Hillary Bell

Senior Seminar
October 18, 2013
Abstract:
Van Tienen FHJ, Praet SFE, De Feyter HM et al. Physical Activity is the Key Determinant of
Skeletal Muscle Mitochondrial Function in Type 2 Diabetes. J Clin Endocrinol Metab.
2012;97(9):3261-3269.
It is known that mitochondrial function is negatively affected by a sedentary lifestyle.
Commonly, patients that suffer from type II diabetes have an inactive lifestyle as well as a
poor diet. This article is about a study that was done with human participants. The purpose
was to determine if an exercise regimen would increase the function of the mitochondria in
patients with type II diabetes and pre-diabetic patients. They used a control group for
comparison as well as a baseline measurement of all the participants. In vivo and ex vivo
measurements were used to record ATP production.
The study involved 12 prediabetic, 11 longstanding type II diabetes mellitus and 12
control subjects. All 35 were Caucasian males except one and 3 subjects discontinued the
study. The type II diabetes mellitus patients were on exogenous insulin and stable medication
regimens prior to the study. All the subjects were put through a body composition, overall
health, and physical performance assessment four weeks prior to the start of the exercise
regimen. Two weeks prior to the exercise beginning the first muscle biopsy and blood sample
was drawn and a magnetic resonance spectroscopy was done. Participants were then put
through one year of a supervised exercise protocol. The magnetic resonance spectroscopy
was done week 22 during the regimen and again 1 week after the exercise protocol had
ended. The blood sample and muscle biopsy were taken at week 11, week 22, and one week
after the protocol was completed. Prior to the blood samples being drawn, patients were given
the same standardized meal, took their medication and then fasted until the morning when the
sample was taken. The muscle biopsy was taken from the vastus lateralis muscle and frozen
in liquid nitrogen. It was then analyzed for citrate synthase, complex I and complex IV.
The results from the study were that the exercise training increased ATP production by
approximately 21 percent and increased related gene expression after exercise in areas such
as the Krebs cycle.
The conclusions from this study were that only longstanding type II diabetes mellitus
patients had lower gene expression of the Krebs cycle and oxidative phosphorylation as well
as dysfunction of the mitochondria. This suggests that there is no direct correlation between
mitochondrial function and insulin resistance. The other conclusion from the study was that
an exercise regimen can, to some degree, reverse mitochondrial dysfunction in those who are
in a longstanding diabetic state.
I think this was a well done study. They worked to really control all of the variables
that could alter their results. The fact that they acknowledge the areas that had no significant
changes makes me confident that the results which showed improvement were accurate. I
think this study would be more reliable if they had more participants. The small group does
not give enough data to make the study noteworthy.
This article is relative to my topic due to the fact that they measured the activity of the
Krebs cycle. They found that the process is increased with exercise. It is valuable to know
that mitochondrial function and other bodily functions can be improved by exercise. The
result of exercise can improve the overall health of type II diabetic patients by increasing
their mitochondrial function.