Coração de atleta

Sistematicamente ouço alunos e professores dizendo que o exercício de força (resistance training) é estímulo que pode modificar negativamente a estrutura cardíaca, ao passo que o exercício de resistência (endurance) poderia alterá-la positivamente.

Isto é viagem.

Primeiro que nem todo atleta de força/potência tem prejuízos na morfologia cardíaca.
Segundo que os que tem, em geral, têm fatores associados (principalmente uso de EAA).
Terceiro, os benefícios não perduram com o destreinamento, ou seja, são irrelevantes para toda a vida se a pessoa não se manter em atividade.

Por quê tantas incongruências? A ciência é dinâmica, as coisas mudam sempre e não há verdade absoluta (a não ser esta…). Assim, o que sempre é sugerido ainda vale: Estude sempre, conhecimento é poder.

Não podemos ser reféns de velhos tótens. Sem medo, sem vergonha, sem timidez. É caminhando e cantando… Ou como o cavalo em desfile em dia da independência.

Boas leituras!

Três resumos para nossa diversão:

Haykowsky MJ, Dressendorfer R, Taylor D, Mandic S, Humen D. Resistance training and cardiac hypertrophy: unravelling the training effect. Sports Med. 2002;32(13):837-49.

Resistance training (RT) is a popular method of conditioning to enhance sport performance as well as an effective form of exercise to attenuate the age-mediated decline in muscle strength and mass. Although the benefits of RT on skeletal muscle morphology and function are well established, its effect on left ventricular (LV) morphology remains equivocal. Some investigations have found that RT is associated with an obligatory increase in LV wall thickness and mass with minimal alteration in LV internal cavity dimension, an effect called concentric hypertrophy. However, others report that short- (18 years) RT does not alter LV morphology, arguing that concentric hypertrophy is not an obligatory adaptation secondary to this form of exertion. This disparity between studies on whether RT consistently results in cardiac hypertrophy could be caused by: (i) acute cardiopulmonary mechanisms that minimise the increase in transmural pressure (i.e. ventricular pressure minus intrathoracic pressure) and LV wall stress during exercise; (ii) the underlying use of anabolic steroids by the athletes; or (iii) the specific type of RT performed. We propose that when LV geometry is altered after RT, the pattern is usually concentric hypertrophy in Olympic weightlifters. However, the pattern of eccentric hypertrophy (increased LV mass secondary to an increase in diastolic internal cavity dimension and wall thickness) is not uncommon in bodybuilders. Of particular interest, nearly 40% of all RT athletes have normal LV geometry, and these athletes are typically powerlifters. RT athletes who use anabolic steroids have been shown to have significantly higher LV mass compared with drug-free sport-matched athletes. This brief review will sort out some of the factors that may affect the acute and chronic outcome of RT on LV morphology. In addition, a conceptual framework is offered to help explain why cardiac hypertrophy is not always found in RT athletes.

Naylor LH, George K, O’Driscoll G, Green DJ.The athlete’s heart: a contemporary appraisal of the ‘Morganroth hypothesis’. Sports Med. 2008;38(1):69-90.

As early as 1975, Morganroth and colleagues hypothesized that the cardiac morphological adaptation observed in athletes corresponded with the nature of the haemodynamic stimulus imposed on the ventricles during repeated exercise bouts. Endurance training purportedly leads to an eccentric form of cardiac hypertrophy, principally characterized by increased left ventricular (LV) cavity dimension, and thus LV mass (LVM), as a consequence of prolonged repetitive volume overload. In contrast, strength training is supposedly associated with a concentric form of hypertrophy where increased ventricular wall thickness, with no change in cavity size, underpins the elevated LVM as a consequence of the pressure overload produced during strenuous resistive exercise. The ‘Morganroth hypothesis’ has been broadly adopted in the scientific and medical literature, partly as a consequence of a large body of cross-sectional evidence suggesting that endurance athletes have greater cavity dimensions than control subjects or resistance athletes. However, in conflict with the ‘Morganroth hypothesis’, several studies suggest that LV wall thickness is increased more in endurance-, than strength-trained athletes and others have reported no morphological changes in resistance-trained athletes. Such controversial data may reflect variability in the training stimuli, with little obvious attempt to quantify these issues in previous research. Further reflection on the ‘Morganroth hypothesis’ may also be pertinent as more sensitive technologies, such as magnetic resonance imaging, are now being employed for the assessment of cardiac morphology. Finally, the process of scaling (or normalizing) cardiac size for between-subject differences in body size and composition has further complicated the description and understanding of cardiac morphology in athletes. Specifically, it is possible that the increased LVM observed in some athletes may merely reflect a ‘larger than normal’ body size. These considerations emphasise the limitations of the predominance of cross-sectional comparisons in the available literature, which assume that differences between groups are due to a training effect per se rather than other between-subject differences. The small number of longitudinal training studies undertaken in athletes suggest that individuals with athlete’s heart can exhibit further cardiac adaptation in response to training resumption. Longitudinal training studies undertaken in previously sedentary subjects generally indicate that exercise results in enlargement of LV cavity size, increases in wall thickness or LVM following training. However, there are currently limited longitudinal data available to comment on the effects of different modalities of exercise training on LV cavity dimension and wall thickness. In summary, significant caveats related to cross-sectional literature, the relative insensitivity of echocardiographic measurements and the paucity of evidence from longitudinal exercise training studies, warrant ongoing research to verify the ‘Morganroth hypothesis’.

Pelliccia A, Maron BJ, De Luca R, Di Paolo FM, Spataro A, Culasso F. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation. 2002 Feb 26;105(8):944-9.

BACKGROUND: The clinical significance and long-term consequences of left ventricular (LV) hypertrophy associated with intensive athletic conditioning remain unresolved.
METHODS AND RESULTS: We prospectively evaluated 40 elite male athletes who had shown marked LV cavity enlargement of > or = 60 mm, wall thickness of > or = 13 mm, or both in a longitudinal fashion with serial echocardiograms, initially at peak training (age 24 +/- 4 years) and subsequently after a long-term deconditioning period (1 to 13 years; mean, 5.6 +/- 3.8). After detraining, LV cavity dimension decreased by 7% (61.2 +/- 2.9 to 57.2 +/- 3.1 mm; P<0.001), maximum wall thickness by 15% (12.0 +/- 1.3 to 10.1 +/- 0.8 mm; P<0.001), and mass normalized to height by 28% (194 +/- 25 to 140 +/- 21 g/m; P or = 60 mm) in 9 athletes (22%); in contrast, wall thickness returned to normal in each athlete. Multiple regression analysis demonstrated that approximately 50% of the incomplete reduction in cavity dimension was explained by increased body weight and recreational physical activity performed during the follow-up period. No athlete had developed cardiac symptoms, impaired exercise performance, or evidence of LV dysfunction.
CONCLUSIONS: LV remodeling was evident after long-term detraining, with significant reduction in cavity size and normalization of wall thickness. Resolution of cavity enlargement was, however, incomplete in most cases, and substantial chamber dilatation persisted in >20% of athletes. The possibility that this residual LV hypertrophy, apparently part of the athlete’s heart syndrome, may have future long-term clinical implications in some individuals cannot be excluded with certainty.


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