Ehud Goldhammer

Exercise Training Improves Diastolic Function in Heart Failure Patients

PURPOSE The studys purpose was to analyze the effects of exercise training on exercise tolerance and left ventricular systolic function and structure in heart failure patients with preserved, mild, and moderate to severe reduction of left ventricular ejection fraction (LVEF). METHODS Ninety-eight patients with moderate to severe (n = 34), mild (n = 33), and preserved (n = 31) LVEF were randomly assigned to exercise training plus usual care (n = 65) or usual care alone (n = 33) in a randomization ratio of 2:1. Left ventricular function, left ventricular dimensions, and exercise tolerance were assessed before and after each intervention. RESULTS Exercise tolerance and LVEF increased with exercise training in all patient groups, whereas they remained unchanged after usual care alone. Exercise training increased the mean ratio of early to late mitral inflow velocities (E/A ratio) and decreased deceleration time (DT) of early filling in patients with mild and preserved LVEF. In patients with moderate to severe systolic dysfunction and advanced diastolic dysfunction (DT < 160 ms), exercise training decreased E/A ratio and increased DT, both of which were unchanged after usual care alone. In the remaining patients (DT > 160 ms), exercise training also improved mitral inflow patterns. Exercise training decreased left ventricular dimensions in patients with mild and moderate to severe reduction of LVEF but not in patients with preserved LVEF. CONCLUSIONS These results indicate that exercise training can improve the course of heart failure independent of the degree of baseline left ventricular dysfunction.

Dilated Inferior Vena Cava: A Common Echocardiographic Finding in Highly Trained Elite Athletes☆☆☆

Typical structural features of the athletes heart as defined by echocardiography have been extensively described; however, information concerning extracardiac structures such as the inferior vena cava (IVC) is scarce. Fifty-eight top-level athletes and 30 healthy members of a matched control group underwent a complete Doppler echocardiographic study. IVC diameter was determined in the subxiphoid approach 10 to 20 mm away from its junction to the right atrium. Measures reflect the median values between maximal inspiratory and expiratory values. IVC respiratory collapsibility index was determined as well. IVC in athletes was 2.31 +/- 0.46 cm compared with 1.14 +/- 0.13 cm in the control group (P <.001). Swimmers had an IVC diameter of 2.66 +/- 0.48 cm compared with 2.17 +/- 0.41 cm in other athletes (P <.05). The IVC was normal (/=2.6 cm) in 24.1% of athletes. The collapsibility index was 58% +/- 6.4% in athletes compared with 70.2% +/- 4.9% in the control group (P <. 001). Correlation was found between IVC size and VO(2) max (r = 0.81, P <.001) and the right ventricle (r = 0.81, P <.001) and with collapsibility index (r = -0.57, P <.05). Multiple regression analysis showed the impact of VO(2) max, cardiac index, and right ventricular and left ventricular end-diastolic dimensions on IVC diameter. IVC dilatation probably represents adaptation of an extracardiac structure to chronic strenuous exercise in top-level, elite athletes.

Is there an interaction between PPARD T294C and PPARGC1A Gly482Ser polymorphisms and human endurance performance

Functional Gly482Ser (rs8192678) and T294C (rs2016520) polymorphisms in the peroxisome proliferator‐activated receptor γ coactivator‐1 (PPARGC1A) and peroxisome proliferator‐activated receptor δ (PPARD) genes, respectively, have been associated with mRNA and/or protein activity. The aim of this study was to determine their frequency distribution among 155 Israeli athletes (endurance athletes and sprinters) and 240 healthy control subjects. There were no differences between the endurance athletes, the sprinters and the control group across the PPARD T294C genotypes (P= 0.62). Similarly, no statistical differences were found between the subgroups of elite‐level endurance athletes (those who had represented Israel in a world track and field championship or in the Olympic Games) and national‐level endurance athletes (P= 0.3), or between elite‐level and national‐level sprinters (P= 0.9). However, a combined influence of these two polymorphisms on endurance performance was found. The PPARD CC +PPARGC1A Gly/Gly genotypes were more frequently found in the elite endurance athletes than in national‐level endurance athletes (P < 0.000). In the cohort of endurance athletes, the odds ratio of the ‘optimal genotype’ for endurance athletes (PPARD CC +PPARGC1A Gly/Gly +PPARGC1A Gly/Ser) being an elite‐level athlete was 8.32 (95% confidence interval 2.2–31.4). In conclusion, the present study suggests that PPARD T294C is not associated with endurance performance. However, a higher frequency of the PPARGC1A Gly/Gly +PPARD CC genotype is associated with elite‐level endurance athletes.

Left ventricular contractility and function at peak aerobic and anaerobic exercises.

PURPOSE The present study compared and evaluated left ventricular function and contractility at peak incremental aerobic type exercise and all-out explosive anaerobic effort in young healthy trained subjects. METHODS Twenty-two young healthy trained subjects (19 +/- 1 yr) were studied by two-dimensional direct M-mode echocardiography at peak aerobic and at peak all-out anaerobic exercises, performed on cycle ergometer. RESULTS All subjects completed the study without any electrocardiographic abnormalities. Significant (P < 0.05) differences between the aerobic and the anaerobic efforts were noted for peak cardiac output (24 +/- 2.0 and 15.0 +/- 1.1 L x min (-1), respectively), left ventricular pressure-volume ratio (5.8 +/- 0.6 and 4.7 +/- 0.5 respectively), end systolic volume (33 +/- 4 and 42 +/- 5 mL, respectively), ejection fraction (79 +/- 7 and 66 +/- 5%, respectively), and total peripheral resistance (TPR) (367 +/- 90 and 704 +/- 90 dynes x s(-1) x cm(- 5), respectively). CONCLUSIONS These data suggest that left ventricular at peak all out anaerobic effort differed markedly from those observed at peak aerobic exercise. These differences are presumably due to the different after-load responses between the two exercise modes. Therefore, it is suggested that anaerobic-type effort should be performed with great caution in normal young healthy subjects.

Paraoxonase activity following exercise-based cardiac rehabilitation program.

PURPOSE: The effect of gender on paraoxonase activity was determined in 37 ischemic heart disease patients who underwent a 12-week aerobic exercise training program. METHODS: Paraoxonase activity was measured by its arylesterase activity (spectrophotometrically, at 250°C, wavelength 270 nm). RESULTS: A 16.7% increase in paraoxonase activity was found following the 12-week exercise program. In addition, there was a significant gender effect with higher mean paraoxonase levels among women during both preexercise (20.8%) and postexercise (24.2%) testing. CONCLUSIONS: Aerobic exercise training was found to be an effective means in inducing plasma levels elevation of the antioxidative, antiatherogenic paraoxonase in patients with coronary artery disease, and particularly in female patients.

Is there an ACE ID-ACTN3 R577X polymorphisms interaction that influences sprint performance?

Functional R577X (rs.1815739) and ID (rs.5186) polymorphisms in the alpha-actinin-3 ( ACTN3) and the angiotensin converting enzyme (ACE) genes, respectively, have been associated with sprint performance. The aim of this study was to determine their effect on sprint performance among 81 Israeli sprinters and 240 healthy controls. Results revealed that the ACE II genotype+ ACTN3 R allele (P=0.003 for sprinters vs. controls), and the ACTN3 RR genotype +ACE I allele (P=0.001 for sprinters vs. controls) might be the genotype for sprinters. In the whole cohort the probability of ACTN3 RR genotype+ ACE I allele being a sprinter (odds ratio 2.67, 95% confidence interval 1.45-4.93) and of ACE II genotype+ ACTN3 R allele being a sprinter (odds ratio 3.57, 95% confidence interval 1.78-7.15) was significantly higher than that in the controls. In conclusion, the above data suggest that ACE ID/ ACTN3 R577X genotype combination is associated with sprint ability. However, ACE ID/ ACTN3 R577X genotype combination is not related to the level of performance.

Effects of low altitude on exercise performance in patients with congestive heart failure after healing of acute myocardial infarction

Patients with chronic congestive heart failure (CHF) have impaired oxygen delivery to working muscles. The Dead Sea, the lowest site on earth, is distinguished by natural oxygen enrichment, low humidity, high barometric pressure, and temperature with increased bromide and magnesium concentrations in the inspired air. The aim of this study is to examine the effects of descent to the Dead Sea on patients with CHF. Twelve patients with CHF and 4 age-matched healthy controls underwent complete echocardiographic studies at rest as well as treadmill and metabolic stress tests, both in Haifa, 130 m above sea level and 3 days after descent to the Dead Sea, 402 m below sea level. Significant changes in parameters at the Dead Sea compared with Haifa included time on treadmill, which increased from 612+/-198 to 672+/-1 86 seconds (p <0.05); the Borg scale decreased by 1 to 2 grades (p <0.05); and oxygen saturation increased by 3% throughout exercise (p <0.05). Systolic blood pressure decreased by 9 mm Hg at rest (p <0.05) and increased by 14 mm Hg at peak exercise at the Dead Sea in patients with CHF (p <0.05). Cardiac output at rest increased by 300 ml/min (p <0.05). Maximum oxygen consumption (VO2max) increased by 126 ml/ min (p <0.05), and even more so in patients with more severe exercise-induced oxygen desaturations, which was associated with lower peak minute ventilation to CO2 production ratio (p <0.05). Thus, descent to the Dead Sea acutely improved exercise performance due to better oxygenation and loading conditions in patients with CHF.

Left ventricular function during strength testing and resistance exercise in patients with left ventricular dysfunction.

PURPOSE Deterioration in left ventricular function is a more sensitive marker of myocardial ischemia during exercise than ST segment depression. The current study was designed to evaluate left ventricular function during one-repetition-maximum (1-RM) strength testing and resistance exercise in cardiac patients with moderate left ventricular dysfunction. METHODS Using echocardiographic methods, left ventricular function was evaluated in 15 patients with left ventricular dysfunction (age, 65 +/- 6.5 years; ejection fraction, 42.1 +/- 5.8). Measurements were performed during 1-RM testing and resistance exercise (20%, 40%, and 60% of 1-RM using 10 to 15 repetitions) on the one-arm biceps curl (BIC) and bilateral knee extension exercises and compared with measurements of left ventricular function during the symptom-limited graded exercise test (SL-GXT). RESULTS During the knee extension exercise, there was a slight but significant reduction (P< or =.05) in ejection fraction values at the end of 60% 1-RM, as compared with rest and previous workloads. Significant increases in systolic blood pressure and left ventricular end-systolic volume ratio values (P< or =.05) from rest to exercise were observed across test modes and for all workloads. The prevalence of new wall motion abnormalities during knee extension and BIC 1-RM strength testing was comparable with that observed during SL-GXT. The greatest increase in new wall motion abnormalities was seen during 60% 1-RM of knee extension exercise, as compared with prior workloads, BIC exercises, and SL-GXT. CONCLUSIONS Despite an increase in occurrence of ischemic changes during the highest resistance exercise workloads and with larger muscle mass, the findings are small in magnitude and do not suggest reduced cardiac performance.

An exercise hemodynamic comparison of verapamil, diltiazem, and amlodipine in coronary artery disease

SummaryA prospective, randomized study compared the effects of equivalent intravenous doses of three slow calciumchannel blockers (verapamil, diltiazem, and amlodipine) on rest and exercise haemodynamics in 30 ischemic heart disease patients. Following a stable control period during which rest and exercise (supine bicycle) hemodynamics were assessed, equivalent hypotensive doses of each compound were administered over 20 minutes and rest/exercise parameters were assessed 10 minutes later. At rest all agents similarly reduced systemic blood pressure; the fall in systemic vascular resistance and the increase in cardiac indices was ranked: amlodipine > diltiazem > verapamil. The heart rate increase for amlodopine differed from verapamil and diltiazem (+19.4% vs. +1.5% vs. −7%; p<0.01).On exercise, similarly greater falls in the systemic vascular resistance index followed amlodipine, compared with verapamil and diltiazem (p<0.05). Only amlodipine significantly reduced the exercise pulmonary artery occlusion pressure (PAOP). Exercise cardiac stroke volume improved after diltiazem and amlodipine. In terms of cardiac performance, both amlodipine and diltiazem produced an improvement, whereas verapamil depressed cardiac pumping activity. Thus, hemodynamic differences between slow-calcium-channel blocking drugs may be demonstrated in humans. These differences would be compatible with a predominant peripheral vascular site of action for amlodipine, in contrast with mixed cardiac and peripheral sites for diltiazem and verapamil.

The effect of long-term beta-adrenergic receptor blockade on the oxygen delivery and extraction relationship in patients with coronary artery disease.

PURPOSE We evaluated the effects of long-term β-blocker treatment on the balance between oxygen delivery and extraction at peak oxygen uptake (VO2) and at target heart rate training (anaerobic threshold). METHODS Fifteen patients with coronary artery disease performed paired peak cardiopulmonary and submaximal exercise tests on a cycle ergometer with and without atenolol treatment. Thirty minutes following the submaximal tests, participants pedaled 10 minutes at a workload corresponding to that of the anaerobic threshold attained. Arterial oxygen was defined from echocardiography and venous oxygen content. RESULTS At rest, stroke volume, heart rate, and cardiac output were lower (P < .05), whereas arteriovenous oxygen difference [(a − v)O2] was higher with the use of atenolol (P < .05). At peak exercise, heart rate, lactate, and systolic blood pressure were lower (P < .05), whereas (a − v)O2 was higher (P < .05) with the use of atenolol. At anaerobic threshold, stroke volume, heart rate, cardiac output, and systolic blood pressure were lower (P < .05), whereas (a − v)O2was higher (P < .05) with the use of atenolol. Absolute VO2 and workload during maximal (P = .67 and P = .49, respectively) and submaximal (P = .13 and P = .44, respectively) exercises were similar between conditions. CONCLUSIONS Results demonstrate that atenolol treatment in patients with coronary artery disease does not alter VO2 and workload at the anaerobic threshold and peak exercise because of an increase in oxygen extraction and stroke volume in the face of reduced heart rate. These findings indicate that with long-term β-adrenergic receptor blockade, there is interplay between oxygen delivery and extraction, suggesting a link between cardiac hemodynamic responses and skeletal muscle metabolic adaptations.