Effects of sleep deprivation on thermoregulation during exercise

1984 ◽  
Vol 246 (1) ◽  
pp. R72-R77 ◽  
Author(s):  
M. N. Sawka ◽  
R. R. Gonzalez ◽  
K. B. Pandolf

Five fit men completed a practice, control, and sleep deprivation exercise test. Two nights of normal sleep preceded the control test, and 33 h of wakefulness preceded the sleep deprivation test. These tests consisted of 20 min of rest followed by 40 min of cycle-ergometer exercise (50% of peak O2 uptake, VO2) in a temperate (ambient temperature, 28 degrees C; relative humidity, 30%)-environment. Esophageal temperature (Tes), local sweat rate (mds), and chest thermal conductance (kch) were continuously measured. During exercise a 0.7 and 0.5 degrees C rise in Tes was found for the sleep deprivation and control tests, respectively. This increase in Tes values from rest to the end of exercise was greater (P = 0.08) for the sleep deprivation than control test. Total body sweat rate, calculated from Potter balance measurements, was 27% less (P less than 0.01) for the sleep deprivation than the control test. Both mds and kch values were lower (P less than 0.05) during the final 20 min of exercise for the sleep deprivation than control test. Final exercise mds values were 19% lower (P less than 0.05) for the sleep deprivation than control test. An asynchronous rather than a normal synchronous mds pattern was frequently observed during the sleep deprivation test. During the sleep deprivation test, the mds sensitivity (delta mds X delta Tes-1) was 38% lower (P less than 0.01) and kch sensitivity (delta kch X delta Tes-1) was 42% lower (P less than 0.05) than during the control test. These data indicate that sleep deprivation decreases evaporative and dry heat loss during moderate-intensity exercise.

1996 ◽  
Vol 21 (4) ◽  
pp. 285-300 ◽  
Author(s):  
Claudette M. St. Croix ◽  
David A. Cunningham ◽  
Donald H. Paterson ◽  
John M. Kowalchuk

The purpose of this study was to measure the contribution of the peripheral chemoreceptor (pRc) to [Formula: see text] during the steady-state of moderate-intensity cycle ergometer exercise using continuous hyperoxic suppression of pRc drive, while stabilizing the drive from the central chemoreceptor by clamping end-tidal PCO2 (PETCO2) at the peak level attained during the hyperoxic period of a poikilocapnic ride. In the isocapnic protocol, the PETCO2 was maintained at a constant level by a negative feedback, open loop system. Five subjects completed four repetitions of each of the poikilocapnic and isocapnic protocols. In the poikilocapnic protocol, [Formula: see text] declined following the step into hyperoxia and then began to increase, whereas the decline in [Formula: see text] was maintained in the isocapnic protocol. However, the mean decrease in [Formula: see text] was not significantly different between the poikilocapnic (16.1 ± 5.0%) and isocapnic (14.9 ± 4.4%) protocols. These results suggest that the declining phase of [Formula: see text] is fully complete before the secondary central stimulating actions of hyperoxia on [Formula: see text] and that the pRc contributes about 15% of the drive to breathe in moderate intensity exercise. Key words: ventilatory control, carotid bodies, hyperoxia


2015 ◽  
Vol 12 (6) ◽  
pp. 808-813 ◽  
Author(s):  
Louisa Beale ◽  
Neil S Maxwell ◽  
Oliver R Gibson ◽  
Rosemary Twomey ◽  
Becky Taylor ◽  
...  

Background:The purpose of this study was to characterize the physiological demands of a riding session comprising different types of recreational horse riding in females.Methods:Sixteen female recreational riders (aged 17 to 54 years) completed an incremental cycle ergometer exercise test to determine peak oxygen consumption (VO2peak) and a 45-minute riding session based upon a British Horse Society Stage 2 riding lesson (including walking, trotting, cantering and work without stirrups). Oxygen consumption (VO2), from which metabolic equivalent (MET) and energy expenditure values were derived, was measured throughout.Results:The mean VO2 requirement for trotting/cantering (18.4 ± 5.1 ml·kg-1·min-1; 52 ± 12% VO2peak; 5.3 ± 1.1 METs) was similar to walking/trotting (17.4 ± 5.1 ml·kg-1·min-1; 48 ± 13% VO2peak; 5.0 ± 1.5 METs) and significantly higher than for work without stirrups (14.2 ± 2.9 ml·kg-1·min-1; 41 ± 12% VO2peak; 4.2 ± 0.8 METs) (P = .001).Conclusion:The oxygen cost of different activities typically performed in a recreational horse riding session meets the criteria for moderate intensity exercise (3-6 METs) in females, and trotting combined with cantering imposes the highest metabolic demand. Regular riding could contribute to the achievement of the public health recommendations for physical activity in this population.


2000 ◽  
Vol 278 (5) ◽  
pp. E949-E957 ◽  
Author(s):  
Stuart H. Kreisman ◽  
Nicholas Ah Mew ◽  
Mylène Arsenault ◽  
Sharon J. Nessim ◽  
Jeffrey B. Halter ◽  
...  

The glucoregulatory response to intense exercise [IE, >80% maximum O2 uptake (V˙o 2 max)] comprises a marked increment in glucose production (Ra) and a lesser increment in glucose uptake (Rd), resulting in hyperglycemia. The Ra correlates with plasma catecholamines but not with the glucagon-to-insulin (IRG/IRI) ratio. If epinephrine (Epi) infusion during moderate exercise were able to markedly stimulate Ra, this would support an important role for the catecholamines' response in IE. Seven fit male subjects (26 ± 2 yr, body mass index 23 ± 0.5 kg/m2,V˙o 2 max 65 ± 5 ml ⋅ kg− 1 ⋅ min− 1) underwent 40 min of postabsorptive cycle ergometer exercise (145 ± 14 W) once without [control (CON)] and once with Epi infusion [EPI (0.1 μg ⋅ kg− 1 ⋅ min− 1)] from 30 to 40 min. Epi levels reached 9.4 ± 0.8 nM (20× rest, 10× CON). Ra increased ∼70% to 3.75 ± 0.53 in CON but to 8.57 ± 0.58 mg ⋅ kg− 1 ⋅ min− 1in EPI ( P < 0.001). Increments in Ra and Epi correlated ( r 2 = 0.923, P ≤ 0.01). In EPI, peak Rd (5.55 ± 0.54 vs. 3.38 ± 0.46 mg ⋅ kg− 1 ⋅ min− 1, P = 0.006) and glucose metabolic clearance rate (MCR, P= 0.018) were higher. The Ra-to-Rdimbalance in EPI caused hyperglycemia (7.12 ± 0.22 vs. 5.59 ± 0.22 mM, P = 0.001) until minute 60 of recovery. A small and late IRG/IRI increase ( P = 0.015 vs. CON) could not account for the Ra increase. Norepinephrine (∼4× increase at peak) did not differ between EPI and CON. Thus Epi infusion during moderate exercise led to increments in Ra and Rd and caused rises of plasma glucose, lactate, and respiratory exchange ratio in fit individuals, supporting a regulatory role for Epi in IE. Epi's effects on Rd and MCR during exercise may differ from its effects at rest.


1990 ◽  
Vol 68 (3) ◽  
pp. 990-996 ◽  
Author(s):  
A. R. Coggan ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
D. M. Bier ◽  
J. O. Holloszy

To assess the effects of endurance training on plasma glucose kinetics during moderate-intensity exercise in men, seven men were studied before and after 12 wk of strenuous exercise training (3 days/wk running, 3 days/wk cycling). After priming of the glucose and bicarbonate pools, [U-13C] glucose was infused continuously during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2) to determine glucose turnover and oxidation. Training increased cycle ergometer peak VO2 by 23% and decreased the respiratory exchange ratio during the final 30 min of exercise from 0.89 +/- 0.01 to 0.85 +/- 0.01 (SE) (P less than 0.001). Plasma glucose turnover during exercise decreased from 44.6 +/- 3.5 mumol.kg fat-free mass (FFM)-1.min-1 before training to 31.5 +/- 4.3 after training (P less than 0.001), whereas plasma glucose clearance (i.e., rate of disappearance/plasma glucose concentration) fell from 9.5 +/- 0.6 to 6.4 +/- 0.8 ml.kg FFM-1.min-1 (P less than 0.001). Oxidation of plasma-derived glucose, which accounted for approximately 90% of plasma glucose disappearance in both the untrained and trained states, decreased from 41.1 +/- 3.4 mumol.kg FFM-1.min-1 before training to 27.7 +/- 4.8 after training (P less than 0.001). This decrease could account for roughly one-half of the total reduction in the amount of carbohydrate utilized during the final 30 min of exercise in the trained compared with the untrained state.


1994 ◽  
Vol 266 (1) ◽  
pp. E136-E143 ◽  
Author(s):  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
D. L. Habash ◽  
A. R. Coggan

We have previously shown that 12 wk of endurance training reduces the rate of glucose appearance (Ra) during submaximal exercise (Coggan, A. R., W. M. Kohrt, R. J. Spina, D. M. Bier, and J. O. Holloszy. J. Appl. Physiol. 68: 990-996, 1990). The purpose of the present study was to examine the time course of and relationship between training-induced alterations in glucose kinetics and endocrine responses during prolonged exercise. Accordingly, seven men were studied during 2 h of cycle ergometer exercise at approximately 60% of pretraining peak oxygen uptake on three occasions: before, after 10 days, and after 12 wk of endurance training. Ra was determined using a primed, continuous infusion of [6,6-2H]glucose. Ten days of training reduced mean Ra during exercise from 36.9 +/- 3.3 (SE) to 28.5 +/- 3.4 mumol.min-1.kg-1 (P < 0.001). Exercise-induced changes in insulin, C-peptide, glucagon, norepinephrine, and epinephrine were also significantly blunted. After 12 wk of training, Ra during exercise was further reduced to 21.5 +/- 3.1 mumol.min-1.kg-1 (P < 0.001 vs. 10 days), but hormone concentrations were not significantly different from 10-day values. The lower glucose Ra during exercise after short-term (10 days) training is accompanied by, and may be due to, altered plasma concentrations of the major glucoregulatory hormones. However, other adaptations must be responsible for the further reduction in Ra with more prolonged training.


1992 ◽  
Vol 72 (3) ◽  
pp. 954-961 ◽  
Author(s):  
W. Stringer ◽  
R. Casaburi ◽  
K. Wasserman

Arterial pH, PCO2, standard bicarbonate, lactate, and ventilation were measured with a high sampling density during rest, exercise, and recovery in normal subjects performing upright cycle ergometer exercise. Three 6-min constant-work exercise tests (moderate, heavy, and very heavy) were performed by each subject. We found a small respiratory acidosis during the moderate-intensity exercise and an early respiratory acidosis followed by a metabolic acidosis for the heavy- and very-heavy-intensity exercise. During recovery, arterial pH rapidly returned to the preexercise value for the moderate-intensity work. However, arterial pH decreased further during the first 2 min of recovery for the heavy- and very-heavy-intensity work, before a slower return toward the resting values. We conclude that arterial acidosis is the consistent arterial pH reaction for moderate-, heavy-, and very-heavy-intensity cycle ergometer exercise in humans and that this acidosis is blunted but not eliminated by the ventilatory response. During recovery, the return to resting arterial pH and PCO2 and standard bicarbonate appears to be determined by the rate of lactate decline.


1992 ◽  
Vol 73 (6) ◽  
pp. 2668-2674 ◽  
Author(s):  
W. C. Adams ◽  
G. W. Mack ◽  
G. W. Langhans ◽  
E. R. Nadel

This study was designed to determine the extent to which changes in the evaporative power of the environment (Emax) affect sweating and evaporative rates. Six male subjects undertook four 60-min bouts of cycle ergometer exercise at 56% maximal O2 uptake (VO2max).Emax was varied by differences in ambient temperature and airflow; two exercise bouts took place at 24 degrees C and two at 35 degrees C, with air velocity at < 0.2 and 3.0 m/s in both. Total sweat production was estimated from body weight loss, whereas whole body evaporative rate was measured continuously from a Potter beam balance. Body core temperature was measured continuously from a thermocouple in the esophagus (T(es)), with mean skin temperature (Tsk) computed each minute from thermocouples at eight sites. Total body sweat loss was significantly greater (P < 0.05) in the 0.2- than in the 3.0-m/s condition at both 24 and 35 degrees C. Tsk was higher (P < 0.05) in the still-air conditions at both temperatures, but final T(es) was significantly higher (P < 0.05) in still air only in the 35 degrees C environment. Thus the reduced Emax in still air caused a greater heat storage, thereby stimulating a greater total sweat loss. However, in part because of reduced skin wettedness, the slope of the sweat rate-to-T(es) relation at 35 degrees C in the 3.0-m/s condition was 118% that at 0.2 m/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 11 ◽  
pp. 204201882092532 ◽  
Author(s):  
Aleksandra Żebrowska ◽  
Marcin Sikora ◽  
Anna Konarska ◽  
Anna Zwierzchowska ◽  
Tomasz Kamiński ◽  
...  

Aim: This study aimed to determine the effect of moderate intensity continuous exercise (Ex) and hypoxia (Hyp) on serum brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1) and its binding protein-3 (IGFBP-3), irisin and cytokines levels in patients with type 1 diabetes (T1D). Methods: A total of 14 individuals with T1D (age: 28.7 ± 7.3 years) and 14 healthy adults (age: 27.1 ± 3.9 years) performed 40-min continuous Ex at moderate intensity (50% lactate threshold) on a cycle ergometer in normoxia (Nor) and Hyp (FiO2 = 15.1%) Biochemical factors, glucose concentrations and physiological variables were measured at rest, immediately and up to 24 h after both Ex protocols. Results: Patients with T1D had significantly lower pre-Ex serum concentrations of BDNF ( p < 0.05, p < 0.01), and total IGF-1 ( p < 0.001, p < 0.05) and significantly higher irisin levels ( p < 0.05, p < 0.01) in Nor and Hyp, compared with healthy subjects. Ex significantly increased in T1D group serum BDNF (in Nor only p < 0.05) and total IGF-1 levels in Nor and Hyp ( p < 0.001 and p < 0.01, respectively). Immediately after Ex in Hyp, freeIGF-1 ( p < 0.05) and irisin levels ( p < 0.001) were significantly higher compared with the levels induced by Ex alone. Free IGF-1 and irisin serum levels remained elevated in 24 h post-Ex in Hyp. In T1D, significant blood glucose (BG) decrease was observed immediately after Ex in Hyp ( p < 0.001) and in 24 h recovery ( p < 0.001) compared with pre-Ex level. Conclusion: The study results suggest that moderate intensity continuous Ex has beneficial effect on BDNF and IGF-1 levels. Ex in hypoxic conditions may be more effective in increasing availability of IGF-1. The alterations in the post-Ex irisin levels and IGF-1 system may be contributing to more effective glycaemia control in patients with T1D.


2010 ◽  
Vol 32 (2) ◽  
pp. 154-175 ◽  
Author(s):  
Amy S. Welch ◽  
Angie Hulley ◽  
Mark Beauchamp

To investigate the relationship between cognitive and affective responses during acute exercise, 24 low-active females completed two 30-min bouts of cycle ergometer exercise at 90% of the ventilatory threshold. In one condition participants had full knowledge of the exercise duration (KD); in the other, exercise duration was unknown (UD). Affect and self-efficacy were measured before and every 3 min during exercise, and affect was also measured postexercise. Affect declined throughout the first half of both conditions, and continued its decline until the end of the UD condition, when a rebound effect was observed. Self-efficacy during exercise displayed a similar pattern. Hierarchical regression analyses demonstrated that during-exercise self-efficacy was a stronger predictor of during-exercise affect than preexercise self-efficacy, and that this relationship was strongest at the end of exercise when duration was unknown. These results indicate that repetitive cognitive appraisal of self and the task could impact the exercise experiences of low-active women during the adoption phase of an exercise program.


2005 ◽  
Vol 98 (4) ◽  
pp. 1371-1378 ◽  
Author(s):  
Brendon J. Gurd ◽  
Barry W. Scheuermann ◽  
Donald H. Paterson ◽  
John M. Kowalchuk

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (τV̇o2) was examined in young adults exhibiting relatively fast (FK; τV̇o2 < 30 s; n = 6) and slow (SK; τV̇o2 > 30 s; n = 6) V̇o2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak V̇o2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. V̇o2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). τV̇o2 was lower ( P < 0.05) in Mod2 than in Mod1 in both FK (20 ± 5 s vs. 26 ± 5 s, respectively) and SK (30 ± 8 s vs. 45 ± 11 s, respectively); linear regression analysis showed a greater “speeding” of V̇o2 kinetics in subjects exhibiting a greater Mod1 τV̇o2. HR, oxyhemoglobin, and total hemoglobin were elevated ( P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced ( P < 0.05) in Mod2, whereas the HHb mean response time was reduced ( P < 0.05) in FK (Mod2, 22 ± 3 s; Mod1, 32 ± 11 s) but not different in SK (Mod2, 36 ± 13 s; Mod1, 34 ± 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of V̇o2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.


Sign in / Sign up

Export Citation Format

Share Document