We examined the effect of ischaemic preconditioning (IPC) on severe-intensity exercise performance, pulmonary oxygen uptake ( VO 2 ) kinetics, skeletal muscle oxygenation (muscle tissue O 2 saturation index) and mitochondrial respiration. Eight men underwent contralateral IPC (4 × 5 min at 220 mmHg) or sham-control (SHAM; 20 mmHg) before performing a cycling time-to-exhaustion test (92% maximum aerobic power). Muscle (vastus lateralis) biopsies were obtained before IPC or SHAM and ∼1.5 min postexercise. The time to exhaustion did not differ between SHAM and IPC (249 ± 37 vs. 240 ± 32 s; P = 0.62). Pre-and postexercise ADP-stimulated (P) and maximal (E) mitochondrial respiration through protein complexes (C) I, II and IV did not differ (P > 0.05). Complex I leak respiration was greater postexercise compared with baseline in SHAM, but not in IPC, when normalized to wet mass (P = 0.01 vs. P = 0.19), mitochondrial content (citrate synthase activity, P = 0.003 vs. P = 0.16; CI+IIP, P = 0.03 vs. P = 0.23) and expressed relative to P (P = 0.006 vs. P = 0.30) and E (P = 0.004 vs. P = 0.26). The VO 2 mean response time was faster (51.3 ± 15.5 vs. 63.7 ± 14.5 s; P = 0.003), with a smaller slow component (270 ± 105 vs. 377 ± 188 ml min −1 ; P = 0.03), in IPC compared with SHAM. The muscle tissue O 2 saturation index did not differ between trials (P > 0.05). Ischaemic preconditioning expedited VO 2 kinetics and appeared to prevent an increase in leak respiration through CI, when expressed proportional to E and P evoked by severe-intensity exercise, but did not improve exercise performance.

IntroductionThis study compared the efficacy of three commercial oral rehydration solutions (ORS) for restoring fluid and electrolyte balance, after exercise-induced dehydration.MethodHealthy, active participants (N = 20; ♀ = 3; age ∼27 y, V˙O2peak ∼52 ml/kg/min) completed three randomised, counterbalanced trials whereby intermittent exercise in the heat (∼36°C, ∼50% humidity) induced ∼2.5% dehydration. Subsequently, participants rehydrated (125% fluid loss in four equal aliquots at 0, 1, 2, 3 h) with a glucose-based (G-ORS), sugar-free (Z-ORS) or amino acid-based sugar-free (AA-ORS) ORS of varying electrolyte composition. Urine output was measured hourly and capillary blood samples collected pre-exercise, 0, 2 and 5 h post-exercise. Sodium, potassium, and chloride concentrations in urine, sweat, and blood were determined.ResultsNet fluid balance peaked at 4 h and was greater in AA-ORS (141 ± 155 ml) and G-ORS (101 ± 195 ml) than Z-ORS (−47 ± 208 ml; P ≤ 0.010). Only AA-ORS achieved positive sodium and chloride balance post-exercise, which were greater for AA-ORS than G-ORS and Z-ORS (P ≤ 0.006), as well as for G-ORS than Z-ORS (P ≤ 0.007) from 1 to 5 h.Conclusionwhen provided in a volume equivalent to 125% of exercise-induced fluid loss, AA-ORS produced comparable/superior fluid balance and superior sodium/chloride balance responses to popular glucose-based and sugar-free ORS.

Purpose: Whilst pre-exercise ischaemic preconditioning (IPC) can improve lower-body exercise performance, its impact on upper-limb performance has received little attention. This study examines the influence of IPC on upper-body exercise performance and oxygen uptake (V ̇O2 ) kinetics. Methods: Eleven recreationally-active males (24 ± 2 years) completed an arm-crank graded exercise test to exhaustion to determine the power outputs at the ventilatory thresholds (VT1 and VT2) and V ̇O2peak (40.0 ± 7.4 ml•kg −1 •min −1 ). Four main trials were conducted, two following IPC (4 × 5-min, 220 mmHg contralateral upper-limb occlusion), the other two following SHAM (4 × 5-min, 20 mmHg). The first two trials consisted of a 15-minute constant work rate and the last two time-to-exhaustion (TTE) arm-crank tests at the power equivalents of 95% VT1 (LOW) and VT2 (HIGH), respectively. Pulmonary V ̇O2 kinetics, heart rate, blood-lactate concentration, and rating of perceived exertion were recorded throughout exercise. Results: TTE during HIGH was longer following IPC than SHAM (459 ± 115 vs 395 ± 102 s, p = .004). Mean response time and change in V ̇O2 between 2-min and end exercise (ΔV ̇O2 ) were not different between IPC and SHAM for arm-cranking at both LOW (80.3 ± 19.0 vs 90.3 ± 23.5 s [p = .06], 457 ± 184 vs 443 ± 245 ml [p = .83]) and HIGH (96.6 ± 31.2 vs 92.1 ± 24.4 s [p = .65], 617 ± 321 vs 649 ± 230 ml [p = .74]). Heart rate, blood-lactate concentration, and rating of perceived exertion did not differ between conditions (all p ≥ .05). Conclusion: TTE was longer following IPC during upper-body exercise despite unchanged V ̇O2 kinetics. Highlights. Whilst pre-exercise ischaemic preconditioning can improve lower-body exercise performance and alter V ̇O2 kinetics, its impact on upper-limb performance has received little attention. . An acute bout of ischaemic preconditioning prior to arm-crank ergometry exercise significantly improved time to exhaustion compared to a sham control condition. . V ̇O2 kinetics in response to ischaemic preconditioning remained unchanged, suggesting alternative mechanisms may explain performance improvements.