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01.12.2007 | Research | Ausgabe 1/2007 Open Access

Cardiovascular Ultrasound 1/2007

Exercise training does not improve myocardial diastolic tissue velocities in Type 2 diabetes

Cardiovascular Ultrasound > Ausgabe 1/2007
Antti Loimaala, Kaj Groundstroem, Marjo Rinne, Arja Nenonen, Heini Huhtala, Ilkka Vuori
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1476-7120-5-32) contains supplementary material, which is available to authorized users.

Competing interests

The author(s) declare that they have no competing interests.

Authors' contributions

AL and KG carried out study design, echocardiography imaging and measurements, data analyses and reporting. MR designed and supervised all exercise programs, and critically revised the manuscript. AN designed and performed all blood analyses and revised the manuscipt. HH designed and performed statistical analyses together with AL, and critically revised the manuscript. IV caried out study design and exercise program planning, and revised the manuscript critically. All authors read and approved the final manuscript.



Myocardial diastolic tissue velocities are reduced already in newly onset Type 2 diabetes mellitus (T2D). Poor disease control may lead to left ventricular (LV) systolic dysfunction and heart failure. The aim of this study was to assess the effects of exercise training on myocardial diastolic function in T2D patients without ischemic heart disease.


48 men (52.3 ± 5.6 yrs) with T2D were randomized to supervised training four times a week and standard therapy (E), or standard treatment alone (C) for 12 months. Glycated hemoglobin (HbA1c), oxygen consumption (VO2max), and muscle strength (Sit-up) were measured. Tissue Doppler Imaging (TDI) was used to determine the average maximal mitral annular early (Ea) and late (Aa) diastolic as well as systolic (Sa) velocities, systolic strain (ε) and strain rate (έ) from the septum, and an estimation of left ventricular end diastolic pressure (E/Ea).


Exercise capacity (VO2max, E 32.0 to 34.7 vs. C 32.6 to 31.5 ml/kg/min, p = .001), muscle strength (E 12.7 to 18.3 times vs. C 14.6 to 14.7 times, p < .001), and HbA1c (E 8.2 to 7.5% vs. C 8.0 to 8.4%, p = .006) improved significantly in the exercise group compared to the controls (ANOVA). Systolic blood pressure decreased in the E group (E 144 to 138 mmHg vs. C 146 to 144 mmHg, p = .04). Contrary to risk factor changes diastolic long axis relaxation did not improve significantly, early diastolic velocity Ea from 8.1 to 7.9 cm/s for the E group vs. C 7.4 to 7.8 cm/s (p = .85, ANOVA). Likewise, after 12 months the mitral annular systolic velocity, systolic strain and strain rate, as well as E/Ea were unchanged.


Exercise training improves endurance and muscle fitness in T2D, resulting in better glycemic control and reduced blood pressure. However, myocardial diastolic tissue velocities did not change significantly. Our data suggest that a much longer exercise intervention may be needed in order to reverse diastolic impairment in diabetics, if at all possible.
Authors’ original file for figure 1
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