English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

A robust and highly responsive autonomic nervous system (ANS) is an invaluable component to human health. The ANS innervates and governs most human organ systems via its two subdivisions, the sympathetic and parasympathetic nerves. For example, patients with differing levels of ANS dysfunction can present with impairments in blood pressure regulation, control of heart rate, and thermoregulation to name a few [6]. While changes in autonomic control have been linked to several chronic diseases and disorders, the large fluctuations in blood glucose levels associated with Type 1 diabetes mellitus (T1DM) tend to place these patients at particularly greater risk [3]. The impairment in ANS function associated with T1DM has been noted in numerous studies, even in those patients who appear to be otherwise ‘‘healthy’’ (i.e., no diagnosed retinopathy, nephropathy, or clinical neuropathy) [11, 12]. A recently published study by Limberg et al. [8] not only eloquently highlights how ANS function is impaired in patients with T1DM at rest, but also how factors as simple as glycemic management can exacerbate impairments in autonomic control. Specifically, these findings were evidenced by marked reductions in heart rate variability, spontaneous cardiac baroreflex sensitivity, and T-wave amplitude along with prolonged QT intervals during and following an acute hypoglycemic episode [8]. Considering that *82 % of patients with T1DM report at least 1 hypoglycemic event each month [4], with greater frequencies reported during physically demanding tasks or physical exercise [14], implementing interventions which can delay and/or reverse ANS dysfunction in these patients is paramount. Along with individualized diet and insulin regimens prescribed for patients with T1DM, exercise has long been considered a key component to diabetes management [2]. Along with the improvements associated with cardiorespiratory health and reductions in the risk for chronic disease, exercise training has clearly been shown to improve ANS function [6]. In fact, the physiological adjustments involving the ANS are believed to play a major role in the systemic protective and therapeutic effects of exercise training [7]. Furthermore, exercise training has been shown to augment baroreflex function and even blunts the agerelated reductions in baroreflex sensitivity [7, 10]. To date, most of these studies have focussed on ‘‘healthy’’ populations; however, the effects and benefits of chronic exercise training in population groups with impaired ANS function (i.e., patients with T1DM) remain largely unknown. Specifically in the study by Limberg et al. [8], fitness of the groups with and without T1DM was not controlled, albeit the authors excluded any individuals who reportedly engaged in regular physical activity programs. Therefore, considering the strong evidence for exercise-induced improvements in ANS function [6], future studies should include separate patient groups with T1DM based on fitness to examine the potential impact of chronic exercise training on blunting and/or reversing impairments in ANS function. Despite the insurmountable evidence for the health benefits associated with chronic exercise training, there remain certain risks related to acute exercise bouts. A recent report by Carter and colleagues [1] revealed that R. McGinn G. P. Kenny (&) Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, ON K1N 6N5, Canada e-mail: gkenny@uottawa.ca

Autonomic dysfunction associated with Type 1 diabetes: a role for fitness?