Journal of Applied Physiology
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J Appl Physiol 87: 2122-2127, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 6, 2122-2127, December 1999

Oxygen-conserving effects of apnea in exercising men

Peter Lindholm, Patrik Sundblad, and Dag Linnarsson

Section of Environmental Physiology, Department of Physiology and Pharmacology, Karolinska Institutet, SE-171 77 Stockholm, Sweden

We sought to determine whether apnea-induced cardiovascular responses resulted in a biologically significant temporary O2 conservation during exercise. Nine healthy men performing steady-state leg exercise carried out repeated apnea (A) and rebreathing (R) maneuvers starting with residual volume +3.5 liters of air. Heart rate (HR), mean arterial pressure (MAP), and arterial O2 saturation (SaO2; pulse oximetry) were recorded continuously. Responses (Delta HR, Delta MAP) were determined as differences between HR and MAP at baseline before the maneuver and the average of values recorded between 25 and 30 s into each maneuver. The rate of O2 desaturation (Delta SaO2/Delta t) was determined during the same time interval. During apnea, Delta SaO2/Delta t had a significant negative correlation to the amplitudes of Delta HR and Delta MAP (r2 = 0.88, P < 0.001); i.e., individuals with the most prominent cardiovascular responses had the slowest Delta SaO2/Delta t. Delta HR and Delta MAP were much larger during A (-44 ± 8 beats/min, +49 ± 4 mmHg, respectively) than during R maneuver (+3 ± 3 beats/min, +30 ± 5 mmHg, respectively). Delta SaO2/Delta t during A and R maneuvers was -1.1 ± 0.1 and -2.2 ± 0.2% units/s, respectively, and nadir SaO2 values were 58 ± 4 and 42 ± 3% units, respectively. We conclude that bradycardia and hypertension during apnea are associated with a significant temporary O2 conservation and that respiratory arrest, rather than the associated hypoxia, is essential for these responses.

hypoxemia; bradycardia; hypertension; breath holding; diving response.


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