Changes in muscle free carnitine and acetylcarnitine with increasing work intensity in the Thoroughbred horse

Summary Treadmill exercise in Thoroughbred horses of 2 min duration and increasing intensity resulted in increased formation and accumulation of acetylcarnitine in the working middle gluteal muscle. At high work intensities a plateau in acetylcarnitine formation was reached corresponding to approximately 70% of the total carnitine pool (approx. 30 mmol · kg^–1 dry muscle). Formation of acetylcarnitine was mirrored by an equal fall in the free carnitine content, which stabilised, at the highest work intensities, at around 8 mmol · kg^– dry muscle. Acetylcarnitine and carnitine reached their point of maximum change at a work intensity just below that resulting in the rapid production and accumulation of lactate and glycerol 3-phosphate. It is possible that the formation of acetylcarnitine is important in the regulation of the intramitochondrial acetyl CoA/CoA ratio; equally these changes may represent a blocking mechanism aimed at preventing the transfer of unwanted free fatty acids (as acylcarnitines) into the mitochondria at work intensities where they could contribute little to energy production.     

Acetyl group accumulation and pyruvate dehydrogenase activity in human muscle during incremental exercise

The changes in the muscle contents of CoASH and carnitine and their acetylated forms, lactate and the active form of pyruvate dehydrogenase complex were studied during incremental dynamic exercise. Eight subjects exercised for 3–4 minutes on a bicycle ergometer at work loads corresponding to 30, 60 and 90% of their V_02max Muscle samples were obtained by percutaneous needle biopsy technique at rest, at the end of each work period and after 10 minutes of recovery. During the incremental exercise test there was a continuous increase in muscle lactate, from a basal value of 4.5 mmol kg^-1 dry weight to 83 mmol kg^-1 at the end of the final period. The active form of pyruvate dehydrogenase complex increased from 0.37 mmol acetyl-CoA formed per minute per kilogram wet weight at rest to 0.80 at 30% V_02max1.28 and 1.25 at 60 and 90% V_02max respectively. Both acetyl-CoA and acetylcarnitine increased at the two highest work loads. The increase of acetyl-CoA was from 12.5 μmol kg^-1 dry weight at rest to 27.3 after the highest work load and for acetylcarnitine from 6.0 mmol kg^-1 dry weight to 15.2. The CoASH and free carnitine contents fell correspondingly. There was a close relationship between acetyl-CoA and acetylcarnitine accumulation in muscle during exercise, with a binding of ? 500 mol acetyl groups to carnitine for each mole of acetyl-CoA accumulated. The results imply that the carnitine store in muscle functions as a buffer for excess formation of acetyl groups from pyruvate catalyzed by the pyruvate dehydrogenase complex.     

Muscle carnitine metabolism during incremental dynamic exercise in humans

The changes in muscle content of carnitine and acetylcarnitine have been studied during incremental dynamic exercise. Six subjects exercised for 10 min on an ergometer at 40 and 75% of their maximal oxygen uptake (VO2 max) and to fatigue at 100% of VO2 max (about 4 min). Muscle samples were taken from the quadriceps femoris muscle at rest and after exercise. Muscle content of free carnitine was (means +/- SE) 15.9 +/- 1.7 mmol kg-1 d.wt (dry weight) at rest and remained unchanged after exercise at low intensity but decreased to 5.9 +/- 0.6 and 4.6 +/- 0.5 mmol kg-1 d.wt after exercise at 75 and 100% of VO2 max respectively. Acetylcarnine content at rest was 6.9 +/- 1.9 mmol kg-1 d.wt and increased during exercise in correspondence with the decrease in free carnitine. Muscle content of pyruvate and lactate was unchanged after exercise at 40% of VO2 max but increased at the higher intensities. The parallel increases in acetylcarnitine, pyruvate and lactate indicate that formation of acetylcarnitine is augmented when the availability of glycolytic three-carbon metabolites is high and is consistent with the idea that acetylcarnitine provides a sink for pyruvate and acetyl CoA. This could be of importance for the maintenance of an adequate level of CoA and thus function of the tricarboxylic acid cycle.     

Acetyl group accumulation and pyruvate dehydrogenase activity in human muscle during incremental exercise.

The changes in the muscle contents of CoASH and carnitine and their acetylated forms, lactate and the active form of pyruvate dehydrogenase complex were studied during incremental dynamic exercise. Eight subjects exercised for 3-4 minutes on a bicycle ergometer at work loads corresponding to 30, 60 and 90% of their VO2max. Muscle samples were obtained by percutaneous needle biopsy technique at rest, at the end of each work period and after 10 minutes of recovery. During the incremental exercise test there was a continuous increase in muscle lactate, from a basal value of 4.5 mmol kg-1 dry weight to 83 mmol kg-1 at the end of the final period. The active form of pyruvate dehydrogenase complex increased from 0.37 mmol acetyl-CoA formed per minute per kilogram wet weight at rest to 0.80 at 30% VO2max, 1.28 and 1.25 at 60 and 90% VO2max, respectively. Both acetyl-CoA and acetylcarnitine increased at the two highest work loads. The increase of acetyl-CoA was from 12.5 mumol kg-1 dry weight at rest to 27.3 after the highest work load and for acetylcarnitine from 6.0 mmol kg-1 dry weight to 15.2. The CoASH and free carnitine contents fell correspondingly. There was a close relationship between acetyl-CoA and acetylcarnitine accumulation in muscle during exercise, with a binding of approximately 500 mol acetyl groups to carnitine for each mole of acetyl-CoA accumulated. The results imply that the carnitine store in muscle functions as a buffer for excess formation of acetyl groups from pyruvate catalyzed by the pyruvate dehydrogenase complex.     

运动状态下脂肪氧化的调节

背景：传递到工作肌群血浆中的脂肪酸主要来自于储存在脂肪组织中的三酰甘油的分解。在大强度运动时,脂肪酸氧化不能支持能量的需要,可能是骨骼肌氧化脂肪酸能力受限。 目的：综述运动时脂肪氧化调节机制方面的研究,提出目前脂肪氧化调节机制方面亟待解决的问题。 方法：以“exercise,fatty acid oxidation,intensity,carnitine,acetylcarnitine,mitochondria”为检索词,检索PubMed数据库1995至2012年发表的相关文章,文献语种限制为英文。纳入与运动时脂肪氧化调节机制相关的内容,排除重复性研究。 结果与结论：计算机初检得到94篇文献,排除无关重复的文献,保留56篇进行综述。运动时脂肪酸氧化存在多种可能调节的步骤,从脂肪组织脂肪分解到骨骼肌线粒体的代谢。目前,最有吸引力的脂肪酸氧化调节候选剂是肌肉代谢物肉碱。它是肉毒碱棕榈酰转移酶1调节和脂肪酸氧化的基本。大强度运动时,糖酵解迅速增加,为线粒体提供过多乙酰辅酶A,并被肉碱缓冲,生成乙酰肉碱。相应地,肌肉自由肉碱下降,降低肉毒碱棕榈酰转移酶1活性,从而降低运输脂肪酸进入线粒体的能力,也降低脂肪酸氧化率。因此,糖原迅速分解和糖酵解对抑制脂肪酸的氧化产生主要影响。     

Non-invasive observation of acetyl-group buffering by 1H-MR spectroscopy in exercising human muscle

The observation of a previously unidentified peak in localized 1H magnetic resonance (MR) spectra of human muscle during and after a work load is reported. Basic NMR properties of this resonance, as well as physiologic circumstances of its observation, suggest that it is due to the acetyl group of acetylcarnitine. The relatively large pool of muscular carnitine acts as a buffering system stabilizing the ratio of acetylated to free coenzyme A. Free carnitine can be acetylated to a large extent whenever a mismatch occurs between the fluxes through pyruvate dehydrogenase and the TCA cycle. Results of initial applications of 1H MR spectroscopy in several muscles and under different exercise regimens are in agreement with earlier invasive measurements of acetylcarnitine. It is demonstrated that the detailed dynamics of acetyl group formation are now likely to be observable non-invasively in humans by localized 1H magnetic resonance spectroscopy on standard MR imaging systems, and that acetylcarnitine buffering as a function of exercise type, oxygenation states, diet and pathology could thus be studied repeatedly and in various muscle groups with much improved temporal resolution.     

New insights concerning the role of carnitine in the regulation of fuel metabolism in skeletal muscle

In skeletal muscle, carnitine plays an essential role in the translocation of long-chain fatty-acids into the mitochondrial matrix for subsequent β-oxidation, and in the regulation of the mitochondrial acetyl-CoA/CoASH ratio. Interest in these vital metabolic roles of carnitine in skeletal muscle appears to have waned over the past 25 years. However, recent research has shed new light on the importance of carnitine as a regulator of muscle fuel selection. It has been established that muscle free carnitine availability may be limiting to fat oxidation during high intensity submaximal exercise. Furthermore, increasing muscle total carnitine content in resting healthy humans (via insulin-mediated stimulation of muscle carnitine transport) reduces muscle glycolysis, increases glycogen storage and is accompanied by an apparent increase in fat oxidation. By increasing muscle pyruvate dehydrogenase complex (PDC) activity and acetylcarnitine content at rest, it has also been established that PDC flux and acetyl group availability limits aerobic ATP re-synthesis at the onset of exercise (the acetyl group deficit). Thus, carnitine plays a vital role in the regulation of muscle fuel metabolism. The demonstration that its availability can be readily manipulated in humans, and impacts on physiological function, will result in renewed business and scientific interest in this compound.     

Effect of carnitine loading on long-chain fatty acid oxidation,maximal exercise capacity,and nitrogen balance

Summary Carnitine has a potential effect on exercise capacity due to its role in the transport of long-chain fatty acids into the mitochondria for-oxidation, the export of acyl-coenzyme A compounds from mitochondria and the activation of branched-chain amino acid oxidation in the muscle. We studied the effect of carnitine supplementation on palmitate oxidation, maximal exercise capacity and nitrogen balance in rats. Daily carnitine supplementation (500 mg - kg^–1 body mass for 6 weeks) was given to 30 rats, 15 of which were on an otherwise carnitine-free diet (group 1) and 15 pair-fed with a conventional pellet diet (group II). A control group (group III,n = 6) was fed ad libitum the pellet diet. Palmitate oxidation was measured by collecting¹⁴CO₂ after an intraperitoneal injection of [1-¹⁴C]palmitate and exercise capacity by swimming to exhaustion. After carnitine supplementation carnitine concentrations in serum were supranormal [group I, total 150.8 (SD 48.5), free 78.9 (SD 18.4); group II, total 170.9 (SD 27.9), free 115.8 (SD 24.6) gmol·1^–1] and liver carnitine concentrations were normal in both groups [group I, total 1.6 (SD 0.3), free 1.2 (SD 0.2); group II, total 1.3 (SD 0.3), free 0.9 (SD 0.2) mol·g^–1 dry mass]. In muscle carnitine concentrations were normal in group I [total 3.8 (SD 1.2), free 3.2 (SD 1.0) mol · g^–1 dry mass] and increased in group II [total 6.6 (SD 0.5), free 4.9 (SD 0.9) mol·g^–1 dry mass]. Despite the difference in muscle carnitine concentrations there were no differences among the groups in cumulative palmitate oxidation after 3 h [group I, 39.7 (SD 11.6)%, group II, 29.6 (SD 14.0)%; group III, 36.5 (SD 10.8)% of injected activity] or swimming time to exhaustion [group I, 9.7 (SD 2.9); group II, 8.4 (SD 3.6); group III, 7.1 (SD 2.8) h]. A borderline increase in nitrogen balance was observed in group II. We concluded that increasing carnitine tissue concentrations by carnitine supplementation had no effect on palmitate oxidation and maximal exercise capacity in the rats studied.     

Effect of sports activity on carnitine metabolism. Measurement of free carnitine, gamma-butyrobetaine and acylcarnitines by tandem mass spectrometry.

The effects of sports activity on carnitine metabolism were studied using mass spectrometry. Serum levels of free carnitine, acylcarnitines (acetylcarnitine, propionylcarnitine, C4-, C5- and C8-acylcarnitine) and gamma-butyrobetaine, a carnitine precursor, were determined by tandem mass spectrometry in liquid secondary ion mass ionization mode. The coefficients of variation at three different concentrations were 2.8-7.9% for gamma-butyrobetaine, and 1.2 to approximately 6.7% for free carnitine. The recoveries added to serum were 109.1% for gamma-butyrobetaine, 89.3% for free carnitine. Sports activity caused increased serum levels of gamma-butyrobetaine, acetylcarnitine, C4- and C8-acylcarnitines and decreased serum levels of free carnitine. This method requires a small amount of sample volume (20 microl of serum) and short total instrumental time for the analysis (1 h for preparation, 2 min per sample for mass spectrometric analysis). Therefore, this method can be applied to study carnitine metabolism under various conditions that affect fatty acid oxidation.     

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

Summary The effects of two types of acute exercise (1 h treadmill running at 20 m· min^–1, or 6 × 10-s periods at 43 m · min^–1, 0° 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 U· 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 snythesis, as well as the sensitivity of this process to insulin at the 24^th following the last training session. It was concluded that in the epitrochlearis muscle, containing mainly FT fibres, both moderate and intensive exercise (acute and repeated) were effective in increasing sensitivity of glucose utilization to insulin. Thus, the response in this muscle type to increased physical activity differs from that reported previously in the soleus muscle, representing the slow-twitch, oxidative fibres in which sprint exercise did not produce any changes in the muscle insulin sensitivity.     

Effects of sprint exercise on oxidative stress in skeletal muscle and liver

Although numerous studies have tested the effects of continuous exercise regimens on antioxidant defences, information on the effect of sprint exercise on the antioxidant defence system and lipid peroxidation levels of tissues is scant. The present study was designed to determine the effects of sprint exercise on the lipid peroxidation and antioxidant enzyme system in liver and skeletal muscle during the post-exercise recovery period in untrained mice. Mice performed 15 bouts of exercise, each comprising running on a treadmill for 30 s at 35 m·min^–1 and a 5° slope, with a 10-s rest interval between bouts. They were then killed by cervical dislocation either immediately (0 h), 0.5 h, 3 h or 24 h after completion of the exercise. Their gastrocnemius muscle and liver tissues were quickly removed. It was found that blood lactate levels increased immediately after the exercise, but had returned to control levels by 0.5 h post-exercise. This exercise regimen had no effect on the activity of superoxide dismutase and glutathione peroxidase in these tissues. Levels of muscle thiobarbituric acid reactive substances (TBARS) had increased at 0.5 and 3 h post-exercise, and then returned to control levels by 24 h post-exercise. In conclusion, acute sprint exercise in mice resulted in an increase in TBARS levels in skeletal muscle; no change was observed in the liver. Antioxidant enzyme activities remained unaffected by acute sprint exercise in these tissues. Electronic Publication     

Changes in carnitine and acetylcarnitine in human semen during cryopreservation.

L-Carnitine and acetylcarnitine concentrations were determined in spermatozoa and seminal plasma from 15 men, in both fresh ejaculate and frozen-thawed semen with cryoprotective medium. Sperm motility was also evaluated. In fresh samples, the levels of carnitine and acetylcarnitine in seminal plasma were comparable whereas in spermatozoa, acetylcarnitine predominated. Cryopreservation did not change the carnitine and acetylcarnitine levels in seminal plasma nor the carnitine concentration in spermatozoa; by contrast, the acetylcarnitine level in spermatozoa was decreased in 14 cases (110 +/- 8 versus 210 +/- 20 nmol/10(8) cells). This decrease in acetylcarnitine content was greater during semen dilution in cryoprotectant than after the freezing/thawing process. Motility was also decreased in all cases after the freezing/thawing process. These results suggest that acetylcarnitine recovery in spermatozoa is further evidence of the deleterious effect of the cryoprotective medium in the cryopreservation of semen.     

Brief intense exercise followed by passive recovery modifies the pattern of fuel use in humans during subsequent sustained intermittent exercise.

The role of work period duration as the principal factor influencing carbohydrate metabolism during intermittent exercise has been investigated. Fuel oxidation rates and muscle glycogen and free carnitine content were compared between two protocols of sustained intermittent intense exercise with identical treadmill speed and total work duration. In the first experiment subjects (n=6) completed 40 min of intermittent treadmill running involving a work : recovery cycle of 6 : 9 s or 24 : 36 s on separate days. With 24 : 36 s exercise a higher rate of carbohydrate oxidation approached significance (P=0.057), whilst fat oxidation rate was lower (P < or = 0.01) and plasma lactate concentration higher (P < or = 0.01). Muscle glycogen was lower post-exercise with 24 : 36 s (P < or = 0.05). Muscle free carnitine decreased (P < or = 0.05), but there was no difference between protocols. In the second experiment a separate group of subjects (n=5) repeated the intermittent exercise protocols with the addition of a 10-min bout of intense exercise, followed by 43 +/- 5 min passive recovery, prior to sustained (40 min) intermittent exercise. For this experiment the difference in fuel use observed previously between 6 : 9 s and 24 : 36 s was abolished. Carbohydrate and fat oxidation, plasma lactate and muscle glycogen levels were similar in 6 : 9 s and 24 : 36 s. When compared with the first experiment, this result was because of reduced carbohydrate oxidation in 24 : 36 s (P < or = 0.05). There was no difference, and no change, in muscle free carnitine between protocols. A 10-min bout of intense exercise, followed by 43 +/- 5 min of passive recovery, substantially modifies fuel use during subsequent intermittent intense exercise.     

Nutrient provision increases signalling and protein synthesis in human skeletal muscle after repeated sprints

The effect of nutrient availability on the acute molecular responses following repeated sprint exercise is unknown. The aim of this study was to determine skeletal muscle cellular and protein synthetic responses following repeated sprint exercise with nutrient provision. Eight healthy young male subjects undertook two sprint cycling sessions (10 × 6 s, 0.75 N m torque kg⁻¹, 54 s recovery) with either pre-exercise nutrient (24 g whey, 4.8 g leucine, 50 g maltodextrin) or non-caloric placebo ingestion. Muscle biopsies were taken from vastus lateralis at rest, and after 15 and 240 min post-exercise recovery to determine muscle cell signalling responses and protein synthesis by primed constant infusion of l-[ring-¹³C₆] phenylalanine. Peak and mean power outputs were similar between nutrient and placebo trials. Post-exercise myofibrillar protein synthetic rate was greater with nutrient ingestion compared with placebo (~48%, P < 0.05) but the rate of mitochondrial protein synthesis was similar between treatments. The increased myofibrillar protein synthesis following sprints with nutrient ingestion was associated with coordinated increases in Akt-mTOR-S6K-rpS6 phosphorylation 15 min post-exercise (~200–600%, P < 0.05), while there was no effect on these signalling molecules when exercise was undertaken in the fasted state. For the first time we report a beneficial effect of nutrient provision on anabolic signalling and muscle myofibrillar protein synthesis following repeated sprint exercise. Ingestion of protein/carbohydrate in close proximity to high-intensity sprint exercise provides an environment that increases cell signalling and protein synthesis.     

Relationships between muscle carnitine,age and oxidative status

Muscle carnitine levels were examined in 31 younger [mean (SD), 27 (5) years] and 27 older [49 (8) years] men. Needle biopsies were obtained from the lateral gastrocnemius or vastus lateralis muscles and assayed for free and total carnitine concentrations via a 5,5-Dithiobis-(2-nitrobenzoic acid) DTNB-linked spectrophotometric procedure. A subgroup of subjects (n = 28) were assessed for citrate synthase (CS) and succinate dehydrogenase (SDH) activity, and type 1 muscle fiber composition (% type I fibers). An additional sub-group of nine subjects was assessed for free and total serum carnitine levels. No mean (SEM) differences in free [21.6 (0.7) vs 20.3 (0.9) mol·g dry weight^-1]] and total [26.4 (0.6) vs 26.1 (0.9) mol·g dry weight^–1) muscle carnitine levels were found between the younger and older subjects, respectively. Correlational data revealed no significant relationships between total muscle carnitine and CS (r = – 0.36), SDH (r = – 0.26), or % type I fibers (r = – 0.16). In addition, there was a low non-significant relationship between serum and muscle total carnitine concentrations (r = – 0.44). These findings suggest that muscle carnitine levels are similar between younger and older males, and there does not appear to be any relationship between muscle carnitine and markers of muscle oxidative potential (i.e., oxidative enzymes, % type I fiber). Since serum carnitine is often used as an indicator of body carnitine status, it is noteworthy that we found a low negative relationship between blood and muscle carnitine concentrations.     

Effect of various types of acute exercise and exercise training on the insulin sensitivity of rat soleus muscle measured in vitro

Effects of acute exercise varying in duration and intensity, as well as of two training regimes (endurance and sprint training) on the sensitivity of the soleus muscle of rat to insulin was measured in vitro and compared in rats. As an index of the muscle insulin sensitivity the hormone concentration in the incubation medium which would produce half maximum stimulation of lactate production (LA) and glycogen synthesis was determined. A single bout of moderate endurance exercise (60 min treadmill running at 20 m×min^–1, 0° inclination) increased the rate of LA production at the hormone concentrations used and increased the sensitivity of the process to insulin at 0.25 and 2 h but not 24 h after termination of exercise. Similar though less pronounced effects were found after heavy endurance exercise (30 min at 25 m×min^–1, 10°), but sprint exercise (6×10 s bouts at 43 m×min^–1, 0°) had no influence on the insulin sensitivity of the soleus muscle. The rate of glycogen synthesis in vitro was accelerated after endurance exercise, but the sensitivity of this process to insulin was unaffected by the preceding exercise. Endurance training for 5 weeks caused marked enhancement of sensitivity of both LA production and glycogen synthesis to insulin, which persisted for at least 48 h after the last training session. No changes in the soleus muscle sensitivity to insulin were found after sprint training. It is concluded that the increased insulin sensitivity of glucose utilization by skeletal muscle which occurs after endurance exercise and particularly during endurance training can substantially contribute to improved carbohydrate tolerance. Sprint exercise does not produce any changes in muscle insulin sensitivity, at least in the soleus muscle of the rat.Dedicated to the late Professor Stanislaw Kozlowski     

Rapid recovery of power output in females

The purpose of the present study was to examine whether the magnitude of the changes in the concentration of muscle metabolites influences the recovery of power output following short-term maximal intensity cycle exercise performed at different average pedalling rates. In part A of the study eight female subjects performed four trials on a cycle ergometer. Two trials involved maximal sprints of 30- and 6-s duration separated by a very short (2–3 s) recovery period. Average pedal rate during the first 30-s sprint was manipulated by employing resistances of either 7.5 or 10.1% of body weight; the second sprint always being performed against 7.5% BW. In two further trials subjects performed only a single 30-s sprint against the two resistances with pre- and post-exercise muscle biopsies and blood samples being taken. Peak power in the second sprint was significantly higher (442 ± 31W vs. 402 ± 33W; P < 0.05) following prior exercise against the greater resistance during which average pedal rate was lower (≈ 26%; P < 0.01) compared with the lesser resistance. However, despite this the muscle metabolite responses to the first sprint were similar (ΔPCr (7.5 vs. 10.1% applied resistance) –55 vs. –59 mmol kg dry muscle^?1: ΔLactate + 104 vs. +107 mmol kg dry muscle^?1: both P > 0.05). In part B of the study six female subjects performed 19 trials in which the recovery interval between a maximal 30-s sprint (where average pedalling rate was manipulated in a manner similar to part A) and a 6-s sprint ranged from 0 to 300 s. The rate of restoration of power output was influenced by the average pedal rate in sprint 1 only for recovery durations of up to 3 s. These findings suggest that the recovery of power is not exclusively determined by muscle metabolites, in particular PCr, when the recovery duration is very short (≤ 3 s). As it has been previously shown that the pattern of muscle activation influences ionic balance it is speculated that ionic factors may be very important in the early and rapid recovery of power.     

Sex difference in plasma ammonia but not in muscle inosine monophosphate accumulation following sprint exercise in humans

Since accumulation of ammonia in plasma has been shown to be lower in females than in males following sprint exercise, we hypothesised that muscle inosine monophosphate (IMP) accumulation would also be smaller in females, especially in type II fibres. A relationship between plasma ammonia and muscle IMP accumulation was expected, since ammonia and IMP are formed in equimolar amounts during the net breakdown of adenine nucleotides. The sprint-exercise-induced IMP accumulation, measured in biopsies from vastus lateralis muscle, did not differ between males (n?=?16) and females (n?=?16) either in type I fibres [males 4.6 (SD 3), females 5.7 (SD 2) mmol?·?kg^?1 dry muscle], type II fibres [males 13.2 (SD 4), females 12.6 (SD 4) mmol?·?kg^?1 dry muscle] or in mixed muscle [males 8.4 (SD 3), females 8.2 (SD 3) mmol?·?kg^?1 dry muscle]. The accumulation of plasma ammonia following the sprint was 35% lower in the females than in the males. The inter-individual variation in plasma ammonia accumulation was explained by the sex but not by the muscle IMP accumulation as tested in a multiple regression analysis. In conclusion, the smaller plasma ammonia accumulation following sprint exercise in females than in males would seem not to be explained by a smaller muscle IMP accumulation per unit muscle during sprint exercise.     

Interspersed normoxia during live high, train low interventions reverses an early reduction in muscle Na+, K+ATPase activity in well-trained athletes

Hypoxia and exercise each modulate muscle Na⁺, K⁺ATPase activity. We investigated the effects on muscle Na⁺, K⁺ATPase activity of only 5 nights of live high, train low hypoxia (LHTL), 20 nights consecutive (LHTLc) versus intermittent LHTL (LHTLi), and acute sprint exercise. Thirty-three athletes were assigned to control (CON, n = 11), 20-nights LHTLc (n = 12) or 20-nights LHTLi (4 × 5-nights LHTL interspersed with 2-nights CON, n = 10) groups. LHTLc and LHTLi slept at a simulated altitude of 2,650 m (F_IO₂ 0.1627) and lived and trained by day under normoxic conditions; CON lived, trained, and slept in normoxia. A quadriceps muscle biopsy was taken at rest and immediately after standardised sprint exercise, before (Pre) and after 5-nights (d5) and 20-nights (Post) LHTL interventions and analysed for Na⁺, K⁺ATPase maximal activity (3-O-MFPase) and content ([³H]-ouabain binding). After only 5-nights LHTLc, muscle 3-O-MFPase activity declined by 2% (P < 0.05). In LHTLc, 3-O-MFPase activity remained below Pre after 20 nights. In contrast, in LHTLi, this small initial decrease was reversed after 20 nights, with restoration of 3-O-MFPase activity to Pre-intervention levels. Plasma [K⁺] was unaltered by any LHTL. After acute sprint exercise 3-O-MFPase activity was reduced (12.9 ± 4.0%, P < 0.05), but [³H]-ouabain binding was unchanged. In conclusion, maximal Na⁺, K⁺ATPase activity declined after only 5-nights LHTL, but the inclusion of additional interspersed normoxic nights reversed this effect, despite athletes receiving the same amount of hypoxic exposure. There were no effects of consecutive or intermittent nightly LHTL on the acute decrease in Na⁺, K⁺ATPase activity with sprint exercise effects or on plasma [K⁺] during exercise.     

Effects of prior heavy exercise,prior sprint exercise and passive warming on oxygen uptake kinetics during heavy exercise in humans

Prior heavy exercise (above the lactate threshold, Th_la) increases the amplitude of the primary oxygen uptake (VO₂) response and reduces the amplitude of the VO₂ slow component during subsequent heavy exercise. The purpose of this study was to determine whether these effects required the prior performance of an identical bout of heavy exercise, or if prior short-duration sprint exercise could cause similar effects. A secondary purpose of this study was to determine the effect of elevating muscle temperature (through passive warming) on VO₂ kinetics during heavy exercise. Nine male subjects performed a 6-min bout of heavy exercise on a cycle ergometer 6 min after: (1) an identical bout of heavy exercise; (2) a 30-s bout of maximal sprint cycling; (3) a 40-min period of leg warming in a hot water bath at 42°C. Prior sprint exercise elevated blood [lactate] prior to the onset of heavy exercise (by ≅5.6 mM) with only a minor increase in muscle temperature (of ≅0.7°C). In contrast, prior warming had no effect on baseline blood lactate concentration, but elevated muscle temperature by ≅2.6°C. Both prior heavy exercise and prior sprint exercise significantly increased the absolute primary VO₂ amplitude (by ≅230 ml·min^–1 and 260 ml·min^–1, respectively) and reduced the amplitude of the VO₂ slow component (by ≅280 ml·min^–1 and 200 ml·min^–1, respectively) during heavy exercise, whereas prior warming had no significant effect on the VO₂ response. We conclude that the VO₂ response to heavy exercise can be markedly altered by both sustained heavy-intensity submaximal exercise and by short-duration sprint exercise that induces a residual acidosis. In contrast, passive warming elevated muscle temperature but had no effect on the VO₂ response. Electronic Publication