Functional test measures as risk indicators for low back pain among fixed-wing military pilots.

PURPOSE: The purpose of this study was to find out the risk value of functional fitness test (FFT) results for low back pain (LBP) among fixed-wing military pilots. METHODS: A total of 104 male military pilots were recruited for this study. The study was conducted with a self-administered questionnaire and FFT. The functional tests were performed in the beginning of study (baseline). The questionnaire was carried out at the baseline and 5 years later. RESULTS: The isometric low back endurance test result was associated with physical activity-related LBP experienced 5 years later. Demographic information was not associated with LBP. The prevalence of overall LBP was 71% and the flight-related LBP prevalence was 31% at the baseline. DISCUSSION: Our findings show that LBP among military pilots is a common problem but it is also associated with tasks other than flying. The functional test results were not associated with flight-related LBP but adequate isometric back endurance may have protective role in LBP caused in physical activities. When trying to find the pilots with increased risk of flight-related LBP, a more sensitive set of tests should be considered.

Deep breathing improves blunted baroreflex sensitivity even after 30 years of type 1 diabetes.

AIMS/HYPOTHESES: Cardiovascular autonomic neuropathy is associated with increased morbidity in patients with type 1 diabetes. Although it is conventionally considered to be an organic, irreversible disorder, we previously demonstrated in patients with short-duration type 1 diabetes that reduced baroreflex sensitivity (BRS) could be corrected by slow, deep breathing, indicating a functional component to the disorder. We have now tested whether autonomic abnormalities in long-term diabetes progress to a stage that cannot be modified by functional manoeuvres, indicating a switch towards predominantly organic dysfunction. METHODS: We studied 117 patients with a short duration (8.9 ± 0.1 years) and 37 patients with a long duration (33.7 ± 0.5 years) of type 1 diabetes, 73 healthy controls and 12 heart-transplanted participants (surgical heart denervation). An autonomic score was calculated from autonomic function tests. Spectral analysis of heart rate and blood pressure variability, and BRS, were obtained from recordings during normal (15 breaths per min) and slow, deep (six breaths per min) controlled breathing. RESULTS: BRS was reduced in all patients, but more in patients with a long duration of diabetes or with increasing autonomic involvement, although the effect of duration disappeared after adjustment for age. Slow breathing increased the BRS to the level of the control participants at a normal rate of breathing (15 per min) in all patients except those with an abnormal autonomic score. CONCLUSIONS/INTERPRETATION: Patients with type 1 diabetes have a blunted BRS that in the majority of patients can be restored by slow breathing, irrespective of disease duration. Even after a long duration of diabetes, the abnormal BRS is at least in part of functional origin.

Early autonomic dysfunction in type 1 diabetes: a reversible disorder?

AIMS/HYPOTHESIS: Cardiac autonomic neuropathy is associated with increased morbidity and mortality rates in patients with type 1 diabetes. The prevalence of early autonomic abnormalities is relatively high compared with the frequency of manifest clinical abnormalities. Thus, early autonomic dysfunction could to some extent be functional and might lead to an organic disease in a subgroup of patients only. If this is true, manoeuvres such as slow deep-breathing, which can improve baroreflex sensitivity (BRS) in normal but not in denervated hearts, could also modify autonomic modulation in patients with type 1 diabetes, despite autonomic dysfunction. METHODS: We compared 116 type 1 diabetic patients with 36 matched healthy control participants and 12 heart-transplanted participants with surgically denervated hearts. Autonomic function tests and spectral analysis of heart rate and blood pressure variability were performed. BRS was estimated by four methods during controlled (15 breaths per minute) and slow deep-breathing (six breaths per minute), and in supine and standing positions. RESULTS: Conventional autonomic function tests were normal, but resting spectral variables and BRS were reduced during normal controlled breathing in patients with type 1 diabetes. However, slow deep-breathing improved BRS in patients with type 1 diabetes, but not in patients with surgically denervated hearts. Standing induced similar reductions in BRS in diabetic and control participants. CONCLUSIONS/INTERPRETATION: Although we found signs of increased sympathetic activity in patients with type 1 diabetes, we also observed a near normalisation of BRS with a simple functional test, indicating that early autonomic derangements are to a large extent functional and potentially correctable by appropriate interventions.

Occurrence, predictors, and clinical significance of autonomic neuropathy in NIDDM. Ten-year follow-up from the diagnosis.

Little is known about the occurrence and predictive factors of autonomic neuropathy and its relationship to cardiovascular mortality in NIDDM patients, and no long-term follow-up studies including nondiabetic control subjects are available. A total of 133 patients with newly diagnosed NIDDM (70 men) and 144 control subjects (62 men) were examined at baseline and after 5 and 10 years of follow-up. Deep-breathing tests (baseline, 5-year, and 10-year) and active orthostatic tests (5- and 10-year) were performed. Criteria for autonomic neuropathy were parasympathetic (expiration-to-inspiration ratio /- 30 mmHg in the orthostatic test), and combined autonomic neuropathy (parasympathetic with sympathetic neuropathy). The frequency of parasympathetic neuropathy (NIDDM patients versus control subjects) was 4.9 vs. 2.2% (P = 0.224) at baseline, 19.6 vs. 8.5% (P = 0.017) at 5 years, and 65.0 vs. 28.0% (P < 0.001) at 10 years of follow-up. The frequency of sympathetic neuropathy was 6.8 vs. 5.6% (P = 0.709) at 5 years and 24.4 vs. 9.0% (P = 0.003) at 10 years of follow- up. These figures for combined autonomic neuropathy were 2.1 vs. 1.8% (P = 0.869) at 5 years and 15.2 vs. 4.2% (P = 0.007) at 10 years of follow-up. NIDDM patients with parasympathetic neuropathy at the 10-year examination showed worse glycemic control and higher insulin values than those without parasympathetic neuropathy. Furthermore, in our subjects, women were more prone to have parasympathetic neuropathy than men. Parasympathetic neuropathy at baseline was more frequent in those who died from a cardiovascular cause than those who did not (13 vs. 3%, P = 0.045). Similarly, sympathetic autonomic nervous dysfunction at the 5-year examination predicted the 10-year cardiovascular mortality. In conclusion, the frequency of autonomic neuropathy in NIDDM patients increases sharply with time. The development of autonomic neuropathy is connected with poor glycemic control. Interestingly, a high insulin level seems to have a predictive role in the development of parasympathetic autonomic neuropathy irrespective of obesity and glycemia.

Noninvasive detection of cardiac sympathetic nervous dysfunction in diabetic patients using [123I]metaiodobenzylguanidine.

The association between clinical autonomic dysfunction and myocardial MIBG accumulation was investigated. The study groups comprised 6 male diabetic patients with autonomic neuropathy (ANP+ group), 6 male diabetic patients without autonomic neuropathy (ANP-group), and 6 male nondiabetic control subjects. The mean age was comparable in all groups, and the subjects had no evidence of coronary heart disease. Reduced heart-rate variation in a deep-breathing test was used as a criterion for autonomic neuropathy. Immediately after injection, the peak net influx rate of MIBG to myocardium was significantly (P less than 0.05) reduced in both diabetic groups. At 6 hr after MIBG injection, the MIBG uptake of the myocardium was significantly (P less than 0.05) smaller in the ANP+ group than in the control group. In the ANP- group, the MIBG uptake of the myocardium was between that of the ANP+ group and that of the control group. Our data show that reduced myocardial MIBG accumulation is associated with autonomic dysfunction in diabetic patients, but it can occur to a lesser extent also in diabetic patients without apparent autonomic neuropathy. The measurement of the myocardial MIBG accumulation is a promising new method to detect cardiac sympathetic nervous dysfunction in diabetic patients.

Angiotensinogen gene M235T polymorphism predicts left ventricular hypertrophy in endurance athletes.

OBJECTIVES: We studied whether left ventricular mass in athletes associates with polymorphisms in genes encoding components of the renin-angiotensin system. BACKGROUND: Adaptive left ventricular hypertrophy is a feature of the athlete's heart. However, similarly training athletes develop left ventricular mass to a different extent, suggesting that genetic factors may modulate heart size. METHODS: We measured left ventricular mass by echocardiography in 50 male and 30 female elite endurance athletes aged 25 +/- 4 (mean +/- SD) years. Deoxyribonucleic acid samples were prepared for genotyping of angiotensinogen (AGT) gene M235T polymorphism, angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and angiotensin II type 1 receptor (AT1) gene A1166C polymorphism. RESULTS: The AGT gene M235T genotypes were significantly associated with left ventricular mass independently of blood pressure in both genders (p = 0.0036 for pooled data). TT homozygotes had greater mass compared with MM homozygotes in both men (147 +/- 12 g/m vs. 132 +/- 15 g/m, p = 0.032) and women (121 +/- 12 g/m vs. 101 +/- 13 g/m, p = 0.019). There was a gender difference in the relation between myocardial mass and AGT genotype, MT heterozygotes resembling MM homozygotes among women and TT homozygotes among men. The other studied gene polymorphisms were not associated with left ventricular mass. CONCLUSIONS: Angiotensinogen gene M235T polymorphism is associated with the variability in left ventricular hypertrophy induced by endurance training, with athletes homozygous for the T allele having the largest hearts. We found no association between ACE gene I/D or AT1 gene A1166C polymorphisms and left ventricular mass.

Impaired endothelium-dependent vasodilation in type 2 diabetes. Relation to LDL size, oxidized LDL, and antioxidants.

OBJECTIVE: To search for determinants of endothelial dysfunction in type 2 diabetes. RESEARCH DESIGN AND METHODS: We performed a comprehensive analysis of cardiovascular risk markers and measured blood flow responses to endothelium-dependent (acetylcholine [ACh] and NG-monomethyl-L-arginine) and -independent (sodium nitroprusside [SNP]) vasoactive agents in 30 nonsmoking men with type 2 diabetes (age 51 +/- 1 years, BMI 27.8 +/- 0.4 kg/m2, HbA1c 7.4 +/- 0.3%) and 12 matched normal control men. RESULTS: ACh-induced vasodilation was 37% lower in type 2 diabetic (6.1 +/- 0.5) than in normal subjects (9.7 +/- 1.5 ml.dl-1.min-1, P < 0.01), while flows during SNP were similar (9.1 +/- 0.6 vs. 9.9 +/- 1.3 ml.dl-1.min-1, NS). The ratio of endothelium-dependent vs. -independent flow (ACh:SNP ratio) was 31% lower in type 2 diabetic (0.70 +/- 0.05) than in normal subjects (1.10 +/- 0.18, P < 0.01). Total (2.2 +/- 0.4 vs. 1.3 +/- 0.2 mmol/l, P < 0.05), VLDL, and intermediate-density lipoprotein triglycerides were significantly higher, and the mean LDL particle diameter was significantly smaller in type 2 diabetic than in normal subjects. The lag times for LDL oxidation by Cu2+ in vitro were similar in patients with type 2 diabetes (183 +/- 7) and in normal subjects (183 +/- 9 min, NS). Measured and calculated (sum of concentration of individual antioxidants in serum) total peroxyl radical-trapping capacities (TRAPs) were comparable between the groups. In the patients with type 2 diabetes, LDL size was significantly correlated with endothelium-dependent vasodilation (r = 0.43, P < 0.05), serum triglycerides (r = -0.75, P < 0.001), and the lag time for LDL oxidation in vitro (r = 0.38, P < 0.05). HbA1c was inversely correlated with the lag time for LDL oxidation in vitro (r = -0.41, P < 0.05) and TRAP. CONCLUSIONS: In summary, patients with type 2 diabetes exhibited impaired endothelium-dependent vasodilation in vivo, elevated serum triglycerides, decreased LDL size, and normal antioxidant capacity. Of these parameters, LDL size was significantly correlated with endothelial function.

Predictors of abnormal cardiovascular autonomic function measured by frequence domain analysis of heart rate variability and conventional tests in patients with type 1 diabetes.

OBJECTIVE: Frequency domain analysis of heart rate variability (HRV) is used to assess cardiovascular autonomic function. There are no prospective data on the sensitivity of its various components to glycemia or other diabetes-related risk factors compared with conventional tests and with other complications of diabetes. RESEARCH DESIGN AND METHODS: In 1985, possible risk factors of future complications were determined in 115 children with type 1 diabetes. In 1996, the presence of complications (HRV analysis, conventional tests of autonomic function, urinary albumin excretion rate [UAER], and retinopathy) were assessed in 83 of these patients (age 32 +/- 1 years, duration of diabetes 22 +/- 1 years). RESULTS: Poor glycemic control (measured as lifetime glycemic exposure or HbA1c in 1985) was the most important independent predictor of decreases in all measures of absolute power of HRV (total power [TP] and very low frequency, low frequency [LF], and high frequency [HF] power) and square root of the mean square of R-R interval differences but not of changes of normalized measures or ratios (normalized HF and LF LF/HF). Other significant independent predictors of autonomic dysfunction were late age of onset of diabetes, female sex, and high BMI. To examine the sensitivity of the various tests to glycemia, the patients were divided into tertiles based on lifetime glycemic exposure (A1c months). Glycemic exposure in the tertiles averaged 194 +/- 25 A1c months (20 years of HbA1c 0.8% above normal), 556 +/- 19 A1c months(20 years of HbA1c 2.3% above normal), and 963 +/- 30 A1c months (20 years of HbA1c 4% above normal). Tests of complications that were significantly abnormal in patients already in the lowest tertile and were correlated with glycemia were TP and severity of retinopathy. Of conventional tests, only the ratio of length of R-R intervals during expiration to inspiration (E/I ratio) was significantly related to glycemic exposure, but it required high glycemic exposure (20 years of HbA1c 4% above normal) to be abnormal. UAER was significantly increased only in the highest tertile of glycemic exposure. CONCLUSIONS: TP and retinopathy score were much more sensitive to antecedent glycemia than conventional tests of autonomic function or UAER and were significantly abnormal in patients exposed to approximately 20 years' duration of an HbA1c 0.8% above normal.

Mechanisms of altered hemodynamic and metabolic responses to insulin in patients with insulin-dependent diabetes mellitus and autonomic dysfunction.

Patients with autonomic neuropathy are more susceptible to insulin-induced hypotension than normal subjects, but the mechanisms are unclear. We quantitated the hemodynamic and metabolic effects of two doses of i.v. insulin (1 and 5 mU/kg.min, 120 min each) and several aspects of autonomic function in 28 patients with insulin-dependent diabetes mellitus (IDDM) and in 7 matched normal subjects under standardized normoglycemic conditions. The autonomic function tests included those predominantly assessing the integrity of vagal heart rate control (the expiration inspiration ratio during deep breathing and high frequency power of heart rate variability) and tests measuring sympathetic nervous function (reflex vasoconstriction to cold and blood pressure responses to standing and handgrip). During hyperinsulinemia, heart rate increased less (2 +/- 1 vs. 6 +/- 2 beats/min; P < 0.04) and diastolic blood pressure fell more (-3.1 +/- 1.2 vs. 0.9 +/- 2.1; P = NS) in the patients with IDDM than in the normal subjects. Forearm vascular resistance decreased significantly in the patients with IDDM [by -7.1 +/- 1.4 mm Hg/(mL/dL.min); P < 0.001 for high vs. low dose insulin], but not in the normal subjects (-0.1 +/- 2.5 mm Hg/(mL/dL.min; P = NS). Reflex vasoconstriction to cold was inversely correlated with the decreases in diastolic (r = -0.51; P < 0.005) and systolic (r = -0.59; P < 0.001) blood pressure and forearm vascular resistance (r = -0.53; P < 0.005), but not with the change in heart rate. The expiration inspiration ratio was, however, directly correlated with the insulin-induced change in heart rate (r = 0.63; P < 0.001), but not with diastolic or systolic blood pressure or forearm vascular resistance. Whole body (48 +/- 2 vs. 67 +/- 5 mumol/kg.min; P < 0.005) and forearm (44 +/- 4 vs. 67 +/- 8 mumol/kg.min; P < 0.05) glucose uptake were significantly lower in the IDDM patients than in the normal subjects. The latter could be attributed to a defect in the forearm glucose arterio-venous difference (1.5 +/- 0.1 vs. 2.2 +/- 0.2 mmol/L, respectively; P < 0.01), but not in blood flow. We conclude that both impaired vagal heart rate control and sympathetic nervous dysfunction exaggerate the hemodynamic effects of insulin in patients with IDDM and could contribute to insulin-induced hypotension.

Autoantibodies against oxidized LDL and endothelium-dependent vasodilation in insulin-dependent diabetes mellitus.

We determined whether autoantibodies against oxidized LDL are increased in patients with IDDM, and if so, whether they are associated with endothelial dysfunction in vivo. Autoantibodies against oxidized LDL (ratio of antibodies against oxidized vs. native LDL, oxLDLab) were determined in 38 patients with IDDM (HbA(1c) 8.4+/-0.2%), who were clinically free of macrovascular disease, and 33 healthy normolipidemic subjects (HbA(1c) 5.1+/-0.1%, P<0.001 vs. IDDM). The groups had comparable serum total-, LDL- (2. 9+/-0.1 vs. 2.8+/-0.1 mmol/l, IDDM vs. controls), and HDL-cholesterol concentrations. OxLDLab were 1.5-fold higher in the IDDM patients (1.8+/-0.1) than in the normal subjects (1.2+/-0.1, P<0.001). OxLDLab were correlated with age in normal subjects, but not with age, duration of disease, LDL-cholesterol, HbA(1c) or degree of microvascular complications in patients with IDDM. To determine whether oxLDLab are associated with endothelial dysfunction in vivo, blood flow responses to intrabrachial infusions of acetylcholine, sodium nitroprusside and L-NMMA were determined in 23 of the patients with IDDM (age 33+/-1 years, body mass index 24. 3+/-0.6 kg/m(2), HbA(1c) 8.5+/-0.3%) and in the 33 matched normal males. OxLDLab were 41% increased in IDDM (1.7+/-0.2 vs. 1.2+/-0.1, P<0.01). Within the group of IDDM patients, HbA(1c) but not oxLDLab or LDL-cholesterol, was inversely correlated with the forearm blood flow response to acetylcholine (r=-0.51, P<0.02), an endothelium-dependent vasodilator, but not to sodium nitroprusside (r=0.06, NS). These data demonstrate that oxLDLab concentrations are increased in patients with IDDM, but show that chronic hyperglycemia rather than oxLDLab, is associated with impaired endothelium-dependent vasodilation in these patients.

Myocardial sympathetic nervous dysfunction detected with iodine-123-MIBG is associated with low heart rate variability after myocardial infarction.

UNLABELLED: The association between myocardial sympathetic innervation and heart rate variability after myocardial infarction was studied in a group of 12 men (aged 30-65 yr) 3 mo after their first myocardial infarction. METHODS: Viable myocardium was imaged using 123I-phenylpentadecanoic acid (pPPA). Functioning myocardial sympathetic nervous tissue was imaged using [123I]-metaiodobenzylguanidine (MIBG). Heart rate variability was measured as the ratio of maximum-to-minimum RR intervals in ECG during deep breathing. RESULTS: The patients were divided into normal (n = 6) and low (n = 6) heart rate variability groups. Myocardial infarction size (pPPA defect) was comparable in the normal and low heart rate variability groups. Even the MIBG defect size was not significantly different in the normal and low groups, the portion of viable myocardium with impaired sympathetic innervation (MIBG defect minus pPPA defect) was significantly greater in the low heart rate variability group than in the normal group. CONCLUSION: The extent of viable myocardium with disturbed sympathetic innervation was greater in patients with low heart rate variability as compared to those with normal heart rate variability 3 mo after myocardial infarction.

Sympathetic reinnervation after acute myocardial infarction.

Myocardial infarction produces sympathetic denervation of the necrotic myocardium and noninfarcted myocardium apical to the injury. Proof of sympathetic reinnervation after myocardial infarction has, however, remained elusive. In this study, we investigated whether cardiac sympathetic reinnervation occurs in men recovering from myocardial infarction. I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid, and Tc-99m sestamibi scintigraphic imaging were conducted in 13 men 3 and 12 months after a first myocardial infarction to determine the extent of denervated myocardium, the size of the infarct, and the size of the myocardium with reduced perfusion, respectively. A defect was determined as regional uptake of < or = 30% of the maximal myocardial activity. The size of the MIBG defect was not significantly different between 3 and 12 months after infarction (17 +/- 8% and 18 +/- 8% of left ventricular mass, respectively). There was also no significant change in the extent of viable but denervated myocardium at 3 and 12 months (average 9 +/- 6% and 10 +/- 5%, respectively). MIBG activity of the infarct zone (expressed as a percentage of MIBG activity of the myocardium with normal perfusion) did not change (17 +/- 13% and 20 +/- 16%), whereas MIBG activity of the periinfarct zone increased during follow-up (32 +/- 11% and 41 +/- 14%, p < 0.01). This was associated with an increase in periinfarct I-123 paraphenylpentadecanoic acid activity (40 +/- 11% and 48 +/- 9%, p < 0.05), but not Tc-99m sestamibi activity (48 +/- 10% and 48 +/- 11%). In conclusion, we did not observe sympathetic reinnervation in the infarct zone between 3 and 12 months after myocardial infarction. However, MIBG activity of the periinfarct zone increased, suggesting partial reinnervation, and this was associated with a recovery of myocardial metabolic activity of the periinfarct zone.

Extent of cardiac autonomic denervation in relation to angina on exercise test in patients with recent acute myocardial infarction.

According to the current concept, anginal pain results from stimulation of sympathetic nerves within the heart. In this study, we evaluated the role of cardiac adrenergic denervation in exercise-induced angina pectoris in 15 men with recent acute myocardial infarction. Before discharge from the hospital, the patients were subjected to a symptom-limited exercise test. Three months after the infarction, cardiac scintigraphic studies using I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid (pPPA), and Tc-99m sestamibi (MIBI) were performed in order to determine the extent of denervated myocardium, the size of infarction, and myocardium with reduced perfusion, respectively. MIBG defect (17.2 +/- 7.6% of left ventricular mass) (defect defined as an activity distribution < or = 30% of the maximal myocardial activity) was larger than pPPA defect (8.3 +/- 8.8%, p < 0.001) in all patients, which indicates that the area of myocardial necrosis was surrounded by viable myocardium with sympathetic denervation. The extent of viable but denervated myocardium was significantly greater in patients who developed angina pectoris than in patients without angina pectoris during the early exercise test (13.3 +/- 4.4% vs 5.0 +/- 2.4%, p < 0.001). In addition, patients with silent ischemia tended to have smaller areas of viable but denervated myocardium than patients with painful ischemia (5.7 +/- 3.8% vs 13.8 +/- 5.1%, p = 0.07). Thus, contrary to expectations, the extent of viable but denervated myocardium seems to be associated with increased pain sensitivity in patients with recent myocardial infarction.

QT interval and QT dispersion in endurance athletes and in power athletes using large doses of anabolic steroids.

We measured electrocardiographic repolarization indexes in athletes. Physiologic adaptive cardiac hypertrophy did not increase QT dispersion in endurance athletes despite long QT intervals due to increased vagal tone. In contrast, power athletes taking large doses of anabolic steroids had increased QT dispersion despite short QT intervals, which seems to reflect altered myocardium in the hypertrophied heart.

Blood pressure reactivity in patients with neurocirculatory asthenia.

The hemodynamic reactions of 30 young men with neurocirculatory asthenia (NCA) were compared to those of 30 healthy controls in isometric handgrip test, orthostatic test, and cold pressor test in order to study the regulation of the central circulation of NCA patients. The measurements were made using sphygmomanometry, ECG, and impedance cardiography. In the isometric handgrip test the heart rate and the diastolic and mean blood pressure increased slightly more (P less than 0.05) in the NCA group than in the controls. In the NCA group the blood pressure rise was, on average, due to an increase in the peripheral vascular resistance, while in the control group it was caused by an elevation in the cardiac output. In the orthostatic and cold pressor tests the hemodynamic alterations were quite similar in the two groups. It is concluded that the NCA patients have in the orthostatic and cold pressor tests a normal ability to elevate the blood pressure by increasing the peripheral vascular resistance. The lack of rise in the cardiac output during the isometric handgrip test in the NCA group is an abnormal reaction, the reason of which remains to be studied.

Left ventricular mass, geometry, and filling in endurance athletes: association with exercise blood pressure.

We studied whether left ventricular (LV) mass and concentricity [relative myocardial volume (RMV)] are associated with exercise blood pressure (BP) in athletes. LV structure and filling were evaluated by Doppler echocardiography and BP in maximal bicycle ergometry and isometric handgrip tests on 32 male endurance athletes and 15 age-matched controls. Indexed LV mass was 145 +/- 14 (SD) g/m in athletes and 93 +/- 20 g/m in controls. Mass was not associated with BP at rest or in low-grade exercise, but with heavier exercise loads this association strengthened in athletes, being maximal at peak exercise (r = 0.65 for mass and 0.58 for indexed mass; P < 0.001). Multivariate analysis indicated that BP at peak exercise accounted for 34% and the amount of training for an additional 11% of the variance in indexed LV mass. RMV was 21% larger in athletes. Only the increase in systolic BP during handgrip explained significantly (19%) the variance in RMV. LV filling velocities were not associated with mass, RMV, or BP. We conclude that in endurance athletes LV mass is associated with BP in heavy dynamic exercise and LV concentricity with BP response in static exercise.

Serum total renin, an independent marker of the activity and severity of retinopathy in patients with IDDM.

BACKGROUND/AIMS: Recent studies have demonstrated marked renin and prorenin concentration gradients between ocular tissues and blood, and local expression of the renin-angiotensin system (RAS) in the eye. The authors determined whether serum total renin, which mostly consists of prorenin, is a marker of the activity and severity of diabetic retinopathy independent of other microvascular complications. METHODS: Total renin concentrations (TRC) were measured with a time resolved immunofluorometric assay in 38 patients with IDDM (age 34 (SD 7) years, duration of disease 22 (7) years, serum creatinine 95 (15) mumol/l, urinary albumin excretion rate (UAER) 207 (829) micrograms/min, HbA1c 8.5% (1.2%)), and in 13 matched normal subjects. All subjects were carefully characterised with respect to the presence and severity of retinopathy (RP score), nephropathy, and neuropathy using seven different tests of autonomic neuropathy. RESULTS: Serum TRC was on average twofold higher in IDDM (396 (SE 211) ng/l) than in normal subjects (201 (88) ng/l, p < 0.001). It was nearly twofold higher in patients with preproliferative or active proliferative retinopathy requiring careful follow up or therapy (TRC 596 (268) ng/l, n = 11) compared with those with quiescent proliferative retinopathy after laser treatment (TRC 338 (183) ng/l, p < 0.01, n = 5); moderately severe non-proliferative retinopathy (337 (106) ng/l, p < 0.01, n = 13), no retinopathy, or only minimal non-proliferative retinopathy (270 (43) ng/l, p < 0.001, n = 9). In multiple linear regression analysis, RP score (p < 0.01), but not the UAER or any index of autonomic neuropathy, was an independent determinant of serum TRC, and explained 32% of its variation (R = 0.57, p < 0.005). CONCLUSIONS: Serum TRC in patients with diabetic retinopathy is increased independent of renal function and autonomic neuropathy especially in those with severe active changes requiring careful follow up or treatment. These findings support the idea that diabetic retinopathy is the most important determinant of serum TRC in patients with IDDM, and that TRC is produced when retinopathy is active.

Individual relationship between heart rate and electromechanic systole in orthostatic test during autonomic blockade.

The aim of this work was to investigate the usefulness of the individual regression coefficients between the HR and the Q-A2 when studying their relationship during simultaneous changes in afterload and preload in combination with autonomic blockade. Twelve healthy male volunteers were studied in an orthostatic test done four times: without drugs (control test), after atropinization, after beta-blockade, as well as after combined beta-blockade and atropinization. The individual regression coefficients showed great inter-individual variation, and in average they were not significantly different in the four tests. However, it was observed that during the control test four, during the atropinization eight, during the beta-blockade three and during the combined beta-blockade and atropinization five individual regression coefficients were greater than -2.1, which is the regression coefficient used for the rate correction of the Q-A2 in males in the Weissler formula. It seems to use that the individual regression coefficents are useful in the evaluation of the relationship between the HR and the Q-A2 in pharmacological or physiological interventions, in which the intra-individual variation is great, and in which the number of subjects is often so small that group regressions are not very informative.

Microcomputer-based monitoring of cardiovascular functions in simulated microgravity.

A microcomputer-based system for non-invasive monitoring of cardiovascular system in simulated microgravity is described. The system evaluates automatically, accurately and interactively heart beat intervals, beat-to-beat non-invasive finger arterial blood pressure (systolic, diastolic, mean and pulse pressure) using a Finapres device and beat-to-beat changes of thoracic blood volume using impedance changes. In addition, beat-to-beat evaluation of cardiac mechanical function including left ventricular ejection time, diastolic time, systolic time intervals, left ventricular ejection fraction estimate and several other contractility parameters, left ventricular volume, stroke volume and cardiac output estimates are performed with high degree of automaticity.

Hormonal responses to 100 km cross-country skiing during 2 days.

AIM: The purposes of this study were to investigate the resting levels and the acute hormonal responses of serum testosterone and cortisol, and with time-resolved immunofluorometric assay of luteinising hormone (LH) and follicle stimulating hormone (FSH), to daily repeated prolonged skiing. METHODS: Quasi-experimental design: short-term follow-up, (reversal) field trial to investigate the daily responses of blood hormones to repeated 50 km skiing during 2 days in men. PARTICIPANTS: 10 physically active men (34.8+/-9.7 y, 1.82+/-0.05 m, 76.1+/-6.6 kg, BMI: 23.0+/-1.5 kg.m(-2)) participating in the Finlandia Ski Race, covering a total distance of 100 km during 2 days. MEASURES: venous blood samples were obtained before and after skiing, and after 1 week's recovery, to determine the concentrations of testosterone, LH, FSH and cortisol in the blood. RESULTS: Testosterone was reduced by over 20% after both days (p=0.016 and 0.002, respectively). LH decreased after the 1( st) race by 37% and after the 2nd race by 44% (p=0.028, both). FSH secretion was stable and cortisol increased 2.2- and 2.6-fold after the races (p<0.001). CONCLUSIONS: The participants in the 2 days' prolonged skiing exercise went through a period of heavy physical stress. They showed changes in their serum testosterone, LH and cortisol concentrations, which, with the exception of the FSH secretion, alter the acute responses of both the adrenal cortex and the hypothalamus-pituitary-testicular axis. When training or competition programmes are planned it should taken into consideration that daily repeated high intensity prolonged skiing without a recovery day may cause hormonal overreaching.