Auditory sEMG biofeedback for reducing muscle co-contraction during pedaling.

Muscle co-contraction between the agonist and antagonist muscles often causes low energy efficiency or movement disturbances. Surface electromyography biofeedback (sEMG-BF) has been used to train muscle activation or relaxation but it is unknown whether sEMG-BF reduces muscle co-contraction. We hypothesized that auditory sEMG-BF improves muscle co-contraction. Our purpose was to investigate whether auditory sEMG-BF is effective in improving muscle co-contraction. Thirteen participants pedaled on a road bike using four different auditory sEMG-BF conditions. We measured the surface electromyography at the lower limb muscles. The vastus lateralis (VL) and the semitendinosus (ST) activities were individually transformed into different beep sounds. Four feedback conditions were no-feedback, VL feedback, ST feedback, and both VL and ST feedback. We compared the co-contraction index (COI) of the knee extensor-flexor muscles and the hip flexor-extensor muscles among the conditions. There were no significant differences in COIs among the conditions (p = 0.83 for the COI of the knee extensor-flexor; p = 0.32 for the COI of the hip flexor-extensor). To improve the muscle co-contraction by sEMG-BF, it may be necessary to convert muscle activation into a muscle co-contraction. We concluded that individual sEMG-BF does not immediately improve muscle co-contraction during pedaling.

Glycosuria medicated with ipragliflozin and nifedipine or ipragliflozin and candesartan: a case report.

INTRODUCTION: Animal studies have reported that treatment with angiotensin II receptor blockers reduced kidney sodium-dependent glucose cotransporter expression. We therefore hypothesized that patients with hypertension treated with an angiotensin II receptor blocker (candesartan) would probably have an increased response to sodium-dependent glucose cotransporter inhibitor therapy (ipragliflozin) compared with patients treated with alternative hypertensive medications such as calcium channel blockers (nifedipine). Although sodium-dependent glucose cotransporter inhibitor (ipragliflozin) is a new anti-diabetic medicine, the clinical efficacy in the Japanese population has not been fully evaluated. We compared the combined effect of angiotensin II receptor blocker candesartan plus ipragliflozin with nifedipine plus ipragliflozin therapy and found that the combination of candesartan plus ipragliflozin was more effective in increasing glycosuria and lowering plasma glucose. CASE PRESENTATION: A 57-year-old Japanese man with essential hypertension was treated with candesartan. Candesartan was switched to nifedipine for the initial 10 days of an observation period and 5 days later he was started on ipragliflozin (day 6 of nifedipine treatment) with nifedipine for the next 5 days. Thereafter (from day 11 to day 20), candesartan was started instead of nifedipine and ipragliflozin was continued. In the last 5 days ipragliflozin was stopped and he was treated with candesartan alone. Neither nifedipine alone (0.038+/-0.004) nor candesartan alone (0.048+/-0.006) produce any trace amount of glycosuria. However, the extent of glycosuria under ipragliflozin with candesartan treatment (37.5+/-8.45) was significantly greater than that of ipragliflozin with nifedipine (23.75+/-0.35; P<0.05). CONCLUSION: Candesartan demonstrated additive actions with ipragliflozin to increase glycosuria compared to ipragliflozin with nifedipine treatment.