Effects of exercise training on mitochondrial function in patients with type 2 diabetes

Larsen, Steen; Skaaby, Stinna; Helge, Jørn Wulff; Dela, Flemming

doi:10.4239/wjd.v5.i4.482

Cited by 15 publications

(11 citation statements)

References 84 publications

(137 reference statements)

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“…In some studies, both regular moderate intensity exercise [ 45 – 48 ] and HIIT [ 10 , 49 , 50 ] have shown to improve insulin sensitivity. However, few research has however demonstrated that insulin sensitivity remained unaltered following HIIT [ 33 ] and moderate intensity exercise [ 33 , 35 , 46 ]In addition, there are multiple studies finding improved insulin sensitivity among sedentary non-diabetic subjects [ 24 , 41 , 51 ]An intriguing study demonstrated that 7 consecutive days of exercise at 60–75% of heart frequency reserve improved ISI composite with additional improvement of AUC in a T2D population [ 45 ]. In our study, ISI composite was unchanged in both groups ( Fig 6A ).…”

Section: Discussionmentioning

confidence: 99%

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High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients

et al. 2015

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Physical activity improves the regulation of glucose homeostasis in both type 2 diabetes (T2D) patients and healthy individuals, but the effect on pancreatic β cell function is unknown. We investigated glycaemic control, pancreatic function and total fat mass before and after 8 weeks of low volume high intensity interval training (HIIT) on cycle ergometer in T2D patients and matched healthy control individuals. Study design/method: Elderly (56 yrs±2), non-active T2D patients (n = 10) and matched (52 yrs±2) healthy controls (CON) (n = 13) exercised 3 times (10×60 sec. HIIT) a week over an 8 week period on a cycle ergometer. Participants underwent a 2-hour oral glucose tolerance test (OGTT). On a separate day, resting blood pressure measurement was conducted followed by an incremental maximal oxygen uptake (O2max) cycle ergometer test. Finally, a whole body dual X-ray absorptiometry (DXA) was performed. After 8 weeks of training, the same measurements were performed. Results: in the T2D-group, glycaemic control as determined by average fasting venous glucose concentration (p = 0.01), end point 2-hour OGTT (p = 0.04) and glycosylated haemoglobin (p = 0.04) were significantly reduced. Pancreatic homeostasis as determined by homeostatic model assessment of insulin resistance (HOMA-IR) and HOMA β cell function (HOMA-%β) were both significantly ameliorated (p = 0.03 and p = 0.03, respectively). Whole body insulin sensitivity as determined by the disposition index (DI) was significantly increased (p = 0.03). During OGTT, the glucose continuum was significantly reduced at -15 (p = 0.03), 30 (p = 0.03) and 120 min (p = 0.03) and at -10 (p = 0.003) and 0 min (p = 0.003) with an additional improvement (p = 0.03) of its 1st phase (30 min) area under curve (AUC). Significant abdominal fat mass losses were seen in both groups (T2D: p = 0.004 and CON: p = 0.02) corresponding to a percentage change of -17.84%±5.02 and -9.66%±3.07, respectively. Conclusion: these results demonstrate that HIIT improves overall glycaemic control and pancreatic β cell function in T2D patients. Additionally, both groups experienced abdominal fat mass losses. These findings demonstrate that HIIT is a health beneficial exercise strategy in T2D patients.Trial RegistrationClinicalTrials.gov NCT02333734 http://clinicaltrials.gov/ct2/show/NCT02333734

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Section: Discussionmentioning

confidence: 99%

“…T2D is linked to endothelial dysfunction and hypertension [ 46 ]. We have demonstrated significant effects on overall blood pressure following 8 weeks of HIIT ( Table 1 ), which may be of pivotal clinical relevance [ 72 ].…”

Section: Discussionmentioning

confidence: 99%

High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients

et al. 2015

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“…Impaired mitochondrial biogenesis is also a possible cause of apoptosis of skeletal muscle cells in T2DM. 18 The goal of this study was to evaluate the effects of LMHFV on glucose homeogenesis, NAFLD and muscle strength as well as the possible mechanisms on mitochondrial biogenesis and lipid metabolism.…”

Section: Introductionmentioning

confidence: 99%

<p>Low-Magnitude High-Frequency Vibration Decreases Body Weight Gain and Increases Muscle Strength by Enhancing the p38 and AMPK Pathways in db/db Mice</p>

Ren¹,

Lan²,

Chen³

et al. 2020

DMSO

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Objective: To evaluate the effect LMHFV on body weight gain, NAFLD and muscle strength and explore effect in mitochondrial biogenesis, AMPKα and p38 pathways. Methods: Vibration platform used in this study provides specific whole-body cyclic mechanical stimulation at low magnitude (0.3 g) and high frequency (50 Hz). Diabetic mice (8-9 mice per group) (C57BL/KsJ-m+/+Lepr db) were randomly divided into untreated group (no vibration) and two vibration groups. Lean mice (8 mice) were used as non-diabetic control for both groups. Two diabetic vibration groups received LMHFV every day for 20 min/day and 40 min/day separately. Results: After 8 weeks of treatment, results showed that body weight, liver weight, fat pad weight, glucose level and insulin level were lower in vibration group when compared with the untreated group. The ratio of fat in liver was significantly decreased after vibration treatment. Muscle strength was significantly increased after vibration. Mitochondrial biogenesis-related gene expression was increased in soleus, gastrocnemius and liver. AMPKα mRNA expression level was increased in soleus and gastrocnemius after vibration treatment. p38 and AMPKα mRNA expression level and protein expression level in liver were enhanced with vibration treatment. Moreover, phosphorylation of p38 and AMPKα was enhanced in liver. Conclusion: LMHFV applied in our study decreases body weight gain and improves muscle strength and NAFLD in diabetic mice which were partly through improving mitochondrial biogenesis by enhancing p38 and AMPKα pathway.

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“…Mitochondrial quality control consists of a series of mechanisms, including reactive oxygen species (ROS) scavenging, mitochondrial dynamics, and mitophagy. Studies have revealed that exercise improves mitochondrial quality both in healthy [ 10 ] and in metabolic and neurodegenerative disorders as well as in aging [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Short-Duration Swimming Exercise after Myocardial Infarction Attenuates Cardiac Dysfunction and Regulates Mitochondrial Quality Control in Aged Mice

Zhao

Sun

Tan

et al. 2018

Oxidative Medicine and Cellular Longevity

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Background Exercise benefits to cardiac rehabilitation (CR) following stable myocardial infarction (MI). The suitable exercise duration for aged patients with coronary heart disease (CHD) remains controversial, and the underlying molecular mechanism is still unclear. Methods and Results 18-Month-old mice after stable MI were randomly submitted to different durations of exercise, including 15 and 60 min swimming training (ST) once per day, five times a week for 8 weeks. Compared to sedentary mice, 15 min ST, rather than 60 min ST, significantly augmented left ventricular function, increased survival rate, and suppressed myocardial fibrosis and apoptosis. 15 min ST improved mitochondrial morphology via regulating mitochondrial fission-fusion signaling. 15 min ST regulated mitophagy signaling via inhibiting LC3-II and P62 levels and increasing PINK/Parkin expression. 15 min ST also inhibited ROS production and enhanced antioxidant SOD2 activity. Notably, 15 min ST significantly increased sirtuin (SIRT) 3 level (2.7-fold) in vivo while the inhibition of SIRT3 exacerbated senescent H9c2 cellular LDH release and ROS production under hypoxia. In addition, SIRT3 silencing impairs mitochondrial dynamics and mitophagy in senescent cardiomyocytes against simulated ischemia (SI) injury. Conclusion Collectively, our study demonstrated for the first time that sustained short-duration exercise, rather than long-duration exercise, attenuates cardiac dysfunction after MI in aged mice. It is likely that the positive regulation induced by a short-duration ST regimen on the elevated SIRT3 protein level improved mitochondrial quality control and decreased apoptosis and fibrosis contributed to the observed more resistant phenotype.

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Effects of exercise training on mitochondrial function in patients with type 2 diabetes

Cited by 15 publications

References 84 publications

High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients

High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients

<p>Low-Magnitude High-Frequency Vibration Decreases Body Weight Gain and Increases Muscle Strength by Enhancing the p38 and AMPK Pathways in db/db Mice</p>

Short-Duration Swimming Exercise after Myocardial Infarction Attenuates Cardiac Dysfunction and Regulates Mitochondrial Quality Control in Aged Mice

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