In order to evaluate the influence of aging on cardiovascular adaptations to endurance training and detraining, 12 young (range 19-25 years) and 12 older (range 50-65 years) male cyclists were examined during the training and after 2 months of detraining. Twelve young and 12 older healthy sedentary males matched for age and body surface area were used as control groups. Each subject underwent a maximal exercise test using a cycle-ergometer in order to measure maximum oxygen consumption, an M-mode and 2D echocardiography in order to assess left ventricle morphology and systolic function, and a Doppler echocardiography for evaluating the diastolic filling pattern. During the training period both groups of athletes showed higher values of maximum oxygen consumption, left ventricular wall thicknesses, end-diastolic diameter and volume, as well as left ventricular mass, than their control subjects; in the older subjects the adaptation of the heart to aerobic training seems to be obtained mainly through a higher increase in left ventricular diastolic filling. In both groups no significant modifications in the ejection fraction and diastolic function parameters were recorded. After the detraining period the wall thicknesses decreased only in young athletes, while left ventricular mass and end-diastolic diameter and volume reduced only in older athletes. In conclusion, training and detraining induced nearly similar left ventricular morphological modifications in the two age groups, even though greater in the older athletes with respect to the ventricular mass and volume. No relevant differences were observed in the Doppler filling pattern between athletes and sedentary controls.
"Body mass, among other factors, is influenced by growth and maturity related changes in size of the lungs, heart and skeletal muscle (Rowland, 2005), but lean body mass represents more closely the active metabolic cell mass than body mass (Sheng & Huggins, 1979). Training is associated with adaptive changes in cardiac structure (Giada et al., 1998). Moreover, heart size is positively correlated with aerobic fitness, cardiac output and stroke volume in childhood , adolescence and adulthood (Osborne et al., 1992). "
[Show abstract][Hide abstract] ABSTRACT: Background: Peak oxygen uptake (VO2peak) is routinely scaled as mL O2 per kilogram body mass despite theoretical and statistical limitations of using ratios. Aim: To examine the contribution of maturity status and body size descriptors to age-associated inter-individual variability in VO2peak and to present static allometric models to normalize VO2peak in male youth soccer players. Subjects and methods: Total body and estimates of total and regional lean mass were measured with dual energy X-ray absorptiometry in a cross-sectional sample of Portuguese male soccer players. The sample was divided into three age groups for analysis: 8–12 years, 13–15 years and 16–18 years. VO2peak was estimated using an incremental maximal exercise test on a motorized treadmill. Static allometric models were used to normalize VO2peak. Results: The independent variables with the best statistical fit explained 72% in the younger group (lean body mass: k = 1.07), 52% in mid-adolescent players (lean body mass: k = 0.93) and 31% in the older group (body mass: k = 0.51) of variance in VO2peak. The inclusion of the exponential term pubertal status marginally increased the explained variance in VO2peak (adjusted R2 = 36–75%) and provided statistical adjustments to the size descriptors coefficients. Conclusion: The allometric coefficients and exponents evidenced the varying inter-relationship among size descriptors and maturity status with aerobic fitness from early to late-adolescence. Lean body mass, lean lower limbs mass and body mass combined with pubertal status explain most of the inter-individual variability in VO2peak among youth soccer players.
Annals of Human Biology 10/2015; 42(2):125-33. DOI:10.3109/03014460.2014.932007 · 1.27 Impact Factor
"Kemi et al. (2004), using preparations of isolated rats myocytes, described that fractional shortening regressed with only 2 weeks of detraining. In humans, it was reported that after detraining, ventricular adaptations returned to conditions similar to those prior to training (Pellicia et al. 2002; Giada et al. 1998; Giannattasio et al. 1992 "
[Show abstract][Hide abstract] ABSTRACT: Exercise training is assumed to improve myocardial function; however, the role of detraining and its effect on myocardial parameters are still unclear. The aim of the present study was to evaluate the effect of detraining on ventricular remodeling and myocardial mechanical parameters after an 8 week (5 days/week, 60 min/day) swimming training period. Forty-three female Wistar rats were distributed into six groups: trained (T, n = 9), detrained 2 weeks (D2, n = 8), detrained 4 weeks (D4, n = 8) and their respective controls: untrained (U, n = 5), untrained 2 weeks (U2, n = 5) and untrained 4 weeks (U4, n = 5). Detrained rats underwent training and then remained sedentary (i.e., "detraining") for 2 or 4 weeks. After training, the T group demonstrated increased physical capacity, left ventricular (LV) posterior wall thickness, and LV end-diastolic diameter, along with decreased heart rate, as evaluated by echocardiogram. In addition, the inotropism and lusitropism parameters studied on papillary muscles showed improvement in the T group (P < 0.05). However, after just 2 weeks of detraining, all parameters regressed back to values which were similar to those of the untrained groups. In conclusion, our results confirmed that exercise training is capable of inducing myocardial remodeling and improving contractile performance; however, these changes are completely lost after a short period of detraining.
"ventricular preload and afterload ( Fleg , 1986 ; Giada et al . 1998 ) . Animal studies using the isolated perfused heart preparation find that contractility declines significantly with advancing age in endurance - trained rats and that the magnitude and the rate of the decline is similar to sedentary rats ( Starnes & Rumsey , 1988 ) . The similarly lower ejection fractions at maximal exercise observed i"
[Show abstract][Hide abstract] ABSTRACT: Older ('Masters') athletes strive to maintain or even improve upon the performance they achieved at younger ages, but declines in athletic performance are inevitable with ageing. In this review, we describe changes in peak endurance exercise performance with advancing age as well as physiological factors responsible for those changes. Peak endurance performance is maintained until approximately 35 years of age, followed by modest decreases until 50-60 years of age, with progressively steeper declines thereafter. Among the three main physiological determinants of endurance exercise performance (i.e. maximal oxygen consumption , lactate threshold and exercise economy), a progressive reduction in appears to be the primary mechanism associated with declines in endurance performance with age. A reduction in lactate threshold, i.e. the exercise intensity at which blood lactate concentration increases significantly above baseline, also contributes to the reduction in endurance performance with ageing, although this may be secondary to decreases in . In contrast, exercise economy (i.e. metabolic cost of sustained submaximal exercise) does not change with age in endurance-trained adults. Decreases in maximal stroke volume, heart rate and arterio-venous O(2) difference all appear to contribute to the age-related reductions in in endurance-trained athletes. Declines in endurance exercise performance and its physiological determinants with ageing appear to be mediated in large part by a reduction in the intensity (velocity) and volume of the exercise that can be performed during training sessions. Given their impressive peak performance capability and physiological function capacity, Masters athletes remain a fascinating model of 'exceptionally successful ageing' and therefore are highly deserving of our continued scientific attention as physiologists.
The Journal of Physiology 02/2008; 586(1):55-63. DOI:10.1113/jphysiol.2007.141879 · 5.04 Impact Factor
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