From this month’s issue of our journal, I am directing attention to two articles concerning Type 1 Diabetes and another concerning oxygen uptake kinetics and aging.
Regular physical activity represents a cornerstone in type 1 diabetes care. However, patients with type 1 diabetes (T1D), especially those with poor glycemic control, may have limitations when they engage in intense aerobic exercise. The study by Tagougui et al. adds to this clinical picture, with their observations that poorly controlled T1D patients displayed a dramatic impairment in oxyhemoglobin desaturation in active muscle during intense exercise in comparison to well-controlled patients. This supports the hypothesis of an increase in oxygen affinity induced by hemoglobin glycation associated with T1D, as previously put forward on the basis of studies in vitro. From a practical perspective, maximal exercise coupled with muscle near-infrared spectroscopy may represent a promising noninvasive method to assess disorders of muscular perfusion occurring even before overt microangiopathy in poorly controlled T1D patients.
In this month’s second highlighted study, Rissanen and colleagues are the first to report the independent contributions of central and peripheral cardiovascular mechanisms to peak O2 uptake (V̇O2peak) in patients with T1D. They show that in addition to reduced V̇O2peak, both cardiac function and active leg muscle blood flow at peak cycling exercise are reduced independently of each other in physically active adults with T1D when compared to well-matched healthy individuals. Importantly, cardiac limitations correlated with glycemic control and peripheral limitations tended to correlate with glycemic control. To complement these reports, we offer a link to a prior, highly cited position statement on type 2 diabetes [American College of Sports Medicine and the American Diabetes Association. Exercise and type 2 diabetes: joint position statement. Med Sci Sports Exerc. 2010;42(12):2282-2303].
I also note the study by Grey et al. Study of older individuals is useful in examining mechanisms controlling V̇O2 kinetics, as this group often displays a slower response compared to young subjects. However, it remains unclear whether the slow V̇O2 kinetics is related to aging per se, or to other partly preventable factors associated with aging (e.g., deteriorated cardiovascular function). This study examined the effects of age and training status, and demonstrated that long-term endurance training prevents the slower V̇O2 kinetics normally associated with aging. The abolishment of the slower V̇O2 kinetics in older trained individuals was related to a preserved matching of O2 delivery to O2 utilization. Finally, this study showed a dissociation between the mechanisms controlling changes in V̇O2max and V̇O2 kinetics with aging and training, as the inevitable decline in V̇O2max with aging was not evident for the V̇O2 kinetics response.
L. Bruce Gladden