase plays a role not only in the mechanisms of ATP recycling through glycogen anaerobic catabolism, but also in the process of ATP depletion.     

The effects of an acute temperature change on the metabolic recovery from exhaustive exercise in luvenile Atlantic salmon (Salmo salar)

This research examined the influence of acute changes of water temperature on the recovery processes following exhaustive exercise in juvenile Atlantic salmon (Salmo salar). White muscle phosphocreatine (PCr), ATP, lactate, glycogen, glucose, pyruvate, plasma lactate, and plasma osmolality were measured during rest and at 0, 1, 2, and 4 h following exhaustive exercise in fish acclimated and exercised at 12 degrees C and acutely exposed to either 6 degrees C or 18 degrees C water during recovery. An acute exposure to 6 degrees C water during the recovery period resulted in a severe reduction of metabolic recovery in salmon. However, metabolites such as muscle PCr and ATP and plasma lactate recovered very quickly (2-4 h) in fish acutely exposed to 18 degrees C during recovery. Overall, differences exist when postexercise metabolite levels are compared between acclimated fish and those fish acutely exposed to different water temperatures (either higher or lower). Taken together, the findings of the acute experiments suggest that at some point following exercise fish may seek warmer environments to speed the recovery process. However, the relationship between behavioural thermoregulation and recovery following exhaustive exercise in fish is not well understood.     

Effect of endurance and sprint exercise on the sensitivity of glucose metabolism to insulin in the epitrochlearis muscle of sedentary and trained rats

The effects of two types of acute exercise (1 h treadmill running at 20 m.min-1, or 6 x 10-s periods at 43 m.min-1, 0 degree inclination), as well as two training regimes (endurance and sprint) on the sensitivity of epitrochlearis muscle [fast twitch (FT) fibres] to insulin were measured in vitro in rats. The hormone concentration in the incubation medium producing the half maximal stimulation of lactate (la) production and glycogen synthesis was determined and used as an index of the muscle insulin sensitivity. A single period of moderate endurance as well as the sprint-type exercise increased the sensitivity of la production to insulin although the rate of la production enhanced markedly only after sprint exercise at 10 and 100 microU.ml-1 of insulin. These effects persisted for up to 2 h after the termination of exercise. Both types of exercise significantly decreased the muscle glycogen content, causing a moderate enhancement in the insulin-stimulated rates of glycogen synthesis in vitro for up to 2 h after exercise. However, a significant increase in the sensitivity of this process to insulin was found only in the muscle removed 0.25 h after the sprint effort. Training of the sprint and endurance types increased insulin-stimulated rates of glycolysis 24 h after the last period of exercise. The sensitivity of this process to insulin was also increased at this instant. Both types of training increased the basal and maximal rates of glycogen synthesis, as well as the sensitivity of this process to insulin at the 24th h following the last training session.(ABSTRACT TRUNCATED AT 250 WORDS)