Separate and combined effects of dehydration and thirst sensation on exercise performance in the heat.

Using intravenous infusion, we separated the physiologic consequences of 3% body mass dehydration from the conscious awareness of fluid replacement on time trial (TT) performance in the heat. Eleven trained cyclists performed 90 min of steady-state (50% V ˙ O 2 peak ) cycling followed by a self-paced 20-km TT in a hot-dry (35 °C, 10% relative humidity, wind speed 3.0 m/s) environment while euhydrated-not thirsty (EU-NT), euhydrated-thirsty (EU-T), dehydrated-not thirsty (DH-NT), or dehydrated-thirsty (DH-T). Thirst was manipulated by providing (NT) or withholding (T) ad libitum 35 °C water oral rinse. Distinct hydration states existed, with 0.4 ± 0.5% dehydration following the 20-km TT (EU) compared with 3.2 ± 0.6% in DH (P < 0.001). Greater perceived thirst existed in T (7 ± 2 on a 1-9 scale) than NT (4 ± 2, P < 0.001) after the TT. No significant differences in power output existed during the TT between hydration (EU 202.9 ± 36.5 W vs DH 207.0 ± 35.9 W, P = 0.362) and thirst conditions (NT 203.3 ± 35.6 W vs T 206.6 ± 36.8 W, P = 0.548), nor were there differences in completion time (P = 0.832) or pacing profile (P = 0.690). Within the range of up to 3% body mass loss, neither the physiologic effects from lowered hydration status nor the perception of thirst, separately or combined, affected sustained submaximal exercise performance in the heat for a healthy and fit population.

Contribution of inflammation to cellular injury in compartment syndrome in an experimental rodent model.

Compartment syndrome, a devastating consequence of limb trauma, is characterised by severe tissue injury and microvascular perfusion deficits. We hypothesised that leucopenia might provide significant protection against microvascular dysfunction and preserve tissue viability. Using our clinically relevant rat model of compartment syndrome, microvascular perfusion and tissue injury were directly visualised by intravital video microscopy in leucopenic animals. We found that while the tissue perfusion was similar in both groups (38.8% (standard error of the mean (sem) 7.1), 36.4% (sem 5.7), 32.0% (sem 1.7), and 30.5% (sem 5.35) continuously-perfused capillaries at 45, 90, 120 and 180 minutes compartment syndrome, respectively versus 39.2% (sem 8.6), 43.5% (sem 8.5), 36.6% (sem 1.4) and 50.8% (sem 4.8) at 45, 90, 120 and 180 minutes compartment syndrome, respectively in leucopenia), compartment syndrome-associated muscle injury was significantly decreased in leucopenic animals (7.0% (sem 2.0), 7.0%, (sem 1.0), 9.0% (sem 1.0) and 5.0% (sem 2.0) at 45, 90, 120 and 180 minutes of compartment syndrome, respectively in leucopenia group versus 18.0% (sem 4.0), 23.0% (sem 4.0), 32.0% (sem 7.0), and 20.0% (sem 5.0) at 45, 90, 120 and 180 minutes of compartment syndrome in control, p = 0.0005). This study demonstrates that the inflammatory process should be considered central to the understanding of the pathogenesis of cellular injury in compartment syndrome.