Megan N. Hawkins

The effect of changes in cardiac output on middle cerebral artery mean blood velocity at rest and during exercise

We examined the relationship between changes in cardiac output and middle cerebral artery mean blood velocity (MCA Vmean) in seven healthy volunteer men at rest and during 50% maximal oxygen uptake steady‐state submaximal cycling exercise. Reductions in were accomplished using lower body negative pressure (LBNP), while increases in were accomplished using infusions of 25% human serum albumin. Heart rate (HR), arterial blood pressure and MCA Vmean were continuously recorded. At each stage of LBNP and albumin infusion was measured using an acetylene rebreathing technique. Arterial blood samples were analysed for partial pressure of carbon dioxide tension (P  a,CO 2. During exercise HR and were increased above rest (P < 0.001), while neither MCA Vmean nor P  a,CO 2 was altered (P > 0.05). The MCA Vmean and were linearly related at rest (P < 0.001) and during exercise (P= 0.035). The slope of the regression relationship between MCA Vmean and at rest was greater (P= 0.035) than during exercise. In addition, the phase and gain between MCA Vmean and mean arterial pressure in the low frequency range were not altered from rest to exercise indicating that the cerebral autoregulation was maintained. These data suggest that the associated with the changes in central blood volume influence the MCA Vmean at rest and during exercise and its regulation is independent of cerebral autoregulation. It appears that the exercise induced sympathoexcitation and the change in the distribution of between the cerebral and the systemic circulation modifies the relationship between MCA Vmean and .

Carotid baroreflex control of leg vasculature in exercising and non-exercising skeletal muscle in humans

Carotid baroreflex (CBR) function was examined in five men and three women (25 ± 1 years) using the variable‐pressure neck collar technique at rest and during dynamic, one‐legged knee extension exercise at 7 W and 25 W. The CBR exhibited control of leg vascular conductance (LVC) at rest and during exercise in both an exercising leg (EL) and a non‐exercising leg (NEL) across a wide range of pressures from +40 Torr neck pressure (NP) to −80 Torr neck suction (NS). Specifically, increases in LVC (% change) in response to NS were no different across −20 to −80 Torr in either EL or NEL compared to rest, P > 0.05. However, CBR‐mediated decreases in percentage LVC in response to NP were attenuated in EL at both 7 W (16 ± 1%) and 25 W (12 ± 1%) compared to rest (40 ± 3%; P < 0.05) as well as compared to responses in the NEL (36 ± 6% at 7 W and 36 ± 7% at 25 W; P < 0.05). This decrease in vascular responsiveness in EL was associated with a reduction in the gain of the percentage muscle sympathetic nerve activity (%MSNA)–%LVC relationship compared to rest (P < 0.05). Collectively, these data indicate that, despite a clear attenuation of the vascular response to MSNA in the exercising leg, CBR‐mediated changes in mean arterial pressure were no different between rest and exercise.

The effects of aerobic fitness and β1-adrenergic receptor blockade on cardiac work during dynamic exercise

The purpose of this investigation was to determine whether cardiovascular adaptations characteristic of long-term endurance exercise compensate more effectively during cardioselective beta(1)-adrenergic receptor blockade-induced reductions in sympathoadrenergic-stimulated contractility. Endurance-trained (ET) athletes (n = 8) and average-trained (AT; n = 8) subjects performed submaximal cycling exercise at moderate [45% maximum oxygen uptake (Vo(2max))] and heavy (70% Vo(2max)) workloads, with and without metoprolol. Cardiac output (Qc), heart rate (HR), and systolic blood pressure were recorded at rest and during exercise. Cardiac work was calculated from the triple product of HR, stroke volume, and systolic blood pressure, and myocardial efficiency is represented as cardiac work for a given total body oxygen consumption. Metoprolol reduced Qc at 45% Vo(2max) (P = 0.004) and 70% Vo(2max) (P = 0.022) in ET subjects, but did not alter Qc in the AT subjects. In ET subjects at 45% Vo(2max), metoprolol-induced reductions in Qc were a result of decreases in HR (P < 0.05) and the absence of a compensatory increase in stroke volume (P > 0.05). The cardiac work and calculated cardiac efficiency were reduced with metoprolol in ET subjects at both exercise intensities and in the AT subjects during the high-intensity workload (P < 0.01). The cardiac work and the calculated cardiac efficiency were not affected by metoprolol in the AT subjects during the 45% Vo(2max) exercise. Therefore, in AT subjects, beta-blockade reduced the amount of pressure generation necessary to produce the same amount of work during moderate-intensity exercise. In patients with heart disease receiving metoprolol, a decrease in the generation of cardiac pressure necessary to perform a given amount of work during mild-to-moderate exercise would prove to be beneficial.