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LETTER TO THE EDITOR The following is the abstract of the article discussed in the subsequent letter:
Subjects with Type 2 diabetes without cardiovascular disease have a reduced exercise capacity compared with nondiabetic subjects. However, the mechanisms responsible for this phenomenon are unknown. The purpose of this study was to evaluate the impact of exercise systolic blood pressure (SBP) response on diverse exercise tolerance parameters in Type 2 diabetic subjects. Twenty-eight sedentary men with Type 2 diabetes were recruited for this study. Subjects were treated with oral hypoglycemic agents and/or diet. Evaluation of glycemic control and peak exercise capacity were performed for each subject. The subjects were divided into two groups according to the median value of peak SBP (210 mmHg) measured in each subject. We observed a 13, 13, and 16% reduction in the relative peak oxygen uptake (
O2 peak), absolute O2 peak, and peak work rate in the low- compared with the high-peak SBP group [26.95 (SD 5.35) vs. 30.96 (SD 3.61) ml·kg–1·min–1, 2.5 (SD 0.4) vs. 2.8 (SD 0.6) l/min, and 169 (SD 34) vs. 202 (SD 32) W; all P < 0.05]. After adjusting for age, relative O2 peak was still significantly different (P < 0.05). There were similar peak respiratory exchange ratio (RER) [1.20 (SD 0.08) vs. 1.16 (SD 0.07); P = 0.24] and peak heart rate [160 (SD 20) vs. 169 (SD 15) beats/min; P = 0.18] between the low- compared with the high-SBP group. No difference in glycemic control was observed between the two groups. The results reported in this study suggest that in subjects with Type 2 diabetes without cardiovascular disease, an elevated exercise SBP is not associated with reduced exercise capacity and its modulation is probably not related to glycemic control
Sympathetic dominance and increased exercise capacity
To the Editor: I have read thoroughly the carefully designed and conducted study by Brassard and colleagues (1). This study evaluated the effect of the presence of elevated systolic blood pressure (SBP) on exercise capacity in patients with Type 2 diabetes. None of the patients exhibited a history of cardiac, vascular, or renal dysfunction or of hypertension. The patients were treated with conventional oral hypoglycemic agents and/or with diet. They were classified according to median peak SBP during exercise into two groups: below 210 mmHg or above 210 mmHg. The authors hypothesized that exercise capacity was reduced in patients with peak SBP above 210 mmHg, and this was attributed to a probable increase an arterial stiffness common to the diabetic state and not to overall glycemic control. As the first study to report how peak SBP in a diabetic cohort impacts exercise performance, the authors conclude that, contrary to their hypothesis, diabetic patients with elevated SBP (>210 mmHg) do not have a compromised exercise capacity. Indeed, after carefully viewing the data, it is clear that diabetic patients in this category have a similar, if not improved, functional capacity adjusted for age, compared with the patients in whom median peak SBP was below 210 mmHg.
The authors have collected their data with their usual attention to detail, and the proposed mechanisms and explanation for the increased exercise capacity of Type 2 diabetes with elevated SBP are both insightful and stimulating for the reader. This rather unusual adaptive effect, the authors stress, is that "a relatively more important LV modeling, induced by diabetes and triggered more specifically by arterial stiffness" may account for the increased performance noted in diabetic patients with SBP >210 mmHg. Furthermore, it is mentioned that this left ventricular (LV) remodeling "might override the deleterious impact induced by diabetes on LV function." As for interpretation to this effect, the authors state that "because there was no significant difference in terms of resting or peak exercise HR, it seems unlikely that sympathetic overactivity might have accounted for our results." Although this may be true for heart rate (HR) if it is the sole index of performance, as the authors contend, I would, however, like to offer alternate interpretations of the importance of an integrated effect engendered by enhanced sympathetic tone during exercise that collectively impacts on exercise capacity.
First, under nonexercise conditions, overcoming the increased afterload imposed by arterial stiffness is invariably facilitated by neurohormonal activation (3). Catecholamine secretion, acting as a double-edge sword, not only selectively increases vascular tone but also "beneficially" induces LV hypertrophy and stimulates contractility of the myocardium. Notwithstanding are the effects of the renin-angiotensin system to further compound, in part, the sympathetic effects on the cardiovascular system. To this point and relating to exercise, I would like to mention that this increased sympathetic tone, besides inducing the Bowditch effect, further enhances the inotropic state of the myocardium, a response that is facilitated by reducing the LV end-systolic volume, thereby improving stroke volume (4). By examining the data in Tables 1 and 2 in the paper of Brassard et al. (1), the pulse pressure, largely determined by LV stroke volume at a given compliance, is calculated as 109 mmHg and 149 mmHg in the <210-mmHg and >210-mmHg groups, respectively. This difference is likely significant because both peak SBP response attained with exercise and change in SBP are higher in the >210-mmHg group. The possibility that compliance of the central arteries may have been altered exists in both patient groups, although no evidence of vascular disease was documented (5). Second, although no need to emphasize, are the well-known systemic effects of the catecholamines on glucose and lipid metabolism on tissues such as liver, adipose tissue, and skeletal muscle, and on pulmonary vasculature to enhance ventilation. But more directly relating to LV performance and of importance to this study, epinephrine, aside from its inotropic effect, is also known to increase myocardial glucose oxidation and ATP production without decreasing efficiency of the myocardium (2). The latter point is perhaps essential under conditions of exercise or of increased exercise capacity despite the chronotropic state of the heart.
REFERENCES
This article has been cited by other articles:
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  P. Brassard and P. Poirier REPLY FROM DRS. BRASSARD AND POIRIER J Appl Physiol, December 1, 2006; 101(6): 1818 - 1818. [Full Text] [PDF]
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