We used intense intermittent exercise to produce a 10% expansion of plasma volume (PV) within 24 h and tested the hypothesis that PV expansion is associated with an increase in plasma albumin content. The protocol consisted of eight 4-min bouts of exercise at 85% maximal O2 uptake with 5-min recovery periods between bouts. PV, plasma concentrations of albumin and total protein (TP), and plasma osmolality were measured before and during exercise and at 1, 2, and 24 h of recovery from exercise. During exercise, PV decreased by 15%, while plasma TP and albumin content remained at control levels. At 1 h of recovery, plasma albumin content was elevated by 0.17 +/- 0.04 g/kg body wt, accounting for the entire increase in plasma TP content. PV returned to control level at 1 h of recovery without fluid intake by the subjects, despite a 820 +/- 120-g reduction in body weight. At 2 h of recovery, plasma TP content remained significantly elevated, and plasma TP and albumin concentration were significantly elevated. At 24 h of recovery, PV was expanded by 4.5 +/- 0.7 ml/kg body wt (10 +/- 1%), estimated from hematocrit and hemoglobin changes, and by 3.8 +/- 1.3 ml/kg body wt (8 +/- 3%), measured by Evans blue dye dilution. Plasma albumin content was increased by 0.19 +/- 0.05 g/kg body wt at 24 h of recovery. If 1 g of albumin holds 18 ml of water, this increase in plasma albumin content can account for a 3.4-ml/kg body wt expansion of the PV. No significant changes in plasma osmolality occurred during recovery, but total plasma osmotic content increased in proportion to PV.(ABSTRACT TRUNCATED AT 250 WORDS)

We examined whether an increase in skin temperature or the rate of increase in core body temperature influences the relationship between minute ventilation (Ve) and core temperature during prolonged exercise in the heat. Thirteen subjects exercised for 60 min on a cycle ergometer at 50% of peak oxygen uptake while wearing a suit perfused with water at 10 degrees C (T10), 35 degrees C (T35), or 45 degrees C (T45). During the exercise, esophageal temperature (Tes), skin temperature, heart rate (HR), Ve, tidal volume, respiratory frequency (f), respiratory gases, blood pressure (BP), and blood lactate were all measured. We found that oxygen uptake, carbon dioxide output, BP, and blood lactate did not differ among the sessions. Tes, HR, Ve, and f remained nearly constant from minute 10 onward in the T10 session, but all of these parameters progressively increased in the T35 and T45 sessions, and significantly higher levels were seen in the T45 than the T35 session. For all but two subjects in the T35 and T45 sessions, plotting Ve as a function of Tes revealed no threshold for hyperventilation; instead, increases in Ve were linearly related to Tes, and there were no significant differences in the slopes or intercepts between the T35 and T45 sessions. Thus, during prolonged submaximal exercise in the heat, Ve increases with core temperature, and the influences of skin temperature and the rate of increase in Tes on the relationship between Ve and Tes are apparently small.

yasu T. Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise. J Appl Physiol 104: 998-1005, 2008. First published January 3, 2008 doi:10.1152/japplphysiol.00146.2007.-We tested the hypothesis that, in humans, hyperthermic hyperpnea elicited in resting subjects differs from that elicited during submaximal, moderate-intensity exercise. In the rest trial, hot-water legs-only immersion and a waterperfused suit were used to increase esophageal temperature (T es) in 19 healthy male subjects; in the exercise trial, T es was increased by prolonged submaximal cycling [50% peak O 2 uptake (V O2)] in the heat (35°C). Minute ventilation (V E), ventilatory equivalent for V O2 (V E/V O2) and CO2 output (V E/V CO2), tidal volume (VT), and respiratory frequency (f) were plotted as functions of T es. In the exercise trial, V E increased linearly with increases (from 37.0 to 38.7°C) in Tes in all subjects; in the rest trial, 14 of the 19 subjects showed a Tes threshold for hyperpnea (37.8 Ϯ 0.5°C). Above the threshold for hyperpnea, the slope of the regression line relating V E and Tes was significantly greater for the rest than the exercise trial. Moreover, the slopes of the regression lines relating V E/V O2, V E/V CO2, and Tes were significantly greater for the rest than the exercise trial. The increase in V E reflected increases in VT and f in the rest trial, but only f in the exercise trial, after an initial increase in ventilation due to VT. Finally, the slope of the regression line relating Tes and VT or f was significantly greater for the rest than the exercise trial. These findings indicate that hyperthermic hyperpnea does indeed differ, depending on whether one is at rest or exercising at submaximal, moderate intensity. thermoregulation; evaporative heat loss; ventilatory pattern IN MANY SPECIES OF MAMMALS and birds, an elevation in body temperature stimulates ventilation and increases evaporative heat loss for thermoregulation with a two-phase panting response (26,33). In animals such as the sheep and dog, this panting response can include two distinct patterns of breathing, often referred to as first-and second-phase panting (7,12,13,26,33). In the first phase, respiratory frequency (f) is maximized, while tidal volume (VT) is minimized, and arterial blood gases are not perturbed (33). The second phase is only evident with an increase in core temperature, and VT and f are increased, so that alveolar ventilation is increased, resulting in hypocapnia and respiratory alkalosis (33). In 1905, Haldane (11) was the first to report that hyperthermia also increases ventilation in humans. The recent review by White (33) suggested that since increased ventilation by hyperthermia in humans increases alveolar ventilation so that respiratory alkalosis occurs, a hyperthermia-induced increase in ventilation in humans is likely to be the second phase of panting. However, the mechanisms and the physiological significance of this response in humans are not fully understood.When body tem...

We measured the changes in heart rate (HR) variability estimated from the standard deviation of the R-R intervals to evaluate cardiac parasympathetic tone noninvasively before and during activation of muscle metaboreflex induced by postexercise muscle ischemia. Eight healthy male subjects performed sustained handgrip at 50% maximal voluntary contraction followed by forearm occlusion. Mean arterial pressure, cardiac stroke volume, and ratio of cardiac preejection period to left ventricular ejection time (PEP/LVET) were also measured. During the 2-min occlusion after 60 s of handgrip with voluntary respiration, HR variability and mean arterial pressure were significantly increased from baseline (54.4 +/- 6.1 to 80.1 +/- 12.8 ms and 81 +/- 1 to 99 +/- 3 mmHg, respectively) and PEP/LVET was decreased from resting level of 0.404 +/- 0.022 to 0.363 +/- 0.036. During occlusion and recovery, HR did not change from baseline level in any experiment. There was no influence of occlusion itself or of cessation of exercise per se on any parameters. Although overall enhanced HR variability was seen, probably due to lower breathing frequency and larger tidal volume, similar results were also obtained from an experiment with controlled respiration, showing that the increase in HR variability was not due to the changes in tidal volume or breathing frequency during occlusion. In conclusion, the HR variability is increased during activation of the muscle metaboreflex induced by postexercise muscle ischemia in humans. This finding shows that the parasympathetic cardiac tone is enhanced during activation of the muscle metaboreflex in humans and balances enhanced cardiac sympathetic activity to result in an unchanged HR.(ABSTRACT TRUNCATED AT 250 WORDS)