Invited Session at ECSS Vienna 2016 “HIT training – Mechanisms and applicability”
Hit Training as a Cure for Type 2 Diabetes
Dela, F.
University of Copenhagen
Type 2 diabetes is characterized by a combination of insulin resistance, insufficient insulin secretory capacity and genetic disposition
combined with excess energy intake and physical. Physical training alleviates insulin resistance, may improve insulin secretory
capacity and improves glycemic control in patients with type 2 diabetes. Large clinical studies lifestyle interventions including weight
loss and increased physical activity have shown fewer hospitalizations, fewer medications, and lower health-care costs, but on
specific cardiovascular endpoints the results have been disappointing in large scale studies.
Thus, while there is no question about the effectiveness of physical training as medicine for insulin resistance, the major problem is
that the patients do not take the medicine. There are many barriers to overcome and motivation, safe environments, convenience and
lack of time are considered to be among the major reasons for not exercising on a regular basis. High intensity interval training (HIIT)
with short periods of intense exercise interspersed with brief periods of rest is a time efficient exercise modality which might surpass
some of the barriers.
As with almost any kind of exercise, an acute high intensity training bout will lower glucose concentrations in patients with type 2
diabetes. However, the longer term (training for 2 weeks or more) studies that have been conducted in patients with type 2 diabetes
have generally used insufficient methods for determining the effect of HIIT on insulin secretion and sensitivity, which are the key
parameters in the pathophysiology of type 2 diabetes. Hence, by using measurements of interstitial glucose concentrations, HOMA or
HbA1c, either marginal or no effect and significant effects of HIIT on glucose homeostasis have been reported.
None of the previous studies have used the gold standard for assessment of insulin sensitivity, the glucose clamp technique and
none have studied specifically skeletal muscle, which the tissue that takes up the vast majority of glucose during insulin stimulation.
Previous studies have addressed the molecular effects of high intensity interval training in skeletal muscle but only one study in
patients with type 2 diabetes. In general these studies shows that HIIT leads to increases in proteins (activity and/or content) related
to mitochondrial biogenesis, such as citrate synthase (CS), complexes in the mitochondrial respiratory chain, silent mating-type
information regulator 2 homolog 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α),
mitofusin (Mfn)-2. Also skeletal muscle GLUT4 protein and glycogen content seem to increase with HIIT, and furthermore, an
increased capacity to fat oxidation (less exercise induced decrease in glycogen and increased hydroxyl-acyl-dehydrogenase (HAD)
activity) takes place after HIIT.