The involvement of quadriceps femoris muscle portions and fibre type recruitment was studied during submaximal knee-extensor exercise without and with thigh occlusion (OCC) and compared with responses during intense exercise. Six healthy male subjects performed 90-s of moderate exercise without (MOD; 29 +/- 4 W) and with thigh OCC, and moderate exercise followed by 90-s of intense exercise (HI; 65 +/- 8 W). Temperatures were continuously measured in m. vastus lateralis (VL), vastus medialis (VM) and rectus femoris (RF) and successive muscle biopsies were obtained from VL. During MOD, muscle temperature increase (delta T(m)) in RF was 0.52 +/- 0.09 degrees C, which was 57% and 73% higher (P < 0.05) than in VL and VM, respectively. During OCC, delta T(m) in RF was 0.39 +/- 0.05 degrees C, which was not different from VM but 54% higher (P < 0.05) than in VL. After MOD, muscle CP in slow twitch (ST) and fast twitch (FT) fibres was 81% and 91% of resting levels, respectively, with lower (P < 0.05) values after OCC (15% and 22%) and HI (24% and 13%). After MOD, OCC and HI, a total of 48%, 93% and 96% of the ST fibres had CP levels below mean-1 SD, respectively, with corresponding values for FT fibres being 41%, 89% and 100%, respectively. In conclusion, a heterogeneous recruitment of the quadriceps muscle portions and muscle fibres was observed during submaximal knee-extensor exercise, whereas recruitment pattern was homogenous during intense exercise. Thigh OCC caused an altered recruitment of fibres and muscle portions, suggesting a significant afferent response affecting the activation of fibres in the contracting muscles.

Background:  After an ischemia time of 1 h during aortic aneurysm surgery, muscle glutathione redox‐status is not altered, indicating that this ischemic insult is well within the scavenging capacity of muscle glutathione, the most important endogenous scavenger. In the present study, the impact of elective aorto‐bifemoral bypass surgery, involving a longer ischemia time, on muscle glutathione and its redox‐status was investigated.

PURPOSE We tested the hypotheses that previous glycogen depletion of slow-twitch (ST) fibers enhances recruitment of fast-twitch (FT) fibers, elevates energy requirement, and results in a slow component of VO2 during moderate-intensity dynamic exercise in humans. METHODS Twelve healthy, male subjects cycled for 20 min at approximately 50% VO2max with normal glycogen stores (CON) and with exercise-induced glycogen depleted ST fibers (CHO-DEP). Pulmonary VO2 was measured continuously and single fiber, muscle homogenate, and blood metabolites were determined repeatedly during each trial. RESULTS ST fiber glycogen content decreased (P < 0.05) during CON (293 +/- 24 to 204 +/- 17 mmol x kg d.w.), but not during CHO-DEP (92 +/- 22 and 84 +/- 13 mmol x kg d.w.). FT fiber CP and glycogen levels were unaltered during CON, whereas FT fiber CP levels decreased (29 +/- 7%, P < 0.05) during CHO-DEP and glycogen content tended to decrease (32 +/- 14%, P = 0.07). During CHO-DEP, VO2 was higher (P < 0.05) from 2 to 20 min than in CON (0-20 min:7 +/- 1%). Muscle lactate, pH and temperature, ventilation, and plasma epinephrine were not different between trials. From 3 to 20 min of CHO-DEP, VO2 increased (P <0.05) by 5 +/- 1% from 1.95 +/- 0.05 to 2.06 +/- 0.08 L x min but was unchanged during CON. In this exercise period, muscle pH and blood lactate were unaltered in both trials. Exponential modeling revealed a slow component of VO2 equivalent to 0.12 +/- 0.04 L x min during CHO-DEP. CONCLUSION This study demonstrates that previous glycogen depletion of ST fibers enhances FT fiber recruitment, elevates O2 cost, and causes a slow component of VO2 during dynamic exercise with no blood lactate accumulation or muscular acidosis. These findings suggest that FT fiber recruitment elevates energy requirement of dynamic exercise in humans and support an important role of active FT fibers in producing the slow component of VO2

1. The role of phosphorylcreatine (PCr) and creatine (Cr) in the regulation of mitochondrial respiration was investigated in permeabilised fibre bundles prepared from human vastus lateralis muscle. 2. Fibre respiration was measured in the absence of ADP (V(0)) and after sequential additions of submaximal ADP (0.1 mM ADP, V(submax)), PCr (or Cr) and saturating [ADP] (V(max)). 3. V(submax) increased by 55 % after addition of saturating creatine (P < 0.01; n = 8) and half the maximal effect was obtained at 5 mM [Cr]. In contrast, V(submax) decreased by 54 % after addition of saturating phosphorylcreatine (P < 0.01; n = 8) and half the maximal effect was obtained at 1 mM [PCr]. V(max) was not affected by Cr or PCr. 4. V(submax) was similar when PCr and Cr were added simultaneously at concentrations similar to those in muscle at rest (PCr/Cr = 2) and at low-intensity exercise (PCr/Cr = 0.5). At conditions mimicking high-intensity exercise (PCr/Cr = 0.1), V(submax) increased to 60 % of V(max) (P < 0.01 vs. rest and low-intensity exercise). 5. Eight of the subjects participated in a 16 day Cr supplementation programme. Following Cr supplementation, V(0) decreased by 17 % (P < 0.01 vs. prior to Cr supplementation), whereas ADP-stimulated respiration (with and without Cr or PCr) was unchanged. 6. For the first time evidence is given that PCr is an important regulator of mitochondrial ADP-stimulated respiration. Phosphorylcreatine decreases the sensitivity of mitochondrial respiration to ADP whereas Cr has the opposite effect. During transition from rest to high-intensity exercise, decreases in the PCr/Cr ratio will effectively increase the sensitivity of mitochondrial respiration to ADP. The decrease in V(0) after Cr supplementation indicates that intrinsic changes in membrane proton conductance occur.

Background: The energy density of a nutrient drink is one of the main factors that affect the gastric emptying of the solution, while osmolality and viscosity are thought to have only a minimal influence. Method: The rate of gastric emptying of two isoenergetic carbohydrate solutions with different osmolality and viscosity was determined using a double sampling gastric aspiration technique. Six healthy male subjects were studied on two occasions using approximately 550 ml of a solution containing 13.5% of carbohydrate either in the form of a mixture of monomeric glucose and short chain glucose oligomers (G-drink) or of long chain glucose polymers composed of 78% amylopectin and 22% amylose (C-drink). Result: The half emptying time (t 1/2, median and range) for the viscous, markedly hypotonic (62 mosmol/kg) C-drink was faster (17.0 (6.2-31.4) min) than for the moderately hypertonic (336 mosmol/kg) G-drink (32.6 (25.2-40.7) min). The amount (median and range) of carbohydrate delivered to the small intestine was greater during the first 10 min after ingestion of C-drink (31.8 (15.8-55.9) g) than after ingestion of G-drink (14.3 (6.8-22.2) g). However, there was no difference in the blood glucose (P = 0.73) or serum insulin (P = 0.38) concentration at any time point after ingestion of the two test drinks. Conclusion: The results of this study show that the carbohydrate present in C-drink, although it has the propensity to form a gel, empties from the stomach faster than that of an isoenergetic carbohydrate solution (G-drink) without potentiating increased circulating blood glucose or insulin levels.

The rate of muscle glycogen synthesis during 2 and 4 h of recovery after depletion by exercise was studied using two energy equivalent carbohydrate drinks, one containing a polyglucoside with a mean molecular mass of 500 000–700 000 (C drink), and one containing monomers and oligomers of glucose with a mean molecular mass of approximately 500 (G drink). The osmolality was 84 and 350 mosmol · l−1, respectively. A group of 13 healthy well-trained men ingested the drinks after glycogen depleting exercise, one drink at each test occasion. The total amount of carbohydrates consumed was 300 g (4.2 g · kg−1) body mass given as 75 g in 500 ml water immediately after exercise and again 30, 60 ad 90-min post exercise. Blood glucose and insulin concentrations were recorded at rest and every 30 min throughout the 4-h recovery period. Muscle biopsies were obtained at the end of exercise and after 2 and 4 h of recovery. Mean muscle glycogen contents after exercise were 52.9 (SD 27.4) mmol glycosyl units · kg−1 (dry mass) in the C group and 58.3 (SD 35.4) mmol glycosyl units · kg−1 (dry mass) in the G group. Mean glycogen synthesis rate was significantly higher during the initial 2 h for the C drink compared to the G drink: 50.2 (SD 13.7) mmol · kg−1 (dry mass) · h−1 in the C group and 29.9 (SD 12.5) mmol · kg−1 (dry mass) · h−1 in the G group. During the last 2 h the mean synthesis rate was 18.8 (SD 33.3) and 23.3 (SD 22.4) mmol · kg−1 (dry mass) · h−1 in the C and G group, respectively (n.s.). Mean blood glucose and insulin concentrations did not differ between the two drinks. Our data indicted that the osmolality of the carbohydrate drink may influence the rate of resynthesis of glycogen in muscle after its depletion by exercise.

In this study we examined the time course of changes in the plasma concentration of oxypurines [hypoxanthine (Hx), xanthine and urate] during prolonged cycling to fatigue. Ten subjects with an estimated maximum oxygen uptake (V˙O2max) of 54 (range 47–67) ml · kg−1 · min−1 cycled at [mean (SEM)] 74 (2)% of V˙O2max until fatigue [79 (8) min]. Plasma levels of oxypurines increased during exercise, but the magnitude and the time course varied considerably between subjects. The plasma concentration of Hx ([Hx]) was 1.3 (0.3) μmol/l at rest and increased eight fold at fatigue. After 60 min of exercise plasma [Hx] was >10 μmol/l in four subjects, whereas in the remaining five subjects it was <5 μmol/l. The muscle contents of total adenine nucleotides (TAN = ATP+ADP+AMP) and inosine monophosphate (IMP) were measured before and after exercise in five subjects. Subjects with a high plasma [Hx] at fatigue also demonstrated a pronounced decrease in muscle TAN and increase in IMP. Plasma [Hx] after 60 min of exercise correlated significantly with plasma concentration of ammonia ([NH3], r = 0.90) and blood lactate (r = 0.66). Endurance, measured as time to fatigue, was inversely correlated to plasma [Hx] at 60 min (r = −0.68, P < 0.05) but not to either plasma [NH3] or blood lactate. It is concluded that during moderate-intensity exercise, plasma [Hx] increases, but to a variable extent between subjects. The present data suggest that plasma [Hx] is a marker of adenine nucleotide degradation and energetic stress during exercise. The potential use of plasma [Hx] to assess training status and to identify overtraining deserves further attention.

This study investigated the effects of muscle glycogen availability on performance and selected physiological and metabolic responses during high-intensity intermittent exercise. Seven male subjects completed a regimen of exercise and dietary intake (48 h) to either lower and keep low (LOW-CHO) or lower and then increase (HIGH-CHO) muscle glycogen stores, on two separate occasions at least a week apart. On each occasion the subjects completed a short-term (<10 min) and prolonged (>30 min) intermittent exercise (IEX) protocol, 24 h apart, which consisted of 6-s bouts of high-intensity exercise performed at 30-s intervals on a cycle ergometer. Glycogen concentration (mean +/- SEM) in m, vastus lateralis before both IEx(short) and IEx(long) was significantly lower following LOW-CHO [180 (14), 181 (17) mmol kg (dw)(-1)] compared with HIGH-CHO [397 (35), 540 (25) mmol kg (dw)(-1)]. In both IEx(short) and IEx(long), significantly less work was performed following LOW-CHO compared with HIGH-CHO. In IEx(long), the number of exercise bouts that could be completed at a pre-determined target exercise intensity increased by 265% from 111 (14) following LOW-CHO to 294 (29) following HIGH-CHO (P < 0.05). At the point of fatigue in IEx(long), glycogen concentration was significantly lower with the LOW-CHO compared with HIGH-CHO [58 (25) vs. 181 (46) mmol kg (dw)(-1), respectively]. The plasma concentrations of adrenaline and nor-adrenaline (in IEx(short) and IEx(long)), and FFA and glycerol (in IEx(long)), increased several-fold above resting values with both experimental conditions. Oxygen uptake during the exercise periods in IEx(long) approached 70% of Vo(2max) These results suggest that muscle glycogen availability can affect performance during both short-term and more prolonged high-intensity intermittent exercise and that with repeated exercise periods as short as 6 s, there can be a relatively high aerobic contribution.

Limitations in energy supply is a classical hypothesis of muscle fatigue. The present paper reviews the evidence available from human studies that energy deficiency is an important factor in fatigue. The maximal rate of energy expenditure determined in skinned fibres is close to the rate of adenosine triphosphate (ATP) utilisation observed in vivo and data suggest that performance during short bursts of exercise (<5 s duration) primarily is limited by other factors than energy supply (e.g. Vmax of myosine adenosine triphosphatase (ATPase), motor unit recruitment, engaged muscle mass). Within 10 s of exercise maximal power output decreases considerably and coincides with depletion of phosphocreatine. During recovery, maximal force and power output is restored with a similar time course as the resynthesis of phosphocreatine. Increases in muscle store of phosphocreatine through dietary supplementation with creatine increases performance during high-intensity exercise. These findings support the hypothesis that energy supply limits performance during high-intensity exercise. It is well documented that pre-exercise muscle glycogen content is related to performance during moderate intensity exercise. Recent data indicates that the interfibre variation in phosphocreatine is large after prolonged exercise to fatigue and that some fibres are depleted to the same extent as after high-intensity exercise. Despite relatively small decreases in ATP, the products of ATP hydrolysis (Pi and free ADP) may increase considerably. Free ADP calculated from the creatine kinase reaction increases 10-fold both after high-intensity exercise and after prolonged exercise to fatigue. It is suggested that local increases in ADP may reach inhibitory levels for the contraction process.

The effect of sustained submaximal exercise on muscle energetics has been studied on the single-fiber level in human skeletal muscle. Seven subjects cycled to fatigue (mean 77 min) at a work rate corresponding to approximately 75% of maximal O2 uptake. Biopsies were taken from the vastus lateralis muscle at rest, at fatigue, and after 5 min of recovery. Muscle glycogen decreased from 444 +/- 40 (SE) mmol glucosyl units/kg dry wt at rest to 94 +/- 16. Postexercise glycogen was inversely correlated (P < 0.01) to muscle content of inosine monophosphate, a catabolite of ATP. Phosphocreatine (PCr) in mixed-fiber muscle decreased at fatigue to 37% but was restored above the initial value (106.5%, P < 0.025) after 5 min of recovery. The overshoot was localized to type I fibers. The rapid reversal of PCr is in contrast to the slow recovery in contraction force. Pi increased at fatigue but less than that expected from the changes in PCr and other phosphate compounds. Mean PCr at rest was approximately 20% higher in type II than in type I fibers (86.4 +/- 3.6 and 71.6 +/- 1.8 mmol/kg dry wt, respectively, P < 0.05), but at fatigue similar PCr contents were observed in the two fiber types. Reduction in PCr in all fibers at fatigue suggests that all fibers were recruited at the end of exercise. PCr content in single fibers showed a great variability in samples at rest, exercise, and recovery. The variability was more pronounced than for ATP, and the data suggest that it is due to interfiber physiological-biochemical differences. At fatigue ATP was maintained relatively high in all single fibers, but a pronounced depletion of PCr was observed in a large number of fibers, and this may contribute to fatigue through the associated increases in Pi or/and free ADP. It is noteworthy that the increase in calculated free ADP at fatigue was similar to that after high-intensity exercise.

The effect of dietary creatine and supplementation on skeletal muscle creatine accumulation and subsequent degradation and on urinary creatinine excretion was investigated in 31 male subjects who ingested creatine in different quantities over varying time periods. Muscle total creatine concentration increased by approximately 20% after 6 days of creatine supplementation at a rate of 20 g/day. This elevated concentration was maintained when supplementation was continued at a rate of 2 g/day for a further 30 days. In the absence of 2 g/day supplementation, total creatine concentration gradually declined, such that 30 days after the cessation of supplementation the concentration was no different from the presupplementation value. During this period, urinary creatinine excretion was correspondingly increased. A similar, but more gradual, 20% increase in muscle total creatine concentration was observed over a period of 28 days when supplementation was undertaken at a rate of 3 g/day. In conclusion, a rapid way to "creatine load" human skeletal muscle is to ingest 20 g of creatine for 6 days. This elevated tissue concentration can then be maintained by ingestion of 2 g/day thereafter. The ingestion of 3 g creatine/day is in the long term likely to be as effective at raising tissue levels as this higher dose.

1. The influence of pre‐exercise muscle glycogen content on ammonia production, adenine nucleotide breakdown and amino acid metabolism was investigated during prolonged exercise in six subjects having one leg with a normal and one leg with a low muscle glycogen content. One‐leg knee‐extensor exercise was performed for 90 min, at a workload of 60‐65% of the maximal power output, first with one leg and then with the other. 2. During exercise ammonia was released in gradually increasing amounts and plateaued after 1 h exercise at a rate of approximately 80 mumol min‐1. The total ammonia production was 9.1 +/‐ 0.4 and 9.5 +/‐ 1.4 mmol (kg dry muscle)‐1 in the normal and low glycogen content leg, respectively. 3. Levels of muscle phosphocreatine (PC), total adenine nucleotides and inosine monophosphate (IMP) were similar at rest and after 90 min of exercise. 4. Only minor differences were observed between rest and exercise and between legs for the muscle concentrations of glutamine, alanine and the branched‐chain amino acids. Muscle glutamate concentration decreased by 60‐70% within the first 10 min of exercise. Glutamate consumption over 90 min quantitatively equalled ammonia production. Most of the glutamate was consumed within the first 10 min of exercise, while ammonia production gradually increased during exercise. Therefore deamination of glutamate cannot be the main source of ammonia production during the later stage of exercise. 5. It is concluded that during prolonged one‐leg exercise at moderate intensity: (a) ammonia production is not affected by pre‐exercise muscle glycogen content, (b) ammonia production exceeds by far the breakdown of adenine nucleotides to IMP and therefore has to be derived from alternative sources, and (c) deamination of amino acids is a likely source of ammonia production during prolonged exercise.

Seven male subjects performed repeated bouts of high-intensity exercise, on a cycle ergometer, before and after 6 d of creatine supplementation (20 g Cr H2O day-1). The exercise protocol consisted of five 6-s exercise periods performed at a fixed exercise intensity, interspersed with 30-s recovery periods (Part I), followed (40 s later) by one 10 s exercise period (Part II) where the ability to maintain power output was evaluated. Muscle biopsies were taken from m. vastus lateralis at rest, and immediately after (i) the fifth 6 s exercise period in Part I and (ii) the 10 s exercise period in Part II. In addition, a series of counter movement (CMJ) and squat (SJ) jumps were performed before and after the administration period. As a result of the creatine supplementation, total muscle creatine [creatine (Cr) + phosphocreatine (PCr)] concentration at rest increased from (mean +/- SEM) 128.7 (4.3) to 151.5 (5.5) mmol kg-1 dry wt (P < 0.05). This was accompanied by a 1.1 (0.5) kg increase in body mass (P < 0.05). After the fifth exercise bout in Part I of the exercise protocol, PCr concentration was higher [69.7 (2.3) vs. 45.6 (7.5) mmol kg-1 dry wt, P < 0.05], and muscle lactate was lower [26.2 (5.5) vs. 44.3 (9.9) mmol kg-1 dry wt, P < 0.05] after vs. before supplementation. In Part II, after creatinine supplementation, subjects were better able to maintain power output during the 10-s exercise period (P < 0.05). There was no change in jump performance as a result of the creatine supplementation (P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Since the exchange of gases, as well as metabolites, is greatly impeded in a paranasal sinus empyema, it is not unlikely that certain organic substances be retained and accumulated in purulent secretion. In this study, secretions aspirated from experimentally infected maxillary sinuses of 26 rabbits were analysed biochemically. Quantitatively, by far the most important acid accumulated in secretions was lactic acid. Lactate induces metabolic acidosis and exerts an inhibitory effect on mammalian defense mechanisms. Lactate may also be used as an energy source by certain microorganisms. In spite of its leukocytic origin lactic acid thus promotes the continuation of a bacterial infection. In addition, certain other organic acids of bacterial origin were found, which, in different ways, contribute to the impediment of antimicrobial defense functions.

1. Muscle biopsy samples were obtained from the vastus lateralis of six healthy volunteers before and after 30 s of treadmill sprinting. A portion of each biopsy sample was used for mixed‐fibre metabolite analysis. Single fibres were dissected from the remaining portion of each biopsy and were used for ATP, phosphocreatine (PCr) and glycogen determination. 2. Before exercise, PCr and glycogen contents were higher in type II fibres (79.3 +/‐ 2.7 and 472 +/‐ 35 mmol (kg dry matter (DM)‐1, respectively) compared with type I fibres (71.3 +/‐ 3.0 mmol (kg DM)‐1, P < 0.01 and 375 +/‐ 25 mmol (kg DM)‐1, P < 0.001, respectively). 3. Peak power output was 885 +/‐ 66 W and declined by 65 +/‐ 3% during exercise. Phosphocreatine and glycogen degradation in type II fibres during exercise (74.3 +/‐ 2.5 and 126.3 +/‐ 15.8 mmol (kg DM)‐1, respectively) was greater than the corresponding degradation in type I fibres (59.1 +/‐ 2.9 mmol (kg DM)‐1, P < 0.001 and 77.0 +/‐ 14.3 mmol (kg DM)‐1, P < 0.01, respectively). The decline in ATP during exercise was similar when comparing fibre types (P > 0.05). 4. Compared with previous studies involving similar durations of maximal cycling exercise, isokinetic knee extension and intermittent isometric contraction, the rates of substrate utilization recorded in type I fibres were extremely high, being close to the rapid rates observed in this fibre type during intense contraction with limb blood flow occluded.

Conference Abstract| January 01 1994 Creatine Supplementation and Electrically Evoked Human Muscle Fatigue SDR Harridge; SDR Harridge 1Dept. of Physiology & Pharmacology, Physiology III, Karolinska Institute, Stockholm, Sweden Search for other works by this author on: This Site PubMed Google Scholar PD Balsom; PD Balsom 1Dept. of Physiology & Pharmacology, Physiology III, Karolinska Institute, Stockholm, Sweden Search for other works by this author on: This Site PubMed Google Scholar K Söderlund K Söderlund 1Dept. of Physiology & Pharmacology, Physiology III, Karolinska Institute, Stockholm, Sweden Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1994) 87 (s1): 124–125. https://doi.org/10.1042/cs087s124a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation SDR Harridge, PD Balsom, K Söderlund; Creatine Supplementation and Electrically Evoked Human Muscle Fatigue. Clin Sci (Lond) 1 January 1994; 87 (s1): 124–125. doi: https://doi.org/10.1042/cs087s124a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu nav search search input Search input auto suggest search filter All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1994 The Biochemical Society and the Medical Research Society1994 Article PDF first page preview Close Modal You do not currently have access to this content.

Conference Abstract| January 01 1994 Carbohydrate Intake and High Intensity Intermittent Exercise PD Balsom; PD Balsom 1Dept. of Physiology and Pharmacology, Physiology III, Karolinska Institute, Stockholm, Sweden Search for other works by this author on: This Site PubMed Google Scholar G Gaitanos; G Gaitanos 1Dept. of Physiology and Pharmacology, Physiology III, Karolinska Institute, Stockholm, Sweden Search for other works by this author on: This Site PubMed Google Scholar K Söderlund; K Söderlund 1Dept. of Physiology and Pharmacology, Physiology III, Karolinska Institute, Stockholm, Sweden Search for other works by this author on: This Site PubMed Google Scholar B Ekblom B Ekblom 1Dept. of Physiology and Pharmacology, Physiology III, Karolinska Institute, Stockholm, Sweden Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1994) 87 (s1): 29–30. https://doi.org/10.1042/cs087s029a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation PD Balsom, G Gaitanos, K Söderlund, B Ekblom; Carbohydrate Intake and High Intensity Intermittent Exercise. Clin Sci (Lond) 1 January 1994; 87 (s1): 29–30. doi: https://doi.org/10.1042/cs087s029a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1994 The Biochemical Society and the Medical Research Society1994 Article PDF first page preview Close Modal You do not currently have access to this content.

Since the discovery of creatine in 1832, it has fascinated scientists with its central role in skeletal muscle metabolism. In humans, over 95% of the total creatine (Crtot) content is located in skeletal muscle, of which approximately a third is in its free (Crf) form. The remainder is present in a phosphorylated (Crphos) form. Crf and Crphos levels in skeletal muscle are subject to individual variations and are influenced by factors such as muscle fibre type, age and disease, but not apparently by training or gender. Daily turnover of creatine to creatinine for a 70kg male has been estimated to be around 2g. Part of this turnover can be replaced through exogenous sources of creatine in foods, especially meat and fish. The remainder is derived via endogenous synthesis from the precursors arginine, glycine and methionine. A century ago, studies with creatine feeding concluded that some of the ingested creatine was retained in the body. Subsequent studies have shown that both Crf and Crphos levels in skeletal muscle can be increased, and performance of high intensity intermittent exercise enhanced, following a period of creatine supplementation. However, neither endurance exercise performance nor maximal oxygen uptake appears to be enhanced. No adverse effects have been identified with short term creatine feeding. Creatine supplementation has been used in the treatment of diseases where creatine synthesis is inhibited.