Linagliptin showed superior glucose-lowering efficacy and comparable safety and tolerability to both placebo and voglibose in Japanese patients with T2DM.

Cerebrovascular reactivity to changes in the partial pressure of arterial carbon dioxide (P a,CO 2 ) via limiting changes in brain [H + ] modulates ventilatory control. It remains unclear, however, how exercise-induced alterations in respiratory chemoreflex might influence cerebral blood flow (CBF), in particular the cerebrovascular reactivity to CO 2 . The respiratory chemoreflex system controlling ventilation consists of two subsystems: the central controller (controlling element), and peripheral plant (controlled element). In order to examine the effect of exercise-induced alterations in ventilatory chemoreflex on cerebrovascular CO 2 reactivity, these two subsystems of the respiratory chemoreflex system and cerebral CO 2 reactivity were evaluated (n = 7) by the administration of CO 2 as well as by voluntary hypo-and hyperventilation at rest and during steady-state exercise. During exercise, in the central controller, the regression line for the P a,CO 2 -minute ventilation (V E ) relation shifted to higherV E and P a,CO 2 with no change in gain (P = 0.84). The functional curve of the peripheral plant also reset rightward and upward during exercise. However, from rest to exercise, gain of the peripheral plant decreased, especially during the hypercapnic condition (−4.1 ± 0.8 to −2.0 ± 0.2 mmHg l −1 min −1 , P = 0.01). Therefore, under hypercapnia, total respiratory loop gain was markedly reduced during exercise (−8.0 ± 2.3 to −3.5 ± 1.0 U, P = 0.02). In contrast, cerebrovascular CO 2 reactivity at each condition, especially to hypercapnia, was increased during exercise (2.4 ± 0.2 to 2.8 ± 0.2% mmHg −1 , P = 0.03). These findings indicate that, despite an attenuated chemoreflex system controlling ventilation, elevations in cerebrovascular reactivity might help maintain CO 2 homeostasis in the brain during exercise.

We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O(2) uptake (VO(2)) after prior heavy exercise of the same muscle group or a different muscle group (i.e., arm). Six healthy male subjects performed two protocols that consisted of two consecutive 6-min exercise bouts separated by a 6-min baseline at 0 W: 1) both bouts of heavy (work rate: 50% of lactate threshold to maximal VO(2)) leg cycling (L1-ex to L2-ex) and 2) heavy arm cranking followed by identical heavy leg cycling bout (A1-ex to A2-ex). Blood lactate concentrations before L1-ex, L2-ex, and A2-ex averaged 1.7 +/- 0.3, 5.6 +/- 0.9, and 6.7 +/- 1.4 meq/l, respectively. An "effective" time constant (tau) of VO(2) with the use of the monoexponential model in L2-ex (tau: 36.8 +/- 4.3 s) was significantly faster than that in L1-ex (tau: 52.3 +/- 8.2 s). Warm-up arm cranking did not facilitate the VO(2) kinetics for the following A2-ex [tau: 51.7 +/- 9.7 s]. The double-exponential model revealed no significant change of primary tau (phase II) VO(2) kinetics. Instead, the speeding seen in the effective tau during L2-ex was mainly due to a reduction of the VO(2) slow component. Near-infrared spectroscopy indicated that the degree of hyperemia in working leg muscles was significantly higher at the onset of L2-ex than A2-ex. In conclusion, facilitation of VO(2) kinetics during heavy exercise preceded by an intense warm-up exercise was caused principally by a reduction in the slow component, and it appears unlikely that this could be ascribed exclusively to systemic lactic acidosis.

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Blood flow (BF) responses in the celiac artery (CA) and superior mesenteric artery (SMA) during and immediately after a meal are poorly understood. We characterized postprandial BF responses in these arteries in the initial phase of digestion. After a baseline measurement in the overnight fasting state, healthy subjects ingested solid food (300 kcal) and water ad libitum within 5 min (4.6 +/- 0.2 min, means +/- SE), and then rested for 60 min in the postprandial state. Mean blood velocities (MBVs) in CA (n = 7) and SMA (n = 9) and mean arterial pressure (MAP) were measured throughout the procedure. The MAP was divided by the MBV to yield the resistance index (RI). The MBV in CA and SMA started increasing within a minute after beginning the meal. The MBV in CA rapidly reached its peak increase (60 +/- 8% change from baseline) at 5 +/- 1 min after the start of the meal, whereas the MBV in SMA gradually reached its peak increase (134 +/- 14%) at 41 +/- 4 min after the start of the meal, reflecting a decrease in the RI for both CA and SMA. These findings suggested an earlier increase in CA and SMA MBV, implying that the increase of BF in some parts of the small intestine precedes the arrival of chyme.