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1 Sports Medicine, Graduate School of Health Sciences, Hiroshima University, Hiroshima, Hiroshima, Japan
2 Physiology, Institute of Health Sciences, Hiroshima University Faculty of Medicine, Hiroshima, Hiroshima, Japan
3 Physiology, Graduate School of Health Sciences, Hiroshima University, Hiroshima, Japan
4 Health and Sports Sciences, Fukuyama Heisei University, Fukuyama, Hiroshima, Japan
* To whom correspondence should be addressed. E-mail: mako2{at}hiroshima-u.ac.jp.
Heart rate (HR) is controlled by the sole mechanism via cardiac parasympathetic outflow in tetraplegic individuals, who lack supraspinal control of sympathetic outflows and circulating catecholamines but have intact vagal pathways. A high-frequency component (HF at 0.15-0.40 Hz) of the power spectrum of HR variability and its relative value against total power (HF/Total) were assessed using a Wavelet transform to identify cardiac parasympathetic outflow. The relative contribution of cardiac parasympathetic and sympathetic outflows to controlling HR was estimated by comparing the HF/Total-HR relationship between age-matched tetraplegic and normal males. Six tetraplegic males with complete cervical spinal cord injury performed static arm exercise at 35% of the maximal voluntary contraction until exhaustion. Although resting cardiac output and arterial blood pressure were lower in tetraplegic than normal subjects, HR, HF, and HF/Total were not statistically different between the two groups. When the tetraplegic subjects developed the same force during exercise as normal subjects, HF and HF/Total decreased to 67-90% of the preexercise control and gradually recovered 1.5 min after exercise. The amount and time course of the changes in HF/Total during and after exercise coincided well between both groups. In contrast, the increase in HR at the start of exercise was blunted in tetraplegic than normal subjects and the HR recovery following exercise was also delayed. It is likely that, although the withdrawal response of cardiac parasympathetic outflow is preserved in tetraplegic subjects, sympathetic decentralization impairs the rapid acceleration of HR at the onset of exercise and the rapid deceleration following exercise.
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