Medicine & Science in Sports & Exercise:
Abstracts: American College of Sports Medicine Conference on Integrative Physiology of Exercise: SATURDAY, SEPTEMBER 30, 2006: POSTER SESSION 3: Metabolic
Zakutansky, Donald W. FACSM; Koceja, David M. FACSM; Wallace, Janet P. FACSM
Indiana University, Bloomington, IN.
Diabetic peripheral neuropathy may be caused by neuronal ischemia and hypoxemia caused by hyperglycemia-induced decreases in neurovascular flow. In humans, H-reflex methodology allows one to localize the effect of ischemia to a single synapse in the spinal cord and may help to uncover how ischemia may produce changes in sensorimotor function. H-reflex and motor threshold decreases with ischemia have been reported in young adults, indicating more excitable sensory and motor nerves (Zakutansky et al 2004). These changes were accompanied by a decrease in H-reflex amplitudes with ischemia. To date, protocols utilizing the H-reflex to examine blood flow implications have not been reported in diabetes.
To examine the effect of limb blood flow on peripheral nerve function in adults with type 2 diabetes and apparently healthy controls. It was hypothesized that acute ischemia would increase excitability of sensory and motor nerves while an increase in blood flow would decrease excitability of the sensory and motor nerves.
Ten adults with type 2 diabetes and 10 age-and BMI-matched controls participated in the study. Soleus H-reflex and motor recruitment curves were determined at baseline, during 10 minutes of ischemia by femoral artery occlusion, and after a 10-minute bout of leg exercise.
At baseline, the H-threshold occurred at 77.44 ± 1.12% and 92.23 ± 0.04% (mean ± SE) of MTc for the diabetic and control groups, respectively. During ischemia, the H-threshold occurred at 72.44 ± 7.19% and 88.79 ± 7.80% of MTc for the diabetic and control groups, respectively. Following exercise, the H-threshold occurred at 64.44 ± 8.47% or 94.93 ± 4.30% of MTc for the diabetic and control groups, respectively, which significantly differed from baseline. Hmax/Mmax ratios were significantly reduced with acute ischemia for controls (4.2 %) and the diabetics (25.1%). These changes were due to a decrease in Hmax during acute ischemia with no change in Mmax. Post-exercise, the Hmax/Mmax returned to baseline for controls while the diabetic group remained significantly lower than at control. Post-exercise, H-reflex and motor responses were hypoexcitable with an accompanying hyperemia for controls. In the diabetic group, the post-exercise period resulted in a hyperexcitable H-reflex and motor response.
Acute ischemia decreases H-reflex thresholds in adults with diabetes and exercise-induced increases in blood flow further decrease these thresholds. These responses are markedly more pronounced than those of their non-diabetic peers and are accompanied by changes in the motorneuron pool.