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% O 2 ) chamber (Colorado Altitude Training, Louisville, CO) including 2hr baseline, 1h low intensity cycling (50% of hypoxic VO 2 max) 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) VO 2 max (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% O 2 • Exercise intensity : 50% of modified VO 2 max Normoxia Trial • 20.9% O 2 • Exercise intensity : 50% of modified VO 2 max 2 hour Resting 1hour Exerci se 2 hour Recovery 0 10 20 30 40 50 60 70 80 90 100 110 120 10 20 30 40 50 60 10 20 30 40 50 60 70 80 90 100 110 120 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

ACSM Poster 2011

Embed Size (px)

Citation preview

Page 1: ACSM Poster 2011

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 90 100 110 120 10 20 30 40 50 60 10 20 30 40 50 60 70 80 90 100 110 120

• 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