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The influence of dehydration on strength after a competitive match of badminton players has been previously studied; however, no research has been done on the effect of milk on performance in badminton. This study therefore aimed to investigate the effects of ad libitum intake of low-fat lactose-free milk (LFM) on subsequent performance of badminton athletes. Eleven collegiate badminton athletes (Mean ± standard deviation for Age = 19.3 ± 1.2 years; Height= 165.4 ± 9.1 cm) participated in this study. A randomized crossover study design was used (with ≥7-day washout between trials) where subjects were assigned to one of the test beverages: lactose-free skim milk (LFM), carbohydrate-electrolyte sports drink (CE) or water (CON). Performance tests were measured before and after subsequent games. Other variables measured included hydration status, perceived recovery and selected subjective perceptions. Palatability and amount ingested was highest for CE and lowest for CON (Mean ± standard deviation for CE 2215.24 ± 690.19 ml >LFM 1530.8 ± 849.9 ml >CON 1341.2 ± 424.2 ml, p = .013) but all beverages affected hydration status and selected performance variables after subsequent games in badminton. Perceived exertion and recovery were similar for the beverages as well. Thirst and gastrointestinal discomfort were however significantly greater for LFM.

This study measured acute physiological responses in pregnant women during short duration exercise in the supine (Sup), side-lying (Side), sitting (Sit), and standing (Std) positions.In a cross-sectional study, 42 healthy pregnant women were divided into 3 groups of 14 persons each: G1, G2, and G3 (first, second, and third trimester, respectively). Baseline assessments were performed following a 30-min rest in the sitting position. Subsequent measurements were then obtained while exercising, without resistance, in the Sup, Side, Sit, and Std, respectively. Physiological parameters, including heart rate (HR), minute ventilation (Comparing resting values, all groups had a significantly increased (1) HR,This study points that acute physiological responses to the positional challenge similarly occur in all trimester of pregnant women. Short duration exercise in the Std positions exerts more physiologic stresses on cardiorespiratory functions than in the Sup, Side, and Sit positions.

The high-affinity choline transporter (CHT1) is responsible for uptake of choline from the synaptic cleft and supplying choline for acetylcholine synthesis. CHT1 internalization by clathrin-coated vesicles is proposed to represent a mechanism by which high-affinity choline uptake can be modulated. We show here that internalized CHT1 is rapidly recycled back to the cell surface in both human embryonic kidney cells (HEK 293 cells) and SH-SY5Y neuroblastoma cells. This rapidly recycling pool of CHT1 comprises about 10% of total CHT1 protein. In the SH-SY5Y neuroblastoma cell line K + -depolarization promotes Ca 2+ -dependent increase in the rate of CHT1 recycling to the plasma membrane without affecting the rate of CHT1 internalization. K + -depolarization also increases the size of the pool of CHT1 protein that can be mobilized to the plasma membrane. Thus, the activity-dependent increase in plasma membrane CHT1 localization appears to be regulated by two mechanisms: (i) an increase in the rate of externalization of the intracellular CHT1 pool; and (ii) the recruitment of additional intracellular transporters to the recycling pool.

The high-affinity choline transporter (CHT1) is responsible for uptake of choline from the synaptic cleft and supplying choline for acetylcholine synthesis. CHT1 internalization by clathrin-coated vesicles is proposed to represent a mechanism by which high-affinity choline uptake can be modulated. We show here that internalized CHT1 is rapidly recycled back to the cell surface in both human embryonic kidney cells (HEK 293 cells) and SH-SY5Y neuroblastoma cells. This rapidly recycling pool of CHT1 comprises about 10% of total CHT1 protein. In the SH-SY5Y neuroblastoma cell line K(+)-depolarization promotes Ca(2+)-dependent increase in the rate of CHT1 recycling to the plasma membrane without affecting the rate of CHT1 internalization. K(+)-depolarization also increases the size of the pool of CHT1 protein that can be mobilized to the plasma membrane. Thus, the activity-dependent increase in plasma membrane CHT1 localization appears to be regulated by two mechanisms: (i) an increase in the rate of externalization of the intracellular CHT1 pool; and (ii) the recruitment of additional intracellular transporters to the recycling pool.

Excess formation of nitric oxide and superoxide by-products (peroxynitrite, reactive oxygen, and reactive nitrogen species) attenuates cholinergic transmission potentially having a role in Alzheimer disease pathogenesis. In this study, we investigated mechanisms by which acute exposure to peroxynitrite impairs function of the sodium-dependent hemicholinium-3 (HC-3)-sensitive choline transporter (CHT) that provides substrate for acetylcholine synthesis. The peroxynitrite generator 3-morpholinosydnonimine (SIN-1) acutely inhibited choline uptake in cells stably expressing FLAG-tagged rat CHT in a dose- and time-dependent manner, with an IC(50) = 0.9 +/- 0.14 mM and t((1/2)) = 4 min. SIN-1 significantly reduced V(max) of choline uptake without altering the K(m). This correlated with a SIN-1-induced decrease in cell surface CHT protein, observed as lowered levels of HC-3 binding and biotinylated CHT at the plasma membrane. It is noteworthy that short-term exposure of cells to SIN-1 accelerated the rate of internalization of CHT from the plasma membrane, but it did not alter return of CHT back to the cell surface. SIN-1 did not disrupt cell membrane integrity or cause cell death. Thus, the inhibitory effect of SIN-1 on choline uptake activity and HC-3 binding was related to enhanced internalization of CHT proteins from the plasma membrane to subcellular organelles.