Abstract

Dear Editor-in-Chief: We thank Dr. Kasikcioglu for his comments regarding our recent paper titled “Altered Cardiac Function and Minimal Cardiac Damage during Prolonged Exercise” (8). Within the paper we reported evidence of a reduction in cardiac function (both systolic and diastolic) concomitant with evidence of minimal cardiac damage, following prolonged exercise in a group of highly trained male triathletes. Dr. Kasikcioglu largely appears to agree with our findings. We do believe however, there are a number of points raised within the letter of Dr. Kasikcioglu that need to be addressed. Dr. Kasikcioglu suggests that few studies have demonstrated changes in diastolic function following prolonged exercise. Within the literature, however, there are numerous studies (3,4,5,6,7,9) demonstrating altered diastolic function following prolonged exercise, some of which demonstrate altered diastolic function in the absence of changes in systolic function (3,9). Dr. Kasikcioglu also makes recognition of the problems associated with the use of standard Doppler techniques in the assessment of diastolic function (load dependence, heart rate) with which we concur. Recent data from our laboratory employing Tissue Doppler Imaging (TDI) further support the notion of altered diastolic function following prolonged exercise. TDI is a novel, relatively load-independent ultrasound technique that may be used to assess cardiac function. Employing TDI, we have recently demonstrated altered diastolic function in the absence of changes in systolic function in a heterogeneous group of athletes following the London Marathon (unpublished findings), thus supporting earlier work employing standard Doppler techniques. Dr. Kasikcioglu suggests that the observed reduction in cardiac function following prolonged exercise is akin to “myocardial stunning.” Myocardial stunning has been widely observed within the clinical setting (2), however, its etiology is yet to be confirmed, and at present without further work we do not believe that myocardial stunning can be compared to exercise induced cardiac fatigue (EICF). Although myocardial stunning is preempted by a period of ischemia, at present the evidence does not support ischemia within the etiology of EICF. Within the available literature no study examining EICF has reported ECG evidence of ischemia preceding cardiac fatigue. In addition to ECG examination, recent work from Apple et al. (1), supported by unpublished data from our laboratory, demonstrates no evidence of ischemia immediately following a marathon using the newly developed ischemia modified albumin (IMA) assay. Further work is required to elucidate the mechanisms responsible for EICF; however, myocardial ischemia is presently not a strong candidate. Robert Shave Department of Sport Science, Brunel University, Uxbridge, United Kingdom Gregory Whyte Olympic Medical Institute, London, United Kingdom Keith George Research Institute for Sport and Exercise Science, John Moores University, Liverpool, United Kingdom

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