Type 2 diabetes (T2D) prevalence has steadily been rising in the past decades and its
complications, including cardiovascular diseases (CVD), are a major public health concern.
Insulin resistance, an important component of T2D, is associated with vascular dysfunctions,
which directly contributes to the pathogenesis of CVD, such as atherosclerosis, and
hypertension, particularly with the elderly. It is also suggested that glucose variability,
measured with continuous glucose monitors (CGM), is an independent risk factor of CVD in T2D
individuals, exposing them to an increased risk of premature death. Moreover, in part because
of immune dysregulation, women with T2D are at a heightened risk of developing CVD compared
to males. Indeed, monocyte inflammatory profile is altered during the aging process and in
women with T2D. This, in turn, causes vascular dysfunction which is associated with a
pro-thrombotic state, and exacerbates atherosclerosis and arterial stiffening.
To lower CVD risk and to maintain an adequate glycemic control, Diabetes Canada recommends
aerobic exercise of high-intensity interval training (HIIT). However, this recommendation is
solely based on the improvement of cardiorespiratory fitness in type 2 diabetes individuals
(level of evidence: grade B, level 2). Furthermore, most of these studies use exercise
protocols with ergocycles, which limit the ecological validity considering that the elderly
population prefers to walk. Though, it is essential to evaluate the impact of different
walking HIIT protocols on clinical targets such as arterial pressure, glycemic
variability/control using ambulatory blood pressure monitors (ABPM) and CGM.
The preliminary data collected in our laboratory shows that a low volume HIIIT program (6 × 1
min) is insufficient to improve glycemic control/variability and ambulatory blood pressure
over 24 hours in elderly diabetic women, despite reducing inflammatory gene expression in
monocytes. Interestingly, pro-inflammatory monocytes are linked with hyperglycemia and play a
crucial role in the atherosclerotic process, while also being associated with arterial
stiffening in individuals with kidney failure, a common T2D complication.
These results raise several questions, including the role played by the length of HIIT
intervals on clinical targets. While our preliminary results didn't impact ambulatory blood
pressure over 24 hours with shorter intervals (6 × 1 min), other studied showed a reduction
of this parameter with longer intervals (4 x 4 min). Therefore, the leading hypothesis of
this study is that longer high intensity intervals (Wisløff protocol: 4 x 4 min) will reduce
ambulatory blood pressure over 24 hours in a greater extent than shorter intervals (10 x 1
min). Indeed, reduced shear stress induced by shorter intervals could damper cellular and
molecular responses to exercise bouts, thereby limiting the effects on arterial stiffness and
blood pressure in the hours following exercise. Moreover, changes in gene expression do not
guarantee changes at the protein level, and proteins are the real effectors of cellular
response. Hence, proteomics will be useful to better understand monocyte response to
different HIIT protocols and, possibly, the clinical benefits of this training method.
Indeed, longer intervals could induce greater variations to the monocytes' proteome, favoring
an anti-inflammatory phenotype, and those changes could be associated with reduced arterial
stiffness and blood pressure.
The primary objective of this study is therefore to compare the effect of two treadmill HIIT
modalities (4x4 min vs. 10x1 min) on arterial stiffness, ambulatory blood pressure over 24
hours and on glycemic variability in elderly women with T2D. The secondary objective is to
assess the proteomic changes in monocytes induced by the two HIIT modalities and to correlate
them with changes in clinical parameters.