Beta2- and beta3-adrenergic receptor polymorphisms and exercise hemodynamics in postmenopausal women.

We sought to determine whether common genetic variations at the beta2 (beta2-AR, Gln27Glu) and beta3 (beta3-AR, Trp64Arg) adrenergic receptor gene loci were associated with cardiovascular (CV) hemodynamics during maximal and submaximal exercise. CV hemodynamics were assessed in 62 healthy postmenopausal women (20 sedentary, 22 physically active, and 20 endurance athletes) during treadmill exercise at 40, 60, 80, and 100% maximal O2 uptake using acetylene rebreathing to quantify cardiac output. The beta2-AR genotype and habitual physical activity (PA) levels interacted to significantly associate with arteriovenous O2 difference (a-vDO2) during submaximal exercise (P = 0.05), with the highest submaximal exercise a-vDO2 in sedentary women homozygous for the beta2-AR Gln allele and no genotype-dependent differences in submaximal exercise a-vDO2 in physically active and athletic women. The beta2-AR genotype also was independently associated with a-vDO2 during submaximal (P = 0.004) and approximately 100% maximal O2 uptake exercise (P = 0.006), with a 1.2-2 ml/100 ml greater a-vDO2 in the Gln/Gln than in the Glu/Glu genotype women. The beta3-AR genotype, independently or interacting with habitual PA levels, was not significantly associated with any CV hemodynamic variables during submaximal or maximal exercise. Thus it appears that the beta2-AR genotype, both independently and interacting with habitual PA levels, is significantly associated with a-vDO2 during exercise in postmenopausal women, whereas the beta3-AR genotype does not appear to be associated with any maximal or submaximal exercise CV hemodynamic responses in postmenopausal women.

Angiotensinogen M235T polymorphism associates with exercise hemodynamics in postmenopausal women.

We sought to determine whether the M235T angiotensinogen (AGT) polymorphism, either interacting with habitual physical activity (PA) levels or independently, was associated with cardiovascular (CV) hemodynamics during maximal and submaximal exercise. Sixty-one healthy postmenopausal women (16 sedentary, 21 physically active, and 24 endurance athletes) had heart rate (HR), blood pressure (BP), cardiac output, stroke volume (SV), total peripheral resistance (TPR), and arteriovenous O2 difference (a-vDO2) assessed during 40, 60, 80, and approximately 100% of VO2 max treadmill exercise. VO2 max did not differ among AGT genotype groups; however, maximal HR was 14 beats/min higher in AGT TT than MM genotype women (P < 0.05). AGT TT genotype women also had 19 beats/min higher HR during approximately 100% VO2 max exercise than AGT MM genotype women (P = 0.008). AGT genotype also interacted with habitual PA levels to associate with systolic BP and a-vDO2 during approximately 100% VO2 max exercise (both P < 0.01). AGT TT genotype women had 11 beats/min higher HR during submaximal exercise than MM genotype women (P < 0.05). AGT genotype interacted with habitual PA levels to associate with systolic BP during submaximal exercise (P = 0.009). AGT genotype, independently or interacting with habitual PA levels, did not associate significantly with diastolic BP, cardiac output, SV, or TPR during maximal or submaximal exercise. Thus this common genetic variant in the renin-angiotensin system appears to associate, both interactively with habitual PA levels and independently, with HR, systolic BP, and a-vDO2 responses to maximal and submaximal exercise in postmenopausal women.

ACE insertion/deletion polymorphism and submaximal exercise hemodynamics in postmenopausal women.

We sought to determine whether the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism is associated with submaximal exercise cardiovascular hemodynamics. Postmenopausal healthy women (20 sedentary, 20 physically active, 22 endurance athletes) had cardiac output (acetylene rebreathing) measured during 40, 60, and 80% VO(2 max) exercise. The interaction of ACE genotype and habitual physical activity (PA) level was significantly associated with submaximal exercise systolic blood pressure, with only sedentary women exhibiting differences among genotypes. No significant effects of ACE genotype or its interaction with PA levels was observed for submaximal exercise diastolic blood pressure. ACE genotype was significantly associated with submaximal exercise heart rate (HR) with ACE II having approximately 10 beats/min higher HR than ACE ID/DD genotype women. ACE genotype did not interact significantly with habitual PA level to associate with submaximal exercise HR. ACE genotype was not independently, but was interactively with habitual PA levels, associated with differences in submaximal exercise cardiac output and stroke volume. For cardiac output, ACE II genotype women athletes had ~25% greater cardiac output than ACE DD genotype women athletes, whereas for stroke volume genotype-dependent differences were observed in both the physically active and athletic women. ACE genotype was not significantly associated, either independently or interactively with habitual PA levels, with submaximal exercise total peripheral resistance or arteriovenous O(2) difference. Thus the common ACE locus polymorphic variation is associated with many submaximal exercise cardiovascular hemodynamic responses.

Pedal and Crank Kinetics in Uphill Cycling.

Alterations in kinetic patterns of pedal force and crank torque due to changes in surface grade (level vs. 8% uphill) and posture (seated vs. standing) were investigated during cycling on a computerized ergometer. Kinematic data from a planar cine analysis and force data from a pedal instrumented with piezoelectric crystals were recorded from multiple trials of 8 elite cyclists. These measures were used to calculate pedal force, pedal orientation, and crank torque profiles as a function of crank angle in three conditions: seated level, seated uphill, and standing uphill. The change in surface grade from level to 8% uphill resulted in a shift in pedal angle (toe up) and a moderately higher peak crank torque, due at least in part to a reduction in the cycling cadence. However, the overall patterns of pedal and crank kinetics were similar in the two seated conditions. In contrast, the alteration in posture from sitting to standing on the hill permitted the subjects to produce different patterns of pedal and crank kinetics, characterized by significantly higher peak pedal force and crank torque that occurred much later in the downstroke. These kinetic changes were associated with modified pedal orientation (toe down) throughout the crank cycle. Further, the kinetic changes were linked to altered nonmuscular (gravitational and inertial) contributions to the applied pedal force, caused by the removal of the saddle as a base of support.