Sodium bicarbonate reduces ventilation without altering core temperature threshold or sensitivity of hyperthermia-induced hyperventilation in exercising humans.

Hyperthermia stimulates ventilation (hyperthermia-induced hyperventilation). In exercising humans, once the core temperature reaches ∼37°C, minute ventilation (V̇e) increases linearly with rising core temperature, and the slope of the relation between V̇e and core temperature reflects the sensitivity of the response. We previously reported that sodium bicarbonate ingestion reduces V̇e during prolonged exercise in the heat without affecting the sensitivity of hyperthermia-induced hyperventilation. Here, we hypothesized that reductions in V̇e associated with sodium bicarbonate ingestion reflect elevation of the core temperature threshold for hyperthermia-induced hyperventilation. Thirteen healthy young males ingested sodium bicarbonate (0.3 g/kg body wt) (NaHCO3 trial) or sodium chloride (0.208 g/kg body wt) (NaCl trial), after which they performed a cycle exercise at 50% of peak oxygen uptake in the heat (35°C and 50% relative humidity) following a pre-cooling. The pre-cooling enabled detection of an esophageal temperature (Tes: an index of core temperature) threshold for hyperthermia-induced hyperventilation. The Tes thresholds for increases in V̇e were similar between the two trials (P = 0.514). The slopes relating V̇E to Tes also did not differ between trials (P = 0.131). However, V̇e was lower in the NaHCO3 than in the NaCl trial in the range of Tes = 36.8-38.4°C (P = 0.007, main effect of trial). These results suggest that sodium bicarbonate ingestion does not alter the core temperature threshold or sensitivity of hyperthermia-induced hyperventilation during prolonged exercise in the heat; instead, it downshifts the exercise hyperpnea.

Sodium bicarbonate ingestion mitigates the heat-induced hyperventilation and reduction in cerebral blood velocity during exercise in the heat.

Hyperthermia during exercise in the heat causes minute ventilation ([Formula: see text]) to increase, which leads to reductions in arterial CO2 partial pressure ([Formula: see text]) and cerebral blood flow. On the other hand, sodium bicarbonate ingestion reportedly results in metabolic alkalosis, leading to decreased [Formula: see text] and increased [Formula: see text] during prolonged exercise in a thermoneutral environment. Here, we investigated whether sodium bicarbonate ingestion suppresses heat-induced hyperventilation and the resultant hypocapnia and cerebral hypoperfusion during prolonged exercise in the heat. Eleven healthy men ingested a solution of sodium bicarbonate (0.3 g/kg body wt) (NaHCO3 trial) or sodium chloride (0.208 g/kg) (NaCl trial). Ninety minutes after the ingestion, the subjects performed a cycle exercise for 60 min at 50% of peak oxygen uptake in the heat (35°C and 40% relative humidity). Esophageal temperature did not differ between the trials throughout (P = 0.56, main effect of trial). [Formula: see text] gradually increased with exercise duration in the NaCl trial, but the increases in [Formula: see text] were attenuated in the NaHCO3 trial (P = 0.01, main effect of trial). Correspondingly, estimated [Formula: see text] and middle cerebral artery blood velocity (an index of anterior cerebral blood flow) were higher in the NaHCO3 than the NaCl trial (P = 0.002 and 0.04, main effects of trial). Ratings of perceived exertion were lower in the NaHCO3 than the NaCl trial (P = 0.02, main effect of trial). These results indicate that sodium bicarbonate ingestion mitigates heat-induced hyperventilation and reductions in [Formula: see text] and cerebral blood velocity during prolonged exercise in the heat.NEW & NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The cerebral hypoperfusion may underlie central fatigue. We demonstrate that sodium bicarbonate ingestion reduces heat-induced hyperventilation and attenuates hypocapnia-related cerebral hypoperfusion during prolonged exercise in the heat. In addition, we show that sodium bicarbonate ingestion reduces ratings of perceived exertion during the exercise. This study provides new insight into the development of effective strategies for preventing central fatigue during exercise in the heat.

Low-intensity exercise delays the shivering response to core cooling.

Hypothermia can occur during aquatic exercise despite production of significant amounts of heat by the active muscles. Because the characteristics of human thermoregulatory responses to cold during exercise have not been fully elucidated, we investigated the effect of low-intensity exercise on the shivering response to core cooling in cool water. Eight healthy young men (24 ± 3 yr) were cooled through cool water immersion while resting (rest trial) and during loadless pedaling on a water cycle ergometer (exercise trial). Before the cooling, body temperature was elevated by hot water immersion to clearly detect a core temperature at which shivering initiates. Throughout the cooling period, mean skin temperature remained around the water temperature (25°C) in both trials, whereas esophageal temperature (Tes) did not differ between the trials (P > 0.05). The Tes at which oxygen uptake (V̇o2) rapidly increased, an index of the core temperature threshold for shivering, was lower during exercise than rest (36.2 ± 0.4°C vs. 36.5 ± 0.4°C, P < 0.05). The sensitivity of the shivering response, as indicated by the slope of the Tes-V̇o2 relation, did not differ between the trials (-441.3 ±177.4 ml·min-1·°C-1 vs. -411.8 ± 268.1 ml·min-1·°C-1, P > 0.05). The thermal sensation response to core cooling, assessed from the slope and intercept of the regression line relating Tes and thermal sensation, did not differ between the trials (P > 0.05). These results suggest that the core temperature threshold for shivering is delayed during low-intensity exercise in cool water compared with rest although shivering sensitivity is unaffected.

Respiratory mechanics and cerebral blood flow during heat-induced hyperventilation and its voluntary suppression in passively heated humans.

We investigated whether heat-induced hyperventilation can be voluntarily prevented, and, if so, how this modulates respiratory mechanics and cerebral blood flow in resting heated humans. In two separate trials, 10 healthy men were passively heated using lower body hot-water immersion and a water-perfused garment covering their upper body (both 41°C) until esophageal temperature (Tes ) reached 39°C or volitional termination. In each trial, participants breathed normally (normal-breathing) or voluntarily controlled minute ventilation (VE ) at a level equivalent to that observed after 5 min of heating (controlled-breathing). Respiratory gases, middle cerebral artery blood velocity (MCAV), work of breathing, and end-expiratory and inspiratory lung volumes were measured. During normal-breathing, VE increased as Tes rose above 38.0 ± 0.3°C, whereas controlled-breathing diminished the increase in VE (VE at Tes  = 38.6°C: 25.6 ± 5.9 and 11.9 ± 1.3 L min-1 during normal- and controlled-breathing, respectively, P < 0.001). During normal-breathing, end-tidal CO2 pressure and MCAV decreased with rising Tes , but controlled-breathing diminished these reductions (at Tes  = 38.6°C, 24.7 ± 5.0 vs. 39.5 ± 2.8 mmHg; 44.9 ± 5.9 vs. 60.2 ± 6.3 cm sec-1 , both P < 0.001). The work of breathing correlated positively with changes in VE (P < 0.001) and was lower during controlled- than normal-breathing (16.1 ± 12.6 and 59.4 ± 49.5 J min-1 , respectively, at heating termination, P = 0.013). End-expiratory and inspiratory lung volumes did not differ between trials (P = 0.25 and 0.71, respectively). These results suggest that during passive heating at rest, heat-induced hyperventilation increases the work of breathing without affecting end-expiratory lung volume, and that voluntary control of breathing can nearly abolish this hyperventilation, thereby diminishing hypocapnia, cerebral hypoperfusion, and increased work of breathing.

Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans.

Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO2 partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (Tes) to reach 39°C. During heating in two separate trials, end-tidal CO2 partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) ( P = 0.005) in the Control trial. This decrease was prevented by breathing CO2-enriched air throughout the heating such that end-tidal CO2 partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating ( P = 1.00). The sensitivity to rising Tes (i.e., slope of the Tes - V̇E relation) did not differ between the Control and CO2-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min-1·°C-1, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO2 breathing increased MCAV relative to Control at the end of heating ( P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia. NEW & NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The last may underlie central fatigue. We are the first to demonstrate that hyperthermia-induced hyperventilation is not suppressed by the resultant hypocapnia and that hypocapnia explains only 36% of cerebral hypoperfusion elicited by hyperthermia. These new findings advance our understanding of the mechanisms controlling ventilation and cerebral blood flow during heat stress, which may be useful for developing interventions aimed at preventing central fatigue during hyperthermia.

Body temperature and cold sensation during and following exercise under temperate room conditions in cold-sensitive young trained females.

We evaluated cold sensation at rest and in response to exercise-induced changes in core and skin temperatures in cold-sensitive exercise trained females. Fifty-eight trained young females were screened by a questionnaire, selecting cold-sensitive (Cold-sensitive, n = 7) and non-cold-sensitive (Control, n = 7) individuals. Participants rested in a room at 29.5°C for ~100 min after which ambient temperature was reduced to 23.5°C where they remained resting for 60 min. Participants then performed 30-min of moderate intensity cycling (50% peak oxygen uptake) followed by a 60-min recovery. Core and mean skin temperatures and cold sensation over the whole-body and extremities (fingers and toes) were assessed throughout. Resting core temperature was lower in the Cold-sensitive relative to Control group (36.4 ± 0.3 vs. 36.7 ± 0.2°C). Core temperature increased to similar levels at end-exercise (~37.2°C) and gradually returned to near preexercise rest levels at the end of recovery (>36.6°C). Whole-body cold sensation was greater in the Cold-sensitive relative to Control group during resting at a room temperature of 23.5°C only without a difference in mean skin temperature between groups. In contrast, cold sensation of the extremities was greater in the Cold-sensitive group prior to, during and following exercise albeit this was not paralleled by differences in mean extremity skin temperature. We show that young trained females who are sensitive to cold exhibit augmented whole-body cold sensation during rest under temperate ambient conditions. However, this response is diminished during and following exercise. In contrast, cold sensation of extremities is augmented during resting that persists during and following exercise.

Wearing graduated compression stockings augments cutaneous vasodilation but not sweating during exercise in the heat.

The activation of cutaneous vasodilation and sweating are essential to the regulation of core temperature during exercise in the heat. We assessed the effect of graduated compression induced by wearing stockings on cutaneous vasodilation and sweating during exercise in the heat (30°C). On two separate occasions, nine young males exercised for 45 min or until core temperature reached ~1.5°C above baseline resting while wearing either (1) stockings causing graduated compression (graduate compression stockings, GCS), or (2) loose-fitting stockings without compression (Control). Forearm vascular conductance was evaluated by forearm blood flow (venous occlusion plethysmography) divided by mean arterial pressure to estimate cutaneous vasodilation. Sweat rate was estimated using the ventilated capsule technique. Core and skin temperatures were measured continuously. Exercise duration was similar between conditions (Control: 42.2 ± 3.6 min vs. GCS: 42.2 ± 3.6 min, P = 1.00). Relative to Control, GCS increased forearm vascular conductance during the late stages (≥30 min) of exercise (e.g., at 40 min, 15.6 ± 5.6 vs. 18.0 ± 6.0 units, P = 0.01). This was paralleled by a greater sensitivity (23.1 ± 9.1 vs. 32.1 ± 15.0 units°C-1, P = 0.043) and peak level (14.1 ± 5.1 vs. 16.3 ± 5.7 units, P = 0.048) of cutaneous vasodilation as evaluated from the relationship between forearm vascular conductance with core temperature. However, the core temperature threshold at which an increase in forearm vascular conductance occurred did not differ between conditions (Control: 36.9 ± 0.2 vs. GCS: 37.0 ± 0.3°C, P = 0.13). In contrast, no effect of GCS on sweating was measured (all P > 0.05). We show that the use of GCS during exercise in the heat enhances cutaneous vasodilation and not sweating.

Effect of voluntary hypocapnic hyperventilation or moderate hypoxia on metabolic and heart rate responses during high-intensity intermittent exercise.

PURPOSE: To investigate the effect of voluntary hypocapnic hyperventilation or moderate hypoxia on metabolic and heart rate responses during high-intensity intermittent exercise. METHODS: Ten males performed three 30-s bouts of high-intensity cycling [Ex1 and Ex2: constant-workload at 80% of the power output in the Wingate anaerobic test (WAnT), Ex3: WAnT] interspaced with 4-min recovery periods under normoxic (Control), hypocapnic or hypoxic (2500 m) conditions. Hypocapnia was developed through voluntary hyperventilation for 20 min prior to Ex1 and during each recovery period. RESULTS: End-tidal CO2 pressure was lower before each exercise in the hypocapnia than control trials. Oxygen uptake ([Formula: see text]) was lower in the hypocapnia than control trials (822 ± 235 vs. 1645 ± 245 mL min-1; mean ± SD) during Ex1, but not Ex2 or Ex3, without a between-trial difference in the power output during the exercises. Heart rates (HRs) during Ex1 (127 ± 8 vs. 142 ± 10 beats min-1) and subsequent post-exercise recovery periods were lower in the hypocapnia than control trials, without differences during or after Ex2, except at 4 min into the second recovery period. [Formula: see text] did not differ between the control and hypoxia trials throughout. CONCLUSIONS: These results suggest that during three 30-s bouts of high-intensity intermittent cycling, (1) hypocapnia reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate during the first but not subsequent exercises; (2) HRs during the exercise and post-exercise recovery periods are lowered by hypocapnia, but this effect is diminished with repeated exercise bouts, and (3) moderate hypoxia (2500 m) does not affect the metabolic response during exercise.

Wearing graduated compression stockings augments cutaneous vasodilation in heat-stressed resting humans.

PURPOSE: We investigated whether graduated compression induced by stockings enhances cutaneous vasodilation in passively heated resting humans. METHODS: Nine habitually active young men were heated at rest using water-perfusable suits, resulting in a 1.0 °C increase in body core temperature. Heating was repeated twice on separate occasions while wearing either (1) stockings that cause graduated compression (pressures of 26.4 ± 5.3, 17.5 ± 4.4, and 6.1 ± 2.0 mmHg at the ankle, calf, and thigh, respectively), or (2) loose-fitting stockings without causing compression (Control). Forearm vascular conductance during heating was evaluated by forearm blood flow (venous occlusion plethysmography) divided by mean arterial pressure to estimate heat-induced cutaneous vasodilation. Body core (esophageal), skin, and mean body temperatures were measured continuously. RESULTS: Compared to the Control, forearm vascular conductance during heating was higher with graduated compression stockings (e.g., 23.2 ± 5.5 vs. 28.6 ± 5.8 units at 45 min into heating, P = 0.001). In line with this, graduated compression stockings resulted in a greater sensitivity (27.5 ± 8.3 vs. 34.0 ± 9.4 units °C-1, P = 0.02) and peak level (25.5 ± 5.8 vs. 29.7 ± 5.8 units, P = 0.004) of cutaneous vasodilation as evaluated from the relationship between forearm vascular conductance with mean body temperature. In contrast, the mean body temperature threshold for increases in forearm vascular conductance did not differ between the Control and graduated compression stockings (36.5 ± 0.1 vs. 36.5 ± 0.2 °C, P = 0.85). CONCLUSIONS: Our results show that graduated compression associated with the use of stockings augments cutaneous vasodilation by modulating sensitivity and peak level of cutaneous vasodilation in relation to mean body temperature. However, the effect of these changes on whole-body heat loss remains unclear.

Diurnal variation in the control of ventilation in response to rising body temperature during exercise in the heat.

We investigated whether heat-induced hyperventilation during exercise is affected by time of day, as diurnal variation leads to higher core temperatures in the evening. Nineteen male subjects were divided into two experiments (protocol 1, n = 10 and protocol 2, n = 9). In protocol 1, subjects performed cycle exercise at 50% peak oxygen uptake in the heat (37°C and 50% RH) in the morning (0600) and evening (1800). Results showed that baseline resting and exercising esophageal temperature (Tes) were significantly (0.5°C) higher in the evening than morning. Minute ventilation (V̇e) increased from 54.3 ± 7.9 and 54.9 ± 6.8 l/min at 10 min to 71.4 ± 8.1 and 76.5 ± 11.8 l/min at 48.5 min in the morning and evening, respectively (both P < 0.01). Time of day had no effect on V̇e (P = 0.44). When V̇e as the output response was plotted against Tes as thermal input, the Tes threshold for increases in V̇e was higher in the evening than morning (37.2 ± 0.7 vs. 36.6 ± 0.6°C, P = 0.009), indicating the ventilatory response to the same core temperature is smaller in the evening. In protocol 2, the circadian rhythm-related higher resting Tes seen in the evening was adjusted down to the same temperature seen in the morning by immersing the subject in cold water. Importantly, the time course of changes in V̇e during exercise were smaller in the evening, but the threshold for V̇e remained higher in the evening than morning (P < 0.001). Collectively, those results suggest that time of day has no effect on time course hyperventilation during exercise in the heat, despite the higher core temperatures in the evening. This is likely due to diurnal variation in the control of ventilation in response to rising core temperature.

Characteristics of hyperthermia-induced hyperventilation in humans.

In humans, hyperthermia leads to activation of a set of thermoregulatory responses that includes cutaneous vasodilation and sweating. Hyperthermia also increases ventilation in humans, as is observed in panting dogs, but the physiological significance and characteristics of the hyperventilatory response in humans remain unclear. The relative contribution of respiratory heat loss to total heat loss in a hot environment in humans is small, and this hyperventilation causes a concomitant reduction in arterial CO2 pressure (hypocapnia), which can cause cerebral hypoperfusion. Consequently, hyperventilation in humans may not contribute to the maintenance of physiological homeostasis (i.e., thermoregulation). To gain some insight into the physiological significance of hyperthermia-induced hyperventilation in humans, in this review, we discuss 1) the mechanisms underlying hyperthermia-induced hyperventilation, 2) the factors modulating this response, and 3) the physiological consequences of the response.

Effect of short-term exercise-heat acclimation on ventilatory and cerebral blood flow responses to passive heating at rest in humans.

Hyperthermia induces hyperventilation and cerebral hypoperfusion in resting humans. We tested the hypothesis that short-term exercise-heat acclimation would alleviate those effects. Twenty healthy male subjects were divided into two groups that performed exercise training in the heat (TR-HEAT, n = 10) or cold (TR-COLD, n = 10). Before and after the training, the subjects in both groups participated in passive-heat tests at rest. Training was performed at 37°C (TR-HEAT) or 10°C (TR-COLD) and entailed four 20-min bouts of cycling at 50% peak oxygen uptake separated by 10-min recoveries daily for 6 consecutive days. After TR-HEAT, esophageal temperature was lowered when measured before and during passive heating, as was the esophageal temperature threshold for cutaneous active vasodilation, whereas plasma volume was increased (all P < 0.05). These traditional indices of successful heat acclimation were not all induced by TR-COLD (all P > 0.05). TR-HEAT had no significant effect on passive heating-induced increases in minute ventilation, even when evaluated as the esophageal temperature threshold for increases in minute ventilation and the slope relating minute ventilation to esophageal temperature (all P > 0.05). By contrast, TR-HEAT attenuated the passive heating-induced reduction in the cerebral vascular conductance index (middle cerebral artery mean blood velocity/mean arterial pressure) (all P < 0.05). TR-COLD did not attenuate the increase in minute ventilation or the decrease in the cerebral vascular conductance index observed during passive heating (all P > 0.05). These data suggest that in resting heated humans, short-term heat acclimation achieved through moderate-intensity exercise training (i.e., 50% peak oxygen uptake) in the heat does not influence hyperthermia-induced hyperventilation, but it does potentially attenuate cerebral hypoperfusion.

Effect of voluntary hypocapnic hyperventilation on the metabolic response during Wingate anaerobic test.

PURPOSE: We evaluated whether hypocapnia achieved through voluntary hyperventilation diminishes the increases in oxygen uptake elicited by short-term (e.g., ~30 s) all-out exercise without affecting exercise performance. METHODS: Nine subjects performed 30-s Wingate anaerobic tests (WAnT) in control and hypocapnia trials on separate days in a counterbalanced manner. During the 20-min rest prior to the 30-s WAnT, the subjects in the hypocapnia trial performed voluntary hyperventilation (minute ventilation = 31 L min(-1)), while the subjects in the control trial continued breathing spontaneously (minute ventilation = 14 L min(-1)). RESULTS: The hyperventilation in the hypocapnia trial reduced end-tidal CO2 pressure from 34.8 ± 2.5 mmHg at baseline rest to 19.3 ± 1.0 mmHg immediately before the 30-s WAnT. In the control trial, end-tidal CO2 pressure at baseline rest (35.9 ± 2.5 mmHg) did not differ from that measured immediately before the 30-s WAnT (35.9 ± 3.3 mmHg). Oxygen uptake during the 30-s WAnT was lower in the hypocapnia than the control trial (1.55 ± 0.52 vs. 1.95 ± 0.44 L min(-1)), while the postexercise peak blood lactate concentration was higher in the hypocapnia than control trial (10.4 ± 1.9 vs. 9.6 ± 1.9 mmol L(-1)). In contrast, there was no difference in the 5-s peak (842 ± 111 vs. 850 ± 107 W) or mean (626 ± 74 vs. 639 ± 80 W) power achieved during the 30-s WAnT between the control and hypocapnia trials. CONCLUSIONS: These results suggest that during short-period all-out exercise (e.g., 30-s WAnT), hypocapnia induced by voluntary hyperventilation reduces the aerobic metabolic rate without affecting exercise performance. This implies a compensatory elevation in the anaerobic metabolic rate.

Voluntary suppression of hyperthermia-induced hyperventilation mitigates the reduction in cerebral blood flow velocity during exercise in the heat.

Hyperthermia during prolonged exercise leads to hyperventilation, which can reduce arterial CO2 pressure (PaCO2 ) and, in turn, cerebral blood flow (CBF) and thermoregulatory response. We investigated 1) whether humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise and 2) the effects of voluntary breathing control on PaCO2 , CBF, sweating, and skin blood flow. Twelve male subjects performed two exercise trials at 50% of peak oxygen uptake in the heat (37°C, 50% relative humidity) for up to 60 min. Throughout the exercise, subjects breathed normally (normal-breathing trial) or they tried to control their minute ventilation (respiratory frequency was timed with a metronome, and target tidal volumes were displayed on a monitor) to the level reached after 5 min of exercise (controlled-breathing trial). Plotting ventilatory and cerebrovascular responses against esophageal temperature (Tes) showed that minute ventilation increased linearly with rising Tes during normal breathing, whereas controlled breathing attenuated the increased ventilation (increase in minute ventilation from the onset of controlled breathing: 7.4 vs. 1.6 l/min at +1.1°C Tes; P < 0.001). Normal breathing led to decreases in estimated PaCO2 and middle cerebral artery blood flow velocity (MCAV) with rising Tes, but controlled breathing attenuated those reductions (estimated PaCO2 -3.4 vs. -0.8 mmHg; MCAV -10.4 vs. -3.9 cm/s at +1.1°C Tes; P = 0.002 and 0.011, respectively). Controlled breathing had no significant effect on chest sweating or forearm vascular conductance (P = 0.67 and 0.91, respectively). Our results indicate that humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise, and this suppression mitigates changes in PaCO2 and CBF.

Effect of voluntary hypocapnic hyperventilation on the relationship between core temperature and heat loss responses in exercising humans.

Two thermolytic thermoregulatory responses, cutaneous vasodilation and sweating, begin when core temperature reaches a critical threshold, after which response magnitudes increase linearly with increasing core temperature; thus the slope indicates response sensitivity. We evaluated the influence of hypocapnia induced by voluntary hyperventilation on the core temperature threshold and sensitivity of thermoregulatory responses. Ten healthy males performed 15 min of cycling at 117 W (29.5°C, 50% RH) under three breathing conditions: 1) spontaneous ventilation, 2) voluntary normocapnic hyperventilation, and 3) voluntary hypocapnic hyperventilation. In the hypocapnic hyperventilation trial, end-tidal CO2 pressure was reduced throughout the exercise, whereas it was maintained around the normocapnic level in the other two trials. Cutaneous vascular conductances at the forearm and forehead were evaluated as laser-Doppler signal/mean arterial blood pressure, and the forearm sweat rate was measured using the ventilated capsule method. Esophageal temperature threshold was higher for the increase in cutaneous vascular conductance in the hypocapnic than normocapnic hyperventilation trial at the forearm (36.88 ± 0.36 vs. 36.68 ± 0.34°C, P < 0.05) and forehead (36.89 ± 0.31 vs. 36.75 ± 0.31°C, P < 0.05). The slope relating esophageal temperature to cutaneous vascular conductance was decreased in the hypocapnic than normocapnic hyperventilation trial at the forearm (302 ± 177 vs. 420 ± 178% baseline/°C, P < 0.05) and forehead (236 ± 164 vs. 358 ± 221% baseline/°C, P < 0.05). Neither the threshold nor the slope for the forearm sweat rate differed significantly between the hypocapnic or normocapnic hyperventilation trials. These findings indicate that in exercising humans, hypocapnia induced by voluntary hyperventilation does not influence sweating, but it attenuates the cutaneous vasodilatory response by increasing its threshold and reducing its sensitivity.

Hypervolemia induced by fluid ingestion at rest: effect of sodium concentration.

PURPOSE: Sodium drink is used as a countermeasure against body fluid loss. However, high concentrations of sodium may cause gastrointestinal upset (e.g., diarrhea). We sought to determine the sodium concentration that induces hypervolemia with a minimal risk of gastrointestinal disturbance. METHODS: Eight healthy active males rested in a chair and ingested a given amount (16-17 ml kg body mass(-1)) of water (W) or solution containing 60, 120 or 180 mmol l(-1) Na(+) (60, 120 and 180Na trials) in 6 equal portions at 10 min intervals. To standardize their hydration status, subjects consumed the same meal and water 2 h before each trial. Drink trials were performed on separate days, and the order was randomized. The change in plasma volume (PV) from pre-drink status was estimated from the hemoglobin concentration and hematocrit every 30 min for 150 min after initiation of drinking. RESULTS: Subjects began trials in a euhydrated state, as reflected by their plasma osmolality (in mmol l(-1): W, 289.4 ± 1.4; 60Na, 287.0 ± 3.5; 120Na, 287.6 ± 2.3; 180Na, 288.9 ± 3.3). At 120 min, PV had not increased from the pre-drink value in the W (-0.8 ± 4.5 %) or 60Na (2.4 ± 4.9 %) trials, but it increased to similar degrees in the 120Na (7.2 ± 4.6 %) and 180Na (9.4 ± 6.6 %) trials. No diarrhea was reported in the W or 60Na trials, but it was reported in the 120Na (n = 1) and 180Na (n = 6) trials. CONCLUSIONS: Beverages containing 120 mmol l(-1) Na(+) induce hypervolemia with a minimum incidence of gastrointestinal problems.

Changes in arterial blood pressure elicited by severe passive heating at rest is associated with hyperthermia-induced hyperventilation in humans.

The arterial blood pressure and ventilatory responses to severe passive heating at rest varies greatly among individuals. We tested the hypothesis that the increase in ventilation seen during severe passive heating of resting humans is associated with a decrease in arterial blood pressure. Passive heating was performed on 18 healthy males using hot water immersion to the level of the iliac crest and a water-perfused suit. We then divided the subjects into two groups: MAP(NOTINC) (n = 8), whose mean arterial blood pressure (MAP) at the end of heating had increased by ≤3 mmHg, and MAP(INC) (n = 10), whose MAP increased by >3 mmHg. Increases in esophageal temperature (T (es)) elicited by the heating were similar in the two groups (+2.3 ± 0.3 vs. +2.4 ± 0.4 °C). Early during heating (increase in T (es) was <1.5 °C), MAP, minute ventilation ([Formula: see text]), and end-tidal CO(2) pressure ([Formula: see text]) were similar between the groups. However, during the latter part of heating (increase in T (es) was ≥1.5 °C), the increase in [Formula: see text] and decrease in [Formula: see text] were significantly greater or tended to be greater, while the increase in MAP was significantly smaller in MAP(NOTINC) than MAP(INC). Among all subjects, heating-induced changes in [Formula: see text] significantly and negatively correlated with heating-induced changes in MAP during the latter part of heating (r = -0.52 to -0.74, P < 0.05). These results suggest that, in resting humans, 25-50 % of the variation in the magnitude of the arterial blood pressure response to severe passive heating can be explained by the magnitude of hyperthermia-induced hyperventilation.

Effect of voluntary hypocapnic hyperventilation on cutaneous circulation in resting heated humans.

Hypocapnia attenuates the sweat response normally seen in hyperthermic resting subjects, but its effect on the blood flow response in their nonglabrous skin under the same hyperthermic conditions remains unclear. In the present study, we investigated whether hypocapnia induced by voluntary hyperventilation affects the blood flow response to heat stress in the nonglabrous skin of resting humans. Nine healthy male subjects were passively heated using legs-only hot water immersion and a water-perfused suit, which caused esophageal temperature (T(es)) to increase by as much as 1.0°C. During normothermia and at +0.6°C T(es) and +1.0°C T(es), the subjects performed two voluntary 7-min hyperventilation (minute ventilation = 40 l/min) trials (hypocapnic and eucapnic) in random order. End-tidal CO(2) pressure was reduced by 23-25 torr during hypocapnic hyperventilation, but it was maintained at the spontaneous breathing level during eucapnic hyperventilation. Cutaneous blood flow was evaluated as the cutaneous red blood cell flux in the forearm (CBF(forearm)) or forehead (CBF(forehead)) and was normalized to the normothermic spontaneous breathing value. Hypocapnic hyperventilation at +0.6°C T(es) was associated with significantly reduced CBF(forearm), compared with eucapnic hyperventilation, after 5-7 min of hyperventilation (395 to 429 vs. 487 to 525% baseline, P < 0.05). No significant difference in CBF(forehead) was seen during hypocapnic hyperventilation compared with eucapnic hyperventilation at +0.6°C T(es) or +1.0°C T(es). These results suggest that in resting humans, hypocapnia achieved through voluntary hyperventilation attenuates the increase in cutaneous blood flow elicited by moderate heat stress in the nonglabrous skin of the forearm, but not the forehead.

Comparison of hyperthermic hyperventilation during passive heating and prolonged light and moderate exercise in the heat.

Elevation of core temperature leads to increases in ventilation in both resting subjects and those engaged in prolonged exercise. We compared the characteristics of the hyperthermic hyperventilation elicited during passive heating at rest and during prolonged moderate and light exercise. Twelve healthy men performed three trials: a rest trial in which subjects were passively heated using hot-water immersion (41°C) and a water-perfused suit and two exercise trials in which subjects exercised at 25% (light) or 50% (moderate) of peak oxygen uptake in the heat (37°C and 50% relative humidity) after first using water immersion (18°C) to reduce resting esophageal temperature (T(es)). This protocol enabled detection of a T(es) threshold for hyperventilation during the exercise. When minute ventilation (Ve) was expressed as a function of T(es), 9 of the 12 subjects showed T(es) thresholds for hyperventilation in all trials. The T(es) thresholds for increases in Ve during light and moderate exercise (37.1 ± 0.4 and 36.9 ± 0.4°C) were both significantly lower than during rest (38.3 ± 0.6°C), but the T(es) thresholds did not differ between the two exercise intensities. The sensitivity of Ve to increasing T(es) (slope of the T(es)-Ve relation) above the threshold was significantly lower during moderate exercise (8.7 ± 3.5 l · min(-1) · °C(-1)) than during rest (32.5 ± 24.2 l · min(-1) · °C(-1)), but the sensitivity did not differ between light (10.4 ± 13.0 l · min(-1) · °C(-1)) and moderate exercise. These results suggest the core temperature threshold for hyperthermic hyperventilation and the hyperventilatory response to increasing core temperature in passively heated subjects differs from that in exercising subjects, irrespective of whether the exercise is moderate or light.