Isolated vasodilated cat hindlimb skeletal muscles were perfused at constant flow and stimulated at 4 Hz for 2-4 min in three studies. Water uptake rates were measured gravimetrically or calculated from venous protein concentration changes. Venous plasma sodium, potassium, chloride, and osmolality were also measured. Maximum water uptake rates averaged 1.8 +/- 0.2 (SE) ml.min-1 x 100 g-1, reaching twice that in some experiments. Water uptake continued after stimulation had ceased. Constant-flow perfusion maintained a constant capillary pressure that was corroborated by measurements of arterial and venous perfusate pressures. Water uptake rate was not influenced by hematocrit but was highly correlated with plasma flow rate. The evidence strongly suggests that small-molecule osmotic pressure was the primary pressure causing the transcapillary water flux. Venous plasma sodium and chloride concentrations increased almost as much as protein (108 and 87% of the protein increase, respectively), as would be expected when water fluxes are driven by small-molecule osmotic pressure. Peak potassium efflux averaged 36 +/- 3 mu eq.min-1 x 100 g-1, but potassium did not contribute significantly to the osmotic gradient.

Anaerobic threshold has been defined as the oxygen uptake (VO2) at which blood lactate (La) begins to rise systematically during graded exercise (Davis et al. 1982). It has become common practice in the literature to estimate the anaerobic threshold by using ventilatory and/or gas exchange alterations. However, confusion exists as to the validity of this practice. The purpose of this study was to examine the precision with which ventilatory and gas exchange techniques for determining anaerobic threshold predicted the anaerobic threshold resolved by La criteria. The anaerobic threshold was chosen using three criteria: (1) systematic increase in blood La (ATLa), (2) systematic increase in ventilatory equivalent for O2 with no change in the ventilatory equivalent for CO2 (ATVE/VO2), and (3) non-linear increase in expired ventilation graphed as a function of VO2 (ATVE). Thirteen trained male subjects performed an incremental cycle ergometer test to exhaustion in which the load was increased by 30 W every 3 minutes. Ventilation, gas exchange measures, and blood samples for La analysis were obtained every 3rd min throughout the test. In five of the thirteen subjects tested the anaerobic threshold determined by ventilatory and gas exchange alterations did not occur at the same VO2 as the ATLa. The highest correlation between a gas exchange anaerobic threshold and ATLa was found for ATVE/VO2 and was r = 0.63 (P less than 0.05). These data provide evidence that the ATLa and ATVE do not always occur simultaneously and suggest limitations in using ventilatory or gas exchange measures to estimate the ATLa.

The purpose of this study was to determine the feasibility of using a positive reinforcement protocol to motivate weight-lifting exercise in rats. Intracranial self-stimulation was used to induce weight-lifting exercise. Bipolar electrodes were implanted in the ventral tegmental area of rats, and the animals were trained to bar press on a continuous reinforcement schedule for electrical brain stimulation. Animals with response rates of 1,200-1,500 presses/h were then trained with a discriminative light stimulus to alternate between a normally positioned bar and an elevated bar that could be reached only by standing on the hindlimbs. The animals were fitted with a weighted jacket at a starting resistance of 5-10% of their body weight. Weight-training sessions were conducted 5 days/wk for 10 wk. Training consisted of 600 presses/session, alternating every 15 presses between the low and high bars. At the beginning of each subsequent week, the resistance was progressively increased, with some animals eventually training at resistances greater than 50% of their body weight. At the end of the training period, the rats were lifting over 550% of the starting weight. Gastrocnemius size and mean fiber diameter were increased in the weight-lifting animals. This model combines exercise with positive incentive and has the advantages of being relatively easy to implement and not producing any apparent physical or mental trauma in the animal.

We developed a mathematical model of human respiration in the awake state that can be used to predict changes in ventilation, blood gases, and other critical variables during conditions of hypocapnia, hypercapnia and these conditions combined with hypoxia. Hence, the model is capable of describing ventilation changes due to the hypocapnic-hypoxia of high altitude. The basic model is that of Grodins et al. [Grodins, F. S., J. Buell, and A. J. Bart. J. Appl. Physiol. 22:260-276, 1967]. We updated the descriptions of (1) the effects of blood gases on cardiac output and cerebral blood flow, (2) acid-base balance in blood and tissues, (3) O2 and CO2 binding to hemoglobin and most importantly, (4) the respiratory-chemostat controller. The controller consists of central and peripheral sections. The central chemoceptor-induced ventilation response is simply a linear function of brain P(CO2) above a threshold value. The peripheral response has both a linear term similar to that for the central chemoceptors, but dependent upon carotid body P(CO2) and with a different threshold and a complex, nonlinear term that includes multiplication of separate terms involving carotid body P(O2) and P(CO2). Together, these terms produce 'dogleg'-shaped curves of ventilation plotted against P(CO2) which form a fan-like family for different values of P(CO2). With this chemical controller, our model closely describes a wide range of experimental data under conditions of solely changes in P(CO2) and for short-term hypoxia coupled with P(CO2) changes. This model can be used to accurately describe changes in ventilation and respiratory gases during ascent and during short-term residence at altitude. Hence, it has great applicability to studying O2-delivery systems in aircraft.