Abstract

The normal heart rate (HR) is linearly related to oxygen consumption (VO 2 ) during aerobic exercise and has been used as the gold standard for rate-adaptive pacing. However, at the onset of constant-workload exercise both VO 2 and the sinus HR increase exponentially before reaching their steady-state levels, producing oxygen and HR deficits. Whether the rate constants ( k ) for VO 2 and HR are related has not been proven. We hypothesized that an instantaneous increase in HR at the onset of exercise to the steady state value ( k = ∞) would reduce oxygen deficit and increase the VO 2 rate constant as compared with normal sinus node function during treadmill exercise. 10 pts with rigorously-proven normal sinus node function and AV block with DDD pacemakers underwent maximal treadmill exercise to determine VCO 2max . Oxygen kinetics were then measured during constant-workload exercise tests (6-min) at 50% VO 2max with pacemakers programmed to 3 modes in random sequence: 1) DDD, with the sinus node controlling pacing rate; 2) Fast an instantaneous increase in HR at onset of exercise to the expected steady-state level for 50% VO 2max ; and 3) Max , an instantaneous increase to the age-predicted maximum at exercise onset. The O 2 deficit was lower in the Fast (434 ± 76 ml) than either the DDD (512 ± 74) (p = 0.01) or Max (503 ± 84) (p = 0.02) pacing modes. The VO 2 rate constant was highest in the Fast mode (2.85 ± 1.38 Fast vs 2.25 ± 0.63 DDD vs 2.38 ± 0.43 Max, p = 0.03). The median Borg perceived exertion score was also lowest in the Fast mode (7.5 Fast vs 8.5 DDD vs 9 Max). Thus , oxygen deficit is improved by an instantaneous increase in HR at the onset of exercise to the steady state level as compared with either the normal sinus node or an overly-aggressive pacing rate. The rate constant for VO 2 is directly related to that for HR.

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