O2 uptake and blood pressure regulation at the onset of exercise: interaction of circadian rhythm and priming exercise.

Circadian rhythm has an influence on several physiological functions that contribute to athletic performance. We tested the hypothesis that circadian rhythm would affect blood pressure (BP) responses but not O(2) uptake (Vo(2)) kinetics during the transitions to moderate and heavy cycling exercises. Nine male athletes (peak Vo(2): 60.5 ± 3.2 ml·kg(-1)·min(-1)) performed multiple rides of two different cycling protocols involving sequences of 6-min bouts at moderate or heavy intensities interspersed by a 20-W baseline in the morning (7 AM) and evening (5 PM). Breath-by-breath Vo(2) and beat-by-beat BP estimated by finger cuff plethysmography were measured simultaneously throughout the protocols. Circadian rhythm did not affect Vo(2) onset kinetics determined from the phase II time constant (τ(2)) during either moderate or heavy exercise bouts with no prior priming exercise (τ(2) moderate exercise: morning 22.5 ± 4.6 s vs. evening 22.2 ± 4.6 s and τ(2) heavy exercise: morning 26.0 ± 2.7 s vs. evening 26.2 ± 2.6 s, P > 0.05). Priming exercise induced the same robust acceleration in Vo(2) kinetics during subsequent moderate and heavy exercise in the morning and evening. A novel finding was an overshoot in BP (estimated from finger cuff plethysmography) in the first minutes of each moderate and heavy exercise bout. After the initial overshoot, BP declined in association with increased skin blood flow between the third and sixth minute of the exercise bout. Priming exercise showed a greater effect in modulating the BP responses in the evening. These findings suggest that circadian rhythm interacts with priming exercise to lower BP during exercise after an initial overshoot with a greater influence in the evening associated with increased skin blood flow.

Prior moderate and heavy exercise accelerate oxygen uptake and cardiac output kinetics in endurance athletes.

Cardiorespiratory interactions at the onset of dynamic cycling exercise are modified by warm-up exercises. We tested the hypotheses that oxygen uptake (Vo(2)) and cardiac output (Q) kinetics would be accelerated at the onset of heavy and moderate cycling exercise by warm-up. Nine male endurance athletes (peak Vo(2): 60.5 +/- 3.2 ml.min(-1).kg(-1)) performed multiple rides of two different 36-min cycling protocols, involving 6-min bouts at moderate and heavy intensities. Breath-by-breath Vo(2) and beat-by-beat stroke volume (SV) and Q, estimated by Modelflow from the finger pulse, were measured simultaneously with kinetics quantified from the phase II time constant (tau(2)). One novel finding was that both moderate (M) and heavy (H) warm-up bouts accelerated phase II Vo(2) kinetics during a subsequent bout of heavy exercise (tau(2): after M = 22.5 +/- 2.7 s, after H = 22.1 +/- 2.9 vs. 26.2 +/- 3.2 s; P < 0.01). Q kinetics in heavy exercise were accelerated by both warm-up intensities (tau(2): M = 22.0 +/- 4.1 s, H = 23.8 +/- 5.6 s vs. 27.4 +/- 7.2 s; P < 0.05). During moderate exercise, prior heavy-intensity warm-up (one or two bouts) accelerated Vo(2) kinetics and elevated Q at exercise onset, with no changes in Q kinetics. A second novel finding was a significant overshoot in the estimate of SV from Modelflow in the first minutes of each moderate and heavy exercise bout. These findings suggest that the acceleration of Vo(2) kinetics during heavy exercise was enabled by the acceleration of Q kinetics, and that rapid increases in Q at the onset of moderate and heavy exercise might result, in part, from an overshoot of SV.

Efficacy of fluid loading as a countermeasure to the hemodynamic and hormonal changes of 28-h head-down bed rest.

After exposure to microgravity, or head-down bed rest (HDBR), fluid loading is often used with the intent of increasing plasma volume and maintaining mean arterial pressure during orthostatic stress. Nine men (aged 18-32 years) underwent three randomized trials with lower body negative pressure (LBNP) before and after: (1) 4-h of sitting with fluid loading (1 g sodium chloride/125 mL of water starting 2.5-h before LBNP), (2) 28-h of 6-degree HDBR without fluid loading, and (3) 28-h of 6-degree HDBR with fluid loading. LBNP was progressive from 0 to -40 mmHg. After 28-h HDBR, fluid loading did not protect against the loss of plasma volume (-280 ± 64 mL without fluid loading, -207 ± 86 with fluid loading, P = 0.472) nor did it protect against a drop of mean arterial pressure (P = 0.017) during LBNP (Post-28 h HDBR response from 0 to -40 mmHg LBNP: 88 ± 4 to 85 ± 4 mmHg without fluid loading and 93 ± 4 to 88 ± 5 mmHg with fluid loading, P = 0.557 between trials). However, fluid loading did protect against the loss of stroke volume index and central venous pressure observed after 28-h HDBR. Fluid loading also attenuated the increase of angiotensin II seen after 28-h HDBR and throughout the LBNP protocol (Post-28 h HDBR response from 0 to -40 mmHg LBNP: 16.6 ± 3.4 to 23.7 ± 5.0 pg/mL without fluid loading and 6.1 ± 0.8 to 12.2 ± 2.3 pg/mL with fluid loading, P < 0.001 between trials). Our results indicate that fluid loading did not protect against plasma volume loss due to HDBR or change blood pressure responses to LBNP. However, changes in central venous pressure, stroke volume and fluid regulatory hormones could potentially influence longer duration studies and those with more severe orthostatic stress.