Beneficial Effects Of Endurance Training Research Articles

Effects and long-term outcomes of endurance versus resistance training as an adjunct to standard medication in patients with stable COPD: a multicenter randomized trial

BackgroundComparisons between endurance training (ET) and resistance training (RT) have produced equivocal findings in chronic obstructive pulmonary disease (COPD) patients. The purpose of our study is to investigate the effectiveness and long-term outcomes of adding ET and RT to conventional medical treatment in patients with COPD. A secondary objective is to investigate the clinical improvements resulting from exercise training in patients with different disease severities.MethodsThe study was a multicenter, prospective trial in people with stable COPD. The cohort was randomized to three groups: individualized medical treatment group (MT), MT + endurance training group (MT + ET) and MT + resistance training group (MT + RT). Exercise was performed 3 times weekly over a 12-week period. The endpoints of exercise capacity, health-related quality of life, COPD symptoms, lung function, and anxiety and depression questionnaires were re-evaluated at baseline, at the completion of the intervention and at 6 and 12-month follow-up. According to the COPD assessment tool offered by GOLD guidelines, patients were stratified into GOLD A and B groups and GOLD C and D groups for further subgroup analysis.ResultsThe intention-to-treat (ITT) population included 366 patients, 328 of them completed the study protocol over 12 months (the PP-population). There were no significant differences in the primary outcome, quality of life, between patients who underwent medical treatment (MT) alone, MT + endurance training (MT + ET), or MT + resistance training (MT + RT) at the completion of the intervention, 6-, or 12-month follow-up. Additionally, no significant differences were observed between MT, MT + RT, or MT + ET groups concerning the primary outcome, exercise capacity (3MWD), after initial 3 months of intervention. However, a small statistically significant difference was noted in favor of MT + ET compared to MT + RT at 12 months (ITT: Δ3MWD in ET vs RT = 5.53 m, 95% confidence interval: 0.87 to 13.84 m, P = 0.03) (PP: Δ3MWD in ET vs RT = 7.67 m, 95% confidence interval: 0.93 to 16.27 m, P = 0.04). For patients in the GOLD C and D groups, improvement in quality of life following ET or RT was significantly superior to medical intervention alone. Furthermore, upon completion of the exercise regimen, RT exhibited a greater improvement in anxiety compared to ET in these patients (ITT: ΔHAD-A at 3-month: RT = -1.63 ± 0.31 vs ET = -0.61 ± 0.33, p < 0.01) (PP: ΔHAD-A at 3-month: RT = -1.80 ± 0.36 vs ET = -0.75 ± 0.37, p < 0.01).ConclusionsOur study presents evidence of the beneficial effects of ET and RT in combination with standard medical treatment, as well as the long-term effects over time after the intervention. While the statistically significant effect favoring ET over RT in terms of exercise capacity was observed, it should be interpreted cautiously. Patients in severe stages of COPD may derive greater benefits from either ET or RT and should be encouraged accordingly. These findings have implications for exercise prescription in patients with COPD.Trial registrationChiCTR-INR-16009892 (17, Nov, 2016).

Oral 3-hydroxybuturate ingestion acutely lowers circulating testosterone concentrations in healthy young males.

Ketone bodies, such as 3-hydroxybutyrate (3-OHB), have been frequently used by endurance athletes, such as cyclists, to enhance performance and recovery and are recognized for their health benefits and therapeutic effects for decades. Testosterone is a potent regulator of red blood cell production. Evidence suggests that ketone bodies can increase the production of erythropoietin, which stimulates red blood cell production. Therefore, we investigated whether an acute increase in 3-OHB levels affects testosterone levels in healthy young men. We studied six healthy, young male participants who fasted overnight and were tested twice: (i) after drinking 37.5 g of Na-D/L-3-OHB dissolved in 500 mL of distilled water (KET), and (ii) after drinking 500 mL of placebo saline water (0.9% NaCl) (CTR). During the KET trial, 3-OHB levels increased to approximately 2.5 mM. Testosterone levels decreased significantly by 20% during KET compared to 3% during CTR. A simultaneous increase in luteinizing hormone was observed in KET. We observed no changes in other adrenal androgens, such as androstenedione and 11-keto androgens. In conclusion, an acute increase in 3-OHB levels decreases testosterone levels. Concomitantly, an increase in luteinizing hormone was observed. This suggests that 3-OHB may counteract some of the beneficial effects of endurance training. Further studies, involving larger sample sizes and performance outcomes, are required to fully understand this phenomenon.

The effects of exercise training on Kinesin and GAP-43 expression in skeletal muscle fibers of STZ-induced diabetic rats

Kinesin-1 and Growth Associated Protein 43 (GAP-43) localization in muscle fiber are crucial for proper skeletal muscle hypertrophy. To evaluate this assumption, we investigated the beneficial effects of endurance training on GAP-43 and Kinesin Family Member 5B (KIF5B) expression in gastrocnemius muscle of streptozotocin (STZ)-induced diabetic rats. Fifty-two male rats were randomly divided into four groups: healthy control (C), healthy trained (T), diabetic control (DC) and diabetic trained (DT). Diabetes was induced by a single intraperitoneal injection of STZ (45 mg/kg). The rats in DT and T groups were subjected to treadmill running for 5 days a week over 6 weeks. The results indicated that the GAP-43 and KIF5B protein levels in the DC group were significantly lower than those in the C group. Additionally, chronic treadmill running in diabetic rats was accompanied by significant increase of GAP-43 and KIF5B protein expression, compared to DC group. Furthermore, the endurance training in healthy rats was associated with a significant increase of GAP-43 and KIF5B protein levels. In addition, we found positive correlation between GAP-43 and KIF5B protein levels and myonuclear number per fiber and average gastrocnemius cross-sectional area (CSA). GAP43 and KIF5B protein levels were decreased in skeletal muscles of diabetic rats, and exercise training had beneficial effects and could restore their abnormal expression. Moreover, there is a strong relationship between muscle hypertrophy and GAP-43 and KIF5B protein levels.

Effect of Endurance Training with Royal Jelly on CRP Gene Expression in Muscle Tissue of Rats with Alzheimer ’s Disease

Background: Studies have shown that Alzheimer’s disease (AD) causes neuromuscular dysfunction by damaging different parts of the central nervous system and inflammation that can increase C-reactive protein (CRP) levels. Nevertheless, the beneficial effects of endurance training (ET) and royal jelly (RJ) on inflammation and reduction of CRP are not fully elucidated. Objectives: The aim of this research was to investigate the effect of ET with RJ on gene expression of CRP in muscle tissues of rats with AD. Methods: In this experimental study, 24 rats with AD (8 mg/kg trimethyltin injection) were randomly divided into four groups of 1-ET, 2-ET + [RJ (100 mg/kg)], 3-RJ and 4-control. Also, six healthy rats were placed in the healthy control group to investigate the effects of AD induction on CRP gene expression. Endurance training groups performed endurance training with a speed of 15 - 20 m/min, 5 sessions per week for eight weeks. Results: Our findings showed ET and RJ significantly decreased CRP gene expression in muscle tissues of rats with AD (P = 0.001) as well as the interaction of ET and RJ was significant in reducing CRP gene expression in muscle tissues of rats with AD (P = 0.001). Conclusions: It appears that ET and RJ have interactive effects on the reduction of CRP in muscle tissues of rats with AD.

Beneficial effects of endurance exercise training on skeletal muscle microvasculature in sickle cell disease patients

AbstractSickle cell disease (SCD) is a genetic hemoglobinopathy leading to 2 major clinical manifestations: severe chronic hemolytic anemia and iterative vaso-occlusive crises. SCD is also accompanied by profound muscle microvascular remodeling. The beneficial effects of endurance training on microvasculature are widely known. The aim of this study was to evaluate the effects of an endurance training program on microvasculature of skeletal muscle in SCD patients. A biopsy of the vastus lateralis muscle and submaximal incremental exercise was performed before and after the training period. Of the 40 randomized SCD patients, complete data sets from 32 patients were obtained. The training group (n = 15) followed a personalized moderate-intensity endurance training program, while the nontraining (n = 17) group maintained a normal lifestyle. Training consisted of three 40-minute cycle ergometer exercise sessions per week for 8 weeks. Histological analysis highlighted microvascular benefits in the training SCD patients compared with nontraining patients, including increases in capillary density (P = .003), number of capillaries around a fiber (P = .015), and functional exchange surface (P < .0001). Conversely, no significant between-group difference was found in the morphology of capillaries. Indexes of physical ability also improved in the training patients. The moderate-intensity endurance exercise training program improved the muscle capillary network and partly reversed the microvascular defects commonly observed in skeletal muscle of SCD patients. This trial was registered at www.clinicaltrials.gov as #NCT02571088.

Endurance Training Counteracts the High-Fat Diet-Induced Profiling Changes of ω-3 Polyunsaturated Fatty Acids in Skeletal Muscle of Middle-Aged Rats.

PurposeTo investigate the effects of endurance training on the content of ω-3 polyunsaturated fatty acids (PUFAs) and their distribution among lipid classes in skeletal muscle in middle aged, high-fat diet fed rats.MethodThirty 10-month old male Sprague Dawley (SD) rats were assigned to four groups. Two groups of rats remained sedentary and were fed chow diet (C group), or high-fat diet (H group), respectively. The other two groups of rats were subjected to endurance training while maintaining their chow diet (EC group), or high-fat diet (EH group). After 16 weeks endurance training and/or diet intervention, the content of ω-3 PUFAs and ω-3 PUFA-containing lipids in rat soleus muscle were analyzed by lipidomics.ResultsRats fed a high-fat diet exhibited decreased overall amount of ω-3 PUFAs in soleus muscle, while endurance training preserved the total amount of ω-3 PUFAs. Both the endurance training and high-fat diet alone changed the profiles of ω-3 PUFAs in different lipid classes. Specifically, the amount of triacylglycerol (TG), lysophosphatidylcholine (LPC), phosphatidylcholine (PC), and phosphatidylglycerol (PG) containing ω-3 PUFAs in soleus muscle was increased by endurance training, but the amount of lysophosphatidylenthanol (LPE), lysophosphatidylinositol (LPI), lysophosphatidylserine (LPS), cardiolipin (CL), phosphatidic acid (PA), and phosphatidylinositol (PI) was decreased. The high-fat diet induced a decrease of ω-3 PUFAs in TG, LPE, LPS, CL, platelet activating factor (PAF), PC, phosphatidylethanolamine (PE), and phosphatidylserine (PS), and an increase in LPC, LPI, PA, and PG. In addition, the effects of the endurance training on ω-3 PUFAs in skeletal muscle was also evident in high-fat diets fed rats, which counteracts the profiling changes caused by high-fat diet feeding.ConclusionThe beneficial effects of endurance training on skeletal muscle may be achieved to some extent through recovering the content of ω-3 PUFAs that has been decreased by high-fat diet feeding.

Ischaemia-induced muscle metabolic abnormalities are poorly alleviated by endurance training in a mouse model of sickle cell disease.

What is the central question of this study? The aim of this study was to evaluate the potential beneficial effects of endurance training during an ischaemia-reperfusion protocol in a mouse model of sickle cell disease (SCD). What is the main finding and its importance? Endurance training did not reverse the metabolic defects induced by a simulated vaso-occlusive crisis in SCD mice, with regard to intramuscular acidosis, mitochondrial dysfunction or anatomical properties. Our results suggest that endurance training would reduce the number of vaso-occlusive crises rather than the complications related to vaso-occlusive crises. The aim of this study was to investigate whether endurance training could limit the abnormalities described in a mouse model of sickle cell disease (SCD) in response to an ischaemia-reperfusion (I/R) protocol. Ten sedentary (HbSS-SED) and nine endurance-trained (HbSS-END) SCD mice were submitted to a standardized protocol of I/R of the leg, during which ATP, phosphocreatine and inorganic phosphate concentrations and intramuscular pH were measured using magnetic resonance spectroscopy. Forty-eight hours later, skeletal muscles were harvested. Oxidative stress markers were then measured. Although the time course of protons accumulation was slightly different between trained and sedentary mice (P<0.05), the extent of acidosis was similar at the end of the ischaemic period. The initial rate of phosphocreatine resynthesis measured at blood flow restoration, illustrating mitochondrial function, was not altered in trained mice compared with sedentary mice. Although several oxidative stress markers were not different between groups (P>0.05), the I/R-related increase of uric acid concentration observed in sedentary SCD mice (P<0.05) was not present in the trained group. The spleen weight, generally used as a marker of the severity of the disease, was not different between groups (P>0.05). In conclusion, endurance training did not limit the metabolic consequences of an I/R protocol in skeletal muscle of SCD mice, suggesting that the reduction in the severity of the disease previously demonstrated in the basal state would be attributable to a reduction of the occurrence of vaso-occlusive crises rather than a decrease of the deleterious effects of vaso-occlusive crises.

Endurance Training Improves Muscle Function And Metabolism In A Sickle Cell Disease Mouse Model

Sickle cell disease (SCD) is an inherited disorder resulting in the synthesis of an abnormal hemoglobin (HbS) and associated with the occurrence of painful vaso-occlusive crisis (VOC). While it has been recently suggested that oxygen supply and use might be impaired due to muscle remodeling, the corresponding metabolic effects in exercising muscle are still unknown. Considering that regular moderate-intensity exercise is known to be beneficial on muscle structure and energetics, endurance training could alleviate the muscle remodelling described in SCD and improve muscle function. PURPOSE: The aim of this study was to characterize in a mouse model of SCD i) the potential abnormalities in muscle energetics and function, and ii) the potential beneficial effects of endurance training. METHODS: Sedentary control (HbAA-SED, n=10), heterozygous (HbAS-SED, n=10) and sickle cell (HbSS-SED, n=10) mice and endurance-trained (8-weeks treadmill running) healthy (HbAA-END, n=10), heterozygous (HbAS-END, n=11) and sickle cell (HbSS-END, n=8) mice were placed in a home-built device designed for a strictly non-invasive study of posterior hindlimb muscles function and metabolism by NMR during a standardized rest - stimulation - recovery protocol. RESULTS: During the stimulation period, HbSS mice developed less force as compared to HbAS mice (p<0.01) and HbAS mice displayed a reduced total force production as compared to HbAA mice (p<0.05). Whatever the genotype, training resulted in a significantly increased force production (p<0.001). Regarding muscle energetics, the exercise-induced phosphocreatine (PCr) depletion and pH decrease were significantly (p < 0.05) larger in HbSS mice as compared to HbAA and HbAS mice. Interestingly, training resulted in a significant (p<0.05) reduction in PCr depletion and intracellular acidosis. CONCLUSIONS: We demonstrated in the present study that SCD was associated with an impaired muscle force production and a larger exercise-induced metabolic consumption. The larger acidosis, which could trigger VOC, might be explained by both an increased non-oxidative glycolytic energy production and an altered protons handling. Interestingly, endurance training improved muscle function and reduced metabolic abnormalities, including acidosis.

Reactive oxygen/nitrogen species and contractile function in skeletal muscle during fatigue and recovery.

The production of reactive oxygen/nitrogen species (ROS/RNS) is generally considered to increase during physical exercise. Nevertheless, direct measurements of ROS/RNS often show modest increases in ROS/RNS in muscle fibres even during intensive fatiguing stimulation, and the major source(s) of ROS/RNS during exercise is still being debated. In rested muscle fibres, mild and acute exposure to exogenous ROS/RNS generally increases myofibrillar submaximal force, whereas stronger or prolonged exposure has the opposite effect. Endogenous production of ROS/RNS seems to preferentially decrease submaximal force and positive effects of antioxidants are mainly observed during fatigue induced by submaximal contractions. Fatigued muscle fibres frequently enter a prolonged state of reduced submaximal force, which is caused by a ROS/RNS-dependent decrease in sarcoplasmic reticulum Ca(2+) release and/or myofibrillar Ca(2+) sensitivity. Increased ROS/RNS production during exercise can also be beneficial and recent human and animal studies show that antioxidant supplementation can hamper the beneficial effects of endurance training. In conclusion, increased ROS/RNS production have both beneficial and detrimental effects on skeletal muscle function and the outcome depends on a combination of factors: the type of ROS/RNS; the magnitude, duration and location of ROS/RNS production; and the defence systems, including both endogenous and exogenous antioxidants.

Endurance training in patients with schizophrenia and healthy controls: differences and similarities.

The aims were to examine the feasibility of and adaptations to endurance training in persons diagnosed with schizophrenia and to address the question whether the principles and beneficial effects of endurance training established in the healthy population apply also to patients with schizophrenia. In this controlled interventional study, 22 patients with schizophrenia and 22 healthy controls performed a standardized aerobic endurance training on bicycle ergometers over 12weeks. Another group of 21 patients with schizophrenia played table soccer. Endurance capacity was measured with incremental cycle ergometry before and after the intervention and 3months later. A specific set of outcome parameters was defined. The training stimuli can be assumed to be similar in both endurance groups. Endurance capacity improved significantly in the endurance groups, but not in the table soccer group. Patients and healthy controls showed comparable adaptations to endurance training, as assessed by physical working capacity and maximal achieved power. Differences were found in changes of performance at a lactate concentration of 3mmol/l. Endurance training was feasible and effective in both groups. The principles and types of training that are usually applied to healthy controls need to be verified in patients with schizophrenia. Nevertheless, patients benefited from endurance training in terms of improvement of endurance capacity and reduction in the baseline deficit in comparison with healthy controls. Therefore, endurance training should be implemented in future therapy programs. These programs need to pay special attention to the differences between patients with schizophrenia and healthy controls.

Leucine supplementation does not affect protein turnover and impairs the beneficial effects of endurance training on glucose homeostasis in healthy mice.

Endurance exercise training as well as leucine supplementation modulates glucose homeostasis and protein turnover in mammals. Here, we analyze whether leucine supplementation alters the effects of endurance exercise on these parameters in healthy mice. Mice were distributed into sedentary (C) and exercise (T) groups. The exercise group performed a 12-week swimming protocol. Half of the C and T mice, designated as the CL and TL groups, were supplemented with leucine (1.5% dissolved in the drinking water) throughout the experiment. As well known, endurance exercise training reduced body weight and the retroperitoneal fat pad, increased soleus mass, increased VO2max, decreased muscle proteolysis, and ameliorated peripheral insulin sensitivity. Leucine supplementation had no effect on any of these parameters and worsened glucose tolerance in both CL and TL mice. In the soleus muscle of the T group, AS-160(Thr-642) (AKT substrate of 160kDa) and AMPK(Thr-172) (AMP-Activated Protein Kinase) phosphorylation was increased by exercise in both basal and insulin-stimulated conditions, but it was reduced in TL mice with insulin stimulation compared with the T group. Akt phosphorylation was not affected by exercise but was lower in the CL group compared with the other groups. Leucine supplementation increased mTOR phosphorylation at basal conditions, whereas exercise reduced it in the presence of insulin, despite no alterations in protein synthesis. In trained groups, the total FoxO3a protein content and the mRNA for the specific isoforms E2 and E3 ligases were reduced. In conclusion, leucine supplementation did not potentiate the effects of endurance training on protein turnover, and it also reduced its positive effects on glucose homeostasis.

Coordinated balancing of muscle oxidative metabolism through PGC-1α increases metabolic flexibility and preserves insulin sensitivity

The peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) enhances oxidative metabolism in skeletal muscle. Excessive lipid oxidation and electron transport chain activity can, however, lead to the accumulation of harmful metabolites and impair glucose homeostasis. Here, we investigated the effect of over-expression of PGC-1α on metabolic control and generation of insulin desensitizing agents in extensor digitorum longus (EDL), a muscle that exhibits low levels of PGC-1α in the untrained state and minimally relies on oxidative metabolism. We demonstrate that PGC-1α induces a strictly balanced substrate oxidation in EDL by concomitantly promoting the transcription of activators and inhibitors of lipid oxidation. Moreover, we show that PGC-1α enhances the potential to uncouple oxidative phosphorylation. Thereby, PGC-1α boosts elevated, yet tightly regulated oxidative metabolism devoid of side products that are detrimental for glucose homeostasis. Accordingly, PI3K activity, an early phase marker for insulin resistance, is preserved in EDL muscle. Our findings suggest that PGC-1α coordinately coactivates the simultaneous transcription of gene clusters implicated in the positive and negative regulation of oxidative metabolism and thereby increases metabolic flexibility. Thus, in mice fed a normal chow diet, over-expression of PGC-1α does not alter insulin sensitivity and the metabolic adaptations elicited by PGC-1α mimic the beneficial effects of endurance training on muscle metabolism in this context.

Does oxidative capacity affect energy cost? An in vivo MR investigation of skeletal muscle energetics

Investigations of training effects on exercise energy cost have yielded conflicting results. The purpose of the present study was to compare quadriceps energy cost and oxidative capacity between endurance-trained and sedentary subjects during a heavy dynamic knee extension exercise. We quantified the rates of ATP turnover from oxidative and anaerobic pathways with (31)P-MRS, and we measured simultaneously pulmonary oxygen uptake in order to assess both total ATP production [i.e., energy cost (EC)] and O(2) consumption (O(2) cost) scaled to power output. Seven sedentary (SED) and seven endurance-trained (TRA) subjects performed a dynamic standardized rest-exercise-recovery protocol at an exercise intensity corresponding to 35% of maximal voluntary contraction. We showed that during a dynamic heavy exercise, the O(2) cost and EC were similar in the SED and endurance-trained groups. For a given EC, endurance-trained subjects exhibited a higher relative mitochondrial contribution to ATP production at the muscle level (84 +/- 12% in TRA and 57 +/- 12% in SED; P < 0.01) whereas the anaerobic contribution was reduced (18 +/- 12% in TRA and 44 +/- 11% in SED; P < 0.01). Our results obtained in vivo illustrate that on the one hand the beneficial effects of endurance training are not related to any reduction in EC or O(2) cost and on the other hand that this similar EC was linked to a change regarding the contribution of anaerobic and oxidative processes to energy production, i.e., a greater aerobic energy contribution associated with a concomitant reduction of the anaerobic energy supply.

Habitual consumption of eggs does not alter the beneficial effects of endurance training on plasma lipids and lipoprotein metabolism in untrained men and women

Changes in plasma lipid and apolipoprotein profiles were evaluated in 12 healthy, unfit subjects (VO 2peak 39.1±2.8 ml·kg -1·min -1; 5 women, 7 men) at baseline and following endurance exercise training. The exercise protocol consisted of a 6-week endurance exercise training program (4–5 days week −1; 60 min·session -1; ≥65% HR max). Subjects were randomly assigned to consume an egg- ( n=6; 12 eggs·week −1) or no-egg ( n=6; 0 eggs·week −1)-based, eucaloric, standardized diet for 8 weeks. Both diets were macronutrient balanced [60% carbohydrate, 30% fat, 10% protein (0.8 g·kg -1·day −1)] and individually designed for weight maintenance. Plasma lipids were measured twice within the same week at baseline and following exercise training. At baseline, subjects were normolipidemic with values of 163.9±41.8, 84.8±36.7, 60.6±15.4 and 93.1±52 mg dl −1 for total cholesterol, LDL cholesterol and HDL cholesterol and triglyceride concentrations, respectively. A two-way ANOVA was used to analyze diet and exercise effects and interactions. In both groups, endurance exercise training resulted in a significant 10% increase in HDL-C ( P<.05), a 19% decrease in Apo B concentrations ( P<.05) and reductions in plasma CETP activity ( P<.05). Plasma LDL-C decreased by 21% ( P=.06). No main effects of diet or interactions with plasma lipids or Apo B concentrations were observed. These data demonstrate that endurance training improved the plasma lipid profiles of previously unfit, normolipidemic subjects independent of dietary cholesterol intake from eggs.

CETP genotypes and HDL-cholesterol phenotypes in the HERITAGE Family Study

Associations between cholesteryl ester transfer protein (CETP) polymorphisms and high-density lipoprotein cholesterol (HDL-c) levels before and after 20 wk of endurance training were investigated in the HERITAGE Family Study. Plasma HDL-c, HDL(2)-c, HDL(3)-c, and apolipoprotein (apo)A1 levels were measured, and 13 CETP single nucleotide polymorphisms (SNPs) were genotyped in 265 blacks and 486 whites. Three haplotypes defined by SNPs at the -1337, -971, and -629 sites were strongly associated with baseline HDL-c levels in whites. Both C-1337T and C-629A were associated with baseline HDL-c (P < 0.001) and apoA1 (P < 0.01) when tested separately. However, only C-629A remained significant in a combined model. G-971A was not associated with HDL phenotypes, but showed significant interactions with C-629A (P = 0.002) on baseline traits. Genotype-by-sex interactions were observed at the -629 locus for HDL(3)-c (P = 0.004) and apoA1 (P = 0.02) training responses in whites. In women, the -629 A/A homozygotes showed greater increases in HDL(3)-c (P = 0.02) and apoA1 (P = 0.02) levels than the other genotypes. Finally, apolipoprotein E (APOE) genotype and the CETP C-629A locus contributed independently and in additive fashion to the HDL traits, explaining 6.0-8.8% of the variance. The CETP -1337T and -629A alleles are associated with higher baseline HDL-c and apoA1 levels. The beneficial effects of endurance training on plasma HDL(3)-c and apoA1 levels are evident in white women homozygous for the -629A allele. The CETP and APOE genotypes account for up to 9% of the variance in HDL-c phenotypes in the HERITAGE Family Study.

Beneficial effects of endurance training on cardiac and skeletal muscle energy metabolism in heart failure

As endurance training improves symptoms and quality of life and decreases mortality rate and hospitalization, it is increasingly recognized as a beneficial practice for heart failure (HF) patients. However, the mechanisms involved in the beneficial effects of exercise training are far from being understood and need further evaluation. Independent of hemodynamics effects, exercise training participates in tissue remodeling. While heart failure induces a generalized metabolic myopathy, adaptation to endurance training mainly improves energetic aspects of muscle function. In the present review, after presenting the main characteristics of cardiac and skeletal muscle energy metabolism and the effects of exercise training, we will discuss the evidence for the beneficial effects of endurance training on cardiac and skeletal muscle oxidative metabolism and intracellular energy transfer in HF. These beneficial effects of exercise training seen in heart failure patients are also relevant to other chronic diseases (chronic obstructive pulmonary disease, diabetes, and obesity) and even for highly sedentary or elderly individuals [Booth F.W., Chakravathy M.V., Spangenburg E.E. Exercise and gene expression: physiological regulation of the human genome through physical activity. J Physiol (Lond) 2002;543:399-411]. Physical rehabilitation is thus a major health issue for populations in industrialized countries.

CETP C&gt;-&gt;−629&gt;A Genotypes and HDL-Cholesterol Phenotypes in the HERITAGE Family Study

PURPOSE: Physical activity is thought to improve high-density lipoprotein cholesterol (HDL-C) metabolism by enhancing reverse cholesterol transport (RCT). Plasma cholesteryl ester transfer protein (CETP) mediates the transfer of cholesteryl esters from HDL particles to triglyceride-rich lipoproteins and is therefore considered a key protein in RCT. METHODS: The aim of this study was to investigate associations between the CETP C>-629>A gene polymorphism and HDL-C profile before and after a 20-week endurance training program in the HERITAGE Family Study. Plasma HDL-C, HDL2- C, HDL3-C and apolipoprotein (apo) A1 levels were measured in 265 Blacks (88 men, 177 women) and 486 Whites (237 men, 249 women). RESULTS: In whites, A/A homozygotes showed significantly higher baseline HDLC (p<0.001), HDL2-C (p<0.001), HDL3-C (p=0.01) and apo A1 (p<0.001) levels compared with C/A heterozygotes and C/C homozygotes. Similar patterns were found in Blacks for baseline HDL-C (p=0.06) and HDL2-C (p=0.004). Significant genotypebysex interactions were observed for HDL3-C (p<0.001) and apo A1 (p<0.002) training responses in Whites. In women, the A/A homozygotes showed greater training-induced increases in HDL3-C (p=0.02) and Apo A1 (p=0.02) levels than the other genotypes, whereas the training responses did not differ between the genotypes in males. The associations were independent of age, sex, baseline BMI and covariates such as smoking, alcohol, endogenous hormones, abdominal fat and plasma triglycerides. CONCLUSIONS: In summary, the CETP −629>A allele is strongly associated with higher baseline HDL-C. Additionally, the beneficial effects of endurance training on plasma HDL3-C and apo A1 levels are particularly evident in white women with the A/A genotype.