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Background. To determine the effects of different haemoglobin (Hb) levels on exercise performance and associated electrolyte changes, a prospective, randomized, double-blinded crossover study was completed in 14 haemodialysis patients. [ABSTRACT FROM PUBLISHER]

This study examined if five sessions of short duration (27 min), high intensity, interval training (HIIT) in the heat over a nine day period would induce heat acclimation in Australian football (AF) players. Fourteen professional AF players were matched for VO2peak (mL·kg(-1)·min(-1)) and randomly allocated into either a heat acclimation (Acc) (n = 7) or Control (Con) group (n = 7). The Acc completed five cycle ergometer HIIT sessions within a nine day period on a cycle ergometer in the heat (38.7 ± 0.5 °C; 34.4 ± 1.3 % RH), whereas Con trained in thermo-neutral conditions (22.3 ± 0.2 °C; 35.8 ± 0. % RH). Four days prior and two days post HIIT participants undertook a 30 min constant load cycling test at 60% V̇O2peak in the heat (37.9 ± 0.1 °C; 28.5 ± 0.7 % RH) during which VO2, blood lactate concentration ([Lac(-)]), heart rate (HR), rating of perceived exertion (RPE), thermal comfort, core and skin temperatures were measured. Heat acclimation resulted in reduced RPE, thermal comfort and [Lac(-)] (all p < 0.05) during the submaximal exercise test in the heat. Heart rate was lower (p = 0.007) after HIIT, in both groups. Heat acclimation did not influence any other measured variables. In conclusion, five short duration HIIT sessions in hot dry conditions induced limited heat acclimation responses in AF players during the in-season competition phase. In practice, the heat acclimation protocol can be implemented in a professional team environment; however the physiological adaptations resulting from such a protocol were limited. Key pointsSome minor heat acclimation adaptations can be induced in professional AF players with five 27 min non-consecutive, short duration HIIT sessions in the heat.The heat acclimation protocol employed in this study was able to be implemented in a professional team sport environment during an actual competitive season.Elevating and maintaining a high core temperature sufficient for heat acclimation likely requires a longer heat training session or some pre-heating prior to exercise.

Background: Postoperatively shed blood salvage is commonly used to reduce allogenic blood transfusion in patients undergoing total hip (THA) and knee arthroplasty (TKA). Autologous blood retransfusion is not devoid of risk. We hypothesized that adding tranexamic acid (TXA) to a restrictive blood transfusion protocol would reduce the need for postoperative autologous blood retransfusion in primary knee and hip arthroplasty., Study Design and Methods: Ninety-eight adult patients undergoing primary THA or TKA were randomly assigned to receive an intraoperative intravenous loading dose of 1.0 g of TXA followed by another 1.0-g dose 3 hours later (TXA group) or a matching volume 0.9% saline placebo (control group). A postoperatively shed autologous blood recovery system was used in all patients and the minimum reinfusion volume set at 250 mL. Red blood cells were transfused if hemoglobin level was less than 8 or if 8 to 10 g/dL with symptoms of anemia., Results: The proportion of patients receiving autologous blood reinfusion was significantly lower in the TXA group (5/49) compared to placebo (42/49) with an absolute difference of -75.5% (adjusted relative risk, 0.005), and none of the patients in the TXA group received more than 400 mL retransfused. Median total external blood loss during the first 24 hours was lower in the TXA group, 320 mL (range, 80-930 mL), compared to 970 mL (range, 100-2600 mL) in the placebo group (p < 0.001). There were no significant differences in homologous blood transfusions and hematologic variables between groups. Treatment differences were consistent by size and significance when the analysis was repeated separately in patients undergoing TKA or THA., Conclusion: Addition of TXA to a restrictive transfusion protocol makes the use of a postoperative blood salvage system in patients undergoing primary hip and knee arthroplasty unnecessary., (© 2013 American Association of Blood Banks.)

Reactive oxygen species (ROS) have been linked with both depressed Na(+),K(+)-pump activity and skeletal muscle fatigue. This study investigated N-acetylcysteine (NAC) effects on muscle Na(+),K(+)-pump activity and potassium (K(+)) regulation during prolonged, submaximal endurance exercise. Eight well-trained subjects participated in a double-blind, randomised, crossover design, receiving either NAC or saline (CON) intravenous infusion at 125 mg kg(-1) h(-1) for 15 min, then 25 mg kg(-1) h(-1) for 20 min prior to and throughout exercise. Subjects cycled for 45 min at 71% , then continued at 92% until fatigue. Vastus lateralis muscle biopsies were taken before exercise, at 45 min and fatigue and analysed for maximal in vitro Na(+),K(+)-pump activity (K(+)-stimulated 3-O-methyfluorescein phosphatase; 3-O-MFPase). Arterialized venous blood was sampled throughout exercise and analysed for plasma K(+) and other electrolytes. Time to fatigue at 92% was reproducible in preliminary trials (c.v. 5.6 +/- 0.6%) and was prolonged with NAC by 23.8 +/- 8.3% (NAC 6.3 +/- 0.5 versus CON 5.2 +/- 0.6 min, P < 0.05). Maximal 3-O-MFPase activity decreased from rest by 21.6 +/- 2.8% at 45 min and by 23.9 +/- 2.3% at fatigue (P < 0.05). NAC attenuated the percentage decline in maximal 3-O-MFPase activity (%Deltaactivity) at 45 min (P < 0.05) but not at fatigue. When expressed relative to work done, the %Deltaactivity-to-work ratio was attenuated by NAC at 45 min and fatigue (P < 0.005). The rise in plasma [K(+)] during exercise and the Delta[K(+)]-to-work ratio at fatigue were attenuated by NAC (P < 0.05). These results confirm that the antioxidant NAC attenuates muscle fatigue, in part via improved K(+) regulation, and point to a role for ROS in muscle fatigue.

Background: Patients with end-stage renal failure (ESRF) exhibit grossly impaired maximal exercise performance. This study investigated whether K+ regulation during exercise is impaired in ESRF and whether this is related to reduced exercise performance., Methods: Nine stable hemodialysis patients and eight controls (CON) performed incremental cycling exercise to volitional fatigue, with measurement of peak oxygen consumption (VO2 peak). Arterial blood was sampled during and following exercise and analyzed for plasma [K+] (PK)., Results: The VO2 peak was approximately 44% less in ESRF than in CON (P < 0.001), whereas peak exercise PK was greater (7.23 +/- 0.38 vs. 6.23 +/- 0.14 mmol x L-1, respectively, P < 0.001). In ESRF, the rate of rise in PK during exercise was twofold greater (0.43 +/- 0.05 vs. 0.23 +/- 0.03 mmol. L-1x min-1, P < 0.005) and the ratio of rise in PK relative to work performed was 3.7-fold higher (90.1 +/- 13.5 vs. 24.7 +/- 3.3 nmol. L-1. J-1, P < 0.001). A strong inverse relationship was found between VO2 peak and the DeltaPK. work-1 ratio (r = -0.80, N = 17, P < 0.001)., Conclusions: Patients with ESRF exhibit grossly impaired extrarenal K+ regulation during exercise, demonstrated by an excessive rise in PK relative to work performed. We further show that K+ regulation during exercise was correlated with aerobic exercise performance. These results suggest that disturbed K+ regulation in ESRF contributes to early muscle fatigue during exercise, thus causing reduced exercise performance.

This study investigated whether fatiguing dynamic exercise depresses maximal in vitro Na(+)-K(+)-ATPase activity and whether any depression is attenuated with chronic training. Eight untrained (UT), eight resistance-trained (RT), and eight endurance-trained (ET) subjects performed a quadriceps fatigue test, comprising 50 maximal isokinetic contractions (180 degrees /s, 0.5 Hz). Muscle biopsies (vastus lateralis) were taken before and immediately after exercise and were analyzed for maximal in vitro Na(+)-K(+)-ATPase (K(+)-stimulated 3-O-methylfluoroscein phosphatase) activity. Resting samples were analyzed for [(3)H]ouabain binding site content, which was 16.6 and 18.3% higher (P < 0.05) in ET than RT and UT, respectively (UT 311 +/- 41, RT 302 +/- 52, ET 357 +/- 29 pmol/g wet wt). 3-O-methylfluoroscein phosphatase activity was depressed at fatigue by -13.8 +/- 4.1% (P < 0.05), with no differences between groups (UT -13 +/- 4, RT -9 +/- 6, ET -22 +/- 6%). During incremental exercise, ET had a lower ratio of rise in plasma K(+) concentration to work than UT (P < 0.05) and tended (P = 0.09) to be lower than RT (UT 18.5 +/- 2.3, RT 16.2 +/- 2.2, ET 11.8 +/- 0.4 nmol. l(-1). J(-1)). In conclusion, maximal in vitro Na(+)-K(+)-ATPase activity was depressed with fatigue, regardless of training state, suggesting that this may be an important determinant of fatigue.