Endurance Exercise Capacity Research Articles

블루베리 추출물과 쌀 단백질의 혼합물이 한계유영운동에 미치는 영향

본 연구에서는 블루베리 추출물과 쌀 단백질을 혼합한 복합물을 마우스에 투여한 후 한계유영운동능력을 평가하였다. 한계유영운동 시간은 비투여(Ex-CON)군보다 혼합물을 투여한(Ex-Mix) 군이 유의적으로 높게 나타났다. 혈중 젖산(lactic acid)과 비에스테르화지방산(NEFA) 모두 Ex-Mix군이 유의적으로 높게 나타나는 것을 확인하였으며, 근육내 글리코겐 함량 및 항산화 능력이 혼합물을 투여한 군에서 운동군보다 유의적으로 높았으며 비운동군과 유의차를 보이지 않았다. 또한, 한계운동으로 높아진 근육 내 MDA 함량은 혼합물 투여에 의해 유의적으로 낮게 나타났으며 비운동군과 유의적 차이를 보이지 않았다. 이상의 결과로 혼합물의 투여가 한계유영운동 능력을 높이고 관련 인자들을 향상시키는 것을 확인하였다.

Pathophysiology of Chronic Systolic Heart Failure. A View from the Periphery.

Heart failure is a common form of heart disease associated with progressive exercise intolerance and high risk of adverse clinical outcome events. The pathophysiology of chronic systolic heart failure is fundamentally determined by the failure of the circulatory system to deliver oxygen sufficient for metabolic needs, and it is best explained by a complex interplay between intrinsic abnormalities of ventricular pump function and extracardiac factors that limit oxygen use in metabolically active tissues. This brief review highlights the role of extracardiac factors (peripheral factors) that may impact exercise capacity in patients with chronic systolic heart failure. Reduced metabolic vasodilation limits delivery of available cardiac output reserve to skeletal muscle during exercise, and it is associated with reduced peak oxygen capacity. Abnormal substrate use in skeletal muscle due to reduced skeletal muscle mass, change in skeletal muscle fiber type, and mitochondrial dysfunction reduces work efficiency and submaximal exercise endurance capacity in patients with systolic heart failure. These extracardiac peripheral mechanisms of impaired exercise tolerance in chronic heart failure may be targets for novel therapeutic development in this patient population.

Ghrelin mediates exercise endurance and the feeding response post-exercise

ObjectiveExercise training has several well-established health benefits, including many related to body weight, appetite control, and blood glucose homeostasis. However, the molecular mechanisms and, in particular, the hormonal systems that mediate and integrate these beneficial effects are poorly understood. In the current study, we aimed to investigate the role of the hormone ghrelin and its receptor, the growth hormone secretagogue receptor (GHSR; ghrelin receptor), in mediating the effects of exercise on food intake and blood glucose following exercise as well as in regulating exercise endurance capacity. MethodsWe used two mouse models of treadmill running to characterize the changes in plasma ghrelin with exercise. We also assessed the role of the ghrelin system to influence food intake and blood glucose after exercise, exercise endurance, and parameters potentially linked to responses to exercise. Mice lacking GHSRs (GHSR-null mice) and wild-type littermates were studied. ResultsAn acute bout of exercise transiently elevated plasma acyl-ghrelin. Without the action of this increased ghrelin on GHSRs (as in GHSR-null mice), high intensity interval exercise markedly reduced food intake compared to control mice. The effect of exercise to acutely raise blood glucose remained unmodified in GHSR-null mice. Exercise-induced increases in plasma ghrelin positively correlated with endurance capacity, and time to exhaustion was reduced in GHSR-null mice as compared to wild-type littermates. In an effort to mechanistically explain their reduced exercise endurance, exercised GHSR-null mice exhibited an abrogated sympathoadrenal response, lower overall insulin-like growth factor-1 levels, and altered glycogen utilization. ConclusionsExercise transiently increases plasma ghrelin. GHSR-null mice exhibit decreased food intake following high intensity interval exercise and decreased endurance when submitted to an exercise endurance protocol. These data suggest that an intact ghrelin system limits the capacity of exercise to restrict food intake following exercise, although it enhances exercise endurance.

Nuclear factor (erythroid derived 2)-like 2 activation increases exercise endurance capacity via redox modulation in skeletal muscles

Sulforaphane (SFN) plays an important role in preventing oxidative stress by activating the nuclear factor (erythroid derived 2)-like 2 (Nrf2) signalling pathway. SFN may improve exercise endurance capacity by counteracting oxidative stress-induced damage during exercise. We assessed running ability based on an exhaustive treadmill test (progressive-continuous all-out) and examined the expression of markers for oxidative stress and muscle damage. Twelve- to 13-week-old Male wild-type mice (Nrf2+/+) and Nrf2-null mice (Nrf2−/−) on C57BL/6J background were intraperitoneally injected with SFN or vehicle prior to the test. The running distance of SFN-injected Nrf2+/+ mice was significantly greater compared with that of uninjected mice. Enhanced running capacity was accompanied by upregulation of Nrf2 signalling and downstream genes. Marker of oxidative stress in SFN-injected Nrf2+/+ mice were lower than those in uninjected mice following the test. SFN produced greater protection against muscle damage during exhaustive exercise conditions in Nrf2+/+ mice than in Nrf2−/− mice. SFN-induced Nrf2 upregulation, and its antioxidative effects, might play critical roles in attenuating muscle fatigue via reduction of oxidative stress caused by exhaustive exercise. This in turn leads to enhanced exercise endurance capacity. These results provide new insights into SFN-induced upregulation of Nrf2 and its role in improving exercise performance.

Air velocity influences thermoregulation and endurance exercise capacity in the heat.

This study examined the effects of variations in air velocity on time to exhaustion and thermoregulatory and perceptual responses to exercise in a hot environment. Eight male volunteers completed stationary cycle exercise trials at 70% peak oxygen uptake until exhaustion in an environmental chamber maintained at 30 °C and 50% relative humidity. Four air velocity conditions, 30, 20, 10, and 0 km/h, were tested, and the headwind was directed at the frontal aspect of the subject by 2 industrial fans, with blade diameters of 1 m and 0.5 m, set in series and positioned 3 m from the subject's chest. Mean ± SD time to exhaustion was 90 ± 17, 73 ± 16, 58 ± 13, and 41 ± 10 min in 30-, 20-, 10-, and 0-km/h trials, respectively, and was different between all trials (P < 0.05). There were progressive elevations in the rate of core temperature rise, mean skin temperature, and perceived thermal sensation as airflow decreases (P < 0.05). Core temperature, heart rate, cutaneous vascular conductance, and perceived exertion were higher and evaporative heat loss was lower without airflow than at any given airflow (P < 0.05). Dry heat loss and plasma volume were similar between trials (P > 0.05). The present study demonstrated a progressive reduction in time to exhaustion as air velocity decreases. This response is associated with a faster rate of core temperature rise and a higher skin temperature and perceived thermal stress with decreasing airflow. Moreover, airflow greater than 10 km/h (2.8 m/s) might contribute to enhancing endurance exercise capacity and reducing thermoregulatory, cardiovascular, and perceptual strain during exercise in a hot environment.

Resistance training and exercise tolerance during high-intensity exercise: moving beyond just running economy and muscle strength.

Resistance training and exercise tolerance during high-intensity exercise: moving beyond just running economy and muscle strength.

Rats bred for low and high running capacity display alterations in peripheral tissues and nerves relevant to neuropathy and pain.

IntroductionDiet and activity are recognized as modulators of nervous system disease, including pain. Studies of exercise consistently reveal a benefit on pain. This study focused on female rats to understand differences related to metabolic status and peripheral nerve function in females.MethodsHere, we investigated parameters of peripheral nerve function relevant to pain in rats selectively bred for high (high‐capacity runners; HCR) or low endurance exercise capacity (low‐capacity runners; LCR) resulting in divergent intrinsic aerobic capacities and susceptibility for metabolic conditions.Results LCR female rats have reduced mechanical sensitivity, higher intraepidermal nerve fiber density and TrkA‐positive epidermal axons, increased numbers of Langerhans and mast cells in cutaneous tissues, and a higher fat content despite similar overall body weights compared to female HCR rats. Sensory and motor nerve conduction velocities, thermal sensitivity, and mRNA expression of selected genes relevant to peripheral sensation were not different.ConclusionsThese results suggest that aerobic capacity and metabolic status influence sensory sensitivity and aspects of inflammation in peripheral tissues that could lead to poor responses to tissue damage and painful stimuli. The LCR and HCR rats should prove useful as models to assess how the metabolic status impacts pain.

Abstract 274: Defective Branched Chain Amino Acid Catabolism Impairs Exercise Endurance

The branched chain amino acids (BCAA), leucine, isoleucine and valine, are essential for mammalians, and they play a positive role in exercise capacity, muscle development, and a lean body phenotype. BCAA supplementation is commonly paired with exercise in order to promote muscle growth, increase resistance to fatigue and reduce muscle soreness. On the other hand, elevated serum BCAA is strongly and positively correlated with the development of insulin resistance, coronary heart disease, and type II diabetes, and is predictive of patient response to therapeutics and intervention outcomes. We have previously shown that defective BCAA catabolism in mice impaired glucose metabolism in the heart and increased susceptibility to stress-induced cardiac damage. In this study we sought to determine the effects of elevated BCAA levels on skeletal muscle performance and response to exercise training using mouse models with systemically elevated BCAA levels. Supplementation of BCAA (1.5mg/g bodyweight/day, ratio of Leu:Ile:Val = 1.5:0.8:1) was administered to mice with impairment of BCAA catabolism due to the deletion of mitochondrial-localized protein phosphatase 2C (KO), a key enzyme in activating BCAA catabolism, and their littermate controls (CON). Mice were subjected to one week of daily exercise training via forced treadmill running and an exercise capacity test was performed at the beginning and end of training. Baseline maximum running time was decreased in the KO compared to CON (mean 73.4 and 82.5 min, respectively). One week of training resulted in increased exercise capacity in CON with an attenuated increase in KO mice (mean 136 and 112 min, respectively). BCAA supplementation did not further improve exercise capacity in CON (mean 131 min) and abrogated the response to training in KO (mean 70.1 min). Reduced exercise capacity positively correlated with elevated serum BCAA levels. Additionally, KO supplemented with BCAAs demonstrated elevated serum succinate, alanine and glutamate levels, which are metabolic markers of physiological stress. We conclude that short term supplementation of BCAA has no benefit for exercise capacity and accumulation of BCAAs has a negative effect on endurance exercise capacity.

Antifatigue effects of troxerutin on exercise endurance capacity, oxidative stress and matrix metalloproteinase-9 levels in trained male rats.

The aim of this study was to investigate effects of troxerutin (TRX) on endurance capacity, oxidative stress and matrix metalloproteinase-9 (MMP-9) levels in trained male rats. Forty male Wistar rats were divided into five groups. The control (Vehicle) and exercise training (5days/week) with vehicle treatment (Exercise), exercise training with TRX treatment at 75 (Ex-TRX75), 150 (Ex-TRX150), and 300mg/kg (Ex-TRX300). The treated groups received TRX by gavage every day while the other groups received water for 30days. On the 30th day, rats were sacrificed immediately after exhaustive swimming test, and some biochemical parameters were measured. Exhaustion swimming time in the Ex-TRX75, Ex-TRX150 and Ex-TRX300 groups significantly increased 1.2-, 1.93- and 2.1-fold compared to the vehicle group, respectively. TRX significantly increased glucose level (P<0.05) and reduced creatine kinase activity (P<0.001) compared to the vehicle and exercise groups. TRX300 significantly reduced alkaline phosphatase and lactate dehydrogenase activities (P<0.05) and blood urea nitrogen (P<0.05) and MMP-9 levels (P<0.05) compared to the vehicle and exercise groups. Additionally, TRX300 and TRX150 significantly increased superoxide dismutase activity compared to the vehicle group (P<0.05). Our results provide experimental evidence in supporting clinical use of TRX as an effective agent against fatigue.

Smooth Muscle Cell Mineralocorticoid Receptors Are Necessary for Cardiovascular Fibrosis with Aging

Vascular aging involves fibrosis leading to stiffening of the vascular wall, an independent predictor of adverse cardiovascular events. Mineralocorticoid receptors (MR) are expressed in vascular smooth muscle cells (SMC) and MR signaling has been implicated in the regulation of cardiovascular fibrosis but has not been explored in cardiovascular aging. We previously demonstrated that aged mice lacking MR in SMCs (SMC‐MR‐KO) have lower blood pressure and reduced responsiveness to angiotensin II. The aim of this study was to investigate the role of SMC‐MR in cardiovascular structural and functional changes with aging and to explore mechanisms by which SMC‐MR contributes to vascular aging by modulating global vascular gene expression in mice. Vascular and cardiac fibrosis, aortic pulse wave velocity (PWV), cardiac echocardiography, intra‐cardiac pressure‐volume loops, and endurance exercise capacity were assessed in 3, 12 and 18 month‐old male MR‐intact and SMC‐MR‐KO mice. Vascular fibrosis in aortas, carotid arteries, and renal arterioles and aortic stiffness increased with aging in MR‐intact mice. Importantly, these aging‐induced increases were attenuated in SMC‐MR‐KO mice. Cardiac hypertrophy, wall thickness, fibrosis and stiffness increased and cardiac function and endurance exercise capacity decreased with aging in MR‐intact mice. Aging‐induced changes in cardiac hypertrophy, wall thickness and function were unaffected by the absence of SMC‐MR, however, SMC‐MR‐KO mice were protected from the aging‐induced increases in cardiac fibrosis and stiffness and the decrease in endurance exercise capacity. There was a significant correlation between aortic PWV and end‐systolic pressure volume relationship, suggesting that the changes in cardiac systolic stiffness are likely secondary to changes in aortic stiffness with aging. Renal fibrosis increased with aging but this increase was independent of the presence of SMC‐MR. To explore the mechanism by which SMC‐MR contributes to vascular fibrosis and stiffness with aging, we characterized global gene expression profiles in aortas from 3 and 12 month‐old MR‐intact and SMC‐MR‐KO mice. 552 and 477 genes were differentially expressed with aging in aortas from MR‐intact and SMC‐MR‐KO, respectively. Only 79 genes were differentially expressed with aging in both MR‐intact and SMC‐MO‐KO mice. Pathway analysis revealed that changes in cardiovascular development pathways with aging are predicted to act in opposing directions in SMC‐MR‐KO mice compared to MR intact mice. We also identified a network of fibrosis‐related genes that are down‐regulated with aging in SMC‐MR‐KO mice, providing a possible mechanism for the reduced vascular fibrosis with aging in SMC‐MR‐KO mice. Our findings provide evidence that SMC‐MR plays a role in aging‐induced increase in vascular fibrosis that contributes to cardiovascular tissue stiffening and dysfunction with aging. Further studies are underway to treat aged mice with MR antagonist to attempt to reverse the aging phenotype.Support or Funding InformationNIH/NHLBI R01 HL119290 and AHA EIA18290005

Prostate Cancer Reduces Endurance Exercise Capacity in the Rat: Possible Roles of Reduced Cardiac Mass and Function

Prostate cancer is the most commonly diagnosed non‐skin cancer in men. Exercise intolerance is common in prostate cancer patients; particularly those subject to androgen deprivation therapy. Whether prostate cancer itself reduces exercise capacity is unknown.ObjectiveWe used a preclinical rat prostate tumor model to test the hypothesis that untreated prostate cancer reduces endurance exercise capacity.MethodsSixteen male Copenhagen rats performed an initial treadmill test to exhaustion. The rats' prostates were subsequently injected with either prostate carcinoma cells (R‐3327 AT‐1 cell line) in Matrigel (cancer, n=9) or Matrigel only (sham, n=7) and the treadmill tests were repeated eight weeks post‐surgery. Following the final treadmill test, left ventricle contractility (left ventricle Δpressure/Δtime) was measured under anesthesia and the heart and gastrocnemius muscles were then dissected and weighed.ResultsAverage prostate tumor mass in the cancer group was 9.8±2.6 g (range: 0.2 to 19.5 g). Initial times to exhaustion were not significantly different between groups (sham: 29.8±1.3, cancer: 28.6±2.5 min, p=0.710). Time to exhaustion at eight weeks post‐surgery was reduced compared to initial values for both groups but the eight‐week time to exhaustion was significantly lower in the cancer group (13.3±1.4 min) compared to the sham group (19.7±2.1 min, p=0.019). Left ventricle Δpressure/Δtime was not significantly different between groups, but within the cancer group prostate tumor mass was significantly inversely correlated to left ventricle Δpressure/Δtime (−0.71, p=0.047). Total body mass was not significantly different between groups (p=0.363) but heart (↓12%, p=0.021), left ventricle (↓16%, p=0.003) and gastrocnemius (↓9%, p=0.005) muscle mass were significantly lower in the cancer group compared to the sham group. Within the cancer group heart (r=−0.74, p=0.22) and left ventricle (r=−0.85, p=0.004) mass, but not gastrocnemius muscle mass (r=−0.15, p=0.696), were inversely correlated with prostate tumor mass. In other words, within the cancer group the rats with the largest prostate tumors had the lowest cardiac contractility, the smallest heart mass, and, more specifically, the smallest left ventricle mass.ConclusionWe found that untreated prostate cancer reduced endurance exercise capacity in rats. Although multiple mechanisms likely contributed to the reduced exercise capacity in rats with prostate cancer, reductions in cardiac muscle function and mass, as well as reductions in gastrocnemius muscle mass, likely played an important role.Support or Funding InformationAmerican Cancer Society (RSG‐14‐150‐01‐CCE to BJB)

Endurance capacity and neuromuscular fatigue following high- vs moderate-intensity endurance training: A randomized trial.

High-intensity exercise induces significant central and peripheral fatigue; however, the effect of endurance training on these mechanisms of fatigue is poorly understood. We compared the effect of cycling endurance training of disparate intensities on high-intensity exercise endurance capacity and the associated limiting central and peripheral fatigue mechanisms. Twenty adults were randomly assigned to 6weeks of either high-intensity interval training (HIIT, 6-8×5minutes at halfway between lactate threshold and maximal oxygen uptake [50%Δ]) or volume-matched moderate-intensity continuous training (CONT, ~60-80minutes at 90% lactate threshold). Two time to exhaustion (TTE) trials at 50%Δ were completed pre- and post-training to assess endurance capacity; the two post-training trials were completed at the pretraining 50%Δ (same absolute intensity) and the "new" post-training 50%Δ (same relative intensity). Pre- and post-exercise responses to femoral nerve and motor cortex stimulation were examined to determine peripheral and central fatigue, respectively. HIIT resulted in greater increases in TTE at the same absolute and relative intensities as pre-training (148% and 43%, respectively) compared with CONT (38% and -4%, respectively) (P≤.019). Compared with pre-training, HIIT increased the level of potentiated quadriceps twitch reduction (-34% vs -43%, respectively, P=.023) and attenuated the level of voluntary activation reduction (-7% vs -3%, respectively, P=.047) following the TTE trial at the same relative intensity. There were no other training effects on neuromuscular fatigue development. This suggests that central fatigue resistance contributes to enhanced high-intensity exercise endurance capacity after HIIT by allowing greater performance to be extruded from the muscle.

Effect of the timing of ice slurry ingestion for precooling on endurance exercise capacity in a warm environment

It has been demonstrated that precooling with ice slurry ingestion enhances endurance exercise capacity in the heat. However, no studies have yet evaluated the optimal timing of ice slurry ingestion for precooling. This study aimed to investigate the effects of varying the timing of ice slurry ingestion for precooling on endurance exercise capacity in a warm environment. Ten active male participants completed 3 experimental cycling trials to exhaustion at 55% peak power output (PPO) after 15min of warm-up at 30% PPO at 30°C and 80% relative humidity. Three experimental conditions were set: no ice slurry ingestion (CON), pre-warm-up ice slurry ingestion (−1°C; 7.5gkg−1) (PRE), and post-warm-up ice slurry ingestion (POST). Rectal and mean skin temperatures at the beginning of exercise in the POST condition (37.1±0.2°C, 33.8±0.9°C, respectively) were lower than those in the CON (37.5±0.3°C; P<0.001, 34.8±0.8°C; P<0.01, respectively) and PRE (37.4±0.2°C; P<0.01, 34.6±0.7°C; P<0.01, respectively) conditions. These reductions increased heat storage capacity and resulted in improved exercise capacity in the POST condition (60.2±8.7min) compared to that in the CON (52.0±11.9min; effect size [ES]=0.78) and PRE (56.9±10.4min; ES=0.34) conditions. Ice slurry ingestion after warm-up effectively reduced both rectal and skin temperatures and increased cycling time to exhaustion in a warm environment. Timing ice slurry ingestion to occur after warm-up may be effective for precooling in a warm environment.

Ice ingestion with a long rest interval increases the endurance exercise capacity and reduces the core temperature in the heat

BackgroundThe timing in which ice before exercise should be ingested plays an important role in optimizing its success. However, the effects of differences in the timing of ice ingestion before exercise on cycling capacity, and thermoregulation has not been studied. The aim of the present study was to assess the effect of length of time after ice ingestion on endurance exercise capacity in the heat.MethodsSeven males ingested 1.25 g kg body mass−1 of ice (0.5 °C) or cold water (4 °C) every 5 min, six times. Under three separate conditions after ice or water ingestion ([1] taking 20 min rest after ice ingestion, [2] taking 5 min rest after ice ingestion, and [3] taking 5 min rest after cold water ingestion), seven physically active male cyclists exercised at 65% of their maximal oxygen uptake to exhaustion in the heat (35 °C, 30% relative humidity).ResultsParticipants cycled significantly longer following both ice ingestion with a long rest interval (46.0 ± 7.7 min) and that with a short rest interval (38.7 ± 5.7 min) than cold water ingestion (32.3 ± 3.2 min; both p < 0.05), and the time to exhaustion was 16% (p < 0.05) longer for ice ingestion with a long rest interval than that with a short rest interval. Ice ingestion with a long rest interval (−0.55 ± 0.07 °C; both p < 0.05) allowed for a greater drop in the core temperature than both ice ingestion with a short rest interval (−0.36 ± 0.16 °C) and cold water ingestion (−0.11 ± 0.14 °C). Heat storage under condition of ice ingestion with a long rest interval during the pre-exercise period was significantly lower than that observed with a short rest interval (−4.98 ± 2.50 W m−2; p < 0.05) and cold water ingestion (2.86 ± 4.44 W m−2).ConclusionsTherefore, internal pre-cooling by ice ingestion with a long rest interval had the greatest benefit on exercise capacity in the heat, which is suggested to be driven by a reduced rectal temperature and heat storage before the start of exercise.

INFLUENCE OF AGE DIFFERENCE IN RESPONSE TO MOTOR SKILL TRAINING ON THE PERFORMANCE OF ACTIVITIES OF DAILY LIVING BY PUPILS WITH CEREBRAL PALSY IN KISUMU KENYA

INTRODUCTION:Cerebral Palsy (CP) is a condition that restricts an individual's ability from independent living. Individuals with cerebral palsy are unable to perform precise movements of both fine and gross motor muscles required for self care activities such as dressing, toileting, feeding, cleaning amoung others. For individuals with cerebral palsy, self care abilities can be improved through training. This study evaluated the influence of age on response to motor skills training on the performance of activities of daily living by learners with cerebral palsy.According to (Olaf, et al., 2009), younger children with cerebral palsy respond faster to exercise on the performance of activities of daily living than adults.(Sekuler, Bennet, & Mamelak, 2005) observed that practice improved performance for both younger and older subjects. However, (Livingston, Stewart, Rosenbaum, & Russel, 2011) revealed that in South Africa, youths with severe physical disabilities have more difficulty performing cognitive skills than self-care skills when compared with younger ones. The study further revealed that most youths with severe physical challenges mastered the skills of activities of daily living even though with a lot of difficulties as compared to younger children with physical challenges. Younger children, more so those with disabilities enjoy self care activities being done for them. The difference between children with physical disabilities and those with Cerebral Palsy is that those with CP have unhealthy brain which may also detorroriate with age, it might therefore not be the age but the state of health of the brain when it comes to the abilities of learning the skills of daily living. In some cases older pupil can learn faster than younger learners and at times it can be vice -versa.LITERATURE REVIEW:(Fisher, 2010) studied cardio respiratory responses to exercise in children and adults in America. The study findings noted that maximum heart rate is a function of age, and children have very high maximal heart rates. Blood flow to working muscles is higher during exercise in children, this may partially compensate for the lower cardiac output. In contrast, during exercise, skeletal muscle oxygen extraction and muscle oxidative capacity are similar in the children and adults. Children require higher minute ventilation at any given oxygen consumption. The reason is the higher respiratory rate and shallower breathing in children. The study further found that respiratory muscles of children must work harder during exercise than those of adults. These differences in the cardio-vascular and respiratory system responses to exercise limit oxygen delivery to working muscles, resulting in a lower endurance exercise capacity in children. This does not mean that children cannot perform endurance exercises or improve endurance exercise capacity; rather it means that children cannot be expected to perform endurance exercises, or train for endurance events at the same level as adults. The study recommends exercise prescription for children which should approximately follow the general recommendations for enhancing motor skill functioning in children with physical disabilities. The reviewed study was done with children and adults with respiratory problems and not with children with cerebral palsy as it is in the present study.(Olaf, et al., 2009) conducted a study on the Gross Motor Function Classification System (GMFCS) among children with cerebral palsy in Europe. The study revealed that younger children with cerebral palsy responded faster to exercise on the performance of activities of daily living than adults.(Sekuler, Bennet, & Mamelak, 2005) carried out a study on age-related learning differences in USA. The study assessed how divided attention costs varied when initial performance levels were equated across the age groups at the start of practice. The result was that practice improved performance for both young and older subjects. …

Ursolic acid induces mitochondrial biogenesis through the activation of AMPK and PGC-1 in C2C12 myotubes: a possible mechanism underlying its beneficial effect on exercise endurance.

Mitochondrial biogenesis, which involves an increase in mitochondrial number and the overall capacity of oxidative phosphorylation, is a critical determinant of skeletal muscle function. Recent findings have shown that some natural products can enhance mitochondrial adaptation to aerobic exercise, which in turn improves exercise performance, presumably by delaying muscle fatigue. Ursolic acid (UA), a natural triterpene, is commonly found in various vegetables and fruits. In the current study, UA was shown to increase mitochondrial mass and ATP generation capacity, with a concomitant production of a low level of mitochondrial reactive oxygen species (ROS) in C2C12 myotubes. Mitochondrial ROS, in turn, activated the redox sensitive adenosine monophosphate-dependent protein kinase (AMPK)/peroxisome proliferator-activated receptor γ coactivator-1(PGC-1) pathway. The activation of AMPK/PGC-1 further increased the expression of cytochrome c oxidase (COX) and uncoupling protein 3. Animal studies showed that UA can also dose-dependently increase the endurance exercise capacity in mice, as assessed by a weight-loaded swimming test and a hanging wire test. Our findings suggest that UA may induce mitochondrial biogenesis through the activation of AMPK and PGC-1 pathways in skeletal muscle, thereby offering a promising prospect for its use to enhance exercise endurance and alleviating fatigue in humans.

Home-based telerehabilitation via real-time videoconferencing improves endurance exercise capacity in patients with COPD: The randomized controlled TeleR Study.

Telerehabilitation has the potential to increase access to pulmonary rehabilitation (PR) for patients with COPD who have difficulty accessing centre-based PR due to poor mobility, lack of transport and cost of travel. We aimed to determine the effect of supervised, home-based, real-time videoconferencing telerehabilitation on exercise capacity, self-efficacy, health-related quality of life (HRQoL) and physical activity in patients with COPD compared with usual care without exercise training. Patients with COPD were randomized to either a supervised home-based telerehabilitation group (TG) that received exercise training three times a week for 8 weeks or a control group (CG) that received usual care without exercise training. Outcomes were measured at baseline and following the intervention. Thirty-six out of 37 participants (mean ± SD age = 74 ± 8 years, forced expiratory volume in 1 s (FEV1 ) = 64 ± 21% predicted) completed the study. Compared with the CG, the TG showed a statistically significant increase in endurance shuttle walk test time (mean difference = 340 s (95% CI: 153-526, P < 0.001)), an increase in self-efficacy (mean difference = 8 points (95% CI: 2-14, P < 0.007)), a trend towards a statistically significant increase in the Chronic Respiratory Disease Questionnaire total score (mean difference = 8 points (95% CI: -1 to 16, P = 0.07)) and no difference in physical activity (mean difference = 475 steps per day (95% CI: -200 to 1151, P = 0.16)). This study showed that telerehabilitation improved endurance exercise capacity and self-efficacy in patients with COPD when compared with usual care.

Overexpression of protein kinase STK25 in mice exacerbates ectopic lipid accumulation, mitochondrial dysfunction and insulin resistance in skeletal muscle

Aims/hypothesisUnderstanding the molecular networks controlling ectopic lipid deposition and insulin responsiveness in skeletal muscle is essential for developing new strategies to treat type 2 diabetes. We recently identified serine/threonine protein kinase 25 (STK25) as a critical regulator of liver steatosis, hepatic lipid metabolism and whole body glucose and insulin homeostasis. Here, we assessed the role of STK25 in control of ectopic fat storage and insulin responsiveness in skeletal muscle.MethodsSkeletal muscle morphology was studied by histological examination, exercise performance and insulin sensitivity were assessed by treadmill running and euglycaemic–hyperinsulinaemic clamp, respectively, and muscle lipid metabolism was analysed by ex vivo assays in Stk25 transgenic and wild-type mice fed a high-fat diet. Lipid accumulation and mitochondrial function were also studied in rodent myoblasts overexpressing STK25. Global quantitative phosphoproteomics was performed in skeletal muscle of Stk25 transgenic and wild-type mice fed a high-fat diet to identify potential downstream mediators of STK25 action.ResultsWe found that overexpression of STK25 in transgenic mice fed a high-fat diet increases intramyocellular lipid accumulation, impairs skeletal muscle mitochondrial function and sarcomeric ultrastructure, and induces perimysial and endomysial fibrosis, thereby reducing endurance exercise capacity and muscle insulin sensitivity. Furthermore, we observed enhanced lipid accumulation and impaired mitochondrial function in rodent myoblasts overexpressing STK25, demonstrating an autonomous action for STK25 within cells. Global phosphoproteomic analysis revealed alterations in the total abundance and phosphorylation status of different target proteins located predominantly to mitochondria and sarcomeric contractile elements in Stk25 transgenic vs wild-type muscle, respectively, providing a possible molecular mechanism for the observed phenotype.Conclusions/interpretationSTK25 emerges as a new regulator of the complex interplay between lipid storage, mitochondrial energetics and insulin action in skeletal muscle, highlighting the potential of STK25 antagonists for type 2 diabetes treatment.

Relationship between FAT/CD36 Protein in Skeletal Muscle and Whole-body Fat Oxidation in Endurance-trained Mice.

[Purpose]We investigated the effects of endurance training on the expression of long-chain fatty acid transport proteins in the skeletal muscle and whole-body fat oxidation during endurance exercise.[Methods]Seven-week-old male ICR mice (n = 12) were divided into 2 groups, namely, Sed (sedentary; non-trained) and Tr (endurance-trained) groups. The Tr group was adapted to treadmill training at a fixed intensity (15 m/min, 8° slope) for 3 days. Next, the exercise intensity was increased while maintaining the 8° slope. In the last week of training, the exercise intensity was set at 25 m/min for 50 min (about 70–75% maximal oxygen uptake for 4 weeks). After the protocol ended, the mice were sacrificed, and tissues were collected for western blot analysis.[Results]Four weeks of endurance training resulted in a significant increase in the protein levels of FAT/CD36 and CPTІ. The FAT/ CD36 protein level in the Tr group was about 1.3-fold greater than that in the Sed group (p < 0.01). Furthermore, the increased CPTІ indicated higher activity (19% upregulation) in the Tr group compared to the Sed group (p < 0.05). The FAT/CD36 protein level and the estimated whole-body fat oxidation rate during 1-h exercise were found to be significantly correlated (r = 0.765, p < 0.01).[Conclusion]We suggest that the increase in FAT/CD36 protein in skeletal muscle by endurance training might be positively associated with whole-body fat oxidation, which might enhance endurance exercise capacity.

Separate and combined effects of exposure to heat stress and mental fatigue on endurance exercise capacity in the heat.

This study investigated the effects of exposure to pre-exercise heat stress and mental fatigue on endurance exercise capacity in a hot environment. Eight volunteers completed four cycle exercise trials at 80% maximum oxygen uptake until exhaustion in an environmental chamber maintained at 30°C and 50% relative humidity. The four trials required them to complete a 90min pre-exercise routine of either a seated rest (CON), a prolonged demanding cognitive task to induce mental fatigue (MF), warm water immersion at 40°C during the last 30min to induce increasing core temperature (WI), or a prolonged demanding cognitive task and warm water immersion at 40°C during the last 30min (MF+WI). Core temperature when starting exercise was higher following warm water immersion (~38°C; WI and MF+WI) than with no water immersion (~36.8°C; CON and MF, P<0.001). Self-reported mental fatigue when commencing exercise was higher following cognitive task (MF and MF+WI) than with no cognitive task (CON and WI; P<0.05). Exercise time to exhaustion was reduced by warm water immersion (P<0.001) and cognitive task (P<0.05). Compared with CON (18±7min), exercise duration reduced 0.8, 26.6 and 46.3% in MF (17±7min), WI (12±5min) and MF+WI (9±3min), respectively. This study demonstrates that endurance exercise capacity in a hot environment is impaired by either exposure to pre-exercise heat stress or mental fatigue, and this response is synergistically increased during combined exposure to them.