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This study examined whether left ventricular function was reduced during 3 h of semi-recumbent ergometer cycling at 70% of maximal oxygen uptake while preload to the heart was maintained via saline infusion. Indices of left ventricular systolic function (end-systolic blood pressure-volume relationship, SBP/ESV) and diastolic filling (ratio of early to late peak filling velocities into the left ventricle, E:A) were calculated during recovery and compared with baseline resting data. During exercise in seven healthy, trained male subjects, an arterial catheter allowed continuous assessment of arterial pressure, stroke volume (SV), cardiac output ( ) and an index of contractility (dP/dt(max)). A venous catheter assessed that central venous pressure (CVP) was maintained throughout rest, exercise and 10 min into recovery. Both systolic blood pressure and heart rate (HR) increased with the onset of exercise (from 132 +/- 5 to 185 +/- 19 mmHg and from 66 +/- 9 to 135 +/- 23 beats min(-1); increases from rest to the end of the first 5 min of exercise in SBP and HR, respectively) but systolic blood pressure did not change from 30 to 180 min of exercise ( approximately 150 mmHg), while heart rate only increased by 8 +/- 9 beats min(-1) (means +/- s.d.; P > 0.05). The attenuated increase in HR compared with other studies suggests that the maintained CVP ( approximately 5 mmHg) helped to prevent cardiovascular drift in this protocol. Stroke volume, and dP/dt(max) were all increased with the onset of exercise (from 85 +/- 8 to 120 +/- 18 ml, from 5.4 +/- 1.3 to 16.5 +/- 3.3 l min(-1) and from 14.4 +/- 4 to 28 +/- 8 mmHg s(-1); values from rest to the end of the first 5 min of exercise for SV, and dP/dt(max), respectively) and were maintained during exercise. There was no difference in the SBP/ESV ratio from pre- to postexercise. Conversely, E:A was reduced from 2.0 +/- 0.4 to 1.6 +/- 0.5 postexercise (P < 0.05), returning to normal values at 24 h postexercise. This change in diastolic filling could not be fully explained (r(2) = 0.39) by an increased heart rate and, with CVP unchanged, it is likely to represent some depression of intrinsic relaxation properties of left ventricular myocytes. Three hours of semi-supine cycling resulted in no evidence of a depression in left ventricular systolic function, while left ventricular diastolic function declined postexercise.

Exercise challenges cerebral autoregulation (CA) by a large increase in pulse pressure (PP) that may make systolic pressure exceed what is normally considered the upper range of CA. This study examined the relationship between systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) and systolic (V(s)), diastolic (V(d)). and mean (V(m)) middle cerebral artery (MCA) blood flow velocity during mild, moderate, and heavy cycling exercise. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated using transfer function analysis. PP increased by 37% and 57% during moderate and heavy exercise, respectively (P < 0.05), and the pulsatility of MCA V increased markedly. Thus exercise increased MCA V(m) and V(s) (P < 0.05) but tended to decrease MCA V(d) (P = 0.06). However, the normalized low-frequency transfer function gain between MAP and MCA V(m) and between SBP and MCA V(s) remained unchanged from rest to exercise, whereas that between DBP and MCA V(d) increased from rest to heavy exercise (P < 0.05). These findings suggest that during exercise, CA is challenged by a rapid decrease rather than by a rapid increase in blood pressure. However, dynamic CA remains able to modulate blood flow around the exercise-induced increase in MCA V(m), even during high-intensity exercise.

We sought to quantify the contribution of cardiac output (Q) and total vascular conductance (TVC) to carotid baroreflex (CBR)-mediated changes in mean arterial pressure (MAP) during mild to heavy exercise. CBR function was determined in eight subjects (25 +/- 1 years) at rest and during three cycle exercise trials at heart rates (HRs) of 90, 120 and 150 beats min-1 performed in random order. Acute changes in carotid sinus transmural pressure were evoked using 5 s pulses of neck pressure (NP) and neck suction (NS) from +40 to -80 Torr (+5.33 to -10.67 kPa). Beat-to-beat changes in HR and MAP were recorded throughout. In addition, stroke volume (SV) was estimated using the Modelflow method, which incorporates a non-linear, three-element model of the aortic input impedance to compute an aortic flow waveform from the arterial pressure wave. The application of NP and NS did not cause any significant changes in SV either at rest or during exercise. Thus, CBR-mediated alterations in Q were solely due to reflex changes in HR. In fact, a decrease in the carotid-HR response range from 26 +/- 7 beats min-1 at rest to 7 +/- 1 beats min-1 during heavy exercise (P = 0.001) reduced the contribution of Q to the CBR-mediated change in MAP. More importantly, at the time of the peak MAP response, the contribution of TVC to the CBR-mediated change in MAP was increased from 74 +/- 14 % at rest to 118 +/- 6 % (P = 0.017) during heavy exercise. Collectively, these findings indicate that alterations in vasomotion are the primary means by which the CBR regulates blood pressure during mild to heavy exercise.