Acetazolamide alters temperature regulation during submaximal exercise

1990 ◽  
Vol 69 (4) ◽  
pp. 1402-1407 ◽  
Author(s):  
W. F. Brechue ◽  
J. M. Stager
Keyword(s):  
Stroke Volume ◽  
Minute Ventilation ◽  
Exercise Bout ◽  
Cycle Ergometer ◽  
Submaximal Exercise ◽  
Whole Body ◽  
Co2 Removal ◽  
O2 Uptake ◽  
Double Blind ◽  
Hypoxic Conditions

Acetazolamide (ACZ), a potent carbonic anhydrase inhibitor, is known to decrease submaximal exercise tolerance under normoxic and hypoxic conditions. These decrements in performance occur despite the maintenance of O2 consumption and CO2 removal. Because ACZ is a diuretic, it induces a moderate hypohydration that may have a role in reducing the ability to sustain exercise through cardiovascular and thermoregulatory impairment. To investigate this potential impairment, seven healthy males between 21 and 35 yr of age were studied in a double-blind crossover design (placebo vs. ACZ). ACZ was administered in three 250-mg oral doses 14, 8, and 2 h before exercise. Subjects exercised at 70% peak O2 uptake for 30 min on a cycle ergometer in a normoxic thermoneutral environment (25 degrees C, 40% relative humidity). Results indicate that exercise minute ventilation was greater but O2 uptake, CO2 output, and respiratory exchange ratio did not differ with ACZ. ACZ led to lower mean skin (0.7 degrees C), higher rectal (0.6 degrees C), and higher mean body temperatures (0.4 degrees C) after 30 min of exercise. Whole-body sweat loss was reduced 23%, and heat storage during the exercise bout was increased 55%. Stroke volume decreased 25%, and arteriovenous O2 difference increased 15%. A significant inverse relationship (r = -0.63) between heart rate and stroke volume was observed. It is concluded that previously reported decreases in the ability to sustain submaximal exercise with ACZ may be related to hypohydration-induced impairment of the cardiovascular and thermoregulatory systems.

Effect of hyperoxia on substrate utilization during intense submaximal exercise

1986 ◽  
Vol 61 (2) ◽  
pp. 523-529 ◽  
Author(s):  
R. P. Adams ◽  
P. A. Cashman ◽  
J. C. Young
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Respiratory Exchange Ratio ◽  
Minute Ventilation ◽  
Exercise Bout ◽  
Substrate Utilization ◽  
Submaximal Exercise ◽  
O2 Uptake ◽  
Co2 Output ◽  
Lactate Levels

Six trained males [mean maximal O2 uptake (VO2max) = 66 ml X kg-1 X min-1] performed 30 min of cycling (mean = 76.8% VO2max) during normoxia (21.35 +/- 0.16% O2) and hyperoxia (61.34 +/- 1.0% O2). Values for VO2, CO2 output (VCO2), minute ventilation (VE), respiratory exchange ratio (RER), venous lactate, glycerol, free fatty acids, glucose, and alanine were obtained before, during, and after the exercise bout to investigate the possibility that a substrate shift is responsible for the previously observed enhanced performance and decreased RER during exercise with hyperoxia. VO2, free fatty acids, glucose, and alanine values were not significantly different in hyperoxia compared with normoxia. VCO2, RER, VE, and glycerol and lactate levels were all lower during hyperoxia. These results are interpreted to support the possibility of a substrate shift during hyperoxia.

Effects of beta-blockade on exercise capacity of trained and untrained men: a hemodynamic comparison

1986 ◽  
Vol 60 (4) ◽  
pp. 1429-1434 ◽  
Author(s):  
M. J. Joyner ◽  
B. J. Freund ◽  
S. M. Jilka ◽  
G. A. Hetrick ◽  
E. Martinez ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Treadmill Exercise ◽  
Cardiovascular Fitness ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
O2 Uptake ◽  
Double Blind ◽  
Beta 2 ◽  
Male Subjects ◽  
Submaximal Heart Rate

To study the effects of cardiovascular fitness on hemodynamic responses to exercise during beta-adrenergic blockade (BAB), submaximal [60% of maximum O2 uptake (VO2max)] and maximal treadmill exercise data were collected in 11 trained (T, VO2max 63.3 ml X kg-1 X min-1, 26.8 yr) and 11 untrained (UT, VO2max 44.5 ml X kg-1 X min-1, 25.0 yr) male subjects. Subjects completed two maximal control tests followed by a randomized, double-blind series of maximal tests after 1-wk treatments with placebo (PLAC), propranolol (PROP, 160 mg/day, beta 1- and beta 2-blockade), and atenolol (ATEN, 100 mg/day, beta 1-blockade). Treatments were separated by 1-wk washout periods. At 60% of control VO2max T and UT subjects experienced no reductions in O2 uptake (VO2) with either drug. Submaximal heart rate (HR, beats/min) was 134.8 PLAC, 107.0 PROP, 107.9 ATEN (P less than 0.05 both drugs vs. PLAC) in T subjects and 141.1 PLAC, 106.1 PROP, and 105.0 ATEN (P less than 0.05 both drugs vs. PLAC) in UT subjects. Cardiac output (1/min) for T was 17.3 PLAC, 16.9 PROP, 16.5 ATEN (P less than 0.05 ATEN vs. PLAC in T only) and for UT it was 12.2 (PLAC), 11.7 (PROP), 11.5 (ATEN) (P less than 0.05 both drugs vs. PLAC in UT). Stroke volume increased from 129.8 ml (PLAC) to 158.6 (PROP) and 156.2 (ATEN) in T (P less than 0.05 both drugs vs. PLAC) and from 86.8 (PLAC) to 110.0 (PROP) and 109.8 (ATEN) (P less than 0.05 both drugs vs. PLAC) in UT. The increases in stroke volume (SV) were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Metabolic, Cardiac, and Hemorheological Responses to Submaximal Exercise under Light and Moderate Hypobaric Hypoxia in Healthy Men

Biology ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 144
Author(s):  
Hun-Young Park ◽  
Jeong-Weon Kim ◽  
Sang-Seok Nam
Keyword(s):  
Oxygen Uptake ◽  
Blood Lactate ◽  
Minute Ventilation ◽  
Random Order ◽  
Cycle Ergometer ◽  
Submaximal Exercise ◽  
Erythrocyte Deformability ◽  
Moderate Hypoxia ◽  
Healthy Men ◽  
Significant Difference

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.

Effect of beta-blockade on the drift in O2 consumption during prolonged exercise

1988 ◽  
Vol 64 (2) ◽  
pp. 753-758 ◽  
Author(s):  
J. K. Kalis ◽  
B. J. Freund ◽  
M. J. Joyner ◽  
S. M. Jilka ◽  
J. Nittolo ◽  
...  
Keyword(s):  
Heart Rate ◽  
Minute Ventilation ◽  
Cycle Ergometer ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Maximal Heart Rate ◽  
O2 Consumption ◽  
Double Blind ◽  
Cycle Ergometer Test ◽  
Ergometer Test

The effect of beta-adrenergic blockade on the drift in O2 consumption (VO2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (VO2max). After an initial maximum cycle ergometer test to determine the subjects' control VO2max, subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control VO2max for 90 min on a cycle ergometer in a warm (31.7 +/- 0.3 degrees C) moderately humid (44.7 +/- 4.7%) environment. beta-Blockade caused significant (P less than 0.05) reductions in VO2max, maximal minute ventilation (VEmax), maximal heart rate (HRmax), and maximal exercise time. Significantly greater decreases in VO2max, VEmax, and HRmax were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, beta-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (VO2) and minute ventilation (VE) were observed with propranolol compared with atenolol or placebo. Furthermore, VO2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential control of ventilation among inbred strains of mice

1994 ◽  
Vol 267 (5) ◽  
pp. R1371-R1377 ◽  
Author(s):  
C. G. Tankersley ◽  
R. S. Fitzgerald ◽  
S. R. Kleeberger
Keyword(s):  
Minute Ventilation ◽  
Inbred Strains ◽  
Whole Body ◽  
Genetic Determinants ◽  
Ventilatory Responses ◽  
Hypoxic Conditions ◽  
Inbred Strains Of Mice ◽  
Genetic Mechanisms ◽  
The Difference ◽  
Differential Control

The role genetic factors play in ventilatory control was examined by challenging eight inbred strains of mice to acute hypercapnia under normoxic and hypoxic conditions. Age-matched mice were exposed for 3-5 min to inspired gases of the following composition (FICO2:FIO2) 0.03:0.10, 2) 0.03:0.21, 3) 0.08:0.10, and 4) 0.08:0.21, with intermittent room air exposures. Breathing frequency (f) and tidal volume (VT) of unanesthetized, unrestrained mice were assessed by whole body plethysmography. During room air breathing, significant (P < 0.01) interstrain differences were noted in the pattern, but minute ventilation (VE) did not differ among the strains. Relative to room air, mild hypercapnia with hypoxia (0.03:0.10) significantly (P < 0.01) elevated VE in each strain, and the percent increase in VE of the DBA/2J strain was significantly (P < 0.05) greater than the other strains. The ventilatory response to these conditions was achieved primarily by a significant (P < 0.01) increase in f among the strains. During severely hypercapnic normoxia (0.08:0.21) and hypoxia (0.08:0.10), the increase in VE was significantly (P < 0.01) greatest in the C57BL/6J (B6) mice and least in the C3H/HeJ (C3) mice. The difference in hypercapnic VE between B6 and C3 strains was largely due to a significantly (P < 0.01) greater increase in VT by B6 mice. On the assumption that environmental factors were identical, these data suggest that genetic determinants govern interstrain variation in the magnitude and pattern of breathing during hypoxia and hypercapnia. Moreover, hypoxic and hypercapnic ventilatory responses appear to be influenced by different genetic mechanisms.

Isotopic estimation of CO2 production during exercise before and after endurance training

1993 ◽  
Vol 75 (1) ◽  
pp. 70-75 ◽  
Author(s):  
A. R. Coggan ◽  
D. L. Habash ◽  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
C. L. Kien
Keyword(s):  
Endurance Training ◽  
Tricarboxylic Acid Cycle ◽  
Cycle Ergometer ◽  
Submaximal Exercise ◽  
Carbohydrate Oxidation ◽  
Whole Body ◽  
Co2 Production ◽  
Acid Oxidation ◽  
Ergometer Exercise ◽  
Before And After

Endurance training reduces the rate of CO2 release (i.e., VCO2) during submaximal exercise, which has been interpreted to indicate a reduction in carbohydrate oxidation. However, decreased ventilation, decreased buffering of lactate, and/or increased fixation of CO2 could also account for a lower VCO2 after training. We therefore used a primed continuous infusion of NaH13CO3 to determine the whole body rate of appearance of CO2 (RaCO2) in seven men during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2peak) before and after endurance training. RaCO2 is independent of the above-described factors affecting VCO2 but may overestimate net CO2 production due to pyruvate carboxylation and subsequent isotopic exchange in the tricarboxylic acid cycle. Training consisted of cycling at 75–100% VO2peak for 45–90 min/day, 6 days/wk, for 12 wk and increased VO2peak by 28% (P < 0.001). VCO2 during submaximal exercise was reduced from 86.8 +/- 3.7 to 76.2 +/- 4.2 mmol/min, whereas RaCO2 fell from 88.9 +/- 4.0 to 76.4 +/- 4.4 mmol/min (both P < 0.001). VCO2 and RaCO2 were highly correlated in the untrained (r = 0.98, P < 0.001) and trained (r = 0.99, P < 0.001) states, as were individual changes in VCO2 and RaCO2 with training (r = 0.88, P < 0.01). These results support the hypothesis that endurance training decreases CO2 production during exercise. The magnitude and direction of this change cannot be explained by reported training-induced alterations in amino acid oxidation, indicating that it must be the result of a decrease in carbohydrate oxidation and an increase in fat oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Systolic and Diastolic Functions After a Brief Acute Bout of Mild Exercise in Normobaric Hypoxia

2021 ◽  
Vol 12 ◽  
Author(s):  
Sara Magnani ◽  
Gabriele Mulliri ◽  
Silvana Roberto ◽  
Fabio Sechi ◽  
Giovanna Ghiani ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Acute Hypoxia ◽  
Exercise Bout ◽  
Tissue Doppler ◽  
Cycle Ergometer ◽  
Left Ventricular ◽  
Normobaric Hypoxia ◽  
Left Ventricular Volumes ◽  
Test Results ◽  
Diastolic Functions

Acute hypoxia (AH) is a challenge to the homeostasis of the cardiovascular system, especially during exercise. Research in this area is scarce. We aimed to ascertain whether echocardiographic, Doppler, and tissue Doppler measures were able to detect changes in systolic and diastolic functions during the recovery after mild exercise in AH. Twelve healthy males (age 33.5 ± 4.8 years) completed a cardiopulmonary test on an electromagnetically braked cycle-ergometer to determine their maximum workload (Wmax). On separate days, participants performed randomly assigned two exercise sessions consisting in 3 min pedalling at 30% of Wmax: (1) one test was conducted in normoxia (NORMO) and (2) one in normobaric hypoxia with FiO2 set to 13.5% (HYPO). Hemodynamics were assessed with an echocardiographic system. The main result was that the HYPO session increased parameters related to myocardial contractility such as pre-ejection period and systolic myocardial velocity with respect to the NORMO test. Moreover, the HYPO test enhanced early transmitral filling peak velocities. No effects were detected for left ventricular volumes, as end-diastolic, end-systolic, and stroke volume were similar between the NORMO and the HYPO test. Results of the present investigation support the hypothesis that a brief, mild exercise bout in acute normobaric hypoxia does not impair systolic or diastolic functions. Rather, it appears that stroke volume is well preserved and that systolic and early diastolic functions are enhanced by exercise in hypoxia.

Enhanced protein breakdown after eccentric exercise in young and older men

1991 ◽  
Vol 71 (2) ◽  
pp. 674-679 ◽  
Author(s):  
R. A. Fielding ◽  
C. N. Meredith ◽  
K. P. O'Reilly ◽  
W. R. Frontera ◽  
J. G. Cannon ◽  
...  
Keyword(s):  
Eccentric Exercise ◽  
Young Men ◽  
Older Men ◽  
Cycle Ergometer ◽  
Whole Body ◽  
Protein Breakdown ◽  
O2 Uptake ◽  
Body Protein ◽  
Fed State ◽  
Effect Of Age

The effects of eccentric exercise on whole body protein metabolism were compared in five young untrained [age 24 +/- 1 yr, maximal O2 uptake (VO2max) = 49 +/- 6 ml.kg-1.min-1] and five older untrained men (age 61 +/- 1 yr, VO2max = 34 +/- 2 ml.kg-1.min-1). They performed 45 min of eccentric exercise on a cycle ergometer at a power output equivalent to 80% VO2max (182 +/- 18 W). Beginning 5 days before exercise and continuing for at least 10 days after exercise, they consumed a eucaloric diet providing 1.5 g.kg-1.day-1 of protein. Leucine metabolism in the fed state was measured before, immediately after, and 10 days after exercise, with intravenous L-[1–13C]leucine as a tracer (0.115 mumol.kg-1.min-1). Leucine flux increased 9% immediately after exercise (P less than 0.011) and remained elevated 10 days later, with no effect of age. Leucine oxidation increased 19% immediately after exercise and remained 15% above baseline 10 days after exercise (P less than 0.0001), with no effect of age. In the young men, urinary excretion of 3-methylhistidine per gram of creatinine did not increase until 10 days postexercise (P less than 0.05), but in the older men, it increased 5 days after exercise and remained high through 10 days postexercise (P less than 0.05), averaging 37% higher than in the young men. These data suggest that eccentric exercise produces a similar increase in whole body protein breakdown in older and young men, but myofibrillar proteolysis may contribute more to whole body protein breakdown in the older group.

Slow component of O2 uptake during heavy exercise: adaptation to endurance training

1995 ◽  
Vol 79 (3) ◽  
pp. 838-845 ◽  
Author(s):  
C. J. Womack ◽  
S. E. Davis ◽  
J. L. Blumer ◽  
E. Barrett ◽  
A. L. Weltman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Power Output ◽  
Slow Component ◽  
Exercise Bout ◽  
Cycle Ergometer ◽  
O2 Uptake ◽  
Heavy Exercise ◽  
Absolute Power ◽  
Exercise Adaptation ◽  
Male Subjects

Seven untrained male subjects [age 25.6 +/- 1.5 (SE) yr, peak O2 uptake (VO2) 3.20 +/- 0.19 l/min] trained on a cycle ergometer 4 days/wk for 6 wk, with the absolute training workload held constant for the duration of training. Before and at the end of each week of training, the subjects performed 20 min of constant-power exercise at a power designed to elicit a pronounced slow component of VO2 (end-exercise VO2-VO2 at minute 3 of exercise) in the pretraining session. An additional 20-min exercise bout was performed after training at this same absolute power output during which epinephrine (Epi) was infused at a rate of 100 ng.kg-1.min-1 between minutes 10 and 20. After 2 wk of training, significant decreases in VO2 slow component, end-exercise VO2, blood lactate ([La-] and glucose concentrations, plasma Epi ([Epi]) and norepinephrine concentrations, ventilation (VE), and heart rate (HR) were observed (P < 0.05). Although the rapid attenuation of the VO2 slow component coincided temporally with reductions in plasma [Epi], blood [La-], and VE, the infusion of Epi after training significantly increased plasma [Epi] (delta 2.22 ng/ml), blood [La-] (delta 2.4 mmol/l) and VE (delta 10.0 l/min) without any change in exercise VO2. We therefore conclude that diminution of the VO2 slow component with training is attributable to factors other than the reduction in plasma [Epi], blood [La-] and VE.

Effects of altitude acclimatization on fluid regulatory hormone response to submaximal exercise

1993 ◽  
Vol 75 (3) ◽  
pp. 1208-1215 ◽  
Author(s):  
P. B. Rock ◽  
W. J. Kraemer ◽  
C. S. Fulco ◽  
L. A. Trad ◽  
M. K. Malconian ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Progressive Increase ◽  
Cycle Ergometer ◽  
Submaximal Exercise ◽  
Plasma Samples ◽  
Hormone Response ◽  
O2 Uptake ◽  
Altitude Acclimatization

To determine the effect of altitude acclimatization on plasma levels of atrial natriuretic peptide (ANP) during submaximal exercise and its relationship with renin and aldosterone, seven male volunteers aged 17–23 yr exercised to exhaustion on a cycle ergometer at 80–85% of their maximum O2 uptake at sea level (SL; 50 m), during 1 h in a hypobaric chamber [acute altitude (AA); 4,300 m], and after 14 or 16 days of residence on the summit of Pikes Peak, CO [chronic altitude (CA); 4,300 m]. Plasma samples taken before exercise, 10 min after the start of exercise, and 5 min postexercise were analyzed for ANP, plasma renin activity (PRA), and aldosterone (ALDO). ANP showed a progressive increase from rest to postexercise [7.49 +/- 1.63 to 11.32 +/- 1.80 (SE) pmol/ml and 6.05 +/- 2.55 to 10.38 +/- 7.20 pmol/ml; P = 0.049, exercise] at SL and AA, respectively, but not at CA (P = 0.039, altitude). Similarly, PRA and ALDO rose from rest to postexercise (P < 0.001, exercise), but the rise in ALDO with exercise was less during AA than during SL and CA (P = 0.002, phase). The decreased ANP levels during exercise after altitude acclimatization, with no change in PRA and ALDO, suggest that ANP has little effect on PRA and ALDO under these conditions.

Sign in / Sign up

Export Citation Format

Share Document