Relationship between ventilatory response and body temperature during prolonged submaximal exercise

2006 ◽  
Vol 100 (2) ◽  
pp. 414-420 ◽  
Author(s):  
Keiji Hayashi ◽  
Yasushi Honda ◽  
Takeshi Ogawa ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu

We examined whether an increase in skin temperature or the rate of increase in core body temperature influences the relationship between minute ventilation (V̇e) 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°C (T10), 35°C (T35), or 45°C (T45). During the exercise, esophageal temperature (Tes), skin temperature, heart rate (HR), V̇e, 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, V̇e, 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 V̇e as a function of Tes revealed no threshold for hyperventilation; instead, increases in V̇e 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, V̇e increases with core temperature, and the influences of skin temperature and the rate of increase in Tes on the relationship between V̇e and Tes are apparently small.

Biology ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 144
Author(s):  
Hun-Young Park ◽  
Jeong-Weon Kim ◽  
Sang-Seok Nam

We compared the effects of metabolic, cardiac, and hemorheological responses to submaximal exercise under light hypoxia (LH) and moderate hypoxia (MH) versus normoxia (N). Ten healthy men (aged 21.3 ± 1.0 years) completed 30 min submaximal exercise corresponding to 60% maximal oxygen uptake at normoxia on a cycle ergometer under normoxia (760 mmHg), light hypoxia (596 mmHg, simulated 2000 m altitude), and moderate hypoxia (526 mmHg, simulated 3000 m altitude) after a 30 min exposure in the respective environments on different days, in a random order. Metabolic parameters (oxygen saturation (SPO2), minute ventilation, oxygen uptake, carbon dioxide excretion, respiratory exchange ratio, and blood lactate), cardiac function (heart rate (HR), stroke volume, cardiac output, and ejection fraction), and hemorheological properties (erythrocyte deformability and aggregation) were measured at rest and 5, 10, 15, and 30 min after exercise. SPO2 significantly reduced as hypoxia became more severe (MH > LH > N), and blood lactate was significantly higher in the MH than in the LH and N groups. HR significantly increased in the MH and LH groups compared to the N group. There was no significant difference in hemorheological properties, including erythrocyte deformability and aggregation. Thus, submaximal exercise under light/moderate hypoxia induced greater metabolic and cardiac responses but did not affect hemorheological properties.


2012 ◽  
Vol 302 (1) ◽  
pp. R94-R102 ◽  
Author(s):  
Bun Tsuji ◽  
Yasushi Honda ◽  
Naoto Fujii ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu

We investigated whether a core temperature threshold for hyperthermic hyperventilation is seen during prolonged submaximal exercise in the heat when core temperature before the exercise is reduced and whether the evoked hyperventilatory response is affected by altering the initial core temperature. Ten male subjects performed three exercise trials at 50% of peak oxygen uptake in the heat (37°C and 50% relative humidity) after altering their initial esophageal temperature (Tes). Initial Tes was manipulated by immersion for 25 min in water at 18°C (Precooling), 35°C (Control), or 40°C (Preheating). Tes after the water immersion was significantly higher in the Preheating trial (37.5 ± 0.3°C) and lower in the Precooling trial (36.1 ± 0.3°C) than in the Control trial (36.9 ± 0.3°C). In the Precooling trial, minute ventilation (V̇e) showed little change until Tes reached 37.1 ± 0.4°C. Above this core temperature threshold, V̇e increased linearly in proportion to increasing Tes. In the Control trial, V̇e increased as Tes increased from 37.0°C to 38.6°C after the onset of exercise. In the Preheating trial, V̇e increased from the initially elevated levels of Tes (from 37.6 to 38.6°C) and V̇e. The sensitivity of V̇e to increasing Tes above the threshold for hyperventilation (the slope of the Tes-V̇e relation) did not significantly vary across trials (Precooling trial = 10.6 ± 5.9, Control trial = 8.7 ± 5.1, and Preheating trial = 9.2 ± 6.9 L·min−1·°C−1). These results suggest that during prolonged submaximal exercise at a constant workload in humans, there is a clear core temperature threshold for hyperthermic hyperventilation and that the evoked hyperventilatory response is unaffected by altering initial core temperature.


2004 ◽  
Vol 96 (4) ◽  
pp. 1365-1370 ◽  
Author(s):  
Colin K. Grissom ◽  
Martin I. Radwin ◽  
Mary Beth Scholand ◽  
Chris H. Harmston ◽  
Mark C. Muetterties ◽  
...  

Previous retrospective studies report a core body temperature cooling rate of 3°C/h during avalanche burial. Hypercapnia occurs during avalanche burial secondary to rebreathing expired air, and the effect of hypercapnia on hypothermia during avalanche burial is unknown. The objective of this study was to determine the core temperature cooling rate during snow burial under normocapnic and hypercapnic conditions. We measured rectal core body temperature (Tre) in 12 subjects buried in compacted snow dressed in a lightweight clothing insulation system during two different study burials. In one burial, subjects breathed with a device (AvaLung 2, Black Diamond Equipment) that resulted in hypercapnia over 30-60 min. In a control burial, subjects were buried under identical conditions with a modified breathing device that maintained normocapnia. Mean snow temperature was -2.5 ± 2.0°C. Burial time was 49 ± 14 min in the hypercapnic study and 60 min in the normocapnic study ( P = 0.02). Rate of decrease in Tre was greater with hypercapnia (1.2°C/h by multiple regression analysis, 95% confidence limits of 1.1-1.3°C/h) than with normocapnia (0.7°C/h, 95% confidence limit of 0.6-0.8°C/h). In the hypercapnic study, the fraction of inspired carbon dioxide increased from 1.4 ± 1.0 to 7.0 ± 1.4%, minute ventilation increased from 15 ± 7 to 40 ± 12 l/min, and oxygen saturation decreased from 97 ± 1 to 90 ± 6% ( P < 0.01). During the normocapnic study, these parameters remained unchanged. In this study, Tre cooling rate during snow burial was less than previously reported and was increased by hypercapnia. This may have important implications for prehospital treatment of avalanche burial victims.


2008 ◽  
Vol 109 (2) ◽  
pp. 318-338 ◽  
Author(s):  
Daniel I. Sessler ◽  
David S. Warner ◽  
Mark A. Warner

Most clinically available thermometers accurately report the temperature of whatever tissue is being measured. The difficulty is that no reliably core-temperature-measuring sites are completely noninvasive and easy to use-especially in patients not undergoing general anesthesia. Nonetheless, temperature can be reliably measured in most patients. Body temperature should be measured in patients undergoing general anesthesia exceeding 30 min in duration and in patients undergoing major operations during neuraxial anesthesia. Core body temperature is normally tightly regulated. All general anesthetics produce a profound dose-dependent reduction in the core temperature, triggering cold defenses, including arteriovenous shunt vasoconstriction and shivering. Anesthetic-induced impairment of normal thermoregulatory control, with the resulting core-to-peripheral redistribution of body heat, is the primary cause of hypothermia in most patients. Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser extent than does general anesthesia. Prolonged epidural analgesia is associated with hyperthermia whose cause remains unknown.


1984 ◽  
Vol 57 (6) ◽  
pp. 1738-1741 ◽  
Author(s):  
T. G. Waldrop ◽  
D. E. Millhorn ◽  
F. L. Eldridge ◽  
L. E. Klingler

Respiratory responses to increased skin temperatures were recorded in anesthetized cerebrate and in unanesthetized decerebrate cats. All were vagotomized, glomectomized, and paralyzed. Core body temperature and end-tidal Pco2 were kept constant with servoncontrollers. Stimulation of cutaneous nociceptors by heating the skin to 46 degrees C caused respiration to increase in both cerebrate and decerebrate cats. An even larger facilitation of respiration occurred when the skin temperature was elevated to 51 degrees C. However, respiration did not increase in either group of cats when the skin was heated to 41 degrees C to activate cutaneous warm receptors. The phenomenon of sensitization of nociceptors was observed. Spinal transection prevented all the respiratory responses to cutaneous heating. We conclude that noxious, but not nonnoxious, increases in skin temperature cause increases in respiratory output.


2017 ◽  
Vol 12 (5) ◽  
pp. 662-667 ◽  
Author(s):  
Matthijs T.W. Veltmeijer ◽  
Dineke Veeneman ◽  
Coen C.C.W. Bongers ◽  
Mihai G. Netea ◽  
Jos W. van der Meer ◽  
...  

Purpose:Exercise increases core body temperature (TC) due to metabolic heat production. However, the exercise-induced release of inflammatory cytokines including interleukin-6 (IL-6) may also contribute to the rise in TC by increasing the hypothalamic temperature set point. This study investigated whether the exercise-induced increase in TC is partly caused by an altered hypothalamic temperature set point.Methods:Fifteen healthy, active men age 36 ± 14 y were recruited. Subjects performed submaximal treadmill exercise in 3 randomized test conditions: (1) 400 mg ibuprofen and 1000 mg acetaminophen (IBU/APAP), (2) 1000 mg acetaminophen (APAP), and (3) a control condition (CTRL). Acetaminophen and ibuprofen were used to block the effect of IL-6 at a central and peripheral level, respectively. TC, skin temperature, and heart rate were measured continuously during the submaximal exercise tests.Results:Baseline values of TC, skin temperature, and heart rate did not differ across conditions. Serum IL-6 concentrations increased in all 3 conditions. A significantly lower peak TC was observed in IBU/APAP (38.8°C ± 0.4°C) vs CTRL (39.2°C ± 0.5°C, P = .02) but not in APAP (38.9°C ± 0.4°C) vs CTRL. Similarly, a lower ΔTC was observed in IBU/APAP (1.7°C ± 0.3°C) vs CTRL (2.0°C ± 0.5°C, P < .02) but not in APAP (1.7°C ± 0.5°C) vs CTRL. No differences were observed in skin temperature and heart-rate responses across conditions.Conclusions:The combined administration of acetaminophen and ibuprofen resulted in an attenuated increase in TC during exercise compared with a CTRL. This observation suggests that a prostaglandin-E2-induced elevated hypothalamic temperature set point may contribute to the exercise-induced rise in TC.


2010 ◽  
Vol 35 (5) ◽  
pp. 691-698
Author(s):  
Robert G. McMurray ◽  
Matthew S. Tenan

Ventilatory control during exercise is a complex network of neural and humoral signals. One humoral input that has received little recent attention in the exercise literature is potassium ions [K+]. The purpose of this study was to examine the relationship between [K+] and ventilation during an incremental cycle test and to determine if the relationship between [K+] and ventilation differs when blood lactate [lac–] is manipulated. Eight experienced triathletes (4 of each sex) completed 2 incremental, progressive (5-min stages) cycle tests to volitional fatigue: 1 with normal glycogen stores and 1 with reduced glycogen. Minute ventilation was measured during the final minute of each stage, and blood [lac–] and [K+] were measured at the end of each exercise stage. Minute ventilation and [K+] increased with exercise intensity and were similar between trials (p > 0.5), despite lower [lac–] during the reduced-glycogen trial. The concordance correlations (Rc) between [lac–] and minute ventilation were stronger for both trials (Rc = ~0.88–0.96), but the slopes of the relationships were different than the relationships between [K+] and minute ventilation (Rc = ~0.76–0.89). The slope of the relationship between [lac–] and minute ventilation was not as steep during the reduced-glycogen trial, compared with the normal trial (p = 0.002). Conversely, the slope of the relationships between [K+] and minute ventilation did not change between trials (p = 0.454). The consistent relationship of minute ventilation and blood [K+] during exercise suggests a role for this ion in the control of ventilation during exercise. Conversely, the inconsistent relationship between blood lactate and ventilation brings into question the importance of the relationship between lactate and ventilation during exercise.


2019 ◽  
Vol 44 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Keiji Hayashi ◽  
Nozomi Ito ◽  
Yoko Ichikawa ◽  
Yuichi Suzuki

Food intake increases metabolism and body temperature, which may in turn influence ventilatory responses. Our aim was to assess the effect of food intake on ventilatory sensitivity to rising core temperature during exercise. Nine healthy male subjects exercised on a cycle ergometer at 50% of peak oxygen uptake in sessions with and without prior food intake. Ventilatory sensitivity to rising core temperature was defined by the slopes of regression lines relating ventilatory parameters to core temperature. Mean skin temperature, mean body temperature (calculated from esophageal temperature and mean skin temperature), oxygen uptake, carbon dioxide elimination, minute ventilation, alveolar ventilation, and tidal volume (VT) were all significantly higher at baseline in sessions with food intake than without food intake. During exercise, esophageal temperature, mean skin temperature, mean body temperature, carbon dioxide elimination, and end-tidal CO2 pressure were all significantly higher in sessions with food intake than without it. By contrast, ventilatory parameters did not differ between sessions with and without food intake, with the exception of VT during the first 5 min of exercise. The ventilatory sensitivities to rising core temperature also did not differ, with the exception of an early transient effect on VT. Food intake increases body temperature before and during exercise. Other than during the first 5 min of exercise, food intake does not affect ventilatory parameters during exercise, despite elevation of both body temperature and metabolism. Thus, with the exception of an early transient effect on VT, ventilatory sensitivity to rising core temperature is not affected by food intake.


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