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J Appl Physiol 101: 1818, 2006; doi:10.1152/japplphysiol.01041.2006
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LETTER TO THE EDITOR

REPLY FROM DRS. BRASSARD AND POIRIER

To the Editor: We would like to thank Dr. Broderick (2a) for his interest and thoughtful comments regarding our manuscript. We agree that sympathetic dominance should not be ruled out for the increased (or preserved) exercise capacity observed in our subjects with high peak systolic blood pressure (SBP). Indeed, we have stated "However, we cannot exclude the possibility that a subtle change in sympathovagal activity, i.e., sympathetic predominance, might have influenced our findings" following the interpretation of our results regarding a possible influence of sympathetic overactivity (2).

This being said, we do not see the comments provided by Dr. Broderick as alternative explanations but rather suggestions that could complete our hypothetic representation of events, in order to explain the higher exercise capacity observed in subjects with elevated peak SBP. One possibility was the presence of a transitory higher cardiac output triggered by arterial stiffness. A plausible parameter that might link this adaptation is indeed the presence of higher catecholamine levels. Accordingly, the latter could positively modulate cardiac work and possibly cardiac output and exercise capacity, via its impact on left ventricular remodeling, i.e. left ventricular hypertrophy, and by its inotropic impact, improving stroke volume as mentioned by Dr Broderick.

However, a question remains: if present, what could explain this difference in catecholamine levels between our groups? More precisely and according to Dr. Broderick’s hypothesis, what could explain these relatively higher catecholamine concentrations in subjects with elevated peak SBP and higher exercise performance? In fact, a higher sympathetic activity is not necessarily associated with enhanced exercise capacity in these subjects. In accordance, a sympathetic predominance has been associated with left ventricular diastolic dysfunction in well-controlled subjects with Type 2 diabetes (5), a condition known to have a negative impact on exercise performance (4). Could this difference represent a reduced catecholamine concentrations in subjects with low vs. high peak SBP rather than the opposite? Diabetic patients with autonomic neuropathy are known to have a low plasma catecholamine’s response to exercise and lower exercise capacity (1, 3). The presence of subclinical symptoms of autonomic dysfunction could thus be associated with a reduction in catecholamine levels and exercise performance. Moreover, it is plausible that subjects with low peak SBP in the presence of subclinical autonomic dysfunction have concomitantly an altered SBP response to exercise, a lower exercise capacity and a comparable chronotropic response to exercise compared to subjects with elevated peak SBP. Finally, the hypothesis that lower catecholamine concentrations in subjects with low peak SBP be related to a more advanced insulin-resistant state compared to subjects with elevated peak SBP seems unlikely because Type 2 diabetic subjects with glucose metabolism influenced by insulin resistance do not seems to be resistant to the sympathetic stimulant effect of insulin (6).

Therefore, several issues regarding the relative impact of the autonomic nervous system on exercise performance in subjects with Type 2 diabetes need further research. The comments highlighted by Dr. Broderick are important and stimulating in our comprehension of the negative impacts of diabetes on exercise capacity.

REFERENCES

  1. Bottini P, Tantucci C, Scionti L, Dottorini ML, Puxeddu E, Reboldi G, Bolli GB, Casucci G, Santeusanio F, Sorbini CA. Cardiovascular response to exercise in diabetic patients: influence of autonomic neuropathy of different severity. Diabetologia 38: 244-250, 1995.[Web of Science][Medline]
  2. Brassard P, Ferland A, Gaudreault V, Bonneville N, Jobin J, Poirier P. Elevated peak exercise systolic blood pressure is not associated with reduced exercise capacity in subjects with Type 2 diabetes. J Appl Physiol 101: 893–897, 2006.[Abstract/Free Full Text]
  3. Broderick TL. Sympathetic dominance and increased exercise capacity. J Appl Physiol 101: 1816–1817, 2006.[Free Full Text]
  4. Kahn JK, Zola B, Juni JE, Vinik AI. Decreased exercise heart rate and blood pressure response in diabetic subjects with cardiac autonomic neuropathy. Diabetes Care 9: 389–394, 1986.[Abstract]
  5. Poirier P, Garneau C, Bogaty P, Nadeau A, Marois L, Brochu C, Gingras C, Fortin C, Jobin J, Dumesnil JG. Impact of left ventricular diastolic dysfunction on maximal treadmill performance in normotensive subjects with well-controlled type 2 diabetes mellitus. Am J Cardiol 85: 473–477, 2000.[CrossRef][Web of Science][Medline]
  6. Poirier P, Bogaty P, Philippon F, Garneau C, Fortin C, Dumesnil JG. Preclinical diabetic cardiomyopathy: relation of left ventricular diastolic dysfunction to cardiac autonomic neuropathy in men with uncomplicated well-controlled type 2 diabetes. Metabolism 52: 1056–1061, 2003.[CrossRef][Web of Science][Medline]
  7. Tack CJ, Smits P, Willemsen JJ, Lenders JW, Thien T, Lutterman JA. Effects of insulin on vascular tone and sympathetic nervous system in NIDDM. Diabetes 45: 15–22, 1996.[Abstract]

Patrice Brassard
Paul Poirier
 Institut Universitaire de Cardiologie et de Pneumologie
Centre de Recherche de l’Hôpital Laval
Université Laval
Québec,,Canada
e-mail: paul.poirier{at}crhl.ulaval.ca





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