The differential anti-inflammatory effects of exercise modalities and their association with early carotid atherosclerosis progression in patients with type 2 diabetes.
OBJECTIVE
Adipokines, visfatin, apelin, vaspin and ghrelin have emerged as novel cardiovascular risk factors. We aimed to evaluate the effects of different exercise modalities on the aforementioned novel adipokines and carotid intima-media thickness in patients with Type 2 diabetes mellitus.


METHODS
One hundred patients with Type 2 diabetes were equivalently (n = 25) randomized into four groups: (1) a control group with patients encouraged to perform self-controlled exercise; (2) a supervised aerobic exercise group (exercise four times/week, 60 min/session, 60-75% of maximum heart rate); (3) a resistance training group (60-80% baseline maximum load achieved in one repetition); and (4) a combined aerobic exercise plus resistance training group, as in groups 2 and 3. All participants had HbA(1c)  levels ≥ 48 mmol/mol (≥ 6.5%), without overt diabetic vascular complications. Blood samples, clinical characteristics, peak oxygen uptake and carotid intima-media thickness measurements were obtained at baseline and at the end of the study, after 6 months.


RESULTS
At baseline, there were non-significant differences between groups. All active groups significantly ameliorated glycaemic profile, insulin sensitivity and triglycerides levels compared with the control group (P < 0.05). Aerobic training further improved lipids, systolic blood pressure and exercise capacity compared with the resistance training and the control groups (P < 0.05). Moreover, high-sensitivity C-reactive protein and visfatin decreased, while vaspin and apelin circulating levels increased within the aerobic exercise group and the aerobic exercise plus resistance training group, and compared with the other groups (P < 0.05). Within- and between-group comparisons showed negligible alterations in ghrelin serum levels and body weight after all exercise modalities. Finally, aerobic training attenuated the carotid intima-media thickness progression (0.017 ± 0.006 mm) compared with the control subjects (0.129 ± 0.042 mm, P < 0.001). That effect was independently associated with visfatin and amelioration of peak oxygen uptake.


CONCLUSIONS
In subjects with Type 2 diabetes, all exercise training modalities improved metabolic profile. Importantly, aerobic training predominantly ameliorated adipokines concentrations and carotid intima-media thickness progression.
Department of Physical Education and Sports Science at Serres, Aristotle University of Thessaloniki. nikoskad@yahoo.com
N P E
NP
Kadoglou
G
G
Fotiadis
A
A
Kapelouzou
A
A
Kostakis
C D
CD
Liapis
I S
IS
Vrabas
D054392:Adipokines / Q000378:metabolism; D000704:Analysis of Variance; D000893:Anti-Inflammatory Agents / Q000378:metabolism*; D000073861:Apelin; D001786:Blood Glucose / Q000378:metabolism*; D002340:Carotid Artery Diseases / Q000097:blood / Q000503:physiopathology* / Q000517:prevention & control; D059168:Carotid Intima-Media Thickness; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D003925:Diabetic Angiopathies / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D018450:Disease Progression; D015444:Exercise; D005215:Fasting; D005260:Female; D054439:Ghrelin / Q000378:metabolism; D006442:Glycated Hemoglobin / Q000378:metabolism*; D006801:Humans; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000378:metabolism; D055070:Resistance Training; D012307:Risk Factors; D015843:Serpins / Q000378:metabolism
D054392:Adipokines; D000893:Anti-Inflammatory Agents; D000073861:Apelin; D001786:Blood Glucose; D054439:Ghrelin; D006442:Glycated Hemoglobin; D036341:Intercellular Signaling Peptides and Proteins; D054409:Nicotinamide Phosphoribosyltransferase; D015843:Serpins; C115436:APLN protein, human; C507339:SERPINA12 protein, human; C517652:hemoglobin A1c protein, human