Practical internal and external cooling methods do not influence rapid recovery from simulated taekwondo performance.

Background/Objectives: The influence of post-exercise cooling on recovery has gained much attention in the empirical literature, however, data is limited in regards to optimizing recovery from taekwondo performance when combat is repeated in quick succession within the same day. The aim of this study was therefore to compare the effects of external and internal cooling after simulated taekwondo combat upon intestinal temperature (Tint), psychomotor skills (reaction time, response time, movement time), and neuromuscular function (peak torque, average power, time to reach peak torque). Methods: Using a randomized counterbalanced crossover design, 10 well-trained male taekwondo athletes completed four recovery methods on separate occasions: passive recovery (CON), a 5-minute thermoneutral water immersion (35°C) (TWI), a 5-min cold water immersion (15°C) (CWI), and ice slurry ingestion (-1°C) (ICE; consumed every 5 min for 30 min). Heart rate (HR), blood lactate (Blac) concentrations, and Tint were determined at rest, immediately after combat, and at selected intervals during a 90-min recovery period. Neuromuscular functional (measured with isokinetic dynamometer) and psychomotor indices were assessed at baseline and after the recovery period. Results: ICE led to a significantly lower Tint at 30 min (P<0.01) and 45 min (P<0.01) after simulated combat; 15-30 min after cessation of ingesting ice slurry, compared with the CON and TWI conditions, respectively. However, there were no differences in Tint across time points between the other conditions (P>0.05). Psychomotor skills and neuromuscular function indices returned to baseline values after the 90 min recovery period (P>0.05) with no differences observed between conditions (P>0.05). Conclusion: The present findings suggest that internal (ICE) and external (CWI) recovery methods appear to have little impact on physiological and functional indices over the time course required to influence repeated taekwondo combat performance.

Acute physiological responses in pregnant women during exercises in different positions.

OBJECTIVE: 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. METHODS: 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 ( V˙E ), oxygen consumption ( V˙O2 ), carbon dioxide production ( V˙CO2 ), and oxygen pulse ( V˙O2 /HR), were collected using the indirect calorimetry. RESULTS: Comparing resting values, all groups had a significantly increased (1) HR, V˙E , and V˙CO2 during the Std, (2) V˙O2 values during the Sit and Std, and (3) O2 pulse values during short duration exercise in all positions except the Std, whereas only G2 and G3 had a significantly decreased HR during the Sup. CONCLUSION: 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.

Activity and subcellular trafficking of the sodium-coupled choline transporter CHT is regulated acutely by peroxynitrite.

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.

Regulated recycling and plasma membrane recruitment of the high-affinity choline transporter.

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.