REVERSAL OF DIASTOLIC DYSFUNCTION IN TYPE 2 DIABETICS AFTER EXERCISE TRAINING: A MATTER OF TIMING?
Patrice Brassard, The Copenhagen Muscle Research Center, Department of Anaesthesia 2041, Rigshospitalet, 2100, Copenhagen, Denmark
28 January 2008
In this manuscript, Loimaala et al.(1) have reported interesting findings regarding the impact of exercise training on indices of myocardial diastolic function in patients with type 2 diabetes. They observed the absence of significant change in myocardial tissue velocities in patients with uncomplicated type 2 diabetes following a one-year endurance and resistance exercise training program. The authors also noted significant improvements in maximal oxygen consumption (VO2max), muscle strength and glycemic control. One of the conclusions provided by the authors as regards to the absence of any influence of chronic exercise on diastolic function indices was that “a much longer non-pharmacological intervention (or aggressive medical therapy) is needed to obtain improvement in myocardial diastolic function”.
These results are of interest since we have recently reported that the normalization of diastolic dysfunction was possible in well-controlled, uncomplicated patients with type 2 diabetes after exercise training (2). Indeed, 45% of our patients with well-controlled type 2 diabetes and diastolic dysfunction who performed 3 months of endurance exercise at 60-70% of VO2max normalized their diastolic dysfunction. In comparison, no control subject with type 2 diabetes who did not perform aerobic exercise training normalized their diastolic dysfunction. In light of these conflicting conclusions, one may argue that the known duration of diabetes as well as the severity of diastolic dysfunction (abnormal relaxation pattern;pseudonormal pattern; restrictive pattern) will have an important influence on whether or not chronic exercise can reverse diastolic dysfunction, and not only the length of the exercise training program.
Potentially longer known duration of diabetes in the cohort of patients studied by Loimaala et al. compared to ours might partly explain why no beneficial impact of exercise training on myocardial diastolic function’s indices was observed. Indeed, their patients had to be diagnosed for three years or less at study enrolment. However, no details are provided about the mean disease duration in each group. In comparison, patients in our exercising group had known diabetes duration of 5+/-7 months. A period of less than three years since diagnosis might be perceived as a relatively short amount of time. However, one need to remember that any significant increase in the period since diagnosis will most likely have an impact on patients’ cardiac function. Indeed, the duration of diabetes is associated with the severity of cardiac dysfunction (3). Accordingly, one possibility could be that the diastolic function related abnormalities present in patients studied by Loimaala et al. were already too advanced to normalize in response to such a chronic exercise stimulus. The presence of hypertension in a majority of patients could also have had a noticeable contribution to the severity of diastolic dysfunction in their cohort.
However, it would have been interesting for Loimaala et al. to include detailed information about the severity of diastolic dysfunction as well as the number of patients with diastolic dysfunction. Smart et al.(4) have recently reported that a 16-week endurance and resistance exercise training program did not positively influence diastolic dysfunction in patients with heart failure, preserved ejection fraction and diastolic dysfunction. Interestingly, a majority of patients from this study had a pseudonormal pattern. In contrast, almost every patient who did normalize its diastolic dysfunction in our study had an abnormal relaxation pattern, therefore a less severe diastolic dysfunction. Accordingly, we might speculate that diabetics with less severe diastolic function impairments still have the possibility to normalize their diastolic dysfunction. However, as one of our patients with a pseudonormal pattern also reversed its diastolic dysfunction, our results also suggest that it may not be necessarily too late for a patient with a more severe diastolic dysfunction to normalize it in response to exercise training.
On the other hand, according to the available information in the manuscript regarding the severity of diastolic dysfunction, another possibility could be that a majority of patients with diabetes studied by Loimaala et al. who exercised had some alterations in diastolic function without overt diastolic dysfunction. One could thus also argue that a near normal diastolic function is difficult to normalize. Taken together, results provided by this study along with ours suggest that the timing for patients with type 2 diabetes to begin an exercise training program is crucial in order to reverse diastolic dysfunction. This being pointed out, I agree with Loimaala et al. that an exercise training program of longer duration might be needed to observe a positive, and probably a more important, influence of this therapeutic approach on diastolic impairments in patients with type 2 diabetes. Clearly, several issues regarding the normalization of diastolic function impairments in patients with type 2 diabetes request further research.
References
1.Loimaala A, Groundstroem K, Rinne M, Nenonen A, Huhtala H, Vuori I. Exercise training does not improve myocardial diastolic tissue velocities in Type 2 diabetes. Cardiovasc Ultrasound 2007; 5:32.
2.Brassard P, Legault S, Garneau C, Bogaty P, Dumesnil JG, Poirier P. Normalization of diastolic dysfunction in type 2 diabetics after exercise training. Med Sci Sports Exerc 2007; 39:1896-1901.
3.Raev DC. Which left ventricular function is impaired earlier in the evolution of diabetic cardiomyopathy? An echocardiographic study of young type I diabetic patients. Diabetes Care 1994; 17:633-639.
4.Smart N, Haluska B, Jeffriess L, Marwick TH. Exercise training in systolic and diastolic dysfunction: effects on cardiac function, functional capacity, and quality of life. Am Heart J 2007; 153:530-536.
REVERSAL OF DIASTOLIC DYSFUNCTION IN TYPE 2 DIABETICS AFTER EXERCISE TRAINING: A MATTER OF TIMING?
28 January 2008
In this manuscript, Loimaala et al.(1) have reported interesting findings regarding the impact of exercise training on indices of myocardial diastolic function in patients with type 2 diabetes. They observed the absence of significant change in myocardial tissue velocities in patients with uncomplicated type 2 diabetes following a one-year endurance and resistance exercise training program. The authors also noted significant improvements in maximal oxygen consumption (VO2max), muscle strength and glycemic control. One of the conclusions provided by the authors as regards to the absence of any influence of chronic exercise on diastolic function indices was that “a much longer non-pharmacological intervention (or aggressive medical therapy) is needed to obtain improvement in myocardial diastolic function”.
These results are of interest since we have recently reported that the normalization of diastolic dysfunction was possible in well-controlled, uncomplicated patients with type 2 diabetes after exercise training (2). Indeed, 45% of our patients with well-controlled type 2 diabetes and diastolic dysfunction who performed 3 months of endurance exercise at 60-70% of VO2max normalized their diastolic dysfunction. In comparison, no control subject with type 2 diabetes who did not perform aerobic exercise training normalized their diastolic dysfunction. In light of these conflicting conclusions, one may argue that the known duration of diabetes as well as the severity of diastolic dysfunction (abnormal relaxation pattern;pseudonormal pattern; restrictive pattern) will have an important influence on whether or not chronic exercise can reverse diastolic dysfunction, and not only the length of the exercise training program.
Potentially longer known duration of diabetes in the cohort of patients studied by Loimaala et al. compared to ours might partly explain why no beneficial impact of exercise training on myocardial diastolic function’s indices was observed. Indeed, their patients had to be diagnosed for three years or less at study enrolment. However, no details are provided about the mean disease duration in each group. In comparison, patients in our exercising group had known diabetes duration of 5+/-7 months. A period of less than three years since diagnosis might be perceived as a relatively short amount of time. However, one need to remember that any significant increase in the period since diagnosis will most likely have an impact on patients’ cardiac function. Indeed, the duration of diabetes is associated with the severity of cardiac dysfunction (3). Accordingly, one possibility could be that the diastolic function related abnormalities present in patients studied by Loimaala et al. were already too advanced to normalize in response to such a chronic exercise stimulus. The presence of hypertension in a majority of patients could also have had a noticeable contribution to the severity of diastolic dysfunction in their cohort.
However, it would have been interesting for Loimaala et al. to include detailed information about the severity of diastolic dysfunction as well as the number of patients with diastolic dysfunction. Smart et al.(4) have recently reported that a 16-week endurance and resistance exercise training program did not positively influence diastolic dysfunction in patients with heart failure, preserved ejection fraction and diastolic dysfunction. Interestingly, a majority of patients from this study had a pseudonormal pattern. In contrast, almost every patient who did normalize its diastolic dysfunction in our study had an abnormal relaxation pattern, therefore a less severe diastolic dysfunction. Accordingly, we might speculate that diabetics with less severe diastolic function impairments still have the possibility to normalize their diastolic dysfunction. However, as one of our patients with a pseudonormal pattern also reversed its diastolic dysfunction, our results also suggest that it may not be necessarily too late for a patient with a more severe diastolic dysfunction to normalize it in response to exercise training.
On the other hand, according to the available information in the manuscript regarding the severity of diastolic dysfunction, another possibility could be that a majority of patients with diabetes studied by Loimaala et al. who exercised had some alterations in diastolic function without overt diastolic dysfunction. One could thus also argue that a near normal diastolic function is difficult to normalize. Taken together, results provided by this study along with ours suggest that the timing for patients with type 2 diabetes to begin an exercise training program is crucial in order to reverse diastolic dysfunction. This being pointed out, I agree with Loimaala et al. that an exercise training program of longer duration might be needed to observe a positive, and probably a more important, influence of this therapeutic approach on diastolic impairments in patients with type 2 diabetes. Clearly, several issues regarding the normalization of diastolic function impairments in patients with type 2 diabetes request further research.
References
1.Loimaala A, Groundstroem K, Rinne M, Nenonen A, Huhtala H, Vuori I. Exercise training does not improve myocardial diastolic tissue velocities in Type 2 diabetes. Cardiovasc Ultrasound 2007; 5:32.
2.Brassard P, Legault S, Garneau C, Bogaty P, Dumesnil JG, Poirier P. Normalization of diastolic dysfunction in type 2 diabetics after exercise training. Med Sci Sports Exerc 2007; 39:1896-1901.
3.Raev DC. Which left ventricular function is impaired earlier in the evolution of diabetic cardiomyopathy? An echocardiographic study of young type I diabetic patients. Diabetes Care 1994; 17:633-639.
4.Smart N, Haluska B, Jeffriess L, Marwick TH. Exercise training in systolic and diastolic dysfunction: effects on cardiac function, functional capacity, and quality of life. Am Heart J 2007; 153:530-536.
Competing interests
No competing interests.