[Show abstract][Hide abstract] ABSTRACT: Abnormal heart rate recovery (HRR) after maximal exercise may indicate autonomic dysfunction and is a predictor for cardiovascular mortality. HRR is attenuated with ageing and in middle-age hypertensive patients but it is unknown if HRR is attenuated in older-age adults with hypertension. This study compared HRR between 16 unmedicated Stage 1 hypertensive (HTN) participants (9M/7F; 68±5 [SD] yrs; awake ambulatory blood pressure [BP] 149±10/87±7mmHg) and 16 normotensive (CON) participants (9M/7F); 67±5 yrs; 122±4/72±5mmHg). Heart rate (HR), BP, oxygen uptake (VO2), cardiac output (Qc) and stroke volume (SV) were measured at rest, at two steady state work rates and graded exercise to peak during maximal treadmill exercise. During 6 minutes of seated recovery the change in HR (ΔHR) was obtained every minute and BP every 2 minutes. In addition HRR and R-R interval (RRI) recovery kinetics were analyzed using a mono-exponential function and the indexes (HRRI and RRII) were calculated. VO2max, HRmax, Qc and SV responses during exercise were not different between groups. ΔHR was significantly different (P<0.001) between the HTN group (26±8) and the CON group (36±12 beats.min(-1)) after 1 min of recovery but less convincing at 2 min (P=0.055). BP recovery was similar between groups. HRRI was significantly lower (P=0.016) and there was a trend of lower RRII (P=0.066) in the HTN group when compared to the CON group. These results show that in older-age adults, HRR is further attenuated with the presence of hypertension, which may be attributable to an impairment of autonomic function.
[Show abstract][Hide abstract] ABSTRACT: Sedentary aging has deleterious effects on the cardiovascular system, including decreased left ventricular compliance and distensibility (LVCD). Conversely, Masters level athletes, who train intensively throughout adulthood, retain youthful LVCD.
Journal of the American College of Cardiology 09/2014; 64(12):1257-66. DOI:10.1016/j.jacc.2014.03.062 · 16.50 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background: Exposure to microgravity causes functional and structural impairment of skeletal muscle. Current exercise regimens are time-consuming and insufficiently effective; an integrated countermeasure is needed that addresses musculoskeletal along with cardiovascular health. High-intensity, short-duration rowing ergometry and supplemental resistive strength exercise may achieve these goals. Methods: 27 healthy volunteers completed 5 weeks of head down tilt bed rest; 18 were randomized to exercise, 9 remained sedentary. Exercise consisted of rowing ergometry 6d/week including interval training, and supplemental strength training 2d/week. Measurements before and after bed rest, and following reambulation included assessment of strength, skeletal muscle volume (MRI), and muscle metabolism (MRS); quadriceps muscle biopsies were obtained to assess muscle fiber types, capillarization and oxidative capacity. Results: Sedentary bed rest (BR) led to decreased muscle volume (quadriceps: -9±4%, p<0.001; plantarflexors: -19±6%, p<0.001). Exercise (ExBR) reduced atrophy in the quadriceps (-5±4%, interaction p=0.018) and calf muscle, though to a lesser degree (-14±6%, interaction p=0.076). Knee extensor and plantarflexor strength was impaired by BR (-14±15%, p=0.014 and -22±7%, p=0.001) but preserved by ExBR (-4±13%, p=0.238 and +13±28%, p=0.011). Metabolic capacity as assessed by VO2max, (31)P-MRS and oxidative chain enzyme activity was impaired in BR but stable or improved in ExBR. Reambulation reversed the negative impact of bed rest. Conclusions: High-intensity, short-duration rowing and supplemental strength training effectively preserved skeletal muscle function and structure while partially preventing atrophy in key antigravity muscles. Due to its integrated cardiovascular benefits, rowing ergometry could be a primary component of exercise prescriptions for astronauts or patients suffering from severe deconditioning.
[Show abstract][Hide abstract] ABSTRACT: An increased "dose" of endurance exercise training is associated with a greater maximal oxygen uptake (VO2max), a larger left ventricular (LV) mass, and improved heart rate and blood pressure control. However, the effect of lifelong exercise dose on metabolic and hemodynamic response during exercise has not been previously examined. Methods and Results: We performed a cross-sectional study on 101 (69 men) seniors (60 yr and older) focusing on lifelong exercise frequency as an index of exercise dose. These included 27 who had performed ≤2 exercise sessions/wk (sedentary), 25 who performed 2-3 sessions/wk (casual), 24 who performed 4-5 sessions/wk (committed) and 25 who performed ≥6 sessions/wk plus regular competitions (Masters athletes) over at least the last 25 yr. Oxygen uptake and hemodynamics (cardiac output [Qc], stroke volume [SV]) were collected at rest, two levels of steady-state submaximal exercise and maximal exercise. Doppler ultrasound measures of LV diastolic filling were assessed at rest and during LV loading (saline infusion) to simulate increased LV filling. Body composition, total blood volume, and heart-rate recovery after maximal exercise were also examined. VO2max increased in a dose-dependent manner (P<0.05). At maximal exercise, Qc and SV were largest in committed exercisers and Masters athletes (P<0.05), while arteriovenous oxygen difference was greater in all trained groups (P<0.05). At maximal exercise, effective arterial elastance, an index of ventricular-arterial coupling, was lower in committed exercisers and Masters athletes (P<0.05). Doppler measures of LV filling were not enhanced at any condition irrespective of lifelong exercise frequency. Conclusion: These data suggest that performing 4 or more weekly endurance exercise sessions over a lifetime results in significant gains in VO2max, SV and heart rate regulation during exercise; however, improved SV regulation during exercise is not coupled with favorable effects on LV filling, even when the heart is fully loaded.
[Show abstract][Hide abstract] ABSTRACT: Background:
Left ventricular assist devices (LVADs) are now widely accepted as an option for patients with advanced heart failure. First-generation devices were pulsatile, but they had poor longevity and durability. Newer generation devices are nonpulsatile and more durable, but remain associated with an increased risk of stroke and hypertension. Moreover, little is understood about the physiological effects of the chronic absence of pulsatile flow in humans.
Methods and results:
We evaluated patients with pulsatile (n=6) and nonpulsatile (n=11) LVADs and healthy controls (n=9) during head-up tilt while measuring hemodynamics and muscle sympathetic nerve activity. Patients with nonpulsatile devices had markedly elevated supine and upright muscle sympathetic nerve activity (mean±SD, 43±15 supine and 60±21 bursts/min at 60° head-up tilt) compared with patients with pulsatile devices (24±7 and 35±8 bursts/min; P<0.01) and controls (11±6 and 31±6 bursts/min; P<0.01); however, muscle sympathetic nerve activity was not different between patients with pulsatile flow and controls (P=0.34). Heart rate, mean arterial pressure, and total peripheral resistance were greater, whereas cardiac output was smaller, in LVAD patients compared with controls in both supine and upright postures. However, these hemodynamic variables were not significantly different between patients with pulsatile and nonpulsatile flow.
Heart failure patients with continuous, nonpulsatile LVADs have marked sympathetic activation, which is likely due, at least in part, to baroreceptor unloading. We speculate that such chronic sympathetic activation may contribute to, or worsen end-organ diseases, and reduce the possibility of ventricular recovery. Strategies to provide some degree of arterial pulsatility, even in continuous flow LVADs may be necessary to achieve optimal outcomes in these patients.
[Show abstract][Hide abstract] ABSTRACT: Doppler ultrasound measures of left ventricular (LV) active relaxation and diastolic suction are slowed with healthy aging. It is unclear to what extent these changes are related to alterations in intrinsic LV properties and/or cardiovascular loading conditions. Seventy carefully screened individuals (38 female, 32 male) aged 21-77 were recruited into four age groups (young: <35; early middle age: 35-49; late middle age: 50-64 and seniors: ≥65 yr). Pulmonary capillary wedge pressure (PCWP), stroke volume, LV end-diastolic volume, and Doppler measures of LV diastolic filling were collected at multiple loading conditions, including supine baseline, lower body negative pressure to reduce LV filling, and saline infusion to increase LV filling. LV mass, supine PCWP, and heart rate were not affected significantly by aging. Measures of LV relaxation, including isovolumic relaxation time and the time constant of isovolumic pressure decay increased progressively, whereas peak early mitral annular longitudinal velocity decreased with advancing age (P < 0.001). The propagation velocity of early mitral inflow, a noninvasive measure of LV suction, decreased with aging with the greatest reduction in seniors (P < 0.001). Age-related differences in LV relaxation and diastolic suction were not attenuated significantly when PCWP was increased in older subjects or reduced in the younger subjects. There is an early slowing of LV relaxation and diastolic suction beginning in early middle age, with the greatest reduction observed in seniors. Because age-related differences in LV dynamic diastolic filling parameters were not diminished significantly with significant changes in LV loading conditions, a decline in ventricular relaxation is likely responsible for the alterations in LV diastolic filling with senescence.
[Show abstract][Hide abstract] ABSTRACT: This study examined the effectiveness of a short-duration but high-intensity exercise countermeasure in combination with a novel oral volume load in preventing bed rest deconditioning and orthostatic intolerance. Bed rest reduces work capacity and orthostatic tolerance due in part to cardiac atrophy and decreased stroke volume. Twenty seven healthy subjects completed 5 wk of -6 degree head down bed rest. Eighteen were randomized to daily rowing ergometry and biweekly strength training while nine remained sedentary. Measurements included cardiac mass, invasive pressure-volume relations, maximal upright exercise capacity, and orthostatic tolerance. Before post-bed rest orthostatic tolerance and exercise testing, nine exercise subjects were given 2 days of fludrocortisone and increased salt. Sedentary bed rest led to cardiac atrophy (125 ± 23 vs. 115 ± 20 g; P < 0.001); however, exercise preserved cardiac mass (128 ± 38 vs. 137 ± 34 g; P = 0.002). Exercise training preserved left ventricular chamber compliance, whereas sedentary bed rest increased stiffness (180 ± 170%, P = 0.032). Orthostatic tolerance was preserved only when exercise was combined with volume loading (-10 ± 22%, P = 0.169) but not with exercise (-14 ± 43%, P = 0.047) or sedentary bed rest (-24 ± 26%, P = 0.035) alone. Rowing and supplemental strength training prevent cardiovascular deconditioning during prolonged bed rest. When combined with an oral volume load, orthostatic tolerance is also preserved. This combined countermeasure may be an ideal strategy for prolonged spaceflight, or patients with orthostatic intolerance.
[Show abstract][Hide abstract] ABSTRACT: Peak oxygen uptake (VO(2)) is diminished in patients with heart failure with preserved ejection fraction (HFpEF) suggesting impaired cardiac reserve. To test this hypothesis, we assessed the haemodynamic response to exercise in HFpEF patients.
Eleven HFpEF patients (73 ± 7 years, 7 females/4 males) and 13 healthy controls (70 ± 4 years, 6 females/7 males) were studied during submaximal and maximal exercise. The cardiac output (Q(c), acetylene rebreathing) response to exercise was determined from linear regression of Q(c) and VO(2) (Douglas bags) at rest, ∼30% and ∼60% of peak VO(2), and maximal exercise. Peak VO(2) was lower in HFpEF patients than in controls (13.7 ± 3.4 vs. 21.6 ± 3.6 mL/kg/min; P < 0.001), while indices of cardiac reserve were not statistically different: peak cardiac power output [CPO = Q(c) × mean arterial pressure (MAP); HFpEF 1790 ± 509 vs. controls 2119 ± 581 L/mmHg/min; P = 0.20]; peak stroke work [SW = stroke volume (SV) × MAP; HFpEF 13 429 ± 2269 vs. controls 13 200 ± 3610 mL/mmHg; P = 0.80]. The ΔQ(c)/ΔVO(2) slope was abnormally elevated in HFpEF patients vs. controls (11.2 ±3.6 vs. 8.3 ± 1.5; P = 0.015).
Contrary to our hypothesis, cardiac reserve is not significantly impaired in well-compensated outpatients with HFpEF. The abnormal haemodynamic response to exercise (decreased peak VO(2), increased ΔQ(c)/ΔVO(2) slope) is similar to that observed in patients with mitochondrial myopathies, suggesting an element of impaired skeletal muscle oxidative metabolism. This impairment may limit functional capacity by two mechanisms: (i) premature skeletal muscle fatigue and (ii) metabolic signals to increase the cardiac output response to exercise which may be poorly tolerated by a left ventricle with impaired diastolic function.
European Journal of Heart Failure 12/2011; 13(12):1296-304. DOI:10.1093/eurjhf/hfr133 · 6.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Sedentary aging leads to increased cardiovascular stiffening, which can be ameliorated by sufficient amounts of lifelong exercise training. An even more extreme form of cardiovascular stiffening can be seen in heart failure with preserved ejection fraction (HFpEF), which comprises ~40~50% of elderly patients diagnosed with congestive heart failure. There are two major interrelated hypotheses proposed to explain heart failure in these patients: 1) increased left ventricular (LV) diastolic stiffness and 2) increased arterial stiffening. The beat-to-beat dynamic Starling mechanism, which is impaired with healthy human aging, reflects the interaction between ventricular and arterial stiffness and thus may provide a link between these two mechanisms underlying HFpEF. Spectral transfer function analysis was applied between beat-to-beat changes in LV end-diastolic pressure (LVEDP; estimated from pulmonary artery diastolic pressure with a right heart catheter) and stroke volume (SV) index. The dynamic Starling mechanism (transfer function gain between LVEDP and the SV index) was impaired in HFpEF patients (n = 10) compared with healthy age-matched controls (n = 12) (HFpEF: 0.23 ± 0.10 ml·m⁻²·mmHg⁻¹ and control: 0.37 ± 0.11 ml·m⁻²·mmHg⁻¹, means ± SD, P = 0.008). There was also a markedly increased (3-fold) fluctuation of LV filling pressures (power spectral density of LVEDP) in HFpEF patients, which may predispose to pulmonary edema due to intermittent exposure to higher pulmonary capillary pressure (HFpEF: 12.2 ± 10.4 mmHg² and control: 3.8 ± 2.9 mmHg², P = 0.014). An impaired dynamic Starling mechanism, even more extreme than that observed with healthy aging, is associated with marked breath-by-breath LVEDP variability and may reflect advanced ventricular and arterial stiffness in HFpEF, possibly contributing to reduced forward output and pulmonary congestion.
[Show abstract][Hide abstract] ABSTRACT: A high prevalence of obesity exists in National Football League (NFL) players as determined by body mass index (BMI). It is not established whether increased BMI is associated with a greater prevalence of cardiovascular (CV) risk factors or coronary atherosclerosis in former NFL players than in nonathletes. This study compared CV risk factors and coronary atherosclerosis in retired NFL players to 2 groups of community controls, the population-based Dallas Heart Study and the preventive medicine cohort, the Aerobics Center Longitudinal Study. Retired NFL players (n = 201) were matched for ethnicity, age, and BMI (Aerobics Center Longitudinal Study, age only). CV risk factors were assessed by survey and screening visit. Coronary atherosclerosis was measured by computed tomography as coronary artery calcium (CAC). Compared to population-based controls, retired NFL players had a significantly lower prevalence of diabetes, hypertension, sedentary lifestyle, and metabolic syndrome, yet a higher prevalence of impaired fasting glucose and hyperlipidemia. However, there was no significant difference in the prevalence of detectable CAC (46% vs 48.3%, p = 0.69) or distribution of CAC (0 to 10, 10 to 100, 100 to 400, > or =400, p = 0.11). Comparing retired NFL players to the physically active preventive medicine controls, there was no difference in the amount of CAC. In retired NFL players, age and hyperlipidemia, not body size, were the most significant predictors of CAC. In conclusion, despite their large body size, retired NFL players do not have a greater prevalence of CV risk factors or amount of CAC than community controls.
The American journal of cardiology 10/2009; 104(6):805-11. DOI:10.1016/j.amjcard.2009.05.008 · 3.28 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Low levels (i.e., </=20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload "selectively" cardiopulmonary baroreceptors in humans, since steady-state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20-54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan-Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and -15- and -30-mmHg LBNP for 6 min each. Application of -15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after approximately 15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at -5- and in all at -10-mmHg LBNP. The delay for left ventricular stroke volume to fall at -15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during -15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at -30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., -10 and -15 mmHg) of LBNP in humans. Thus "selective" unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.
[Show abstract][Hide abstract] ABSTRACT: Cardiovascular diseases increase with advancing age, associated with left ventricular and arterial stiffening in humans. In contrast, daily exercise training prevents and/or improves both ventricular and arterial stiffening with ageing. We propose a new approach to quantify the dynamics of the Starling mechanism, namely the beat-to-beat modulation of stroke volume (SV) caused by beat-to-beat alterations in left ventricular filling, which we propose reflects the complex interaction between ventricular and arterial stiffness. We hypothesized that the dynamic Starling mechanism would be impaired with ageing, and that this impairment would be prevented and restored by daily exercise training. Two different approaches were employed: (1) a cross-sectional study to assess the effects of ageing and life-long exercise training; and (2) a longitudinal study to assess the effects of one-year endurance training in the elderly. Spectral transfer function gain between beat-to-beat changes in left ventricular end-diastolic pressure and SV was used as an index of the dynamic Starling mechanism. Gain was significantly lower in the sedentary elderly (70 +/- 3 years) than in both young individuals (27 +/- 6 years) and Masters athletes (68 +/- 3 years), and it was significantly lower in Masters athletes than in young controls (elderly: 0.37 +/- 0.11; Masters athletes: 0.96 +/- 0.55; young: 1.52 +/- 0.42 ml m(-2) mmHg(-1), mean +/- s.d.). Gain increased by 65% after one-year exercise training in the elderly, although the response was quite variable (P = 0.108). These findings suggest that the dynamic Starling mechanism is impaired with human ageing possibly due to ventricular-arterial stiffening. Life-long daily exercise training may minimize this impairment, although the effect may be limited particularly when started later in life.
The Journal of Physiology 05/2008; 586(7):1951-62. DOI:10.1113/jphysiol.2007.143651 · 5.04 Impact Factor