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THE EFFECT OF ACUTE NORMOBARIC HYPOXIA ON HEART RATE AND
MEAN ARTERIAL PRESSURE AT REST, DURING AND POST EXERCISE
YongSuk Seo, Chul-Ho Kim, Corey A. Peacock, Edward J. Ryan, Zachary Sax,
John Gunstad, and Ellen L. Glickman FACSM
These results suggest that normobaric hypoxia causes a differential hemodynamic response from normoxia in apparently healthy middle aged
males at rest and post-exercise.
.
.
.
ABSTRACT
•  Grover, R.F., Weil, J.V., & Reeves, J.T. (1986). Cardiovascular adaptation to exercise at high altitude. Exerc Sport Sci Rev, 14: 269-302
• Leunberger, U.A., Gray, K., & Herr, M. D. (1999). Adenosine contributes to hypoxia-induced forearm vasodilation in human. J Appl Physiol, 87:
2218- 2224.
• Fulco, C. S., Rock, P. B., Trad, L. A., Beidleman, B., Smith, S., Muza, S. R., & Cymerman, A. (1994). Increased physical activity augments the
incidence and severity of acute mountain sickness (AMS) during a simulated ascent to 4,600m (Abstract). FASEBJ, 8, A298.
PURPOSE: To determine the effect of acute normobaric hypoxia on heart rate and mean arterial pressure at rest, during and post-exercise in middle-aged males.
METHODS: Eight apparently healthy (35.9 ± 5.7 ml·kg-1·min-1), middle-aged (40.5 ± 2 yr) males volunteered to participate in the present investigation.
Participants reported to the exercise physiology laboratory on three separate occasions. On the first visit, subjects underwent a graded exercise test (Excalibur
1300W cycle ergometer) to determine maximal oxygen consumption. The next two visits were separated by a one week washout period. Participants underwent
normoxia with exercise (N+E) and hypoxia with exercise (H+E) in a hypoxia (20.9% vs. 12.5% O2) chamber (Colorado Altitude Training, Louisville, CO) including
2hr baseline, 1h low intensity cycling (50% of hypoxic VO2max) and 2h recovery. Heart rate (HR) measures were obtained every 10 min, and mean arterial pressure
(MAP) measures were obtained every 30min throughout the experimental trials.
RESULTS: A repeated measures ANOVA revealed a trial (N+E and H+E) by time interaction for heart rate (p<0.01), and a pair-sample t-test demonstrated that
the difference in post exercise HR between H+E and N+E is greater than pre exercise (p<0.05). MAP demonstrated a trial by time interaction (p<0.05); MAP
decreased greater in hypoxia than normoxia post exercise.
CONCLUSION: These data suggest that normobaric hypoxia causes a differential hemodynamic response from normoxia in apparently healthy middle-aged
males at rest and post-exercise.
Hypoxia is a potent stressor that induces various physiological changes. Although modifications in autonomic regulation and vascular tone are responses to
hypoxia, changes in heart rate and blood pressure may vary depending on individual characteristics, severity of hypoxia and exercise intensity and duration.
The purpose of the current study was to determine the effect of acute normobaric hypoxia on heart rate and mean arterial pressure at rest, during and post-
exercise in middle-aged males.
Participants
Table 1. Subjects' Physical Characteristics
Age
(yrs)
Height
(cm)
Weight
(kg)
VO2max
(ml/kg/min)
Workload
(W)
40.5±2.3
 179.3±4.7
 80.2±9.9
 35.9±9.4
 45.8±23.6
Preliminary testing
• Physical characteristics measurements
• Maximal oxygen capacity test on bike ergometer
Experimental Design
• Two trials with one week washout period:
hypoxia with exercise (H+E) & normoxia with exercise (N+E)
• Normobaric Hypoxia Chamber (Colorado Altitude Training, Louisville, CO)
• VO2max is decreased by 26% at 4300m (12.5% O2) (Fulco, Rock and Cymerman, 1998).
Hypoxia Trial
• 12.5% O2
• Exercise intensity : 50% of modified VO2max
Normoxia Trial
• 20.9% O2
• Exercise intensity : 50% of modified VO2max
2 hour Resting
1hour Exerci
se
2 hour Recovery
0 10 20 30 40 50 60 70 80 90 100110120 10 20 30 40 50 60 10 20 30 40 50 60 70 80 90 100110120
• Heart rate (HR) measures were obtained every 10 min
• Mean arterial pressure (MAP) measures were obtained every 30min
throughout the experimental trials
Timeline for measurement
Figure 1. Heart Rate
Significant main effect of time (p=0.000) and trial (p=0.007)
Significant trial by time interaction (p=0.000)
Figure 2. Mean Heart Rate during Base, Exercise and Recovery
Significant difference between H+E and N+E(p<0.05)
Figure 3. Mean Arterial Pressure
Significant main effect of time (p=0.010)
Significant trial by time interaction (p=0.017)
METHODS and PROCEDURES
INTRODUCTION
CONCLUSIONS
RESULTS
REFERENCE

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Effect of Hypoxia on Heart Rate and Blood Pressure

  • 1. THE EFFECT OF ACUTE NORMOBARIC HYPOXIA ON HEART RATE AND MEAN ARTERIAL PRESSURE AT REST, DURING AND POST EXERCISE YongSuk Seo, Chul-Ho Kim, Corey A. Peacock, Edward J. Ryan, Zachary Sax, John Gunstad, and Ellen L. Glickman FACSM These results suggest that normobaric hypoxia causes a differential hemodynamic response from normoxia in apparently healthy middle aged males at rest and post-exercise. . . . ABSTRACT •  Grover, R.F., Weil, J.V., & Reeves, J.T. (1986). Cardiovascular adaptation to exercise at high altitude. Exerc Sport Sci Rev, 14: 269-302 • Leunberger, U.A., Gray, K., & Herr, M. D. (1999). Adenosine contributes to hypoxia-induced forearm vasodilation in human. J Appl Physiol, 87: 2218- 2224. • Fulco, C. S., Rock, P. B., Trad, L. A., Beidleman, B., Smith, S., Muza, S. R., & Cymerman, A. (1994). Increased physical activity augments the incidence and severity of acute mountain sickness (AMS) during a simulated ascent to 4,600m (Abstract). FASEBJ, 8, A298. PURPOSE: To determine the effect of acute normobaric hypoxia on heart rate and mean arterial pressure at rest, during and post-exercise in middle-aged males. METHODS: Eight apparently healthy (35.9 ± 5.7 ml·kg-1·min-1), middle-aged (40.5 ± 2 yr) males volunteered to participate in the present investigation. Participants reported to the exercise physiology laboratory on three separate occasions. On the first visit, subjects underwent a graded exercise test (Excalibur 1300W cycle ergometer) to determine maximal oxygen consumption. The next two visits were separated by a one week washout period. Participants underwent normoxia with exercise (N+E) and hypoxia with exercise (H+E) in a hypoxia (20.9% vs. 12.5% O2) chamber (Colorado Altitude Training, Louisville, CO) including 2hr baseline, 1h low intensity cycling (50% of hypoxic VO2max) and 2h recovery. Heart rate (HR) measures were obtained every 10 min, and mean arterial pressure (MAP) measures were obtained every 30min throughout the experimental trials. RESULTS: A repeated measures ANOVA revealed a trial (N+E and H+E) by time interaction for heart rate (p<0.01), and a pair-sample t-test demonstrated that the difference in post exercise HR between H+E and N+E is greater than pre exercise (p<0.05). MAP demonstrated a trial by time interaction (p<0.05); MAP decreased greater in hypoxia than normoxia post exercise. CONCLUSION: These data suggest that normobaric hypoxia causes a differential hemodynamic response from normoxia in apparently healthy middle-aged males at rest and post-exercise. Hypoxia is a potent stressor that induces various physiological changes. Although modifications in autonomic regulation and vascular tone are responses to hypoxia, changes in heart rate and blood pressure may vary depending on individual characteristics, severity of hypoxia and exercise intensity and duration. The purpose of the current study was to determine the effect of acute normobaric hypoxia on heart rate and mean arterial pressure at rest, during and post- exercise in middle-aged males. Participants Table 1. Subjects' Physical Characteristics Age (yrs) Height (cm) Weight (kg) VO2max (ml/kg/min) Workload (W) 40.5±2.3 179.3±4.7 80.2±9.9 35.9±9.4 45.8±23.6 Preliminary testing • Physical characteristics measurements • Maximal oxygen capacity test on bike ergometer Experimental Design • Two trials with one week washout period: hypoxia with exercise (H+E) & normoxia with exercise (N+E) • Normobaric Hypoxia Chamber (Colorado Altitude Training, Louisville, CO) • VO2max is decreased by 26% at 4300m (12.5% O2) (Fulco, Rock and Cymerman, 1998). Hypoxia Trial • 12.5% O2 • Exercise intensity : 50% of modified VO2max Normoxia Trial • 20.9% O2 • Exercise intensity : 50% of modified VO2max 2 hour Resting 1hour Exerci se 2 hour Recovery 0 10 20 30 40 50 60 70 80 90 100110120 10 20 30 40 50 60 10 20 30 40 50 60 70 80 90 100110120 • Heart rate (HR) measures were obtained every 10 min • Mean arterial pressure (MAP) measures were obtained every 30min throughout the experimental trials Timeline for measurement Figure 1. Heart Rate Significant main effect of time (p=0.000) and trial (p=0.007) Significant trial by time interaction (p=0.000) Figure 2. Mean Heart Rate during Base, Exercise and Recovery Significant difference between H+E and N+E(p<0.05) Figure 3. Mean Arterial Pressure Significant main effect of time (p=0.010) Significant trial by time interaction (p=0.017) METHODS and PROCEDURES INTRODUCTION CONCLUSIONS RESULTS REFERENCE