Training-induced elevation in FABP(PM) is associated with increased palmitate use in contracting muscle.
(25/2144)
To evaluate the effects of endurance training in rats on fatty acid metabolism, we measured the uptake and oxidation of palmitate in isolated rat hindquarters as well as the content of fatty acid-binding proteins in the plasma membranes (FABP(PM)) of red and white muscles from 16 trained (T) and 18 untrained (UT) rats. Hindquarters were perfused with 6 mM glucose, 1,800 microM palmitate, and [1-(14)C]palmitate at rest and during electrical stimulation (ES) for 25 min. FABP(PM) content was 43-226% higher in red than in white muscles and was increased by 55% in red muscles after training. A positive correlation was found to exist between succinate dehydrogenase activity and FABP(PM) content in muscle. Palmitate uptake increased by 64-73% from rest to ES in both T and UT and was 48-57% higher in T than UT both at rest (39.8 +/- 3.5 vs. 26.9 +/- 4. 4 nmol. min(-1). g(-1), T and UT, respectively) and during ES (69.0 +/- 6.1 vs. 43.9 +/- 4.4 nmol. min(-1). g(-1), T and UT, respectively). While the rats were resting, palmitate oxidation was not affected by training; palmitate oxidation during ES was higher in T than UT rats (14.8 +/- 1.3 vs. 9.3 +/- 1.9 nmol. min(-1). g(-1), T and UT, respectively). In conclusion, endurance training increases 1) plasma free fatty acid (FFA) uptake in resting and contracting perfused muscle, 2) plasma FFA oxidation in contracting perfused muscle, and 3) FABP(PM) content in red muscles. These results suggest that an increased number of these putative plasma membrane fatty acid transporters may be available in the trained muscle and may be implicated in the regulation of plasma FFA metabolism in skeletal muscle. (+info)
Validity of the heart rate deflection point as a predictor of lactate threshold during running.
(26/2144)
During an incremental run test, some researchers consistently observe a heart rate (HR) deflection at higher speeds, but others do not. The present study was designed to investigate whether differences in test protocols could explain the discrepancy. Additionally, we sought to determine whether the HR deflection point accurately predicts lactate threshold (LT). Eight trained runners performed four tests each: 1) a treadmill test for maximal O(2) uptake, 2) a Conconi test on a 400-m track with speeds increasing approximately 0.5 km/h every 200 m, 3) a continuous treadmill run with speeds increasing 0.5 km/h every minute, and 4) a continuous LT treadmill test in which 3-min stages were used. All subjects demonstrated an HR deflection on the track, but only one-half of the subjects showed an HR deflection on the treadmill. On the track the shortening of stages with increasing speeds contributed to a loss of linearity in the speed-HR relationship. Additionally, the HR deflection point overestimated the LT when a continuous treadmill LT protocol was used. In conclusion, the HR deflection point was not an accurate predictor of LT in the present study. (+info)
Female-related skeletal muscle phenotype in patients with moderate chronic heart failure before and after dynamic exercise training.
(27/2144)
This study hypothesized that female patients with chronic heart failure (CHF), similarly as previously reported for male patients, have a decreased proportion of type I (slow twitch) muscle fibers combined with fiber atrophy, and respond to exercise training with an increased muscular fiber area and performance, and with an unaltered fiber type distribution. METHODS: Sixteen women [age 62 +/- 10 years (mean +/- SD)] with stable, moderate CHF (left ventricular ejection fraction 28 +/- 8%) underwent percutaneous needle biopsies of the lateral vastus muscle, and assessments of isokinetic muscle strength and exercise tests with respiratory gas and blood lactate analyses, before and after 8 weeks of intensive knee extensor endurance training. RESULTS: When compared to healthy age-matched women, the women with CHF unexpectedly had a normal proportion of type I fibers (51 +/- 15%), but a decreased cross-sectional area in both type I and II fibers. Exercise training increased the cross-sectional area of muscle fibers up to the reference range (21%, p < 0.04), while the relative number of type I fibers decreased (12%, p < 0.03). Training also increased muscle strength (16%, p < 0.0001) and peak oxygen uptake (20%, p < 0.0001). The increase in peak oxygen uptake was directly related to the training-induced increase in fiber areas (r = 0.63; p < 0.03), and decrease in lactate accumulation was inversely related to the training-induced decrease in the relative number of type I fibers (r = -0.62; p < 0.02). CONCLUSIONS: As for men with CHF, a skeletal muscle atrophy was found in women, but contrary to the hypothesis, the proportion of type I muscle fibers was normal. Exercise training counteracted the atrophy suggesting skeletal muscle trainability in female CHF patients. (+info)
Angiotensinogen gene M235T polymorphism predicts left ventricular hypertrophy in endurance athletes.
(28/2144)
OBJECTIVES: We studied whether left ventricular mass in athletes associates with polymorphisms in genes encoding components of the renin-angiotensin system. BACKGROUND: Adaptive left ventricular hypertrophy is a feature of the athlete's heart. However, similarly training athletes develop left ventricular mass to a different extent, suggesting that genetic factors may modulate heart size. METHODS: We measured left ventricular mass by echocardiography in 50 male and 30 female elite endurance athletes aged 25 +/- 4 (mean +/- SD) years. Deoxyribonucleic acid samples were prepared for genotyping of angiotensinogen (AGT) gene M235T polymorphism, angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and angiotensin II type 1 receptor (AT1) gene A1166C polymorphism. RESULTS: The AGT gene M235T genotypes were significantly associated with left ventricular mass independently of blood pressure in both genders (p = 0.0036 for pooled data). TT homozygotes had greater mass compared with MM homozygotes in both men (147 +/- 12 g/m vs. 132 +/- 15 g/m, p = 0.032) and women (121 +/- 12 g/m vs. 101 +/- 13 g/m, p = 0.019). There was a gender difference in the relation between myocardial mass and AGT genotype, MT heterozygotes resembling MM homozygotes among women and TT homozygotes among men. The other studied gene polymorphisms were not associated with left ventricular mass. CONCLUSIONS: Angiotensinogen gene M235T polymorphism is associated with the variability in left ventricular hypertrophy induced by endurance training, with athletes homozygous for the T allele having the largest hearts. We found no association between ACE gene I/D or AT1 gene A1166C polymorphisms and left ventricular mass. (+info)
Endurance exercise training does not alter lipolytic or adipose tissue blood flow sensitivity to epinephrine.
(29/2144)
We evaluated the relationship between lipolysis and adipose tissue blood flow (ATBF) in response to epinephrine and the effect of endurance exercise training on these responses. Five healthy untrained men underwent a four-stage incremental epinephrine infusion (0.00125, 0.005, 0.0125, and 0.025 microgram. kg fat free mass(-1). min(-1)) plus hormonal clamp before and after 16 wk of cycle ergometry exercise training. Whole body glycerol and free fatty acid (FFA) rates of appearance (R(a)) in plasma were determined by stable isotope methodology, and ATBF was assessed by (133)Xe clearance. After each training session, subjects were fed the approximate number of calories expended during exercise to prevent changes in body weight. Glycerol R(a), FFA R(a), and ATBF increased when plasma epinephrine concentration reached 0.8 nM, but at plasma epinephrine concentrations >1.6 nM ATBF plateaued, whereas lipolysis continued to increase. Exercise training increased peak oxygen uptake by 24 +/- 7% (2.9 +/- 0.2 vs. 3.6 +/- 0.1 l/min; P < 0. 05) but did not alter body weight [70.5 +/- 3.8 vs. 72.0 +/- 3.8 kg; P = nonsignificant (NS)] or percent body fat (18.4 +/- 1.6 vs. 17.8 +/- 1.9%; P = NS). Lipolytic and ATBF responses to epinephrine were also the same before and after training. We conclude that the lipolytic and ATBF responses to epinephrine are coordinated when plasma epinephrine concentration is +info)
A metabolic limit on the ability to make up for lost time in endurance events.
(30/2144)
It has been repeatedly demonstrated that the tolerable duration (t) of high-intensity cycling is well characterized as a hyperbolic function of power (P) with an asymptote that has been termed the "fatigue threshold" and with a curvature constant. This hyperbolic P-t relationship has also been confirmed in running and swimming, when speed (V) is used instead of P; that is, (V - V(F)). t = D', where V(F) is the V at the fatigue threshold, and D' is the curvature constant. Therefore, we theoretically analyzed herein the consequences of an athlete performing the initial part of an endurance event at a V different from the constant rate that would allow the performance time to be determined by the hyperbolic V-t relationship. We considered not only the V-t constraints that limit the athlete's ability to make up the time lost by too slow an early pace but also the consequences of a more rapid early pace. Our analysis demonstrates that both the V(F) and D' parameters of the athlete's V-t curve play an important role in the pace allocation strategy of the athlete. That is, 1) when the running V during any part of the whole running distance is below V(F), the athlete can never attain the goal of achieving the time equivalent to that of running the entire race at constant maximal V (i.e., that determined by one's own best V-t curve); and 2) the "endurance parameter ratio" D'/V(F) is especially important in determining the flexibility of the race pace that the athlete was able to choose intentionally. (+info)
Acute changes in serum lipids and lipoprotein subclasses in triathletes as assessed by proton nuclear magnetic resonance spectroscopy.
(31/2144)
Exercise is associated with changes in lipids that may protect against coronary heart disease (CHD). In this study of 28 triathletes, we analyzed acute changes in serum lipid and lipoprotein concentrations after completion of the 1995 World Championship Hawaii Ironman Triathlon. With standard laboratory assays, we demonstrate significant decreases in total cholesterol, VLDL cholesterol, ApoB100, and Lp(a). Total HDL cholesterol increased significantly immediately after the race. With a novel proton NMR spectroscopy assay, we demonstrate that smaller diameter LDL particles, corresponding to small, dense LDL, declined by 62%. Moreover, larger HDL subclasses, whose levels are inversely associated with CHD, increased significantly by 11%. Smaller HDL subclasses, which have been directly associated with CHD in some studies, acutely decreased by 16%. Therefore, exercise not only acutely induces changes in lipoprotein concentrations among the standard species in a manner that favorably affects CHD risk, but also induces favorable changes in specific lipoprotein subclass size distribution that also may alter CHD risk independently of the total lipoprotein serum concentration. (+info)
Heart failure-related myopathy. Clinical and pathophysiological insights.
(32/2144)
AIMS: To evaluate the relationship of skeletal and respiratory muscular dysfunction with the degree of clinical severity, cardiac impairment and exercise intolerance in patients with chronic heart failure. METHODS AND RESULTS: Ninety-one patients (age 52.7+/-8 years) on standard therapy and in a stable clinical condition with normal nutritional status underwent evaluation of (1) clinical severity and metabolic status (NYHA class, weight, albuminaemia, natraemia, cortisol, insulin, neurohormones), (2) cardiac function (Echo, right heart catheterization), (3) exercise tolerance (peak VO(2)), (4) dynamic isokinetic forces of the quadriceps and hamstring (Cybex method), and respiratory muscle strength (maximal inspiratory and expiratory pressures). Fifty patients had a peak VO(2)<14 ml x kg(-1) x min(-1)(10.6+/-2) and 41 had values >/=14 (18.3+/-4). In the former group, leg and respiratory strength were significantly lower (extensors: 80+/-24 vs 100.9+/-22 Nm; flexors: 48.5+/-24 vs 75.3+/-22, both P<0.001; maximal expiratory pressure: 85.5+/-30 vs 104.8+/-31, P<0.01). Muscular strength was not related to indices of clinical severity, metabolic status, neurohormones or to the degree of systolic/diastolic cardiac function, but it was related to weight and age. Multivariate analysis of the peak VO(2)with clinical, haemodynamic and peripheral indicators showed weight (beta= 0.32, P = 0.007), muscular strength (beta= 0.32, P = 0.01) and NYHA class (beta= 0.31, P = 0.001) as the only independent predictors. The joint adjusted R(2)value was 0.48 (P<0.001). CONCLUSION: Muscular dysfunction is part of the syndrome of heart failure. Together with symptom perception, it predicts nearly half of the variation in exercise tolerance. (+info)