Sports medicine - open · 2017
Salivary alpha amylase not chromogranin A reflects sympathetic activity: exercise responses in elite male wheelchair athletes with or without cervical spinal cord injury.
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Leicht Christof A, Paulson Thomas A W, Goosey-Tolfrey Victoria L, Bishop Nicolette C
Аннотация
BACKGROUND: Salivary alpha amylase (sAA) and chromogranin A (sCgA) have both been suggested as non-invasive markers for sympathetic nervous system (SNS) activity. A complete cervical spinal cord injury leading to tetraplegia is accompanied with sympathetic dysfunction; the aim of this study was to establish the exercise response of these markers in this in vivo model.
METHODS: Twenty-six elite male wheelchair athletes (C6-C7 tetraplegia: N = 8, T6-L1 paraplegia: N = 10 and non-spinal cord injured controls: N = 8) performed treadmill exercise to exhaustion. Saliva and blood samples were taken pre, post and 30 min post exercise and analysed for sAA, sCgA and plasma adrenaline concentration, respectively.
RESULTS: In all three subgroups, sAA and sCgA were elevated post exercise (P < 0.05). Whilst sCgA was not different between subgroups, a group × time interaction for sAA explained the reduced post-exercise sAA activity in tetraplegia (162 ± 127 vs 313 ± 99 (paraplegia) and 328 ± 131 U mL-1 (controls), P = 0.005). The post-exercise increase in adrenaline was not apparent in tetraplegia (P = 0.74). A significant correlation was found between adrenaline and sAA (r = 0.60, P = 0.01), but not between adrenaline and sCgA (r = 0.06, P = 0.79).
CONCLUSIONS: The blunted post-exercise rise in sAA and adrenaline in tetraplegia implies that both reflect SNS activity to some degree. It is questionable whether sCgA should be used as a marker for SNS activity, both due to the exercise response which is not different between the subgroups and its non-significant relationship with adrenaline.
METHODS: Twenty-six elite male wheelchair athletes (C6-C7 tetraplegia: N = 8, T6-L1 paraplegia: N = 10 and non-spinal cord injured controls: N = 8) performed treadmill exercise to exhaustion. Saliva and blood samples were taken pre, post and 30 min post exercise and analysed for sAA, sCgA and plasma adrenaline concentration, respectively.
RESULTS: In all three subgroups, sAA and sCgA were elevated post exercise (P < 0.05). Whilst sCgA was not different between subgroups, a group × time interaction for sAA explained the reduced post-exercise sAA activity in tetraplegia (162 ± 127 vs 313 ± 99 (paraplegia) and 328 ± 131 U mL-1 (controls), P = 0.005). The post-exercise increase in adrenaline was not apparent in tetraplegia (P = 0.74). A significant correlation was found between adrenaline and sAA (r = 0.60, P = 0.01), but not between adrenaline and sCgA (r = 0.06, P = 0.79).
CONCLUSIONS: The blunted post-exercise rise in sAA and adrenaline in tetraplegia implies that both reflect SNS activity to some degree. It is questionable whether sCgA should be used as a marker for SNS activity, both due to the exercise response which is not different between the subgroups and its non-significant relationship with adrenaline.