Moderate-intensity resistance exercise training in patients with chronic heart failure improves strength, endurance, heart rate variability, and forearm blood flow

Thirty-nine CHF patients (New York Heart Association Functional Class = 2.3±0.5; left ventricular ejection fraction 28%±7%; age 65±11 years; 33:6 male:female) underwent 2 identical series of tests, 1 week apart, for strength and endurance of the knee and elbow extensors and flexors, VO_2peak, HRV, FBF at rest, and FBF activated by forearm exercise or limb ischemia. Patients were then randomized to 3 months of resistance training (EX, n = 19), consisting of mainly isokinetic (hydraulic) ergometry, interspersed with rest intervals, or continuance with usual care (CON, n = 20), after which they underwent repeat endpoint testing. Combining all 4 movement patterns, strength increased for EX by 21±30% (mean±SD, P<.01) after training, whereas endurance improved 21±21% (P<.01). Corresponding data for CON remained almost unchanged (strength P<.005, endurance P<.003 EX versus CON). VO_2peak improved in EX by 11±15% (P<.01), whereas it decreased by 10±18% (P<.05) in CON (P<.001 EX versus CON). The ratio of low-frequency to high-frequency spectral power fell after resistance training in EX by 44±53% (P<.01), but was unchanged in CON (P<.05 EX versus CON). FBF increased at rest by 20±32% (P<.01), and when stimulated by submaximal exercise (24±32%, P<.01) or limb ischemia (26±45%, P<.01) in EX, but not in CON (P<.01 EX versus CON).

Increased insulin-stimulated Akt pSer473 and cytosolic SHP2 protein abundance in human skeletal muscle following acute exercise and short-term training.

The purpose of the present study was to determine in human skeletal muscle whether a single exercise bout and 7 days of consecutive endurance (cycling) training 1) increased insulin-stimulated Akt pSer473and 2) altered the abundance of the protein tyrosine phosphatases (PTPases), PTP1B and SHP2. In healthy, untrained men (n = 8; 24 ± 1 yr), glucose infusion rate during a hyperinsulinemic euglycemic clamp, when compared with untrained values, was not improved 24 h following a single 60-min bout of endurance cycling but was significantly increased (~30%; P < 0.05) 24 h following completion of 7 days of exercise training. Insulin-stimulated Akt pSer473was ~50% higher (P < 0.05) 24 h following the acute bout of exercise, with this effect remaining after 7 days of training (P < 0.05). Insulin-stimulated insulin receptor and insulin receptor substrate-1 tyrosine phosphorylation were not altered 24 h after acute exercise and short-term training. Insulin did not acutely regulate the localization of the PTPases, PTP1B or SHP2, although cytosolic protein abundance of SHP2 was increased (P < 0.05; main effect) 24 h following acute exercise and short-term training. In conclusion, insulin-sensitive Akt pSer473and cytosolic SHP2 protein abundance are higher after acute exercise and short-term training, and this effect appears largely due to the residual effects of the last bout of prior exercise. The significance of exercise-induced alterations in cytosolic SHP2 and insulin-stimulated Akt pSer473on the improvement in insulin sensitivity requires further elucidation.

Muscle Na+ -K+ -ATPase activity and isoform adaptions to intense interval exercise and training in well-trained athletes

The Na⁺-K⁺-ATPase enzyme is vital in skeletal muscle function. We investigated the effects of acute high-intensity interval exercise, before and following high-intensity training (HIT), on muscle Na⁺-K⁺-ATPase maximal activity, content, and isoform mRNA expression and protein abundance. Twelve endurance-trained athletes were tested at baseline, pretrain, and after 3 wk of HIT (posttrain), which comprised seven sessions of 8 x 5-min interval cycling at 80% peak power output. Vastus lateralis muscle was biopsied at rest (baseline) and both at rest and immediately postexercise during the first (pretrain) and seventh (posttrain) training sessions. Muscle was analyzed for Na⁺-K⁺-ATPase maximal activity (3-O-MFPase), content ([³H]ouabain binding), isoform mRNA expression (RT-PCR), and protein abundance (Western blotting). All baseline-to-pretrain measures were stable. Pretrain, acute exercise decreased 3-O-MFPase activity [12.7% (SD 5.1), P < 0.05], increased α₁, α₂, and α₃ mRNA expression (1.4-, 2.8-, and 3.4-fold, respectively, P < 0.05) with unchanged ß-isoform mRNA or protein abundance of any isoform. In resting muscle, HIT increased (P < 0.05) 3-O-MFPase activity by 5.5% (SD 2.9), and α₃ and ß₃ mRNA expression by 3.0- and 0.5-fold, respectively, with unchanged Na+-K+-ATPase content or isoform protein abundance. Posttrain, the acute exercise induced decline in 3-O-MFPase activity and increase in α₁ and α₃ mRNA each persisted (P < 0.05); the postexercise 3-O-MFPase activity was also higher after HIT (P < 0.05). Thus HIT augmented Na⁺-K⁺-ATPase maximal activity despite unchanged total content and isoform protein abundance. Elevated Na⁺-K⁺-ATPase activity postexercise may contribute to reduced fatigue after training. The Na⁺-K⁺-ATPase mRNA response to interval exercise of increased α - but not ß-mRNA was largely preserved posttrain, suggesting a functional role of α mRNA upregulation.

Slow component of VO2 kinetics: the effect of training status, fibre type, UCP3 mRNA and citrate synthase activity

Examines the relationship between the magnitude of the relative slow component (SC) of pulmonary oxygen uptake VO[sub 2], citrate synthase activity, UCP2 and UCP3 mRNA levels and muscle fiber composition in both endurance-trained and recreationally active subjects. Magnitude of the relative SC of the Tr group; Indicators of aerobic fitness; High negative correlations between the magnitude of the relative SC and citrate synthase activity and VO[sub 2] peak.

UCP3 protein expression is lower in type I, IIa and IIx muscle fiber types of endurance-trained compared to untrained subjects

Uncoupling protein 3 (UCP3) is a muscle mitochondrial protein believed to uncouple the respiratory chain, producing heat and reducing aerobic ATP production. Our aim was to quantify and compare the UCP3 protein levels in type I, IIa and IIx skeletal muscle fibers of endurance-trained (Tr) and healthy untrained (UTr) individuals. UCP3 protein content was quantified using Western blot and immunofluorescence. Skeletal muscle fiber type was determined by both an enzymatic ATPase stain and immunofluorescence. UCP3 protein expression measured in skeletal muscle biopsies was 46% lower ( P=0.01) in the Tr compared to the UTr group. UCP3 protein expression in the different muscle fibers was expressed as follows; IIx>IIa>I in the fibers for both groups ( P<0.0167) but was lower in all fiber types of the Tr when compared to the UTr subjects ( P<0.001). Our results show that training status did not change the skeletal muscle fiber hierarchical UCP3 protein expression in the different fiber types. However, it affected UCP3 content more in type I and type IIa than in the type IIx muscle fibers. We suggest that this decrease may be in relation to the relative improvement in the antioxidant defense systems of the skeletal muscle fibers and that it might, as a consequence, participate in the training induced improvement in mechanical efficiency.

Effects of creatine loading and prolonged creatine supplementation of body composition, fuel selection, sprint and endurance performance in humans

Most research on creatine has focused on short-term creatine loading and its effect on high-intensity performance capacity. Some studies have investigated the effect of prolonged creatine use during strength training. However, studies on the effects of prolonged creatine supplementation are lacking. In the present study, we have assessed the effects of both creatine loading and prolonged supplementation on muscle creatine content, body composition, muscle and whole-body oxidative capacity, substrate utilization during submaximal exercise, and on repeated supramaximal sprint, as well as endurance-type time-trial performance on a cycle ergometer. Twenty subjects ingested creatine or a placebo during a 5-day loading period (20g·day^-1) after which supplementation was continued for up to 6 weeks (2g·day^-1). Creatine loading increased muscle free creatine, creatine phosphate (CrP) and total creatine content (P<0.05). The subsequent use of a 2g·day^-1 maintenance dose, as suggested by an American College of Sports Medicine Roundtable, resulted in a decline in both the elevated CrP and total creatine content and maintenance of the free creatine concentration. Both short- and long-term creatine supplementation improved performance during repeated supramaximal sprints on a cycle ergometer. However, whole-body and muscle oxidative capacity, substrate utilization and time-trial performance were not affected. The increase in body mass following creatine loading was maintained after 6 weeks of continued supplementation and accounted for by a corresponding increase in fat-free mass. This study provides definite evidence that prolonged creatine supplementation in humans does not increase muscle or whole-body oxidative capacity and, as such, does not influence substrate utilization or performance during endurance cycling exercise. In addition, our findings suggest that prolonged creatine ingestion induces an increase in fat-free mass.

Interaction of contractile activity and training history on mRNA abundance in skeletal muscle from trained athletes

Skeletal muscle displays enormous plasticity to respond to contractile activity with muscle from strength- (ST) and endurance-trained (ET) athletes representing diverse states of the adaptation continuum. Training adaptation can be viewed as the accumulation of specific proteins. Hence, the altered gene expression that allows for changes in protein concentration is of major importance for any training adaptation. Accordingly, the aim of the present study was to quantify acute subcellular responses in muscle to habitual and unfamiliar exercise. After 24-h diet/exercise control, 13 male subjects (7 ST and 6 ET) performed a random order of either resistance (8 x 5 maximal leg extensions) or endurance exercise (1 h of cycling at 70% peak O2 uptake). Muscle biopsies were taken from vastus lateralis at rest and 3 h after exercise. Gene expression was analyzed using real-time PCR with changes normalized relative to preexercise values. After cycling exercise, peroxisome proliferator-activated receptor- coactivator-1 (ET 8.5-fold, ST 10-fold, P < 0.001), pyruvate dehydrogenase kinase-4 (PDK-4; ET 26-fold, ST 39-fold), vascular endothelial growth factor (VEGF; ET 4.5-fold, ST 4-fold), and muscle atrophy F-box protein (MAFbx) (ET 2-fold, ST 0.4-fold) mRNA increased in both groups, whereas MyoD (3-fold), myogenin (0.9-fold), and myostatin (2-fold) mRNA increased in ET but not in ST (P < 0.05). After resistance exercise PDK-4 (7-fold, P < 0.01) and MyoD (0.7-fold) increased, whereas MAFbx (0.7-fold) and myostatin (0.6-fold) decreased in ET but not in ST. We conclude that prior training history can modify the acute gene responses in skeletal muscle to subsequent exercise.

Optimizing training adaptations by manipulating glycogen

For decades, glycogen has been recognized as a storage form of glucose within the liver and muscles. Only recently has a greater role for glycogen as a regulator of metabolic signalling been suggested. Glycogen either directly or indirectly regulates a number of signalling proteins, including the adenosine-5'-phosphate- (AMP-) activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (MAPK). AMPK and p38 MAPK play a significant role in controlling the expression and activity of the peroxisome proliferator activated receptor γ coactivators (PGCs), respectively. The PGCs can directly increase muscle mitochondrial mass and endurance exercise performance. As low muscle glycogen is generally associated with greater activation of these pathways, the concept of training with low glycogen to maximize the physiological adaptations to endurance exercise is gaining acceptance in the scientific community. In this review, we evaluate the scientific basis for this philosophy and propose some practical applications of this philosophy for the general population as well as elite endurance athletes.

Monitoring voluntary food intake in female endurance athletes

Female athletes may demonstrate a poor ability to quantify portion sizes and educational sessions using food models do not always improve accuracy. Female cyclists with the highest body fat do not report the highest energy intakes during 70 days of training and racing. Training loads can influence reported daily energy intake.

Exercise and Sports Science Australia position statement on exercise training and chronic heart failure

Chronic heart failure (CHF) is a complex syndrome characterised by progressive decline in left ventricular function, low exercise tolerance and raised mortality and morbidity. Regular exercise participation has been shown to be a safe and effective treatment modality in the majority of CHF patients, partially reversing some of the maladaptations evident in myocardial and skeletal muscle function, and resulting in improvements in physical fitness and quality of life, and perhaps reduced mortality. The volume and intensity of exercise that is recommended depends on the syndrome severity, however in most patients it should consist of a combination of low-to-moderate intensity aerobic (endurance) exercise on most days of the week and individually prescribed low-to-moderate intensity resistance (strength) training at least twice per week. Additionally, all patients should be closely monitored prior to and during exercise for contraindications by an appropriately trained health professional. The purpose of this statement is to inform and guide exercise practitioners and health professionals in the safe and effective prescription and supervision of exercise for patients with CHF.

Differential response to resistance training in CHF according to ACE genotype

Background : The Angiotensin Converting Enzyme (ACE) gene may influence the risk of heart disease and the response to various forms of exercise training may be at least partly dependent on the ACE genotype. We aimed to determine the effect of ACE genotype on the response to moderate intensity circuit resistance training in chronic heart failure (CHF) patients.

Methods : The relationship between ACE genotype and the response to 11 weeks of resistance exercise training was determined in 37 CHF patients (New York Heart Association Functional Class = 2.3 ± 0.5; left ventricular ejection fraction 28 ± 7%; age 64 ± 12 years; 32:5 male:female) who were randomised to either resistance exercise (n = 19) or inactive control group (n = 18). Outcome measures included VO_2peak power output and muscle strength and endurance. ACE genotype was determined using standard methods.

Results : At baseline, patients who were homozygous for the I allele had higher VO_2peak (p = 0.02) and peak power (p = 0.003) compared to patients who were homozygous for the D allele. Patients with the D allele, who were randomised to resistance training, compared to non-exercising controls, had greater peak power increases (ID p < 0.001; DD p < 0.001) when compared with patients homozygous for the I allele, who did not improve. No significant genotype-dependent changes were observed in VO_2peak, muscle strength, muscle endurance or lactate threshold.

Conclusion : ACE genotype may have a role in exercise tolerance in CHF and could also influence the effectiveness of resistance training in this condition.