Maximal aerobic capacity is an important indicator of physiological functional capacity. Individuals with Down syndrome have extremely low maximal aerobic capacity relative to the general population. Their values are even much lower than those of people with an intellectual disability who do not have Down syndrome (1). Average maximal aerobic capacity for college-aged individuals with Down syndrome is approximately 20 mL·kg−1·min−1 and is close to the critical values of 15 to 18 mL·kg−1·min−1 that are required for functional independence (2). Why is average maximal aerobic capacity for these individuals so low? It is not caused by a lack of effort during graded exercise, as criteria for reaching maximal exertion were achieved properly. It cannot be explained by congenital heart disease either. Extreme deconditioning associated with a lack of motivation to exercise was thought to be a factor, along with some contributions from higher body fatness, lower muscle mass, and muscle hypotonia (poor muscle tone) that often coexist in Down syndrome.
In this issue of Exercise and Sport Sciences Reviews, Fernhall and colleagues (1) dispel such a notion and make the argument that autonomic dysfunction leading to chronotropic incompetence is the primary contributor to the extremely low physical work capacity in individuals with Down syndrome. Based on a series of studies using a variety of perturbations to activate autonomic nervous system (e.g., cold pressor test, isometric exercise), they built a convincing case that Down syndrome is associated strongly with autonomic dysfunction. As autonomic nervous system plays a critical role in determining maximal heart rate and maximal aerobic capacity, it is not surprising that peak heart rate is lower in individuals with Down syndrome than in age-matched healthy peers (3), but the magnitude of reduction is rather substantial (25–30 beats·min−1). In healthy adults, the lower maximal heart rate can be compensated by augmented stroke volume so that maximal cardiac output and maximal oxygen consumption could remain unchanged (4). Presumably, autonomic dysfunction and its sequela (e.g., failure to augment contractility via sympathetic activation, cardiac dysfunction) may not allow them to increase stroke volume, contributing to the poor work capacity. Although the research findings presented are interesting and thought provoking, most of the available data in this area are derived using rather indirect measures of autonomic function (e.g., heart rate variability). Future studies using more direct assessment of autonomic nervous system function (e.g., pharmacological blockade) are warranted.
Down syndrome often is described as premature or accelerated biological aging. As such, it is critical to understand how functional capacity that is quite low, even at young age, changes with advancing age in this population. The life expectancy for individuals with Down syndrome is increasing dramatically from 12 yr in 1912 to 25 yr in 1983 to the current 55 to 60 yr of age, with the oldest people living now past 80 yr. Interestingly, the age-associated decline in maximal aerobic capacity seems to be absent in individuals with Down syndrome at least to approximately 40 yr of age (1). It is not known if and how much maximal aerobic capacity declines after 40 yr of age. Unfortunately, very limited data are available currently to examine “older” individuals with Down syndrome because most of the available data focus on adolescents and young adults with Down syndrome. It will be interesting to see whether the autonomic dysfunction and its impact on maximal aerobic capacity persist or worsen to older age, considering that aging is associated with marked and sustained increases in sympathetic nervous system activity.
Department of Kinesiology and Health Education
University of Texas at Austin
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