The data demonstrate that relatively modest hypohydration ( approximately 2.7%) as a result of EID, significantly slows 5- and 10-m sprint times. Furthermore, although the glycerol hydration regimen provided a better hydration status than the placebo hydration regimen, no performance benefits were observed.
The purpose of the present investigation was to test the hypotheses that the mechanomyographic (MMG) signal would be affected by hydration status due to changes in the intra- and extracellular fluid content (which could affect the degree of fluid turbulence), changes in the filtering properties of the tissues between the MMG sensor and muscle, and changes in torque production that may accompany dehydration. Ten subjects (age 22.5 +/- 1.6 years) were tested for maximal isometric (MVC), submaximal isometric (25, 50, and 75%MVC), and maximal concentric isokinetic muscle strength of the biceps brachii in either a euhydrated or dehydrated state while the electromyographic (EMG) and MMG signals were recorded. Separate three-way and two-way ANOVAs indicated no change in torque, EMG amplitude, EMG mean power frequency (MPF), MMG amplitude, and MMG MPF with dehydration. The lack of dehydration effect suggests that MMG may be more reflective of the intrinsic contractile processes of a muscle fiber (torque production) or the motor control mechanisms (reflected by the EMG) than the tissues and fluids surrounding the muscle fiber.
The aim of the present study was to examine the effects of sodium bicarbonate (NaHCO(3)) administration on lower-body, hypertrophy-type resistance exercise (HRE). Using a double-blind randomized counterbalanced design, 12 resistance-trained male participants (mean ± SD; age = 20.3 ± 2 years, mass = 88.3 ± 13.2 kg, height = 1.80 ± 0.07 m) ingested 0.3 g kg(-1) of NaHCO(3) or placebo 60 min before initiation of an HRE regimen. The protocol employed multiple exercises: squat, leg press, and knee extension, utilizing four sets each, with 10-12 repetition-maximum loads and short rest periods between sets. Exercise performance was determined by total repetitions generated during each exercise, total accumulated repetitions, and a performance test involving a fifth set of knee extensions to failure. Arterialized capillary blood was collected via fingertip puncture at four time points and analyzed for pH, [HCO(3)(-)], base excess (BE), and lactate [Lac(-)]. NaHCO(3) supplementation induced a significant alkaline state (pH: NaHCO(3): 7.49 ± 0.02, placebo: 7.42 ± 0.02, P < 0.05; [HCO(3)(-)]: NaHCO(3): 31.50 ± 2.59, placebo: 25.38 ± 1.78 mEq L(-1), P < 0.05; BE: NaHCO(3): 7.92 ± 2.57, placebo: 1.08 ± 2.11 mEq L(-1), P < 0.05). NaHCO(3) administration resulted in significantly more total repetitions than placebo (NaHCO(3): 139.8 ± 13.2, placebo: 134.4 ± 13.5), as well as significantly greater blood [Lac(-)] after the exercise protocol (NaHCO(3): 17.92 ± 2.08, placebo: 15.55 ± 2.50 mM, P < 0.05). These findings demonstrate ergogenic efficacy for NaHCO(3) during HRE and warrant further investigation into chronic training applications.
Although both hypokalemia and hypomagnesemia have been linked with life-threatening cardiac arrhythmias, published studies disagree regarding the frequency of simultaneously low serum potassium and magnesium concentrations. To investigate the possible associations between the concentrations of these ions in serum, we carried out a retrospective study of all paired magnesium-potassium measurements reported from our laboratory during two separate two-week periods. Of 963 paired measurements in 421 patients, 12% of the samples were hypokalemic and 26% were hypomagnesemic. The frequency of hypomagnesemia was significantly greater in hypokalemic samples (38%) compared with nonhypokalemic samples (25%). The potential clinical importance of this relationship requires further investigation.
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