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Sedentary Subjects (sedentary + subject)

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Medical Sciences	80%

Selected Abstracts

"Supranormal" Cardiac Function in Athletes Related to Better Arterial and Endothelial Function

ECHOCARDIOGRAPHY, Issue 6 2010
Maria Florescu M.D.
Objective: Athlete's heart is associated with left ventricular (LV) hypertrophy (LVH), and "supranormal" cardiac function, suggesting that this is a physiological process. Hypertrophy alone cannot explain increase in cardiac function, therefore, other mechanisms, such as better ventriculo-arterial coupling might be involved. Methods: We studied 60 male (21 ± 3 years) subjects: 27 endurance athletes, and a control group of 33 age-matched sedentary subjects. We assessed global systolic and diastolic LV function, short- and long-axis myocardial velocities, arterial structure and function and ventriculo-arterial coupling, endothelial function by flow-mediated dilatation, and amino-terminal pro-brain natriuretic peptide (NT-proBNP) and biological markers of myocardial fibrosis and of oxidative stress. Results: Athletes had "supranormal" LV longitudinal function (12.4 ± 1.0 vs 10.1 ± 1.4 cm/s for longitudinal systolic velocity, and 17.4 ± 2.6 vs 15.1 ± 2.4 cm/s for longitudinal early diastolic velocity, both P < 0.01), whereas ejection fraction and short-axis function were similar to controls. Meanwhile, they had better endothelial function (16.7 ± 7.0 vs 13.3 ± 5.3%, P < 0.05) and lower arterial stiffness (pulse wave velocity 7.1 ± 0.6 vs 8.8 ± 1.1 m/s, P = 0.0001), related to lower oxidative stress (0.259 ± 0.71 vs 0.428 ± 0.88 nmol/mL, P = 0.0001), with improved ventriculo-arterial coupling (37.1 ± 21.5 vs 15.5 ± 13.4 mmHg.m/s3× 103, P = 0.0001). NT-proBNP and markers of myocardial fibrosis were not different from controls. LV longitudinal function was directly related to ventriculo-arterial coupling, and inversely related to arterial stiffness and to oxidative stress. Conclusions: "Supranormal" cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete's heart is purely a physiological phenomenon, associated with "supranormal" cardiac function, and there are no markers of myocardial fibrosis. (Echocardiography 2010;27:659-667) [source]

Inspiratory muscle performance in endurance athletes and sedentary subjects

RESPIROLOGY, Issue 2 2001
Peter R. Eastwood
Objective: The aim of this study was to determine whether whole-body endurance training is associated with increased respiratory muscle strength and endurance. Methodology: Respiratory muscle strength (maximum inspiratory pressure (PImax)) and endurance (progressive threshold loading of the inspiratory muscles) were measured in six marathon runners and six sedentary subjects. Results: PImax was similar between the two groups of subjects but the maximum threshold pressure achieved was greater in marathon runners (90 ± 8 vs 78 ± 10% of PImax, respectively, mean ± SD, P < 0.05). During progressive threshold loading, marathon runners breathed with lower frequency, higher tidal volume, and longer inspiratory and expiratory time. At maximum threshold pressure, marathon runners had lower arterial O2 saturation, but perceived effort (Borg scale) was maximal in both groups. Efficiency of the respiratory muscles was similar in both groups being 2.0 ± 1.7% and 2.3 ± 1.8% for marathon runners and sedentary subjects, respectively. Conclusions: The apparent increase in respiratory muscle endurance of athletes was a consequence of a difference in the breathing pattern adopted during loaded breathing rather than respiratory muscle strength or efficiency. This implies that sensory rather than respiratory muscle conditioning may be an important mechanism by which whole-body endurance is increased. [source]

Exercise prevents age-related decline in nitric-oxide-mediated vasodilator function in cutaneous microvessels

THE JOURNAL OF PHYSIOLOGY, Issue 14 2008
Mark A. Black
Ageing is associated with impaired endothelium-derived nitric oxide (NO) function in human microvessels. We investigated the impact of cardiorespiratory fitness and exercise training on physiological and pharmacological NO-mediated microvascular responses in older subjects. NO-mediated vasodilatation was examined in young, older sedentary and older fit subjects who had two microdialysis fibres embedded into the skin on the ventral aspect of the forearm and laser Doppler probes placed over these sites. Both sites were then heated to 42°C, with Ringer solution infused in one probe and N -nitro- l -arginine methyl ester (l -NAME) through the second. In another study, three doses of ACh were infused in the presence or absence of l -NAME in similar subjects. The older sedentary subjects then undertook exercise training, with repeat studies at 12 and 24 weeks. The NO component of the heat-induced rise in cutaneous vascular conductance (CVC) was diminished in the older sedentary subjects after 30 min of prolonged heating at 42°C (26.9 ± 3.9%CVCmax), compared to older fit (46.2 ± 7.0%CVCmax, P < 0.05) and young subjects (41.2 ± 5.2%CVCmax, P < 0.05), whereas exercise training in the older sedentary group enhanced NO-vasodilator function in response to incremental heating (P < 0.05). Similarly, the NO contribution to ACh responses was impaired in the older sedentary versus older fit subjects (low dose 3.2 ± 1.3 versus 6.6 ± 1.3%CVCmax; mid dose 11.4 ± 2.4 versus 21.6 ± 4.5%CVCmax; high dose 35.2 ± 6.0 versus 52.6 ± 7.9%CVCmax, P < 0.05) and training reversed this (12 weeks: 13.7 ± 3.6, 28.9 ± 5.3, 56.1 ± 3.9%CVCmax, P < 0.05). These findings indicate that maintaining a high level of fitness, or undertaking exercise training, prevents age-related decline in indices of physiological and pharmacological microvascular NO-mediated vasodilator function. Since higher levels of NO confer anti-atherogenic benefit, this study has potential implications for the prevention of microvascular dysfunction in humans. [source]

Scaling of lactate threshold by peak oxygen uptake and by fat-free mass0·67

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 3 2007
James A. Davis
Summary The lactate threshold (LT) represents the onset of metabolic acidosis during cardiopulmonary exercise testing (CPET). It is measured as a O2 in the units of ml min,1. In order to make comparisons among subjects, LT is often scaled or normalized by O2 peak resulting in the LT/O2 peak ratio. Ratio variables have underlying assumptions. One assumption is that the relationship between the numerator and denominator is linear with a zero y -intercept. If the relationship has a positive y -intercept, then the ratio will decrease with increasing values of the scaling variable thereby penalizing subjects with larger values of the scaling variable. Our purpose was to examine the validity of scaling LT by O2 peak and by fat-free mass raised to 0·67 power (FFM0·67) as dimensional analysis predicts that LT is proportional to FFM0·67. Cycle ergometer CPET was administered to 204 healthy, sedentary subjects (103 males) to the limit of tolerance. Lactate threshold was estimated noninvasively using the V-slope technique. Fat-free mass was assessed by skinfolds. The relationship of LT versus O2 peak was linear with a positive y -intercept for both sexes. Consequently, the LT/O2 peak ratio decreased as O2 peak increased for both sexes. The relationship of LT versus FFM0·67was linear with a zero y -intercept for both sexes. Consequently, the plot of the LT/FFM0·67 ratio versus FFM resulted in a straight line with a slope of zero for both sexes. The results of this study support the conclusion that FFM0·67, but not O2 peak, is a valid scaling variable for LT. [source]