Six male subjects (26.0+3.1 years), performed an exercise regimen of repeated knee extension exercises in an attempt to induce size and strength changes in the quadriceps muscle (thigh). Their left thigh was trained using an isotonic (IST) lifting protocol and the right thigh was trained using an isokinetic (ISK) device. The total amount of torque produced by each protocol was the same and knee extensions were performed at a common velocity (120 deg/sec). Training was performed 3 days per week for a period of 8 weeks. Data were presented as means (±SD) for pre-and post-training values with a level of significance set at P<0.05.Girth measurements, corrected for subcutaneous fat and expressed as thigh volumes (cc), showed a significant hypertrophy of the IST thigh (3300.67+526.67) after training as compared to that of the IST thigh (3044.13±448.50) before training. No significant difference was found between pre-and post-training ISK thigh volumes. Computed tomography (CT) data were also obtained but could not be statistically analyzed because of technical errors.The mean IST (36.0+0.0) and ISK repetitions (64.54±13.61) necessary to produce equal work bouts (based on total torque produced) were significantly different, resulting in a greater training intensity for the isotonic training.Strength gains as measured isotonically and isokinetically were specific to the training mode. The IST thigh showed a significant strength (Kg) gain when tested on an IST device; the ISK thigh did not. However, the ISK thigh gained significant strength (Kg-m) at all testing velocities (60,180 and 240 deg/sec) while the IST thigh did not.These data would indicate: 1) IST training is superior to ISK training for producing hypertrophy of the thigh; 2) IST training is more intense than ISK training for equal workbouts; and 3) strength gains are specific to training and to the mode of testing.

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Left ventricular hypertrophy (LVH), the detection of which is recommended for routine risk prediction by all guidelines, is more prevalent in groups of African ancestry. This is in-part attributed to higher prevalence rates of obesity. The ability to detect LVH using electrocardiographic (ECG) criteria may be modified in groups of African ancestry. The impact of co-existent obesity on the ability to detect ECG-LVH in this ethnic group has not been determined. Moreover, whether estimated glomerular filtration rate (eGFR) or serum C-reactive protein (CRP concentrations are independently associated with LV mass index (LVMI) and can therefore be used to complement ECG criteria for LVH detection is uncertain. ECG voltage criteria for the detection of echocardiographic LVH were evaluated in 661 participants from a community sample of African ancestry (43% obese). Body mass index (BMI) was inversely associated with Sokolow-Lyon (SL) voltages (partial r=-0.27, p<0.0001) and no BMI-Cornell voltage relations were noted (p=0.21). BMI was associated with voltage criteria that incorporate only limb lead recordings (r=0.17-0.23), but these relationships were weaker than BMI-LVMI relations (r=0.36, p<0.01-p<0.0001 for comparisons of r values). All ECG criteria were as strongly related to blood pressure (BP) as LVMI. Sokolow-Lyon voltage-LVMI relations were noted only after adjustments for BMI (p<0.02) and SL voltages showed no performance for LVH detection. Cornell voltages showed significant performance in the non-obese (area under the receiver operating curve [AUC]=0.67±0.04, p<0.0005), but not the obese (AUC=0.56±0.04, p=0.08). ECG criteria which employ limb-lead recordings only (e.g. RaVL) showed better performance in non-obese than obese (AUC=0.75±0.04 and 0.59±0.04 respectively, p<0.005 for comparison) and markedly reduced specificity for LVH detection in obese (76%) than non-obese (92%, p<0.0001) despite similar sensitivities (32 vs 29%). Thus, in groups of African ancestry, obesity contributes toward a poor validity and performance of all voltage criteria for the detection of LVH. None of the current criteria are recommended for use in obesity in groups of African descent. Alternative approaches are required for LVH detection in these groups.In 621 randomly selected participants from the community sample [332 were normotensive (NT)], eGFR was associated with LVMI and LVM in excess of that predicted from stroke work (inappropriate LVM, LVMinappr) in all participants (LVMI: partial r=-0.18, p<0.0001; LVMinappr: partial r=-0.17, p<0.0001) and NT (LVMI: partial r=-0.23,p<0.0001; LVMinappr: partial r=-0.22, p<0.0001) separate from hypertensives. When replacing clinic BP with either aortic systolic BP (applanation tonometry and SphygmoCor software), 24-hour BP, aortic pulse wave velocity (PWV) (applanation tonometry and SphygmoCor software), stroke work (for LVMI), LV end diastolic diameter (LVEDD), or circumferential wall stress in the regression models, eGFR retained strong associations with LVMI (p=0.01 to <0.0001) and LVMinappr (p<0.005 to <0.0001). Thus, strong relationships between eGFR and LVM occur at a community level irrespective of the presence of hypertension and independent of 24-hour and aortic BP, PWV, LVEDD,stroke work and wall stress. The independent relationships between eGFR and LVMI, support the notion that eGFR may be evaluated for LVH detection. In 361 randomly selected participants from a community with a high prevalence of CRP concentrations considered to be high-risk (54.0%), but without cardiovascular or renal disease, serum CRP concentrations were correlated with both LVMI and LVMinappr (p<0.0001). With adjustments for a number of potential confounders including age, systolic BP, waist circumference (or BMI), and glucose control (glycated haemoglobin), the relationships between serum CRP concentrations and both LVMI and LVMinappr (partial r=0.11, p<0.05 for both) persisted. The independent relationship between CRP and LVMI or LVMinappr translated into a higher multivariate-adjusted LVMI and LVMinappr values in the highest as compared to the lowest quartile of CRP (LVMI; highest quartile CRP=48.8±10.7, lowest quartile CRP=45.0±11, p<0.05; LVMinappr; highest quartile CRP=137±24, lowest quartile CRP=127±24, p<0.05). The independent relationships between CRP and LVMI, support the notion that CRP may also be evaluated for LVH detection. In 358 participants from a randomly selected community sample with a high prevalence of obesity (41%), a combination of CRP concentrations and eGFR above or below the median for the sample respectively showed significant performance (AUC=0.61±0.03, p<0.0005), but a low specificity for LVH detection (77%). When eGFR and CRP concentrations were employed to complement RaVL, although the overall performance did not improve (AUC=0.71±0.03, p<0.0005, RaVL alone: AUC=0.70±0.03), the specificity increased (93%) whilst sensitivity (25%) was in-line with previously reported sensitivities for LVH detection using ECG criteria in alternative population samples. Without changing overall performance, eGFR together with RaVL increased the specificity to 88% and CRP concentrations when considered together with RaVL increased the specificity to 87%. Thus, in a community sample where the specificity and performance of ECG criteria for LVH detection are poor, the use of eGFR and/or CRP concentrations to complement ECG criteria increase the specificity without altering the overall performance. In conclusion, the present thesis provides evidence to indicate that current ECG criteria for the detection of LVH are invalid in obese individuals of African ancestry, but that clinical markers of renal dysfunction and systemic inflammation, which are associated with LVMI independent of haemodynamic factors and co-morbidities may be employed to complement ECG criteria to improve the specificity for LVH detection.

M.Sc.(Med.), Faculty of Health Sciences, University of the Witwatersrand, 2010 / The progression from compensated cardiac hypertrophy to decompensation and cardiac failure is accompanied by cardiac dilatation. As cardiac failure has a poor prognosis, it is imperative to prevent the progression to cardiac dilatation and heart failure. In this regard, an understanding of the mechanisms of cardiac dilatation is vital to guide optimal therapy to prevent heart failure. Although a number of factors have been shown to contribute to the development of cardiac dilatation, to date the role of alterations in cardiac myocyte dimensions remains unclear. Hence, the aim of the current study was to determine whether changes in cardiac myocyte dimensions contribute to the process of cardiac dilatation. Methods: Two models of cardiac dilatation in pressure-overload induced cardiac hypertrophy were assessed. One model was a natural progression model, in which 18 spontaneously hypertensive rats (SHR), were assessed at 23 months of age (an age when left ventricular hypertrophy is noted to have progressed to left ventricular decompensation, dilatation and heart failure in approximately 50% of rats). The second model, a pharmacological model, was induced in 14 month old SHR (n=9) by chronic beta-adrenoreceptor activation [0.02mg/kg isoproterenol (ISO) twice daily for 4.5 months]. Chronic beta-adrenoreceptor activation in SHR, enhances the progression from compensated left ventricular hypertrophy to left ventricular dilatation. Nine normotensive Wistar Kyoto (WKY) rats were the controls for both models. Left ventricular dilatation was defined as an increase in left ventricular radius determined at controlled filling pressures using piezo-electric transducers. The classification of rats as being in heart failure was based upon the presence of pleuropericardial effusions and / or atrial thrombi. Cardiac myocytes were isolated and dimensions determined using both light microscopy and flow cytometry. Results: Left ventricular radius was increased in SHR-Failure compared to SHR-Non-Failure (p<0.01), and in SHR-ISO compared to SHR-Control (saline administration) (p<0.01), hence confirming the presence of cardiac dilatation in both models. Although, cardiac myocyte length vi was increased in all SHR groups compared to WKY (p<0.001), no differences were observed between SHR-Failure and SHR-Non-Failure, or between SHR-ISO and SHR-Control. No differences in cell length:width ratios or in cell widths were evident between the groups. The flow cytometry data confirmed the results obtained for cardiac myocyte lengths using microscopy. Moreover, a linear correlation (r=0.46, p=0.002) between flow cytometry and microscopy cardiac myocyte lengths was observed. Importantly, no relationships were evident between left ventricular radius and cardiac myocyte length (r=0.12, p=0.42 and r=0.14, p=0.35 for microscopic and flow cytometry lengths respectively). Conclusion: The results from the present study show that although pressure-overload hypertrophy is associated with lengthening of cardiac myocytes, no further changes occur with cardiac dilatation. Hence, alterations in cardiac myocyte dimensions do not contribute to the development of cardiac dilatation in pressure-overload models.