Effect of 2 weeks of endurance training on uncoupling protein 3 content in untrained human subjects

AIM: The mitochondrial uncoupling protein-3 (UCP3) is able to lower the proton gradient across the inner mitochondrial membrane, thereby uncoupling substrate oxidation from ATP production and dissipating energy as heat. What the effect of endurance training on UCP3 is, is still controversial. Endurance-trained athletes are characterized by lower levels of UCP3, but longitudinal studies in rodents reported no effect of endurance training on muscular UCP3 levels. Here, we examined the effect of a 2-week training programme on skeletal muscle UCP3 protein content in untrained human subjects, and hypothesized that UCP3 will be reduced after the training programme. METHODS: Nine untrained men [age: 23.3 +/- 3.2 years; BMI: 22.6 +/- 2.6 kg m(-2); maximal power output (W(max)): 3.8 +/- 0.6 W kg(-1) body weight] trained for 2 weeks. Before and at least 72 h after the training period, muscle biopsies were taken for determination of UCP3 protein content. RESULTS: UCP3 protein content tended to be lower after the training programme [95 +/- 10 vs. 109 +/- 12 arbitrary units (AU), P = 0.08]. Cytochrome c content tended to increase with 33% in response to endurance training (52 +/- 6 vs. 39 +/- 6 AU, P = 0.08). The ratio UCP3 relative to cytochrome c tended to decrease significantly upon endurance training (2.0 +/- 0.4 vs. 3.2 +/- 0.6 AU, P = 0.01). CONCLUSION: A short-term (2-week) endurance training programme decreased UCP3 protein levels and significantly reduced the ratio of UCP3 to cytochrome c.     

Effect of epigallocatechin gallate on uncoupling protein 2 in acute liver injury

Background: The aim of this study was to investigate the effect of epigallocatechin gallate (EGCG) on uncoupling protein 2 regulation in an acute liver injury-animal model. Methods: Twenty seven male Wistar rats were divided into three groups: control group (n = 9), TAA group (n = 9): acute liver injury was induced by the intraperitoneal injection of thioacetamide (200 mg/kg) and EGCG/TAA (n = 9 rats): Epigallocatechin gallate was given two weeks prior to the induction of acute liver injury by thioacetamide. The levels of uncoupling protein 2, CRP, TNF-α and interleukins (IL) 6 and 18 were analyzed in the liver using PCR analysis. Results: Q-PCR analysis showed that the genetic expression of UCP2, TNF-α and CRP in the EGCG/TAA group was the least in comparison to other groups (P ≤ 0.005). The IL-6 and IL-18 were upregulated after induction of acute liver injury, but this upregulation was significantly less in the group that received epigallocatechin gallate (EGCG/TAA) compared to the TAA group. In addition, histological examination showed a reduction in hepatocyte injury in EGCG/TAA compared to the TAA group. Conclusion: Epigallocatechin gallate administration prior to induction of acute liver injury down-regulates uncoupling protein 2 expression and reduces IL-6, IL-18, TNF-α and CRP.     

解偶联蛋白3基因启动子区-55（C〉T）多态与中国人静息能量消耗及体脂含量与分布的关系

目的 研究解偶联蛋白3基因（UCP3）启动子区-55（C〉T）多态与中国人静息能量消耗、体脂参数的关系。方法 在300名中国人（正常体重91人，超重／月巴胖209人）中，用聚合酶链反应一限制性片段长度多态性（polymemse chain reaction-restriction fragment length polymorphisms，PCR—RFLP）检测伙巧基因启动子区-55（C〉T）变异，并测定其静息能量消耗、体脂含量及分布。结果 UCP3基因启动子区-55（C〉T）多态基因型频率与肥胖及肥胖类型均无相关。正常体重组1T基因型者静息能量消耗水平显著高于CT及CC基因型者（P〈0．05）；超重／肥胖组各基因型者间比较亦有同样趋势。在超重／肥胖组，TT基因型者FM／FFM值与CT及CC基因型者差异有显著意义（P〈0．01）。结论 UCP3基因启动子区-55（C〉T）多态与中国人静息能量消耗相关，该变异可能通过对静息能量消耗的影响调节机体的能量代谢。     

解偶联蛋白3基因启动子区-55(C>T)多态与中国人静息能量消耗及体脂含量与分布的关系

目的研究解偶联蛋白3基因(UCP3)启动子区-55(C>T)多态与中国人静息能量消耗、体脂参数的关系。方法在300名中国人(正常体重91人,超重/肥胖209人)中,用聚合酶链反应-限制性片段长度多态性(polymerase chain reaction-restrictionfragment length polymorphisms ,PCR-RFLP)检测UCP3基因启动子区-55(C>T)变异,并测定其静息能量消耗、体脂含量及分布。结果UCP3基因启动子区-55(C>T)多态基因型频率与肥胖及肥胖类型均无相关。正常体重组TT基因型者静息能量消耗水平显著高于CT及CC基因型者(P<0·05) ;超重/肥胖组各基因型者间比较亦有同样趋势。在超重/肥胖组,TT基因型者FM/FFM值与CT及CC基因型者差异有显著意义(P<0·01)。结论UCP3基因启动子区-55(C>T)多态与中国人静息能量消耗相关,该变异可能通过对静息能量消耗的影响调节机体的能量代谢。     

Bio-energetic changes in human gastrocnemius muscle 1–2 days after strenuous exercise

[³¹P]magnetic resonance spectroscopy was used to study the metabolic sequelae of intense muscular activity in gastrocnemius of seven subjects 1–2 days after a 67-mile bicycle ride. The muscle was examined at rest, during a test exercise and during recovery from test exercise. Post-ride and pre-ride results were compared. At rest, the ratio of phosphocreatine to ATP (PCr/ATP) was increased post-ride; during test exercise PCr/(PCr + Pi) was lower post-ride; and the recoveries of PCr, Pi and PCr/(PCr + Pi) after test exercise were delayed, with decreased ‘overshoot’ of PCr/(PCr + Pi) (which is due to recovery of Pi to below its resting value). Mild mitochondrial damage (perhaps due to exposure to high cytosolic [Pi] during the bicycle ride) may explain some of these results. In contrast to reports of largely eccentric exercise there was no increase in resting Pi/ATP. We have thus demonstrated perturbations of muscle bio-energetics 1–2 days after strenuous exercise, in the absence of convincing enzymological evidence of muscle damage.     

Effect of endurance training and/or fish oil supplemented diet on cytoplasmic fatty acid binding protein in rat skeletal muscles and heart

Endurance training and/or a fish oil supplemented diet affect cytoplasmic fatty acid binding protein (FABP_c) content in rat skeletal muscles and heart. After 8 weeks of swimming, trained rats exhibited higher FABP_c content in the extensor digitorum longus (EDL) and in the gastrocnemius than did control rats (30%). The FABP_c increase was associated with an increase of citrate synthase activity (85% and 93%, respectively, in the two muscles), whereas lactate dehydrogenase activity decreased significantly. In contrast, in the soleus and in the heart we did not observe any effect of exercise either on FABP_c or on the metabolic profile. Therefore, increasing oxidative capacities of muscle by exercise resulted in a concomitant increase of the FABP_c content. Giving a polyunsaturated fatty acid (ω-3) supplemented diet for eight weeks induced a large rise of the FABP_c in EDL (300%), gastrocnemius (250%), soleus (50%) and heart (15%) without a concurrent accumulation of intramuscular triglycerides or modification of the citrate synthase activity, suggesting that polyunsaturated fatty acids may increase FABP_c content by up-regulating fatty acid metabolism genes via peroxisome proliferator-activated receptor alpha activation. Endurance trained rats fed with an ω-3 diet had similar FABP_c content in the gastrocnemius muscle when compared to sedentary ω-3 fed rats, whereas an additive effect of exercise and diet was observed in the EDL. The FABP_c in the soleus and in the heart of rats fed with ω-3 supplements remained constant whether rats performed exercise or not. As a result, both exercise and ω-3-enriched diet influenced FABP_c content in muscle. These two physiological treatments presumably acted on FABP_c content by increasing fatty acid flux within the cell. Electronic Publication     

Effects of high‐intensity intermittent swimming on PGC‐1α protein expression in rat skeletal muscle

Aim: The aim of the present investigation was to elucidate the effects of exercise intensity on exercise‐induced expression of peroxisome proliferator‐activated receptor γ coactivator‐1α (PGC‐1α) protein in rat skeletal muscle. Methods: We measured PGC‐1α content in the skeletal muscles of male Sprague–Dawley rats (age: 5–6 weeks old; body weight: 150–170 g) after a single session of high‐intensity intermittent exercise (HIE) or low‐intensity prolonged swimming exercise (LIE). During HIE, the rats swam for fourteen 20‐s periods carrying a weight (14% of body weight), and the periods of swimming were separated by a 10‐s pause. LIE rats swam with no load for 6 h in two 3‐h sessions, separated by 45 min of rest. Results: After HIE, the PGC‐1α protein content in rat epitrochlearis muscle had increased by 126, 140 and 126% at 2, 6 and 18 h, respectively, compared with that of the age‐matched sedentary control rats’ muscle. Immediately, 6 and 18‐h after LIE, the PGC‐1α protein content in the muscle was significantly elevated by 84, 95 and 67% respectively. The PGC‐1α protein content observed 6 h after HIE tended to be higher than that observed after LIE. However, there was no statistically significant difference between the two values (P = 0.12). Conclusion: The present investigation suggests that irrespective of the intensity of the exercise, PGC‐1α protein content in rat skeletal muscle increases to a comparable level when stimuli induced by different protocols are saturated. Further, HIE is a potent stimulus for enhancing the expression of PGC‐1αprotein, which may induce mitochondrial biogenesis in exercise‐activated skeletal muscle.     

Responses of rat myocardial antioxidant defences and heat shock protein HSP72 induced by 12 and 24‐week treadmill training

Aim: The purpose of this study was to determine the effects of both a short (12 weeks) and a long‐term (24 weeks) endurance treadmill‐training programme on the levels of oxidative stress markers, the activity of the enzymatic antioxidants, and the content of the 72 kDa heat shock protein (HSP72) in rat myocardium. Methods: Thirty male Wistar rats were randomly assigned to exercise trained (n = 16) and sedentary (n = 14) groups. After 12 week of training, eight rats were killed while the remaining eight continued the training programme until 24 week. Results: Seven sedentary controls were killed together with each trained group. Levels of thiobarbituric acid‐reactive substances (TBARS), protein carbonyls, and total and oxidized glutathione (tGSH and GSSG) in myocardial homogenates were unchanged by training irrespective of the protocol duration. However, an increased content of the oxidative stress biomarkers was detected in hearts from both the 24‐week trained rats and their sedentary controls when compared with their corresponding 12‐week groups. The antioxidant enzymatic activities total and mitochondrial superoxide dismutase (tSOD and mtSOD, respectively), glutathione peroxidase (GPX) and glutathione reductase (GR), remained unchanged after the 12‐week training period whereas a significant increase in tSOD and mtSOD activities (18%, P < 0.05) was observed in heart homogenates of 24‐week trained animals as compared with their sedentary controls. HSP72 expression levels were not significantly modified after 12 week of training but a threefold increase was detected after 24 week (P < 0.05). Conclusion: These results demonstrate that a long‐term endurance training (24 weeks) induced discrete increases in antioxidant enzyme activities in rat myocardium and elicited a marked enhancement in HSP72 expression levels. However, a shorter training programme (12 weeks), was not effective in increasing heart antioxidant defences.     

IGF-1 regulate the expression of uncoupling protein 2 via FOXO1

Abstract

Mitochondria uncoupling protein2 (UCP2) expressed ubiquitously is a key molecule of energy metabolism. Insulin-like growth factor-1 (IGF-1) is a hormone, a target molecule of growth hormone (GH) signal pathway, which is also known as the drug “mecasermin” for clinical usages. IGF-1 is seemed to be closely related to metabolic diseases, such as adult GH deficiency. However, there has not been reports depicted possible relationship with each other. So, we sought to elucidate the mechanisms by which expression of UCP2 is regulated by IGF-1 via FOXO1. The findings suggested that three sequences in the consensus UCP2 promoter play complementary functional roles in the functional expression of FOXO1. So, we found that FOXO1 is involved in IGF-1-mediated energy metabolism greater than that of direct action of GH via STAT5. Our findings suggested that IGF-1 was involved in energy metabolism by regulating the expression of UCP2 via the PI3K/Akt/FOXO1 pathway.     

Combined effects of hypoxia and endurance training on lipid metabolism in rat skeletal muscle

Aim: To determine whether endurance training can counterbalance the negative effects of hypoxia on mitochondrial phosphorylation and expression of the long chain mitochondrial fatty acid transporter muscle carnitine palmitoyl transferase 1 (mCPT‐1). Methods: Male Wistar rats were exposed either to hypobaric hypoxia (at a simulated altitude of ≈4000 m, PIO₂ ≈ 90 mmHg) or to normoxia (sea level) for 5 weeks. In each environment, rats were randomly assigned to two groups. The trained group went through a 5‐week endurance training programme. The control group remained sedentary for the same time period. Muscle fatty acid oxidation capacity was evaluated after the 5‐week period on isolated mitochondria prepared from quadriceps muscles with the use of palmitoylcarnitine or pamitoylCoA + carnitine. Results: Chronic hypoxia decreased basal (V₀, ?31% with pamitoylCoA + carnitine and ?21% with palmitoylcarnitine, P < 0.05) and maximal (V_max, ?31% with pamitoylCoA + carnitine, P < 0.05) respiration rates, hydroxyacylCoA dehydrogenase activity (?48%, P < 0.05), mCPT‐1 activity index (?34%, P < 0.05) and mCPT‐1 protein content (?34%, P < 0.05). Five weeks of endurance training in hypoxia brought V₀, mCPT‐1 activity index and mCPT‐1 protein content values back to sedentary normoxic levels. Moreover, in the group trained in hypoxia, V_max reached a higher level than in the group that maintained a sedentary lifestyle in normoxia (24.2 nmol O₂· min^?1 · mg^?1 for hypoxic training vs. 19.9 nmol O₂ · min^?1 · mg^?1 for normoxic sedentarity, P < 0.05). Conclusion: Endurance training can attenuate chronic hypoxia‐induced impairments in mitochondrial fatty acid oxidation. This training effect seems mostly mediated by mCPT‐1 activity rather than by mCPT‐1 content.     

运动产生鸢尾素对心肌纤维化的影响

文题释义： 心肌纤维化(myocardial fibrosis,MF)：心脏作为人体全身最重要的器官之一,其主要功能是为血流提供动力,把血液运行至身体各个部分。而心脏的泵血功能有赖于心肌的收缩和舒张能力。心肌纤维化是指心脏成纤维细胞的活化和过度增殖,导致胶原纤维过度积聚, 胶原含量升高和胶原容积增高的病理性变化,此过程会使心肌僵硬度提高,收缩和舒张能力降低。鸢尾素(irisin)：属于一种肌肉因子,它于2012年被首次发现,其主要功能是使白色脂肪组织转化为棕色脂肪,增加产热和能量消耗。运动训练可以升高血液鸢尾素水平,且不同运动方式对其影响结果存有差异,血清鸢尾素通过作用于解偶联蛋白2和线粒体稳态调控氧化应激和炎症反应从而对心肌起保护作用。背景：心肌纤维化是现代医学研究的一个重要议题,与心律失常、慢性心力衰竭等常见心脏疾病密切相关。运动介入对心肌纤维化有显著改善作用,但运动改善心肌纤维化的机制及不同运动类型对心肌纤维化的影响缺乏系统、全面的认识。运动如何触发鸢尾素的产生而对心肌纤维化起作用？这个问题目前尚不清楚。 目的：针对国内外学者有关运动刺激诱导鸢尾素的产生及其对心肌纤维化的影响进行全面综述,揭示其对心肌的保护作用机制,从而为提高心脏功能,预防心律失常、慢性心力衰竭等常见心脏疾病提供理论基础及实践参考。 方法：搜寻ELSEVIER、Web of Science、CNKI资料总库、万方数据、维普中文期刊服务平台及台湾学术文献数据库,检索与运动训练、鸢尾素、心肌纤维化等相关的中英文文献,发表时间截止至2019年8月,根据研究需要确立相应的入选标准,对最终筛选所得的58篇文献进行论述。 结果与结论：①人体试验中已证实长时间及单次运动均可提高肌肉及循环鸢尾素水平,而这一结果也在动物实验中得到较好验证;少数试验结果表明长时运动对血液鸢尾素水平无显著影响;出现不同结果的原因可能是选择的研究对象、运动方式、运动强度、运动频率不同,而具体机制尚不明确;②运动可通过鸢尾素作用于心肌线粒体稳定、能量代谢、氧化应激和炎症反应对心肌起保护作用,从而改善心肌纤维化;③心肌纤维化的发生受神经内分泌的调节和氧化应激及炎症反应的影响,鸢尾素可通过抑制ROS/p38MAPK/NFKB信号通路、内源性活性氧和ROS-NLRP3炎症信号通路、调节解偶联蛋白2的表达和线粒体稳态,从而影响心肌纤维化形成机制里的氧化应激反应和炎症反应过程,因此运动改善心肌纤维化可能和运动提高鸢尾素表达从而对心肌起保护作用有关。 ORCID:0000-0003-0990-2396(尹练)中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

Exercise-induced decreases in sarcoplasmic reticulum Ca2+–ATPase activity attenuated by high-resistance training

Muscle biopsies were performed on the vastus lateralis muscle prior to and during a high-resistance training (HRT) programme in order to examine the effects of hypertrophy on sarcoplasmic reticulum Ca²⁺ ATPase activity at rest and during exercise. In six male untrained volunteers (peak aerobic power, V˙O ₂ peak = 3.39 ± 0.13 L min^?1, mean ± SE), the resting Ca²⁺ ATPase activity (μmol min^?1 g wet wt^?1) at 0 (4.89 ± 0.20), 4 (5.62 ± 0.56), 7 (5.15 ± 0.41) and 12 (4.82 ± 0.11) weeks was unchanged by HRT. During cycle ergometer exercise, prior to training, Ca²⁺-ATPase was reduced (P < 0.05) by 14% during the initial 30 min at 58% VO ₂ peak and (P < 0.05) a further 19% during 30 min at 72% VO ₂ peak. Following 7 and 12 weeks of training, the decreases in SR Ca²⁺-ATPase were less pronounced (P < 0.05). These results indicate that muscle hypertrophy, although incapable of altering Ca²⁺-ATPase pump activity at rest, can attenuate the decrease observed in exercise by mechanism(s) as yet unknown.     

解耦联蛋白2在人卵巢的表达及与年龄的关系

目的探讨解耦联蛋白2（UCP2）在卵巢组织的表达及其与年龄的关系。方法用原位杂交和Western blot检测33例,其中〈36岁11例,≥36岁22例。手术切除的卵巢组织UCP2 mRNA和蛋白的表达,结果UCP2主要表达于人类卵巢生长卵泡的颗粒细胞和卵巢血管壁细胞内,在蛋白水平,年长女性UCP2表达水平显著低于年轻女性。结论UCP2可能参与卵泡发育调控,年长女性颗粒细胞UCP2表达降低可能是年龄相关卵母细胞改变的机制之一。     

解偶联蛋白3基因 -55 C→T变异与中国人体脂代谢、含量、分布及2型糖尿病的关系

目的 研究解偶联蛋白3（uncoupling protein 3,UCP3）基因－55C→T变异与中国人体脂含量、体脂代谢、体脂分布及2型糖尿病的关系。方法 用聚合酶链反应－限制性片段长度多态性检测了165名糖耐量正常者（男／女为69／96）及151例2型糖尿病患者（男／女为62／89）UCP3基因－55C→T变异的基因型，核磁共振8检测局部体脂含量，酶法及硫酸葡聚糖－锰沉淀法测血总胆固醇及血高密度脂蛋白胆固醇，并用公工密度脂蛋白胆固醇。结果 （1）非糖尿病中国人与白种人比较等位基因频率及基因型频率差异均无显著性（P分别为0.1120和0.0646），与Pima印地安人比较差异均有显著性（P分别为0.0105及0.0314）。（2）逐步回归分析发现，UCP3基因－55C→T变异的独立相关变量：糖耐量正常男性组为血高密度脂蛋白胆固醇及低密度脂蛋白胆固醇，糖耐量正常女性组为股部脂肪面积，2型糖尿病男性组为血甘油三酯，2型糖尿病妇性组为腰臀比。（3）2型糖尿病组与糖耐量正常组相比，等位基因频率的差异有显著性（P为0.0358）。携带T等位基因发生2型糖尿病的相对风险的比数比为1.434（95％可信区间为1.031-1.995）。结论 UCP3基因－55C→T变异与中国人局部体脂含量、体脂代谢及分布相关，但存在性别及疾病状态的差异。该变异与中国人2型糖尿病的发生相关。     

Effects of strength and endurance training on isometric muscle strength and walking speed in elderly women

The separate effects of 18 weeks of intensive strength and endurance training on isometric knee extension (KE) and flexion (KF) strength and walking speed were studied in 76-to 78-year-old women. Maximal voluntary isometric force for both KE and KF was measured in a sitting position on a custom-made dynamometer chair at a knee angle of 60° from full extension. Maximal walking speed was measured over a distance of 10 m. The endurance-trained women increased KE torque and KE torque/body mass after the first 9 weeks of training when compared with the controls. When comparing the baseline, 9 week and 18 week measurements within the groups separately, both the endurance- and strength-training groups increased KE torque, KE torque/body mass and walking speed. Individual changes in KE torque/body mass before and after 18 weeks of training averaged 19.1% in the strength group, 30.9% in the endurance group and 2.0% in the controls. This study indicates that in elderly women the effects of physical training on muscle strength and walking speed occur after endurance as well as strength training. The considerable interindividual variation in change of muscle performance is also worth noticing.     

Effects of endurance training on hyperammonaemia during a 45-min constant exercise intensity

Summary Eleven laboratory-pretrained subjects (initial =54 ml·kg⁻¹·min⁻¹) took part in a study to evaluate the effect of a short endurance training programme [8–12 sessions, 1 h per session, with an intensity varying from 60% to 90% maximal oxygen consumption ] on the responses of blood ammonia (b[NH ₄ ⁺ ]) and lactate (b[la]) concentrations during progressive and constant exercise intensities. After training, during which did not increase, significant decreases in b[NH ₄ ⁺ ], b[la] and muscle proton concentration were observed at the end of the 80% constant exercise intensity, although b[NH ₄ ⁺ ] and b[la] during progressive exercise were unchanged. On the other hand, no correlations were found between muscle fibre composition and b[NH ₄ ⁺ ] in any of the exercise procedures. This study demonstrated that a constant exercise intensity was necessary to reveal the effect of training on muscle metabolic changes inducing the decrease in b[NH ₄ ⁺ ] and b[la]. At a relative power of exercise of 80% , there was no effect of muscle fibre composition on b[NH ₄ ⁺ ] accumulation.     

Effects of strength, endurance and combined training on myosin heavy chain content and fibre-type distribution in humans

This study investigated the effect of strength training, endurance training, and combined strength plus endurance training on fibre-type transitions, fibre cross-sectional area (CSA) and MHC isoform content of the vastus lateralis muscle. Forty volunteers (24 males and 16 females) were randomly assigned to one of four groups: control (C), endurance training (E), strength training (S), or concurrent strength and endurance training (SE). The S and E groups each trained three times a week for 12 weeks; the SE group performed the same S and E training on alternate days. The development of knee extensor muscle strength was S>SE>E (P<0.05) and has been reported elsewhere. The reduction in knee extensor strength development in SE as compared to S corresponded to a 6% increase in MHCIIa content (P<0.05) in SE at the expense of the faster MHCIId(x) isoform (P<0.05), as determined by electrophoretic analyses; reductions in MHCIId/x content after S or E training were attenuated by comparison. Both S and SE induced three- to fourfold reductions (P<0.05) in the proportion of type IIA/IID(X) hybrid fibres. S also induced fourfold increases in the proportion of type I/IIA hybrid fibres within both genders, and in a population of fibres expressing a type I/IID(X) hybrid phenotype within the male subjects. Type I/IIA hybrid fibres were not detected after SE. Both S and SE training paradigms induced similar increases (16–19%, P<0.05) in the CSA of type IIA fibres. In contrast, the increase in CSA of type I fibres was 2.9-fold greater (P<0.05) in S as compared to SE after 12 weeks. We conclude that the interference of knee extensor strength development in SE versus S was related to greater fast-to-slow fibre-type transitions and attenuated hypertrophy of type I fibres. Data are given as mean (SEM) unless otherwise stated.     

Extreme endurance training evidence of capillary and mitochondria compartmentalization in human skeletal muscle

Summary Biopsies from the medial gastrocnemius muscle of three experienced endurance runners who had completed an ultramarathon run (160 km) the previous day were assessed for their oxidative characteristics (fibre types, capillarization and mitochondria content). Also, a regional comparison was made for fibres located centrally (completely surrounded by other fibres) versus fibres located peripherally (next to the interfascicular space) and the capillarization of these peripheral fibres was determined. Subsarcolemmal mitochondria were abundant and compartmentalized close to the capillaries. The number of capillaries around fibres ranged from 5.8 to 8.5 and 5.7 to 8.5, and the number of capillaries·mm^–2 ranged from 665 to 810 and 727 to 762, for type I (slow twitch) and type 11 (fast twitch) fibres, respectively. Central fibres contained a greater number of capillaries and more capillaries·mm^–2 than their peripheral counterparts. Peripheral fibres contained more capillaries · m^–1 between fibres than at the interfascicular space. Type I fibres were more distributed (63%–78%) and larger than type II fibres. An abundance of subsarcolemmal mitochondria located close to the capillaries, efficient capillary proliferation between fibres where sharing can occur and greater relative distribution and size of type I fibres are, collectively, efficient characteristics of extreme endurance training.     

Effects of endurance training on oxidative capacity and structural composition of human arm and leg muscles

Six healthy subjects performed endurance training of the same duration with legs and arms consecutively. Performance and muscle structure were measured before and after training in lower and upper limbs. Training induced similar increases in maximal oxygen consumption (6 ± 1 vs. 7 ± 2 mL min^?1 kg^?1: legs vs. arms, P > 0.05) and mitochondrial volume in leg and arm muscles (42 ± 12 vs. 31 ± 11%: legs vs. arms, P > 0.05). The gain in mitochondrial volume after training was achieved solely by increasing the fraction of mitochondria (+40 ± 11%, P < 0.05) in the same muscle volume (+2 ± 2%, P > 0.05) in the legs. In contrast, increased muscle volume (+14 ± 3%, P < 0.05), in addition to a tendency for an increase in mitochondrial fraction (+16 ± 11%, P > 0.05), occurred in the arms after training. Thus, similar improvements in muscle oxidative capacity in upper and lower limbs were brought about by different mechanisms. It is suggested that due to infrequent use and a lack of load-bearing function, arm muscle volume is underdeveloped in untrained, sedentary or detrained/injured subjects and that the mode of endurance training used in this study is sufficient to enlarge arm muscle volume as well as aerobic capacity.