Effects of resistance training on cardiovascular responses to lower body negative pressure in the elderly

The purpose of the present study was to determine whether resistance training alters the cardiovascular responses to submaximal lower body negative pressure (LBNP) in the elderly. Twenty‐one subjects were randomized into a control (C: n=10; 70 ± 3 years, mean ± SD) or a resistance training (TR: n=11; 67 ± 7 years) group. Subjects in the TR underwent 12 weeks of training consisting of three sets of 8–12 contractions at ?60–80% of their initial maximal one repetition, three times per week, on 10 different machines. Before (Pre) and after (Post) training, all subjects underwent exposures of LBNP of ?10, ?20 and ?40 Torr and muscle biopsy sampling at the vastus lateralis. TR increased (P≤0·05) knee extension (Pre=379 ± 140 N, Post=534 ± 182 N) and chest press (Pre=349 ± 137 N, Post=480 ± 192 N) strength. Neither body weight nor percentage body fat were altered (P >0·05) by training. Resistance training increased (P≤0·05) cross‐sectional area in both Type I (4203 ± 1196 to 5248 ± 1728 μm²) and Type II (3375 ± 1027 to 4286 ± 1892 μm²) muscle fibres. Forearm blood flow, forearm vascular conductance, mean arterial pressure, and heart‐rate responses to LBNP were not altered by the training. These data suggest that the cardiovascular responses of elderly to LBNP are unaffected by 12 weeks of whole‐body resistance training despite increases in muscle strength and size.     

Middle cerebral artery blood flow velocity in response to lower body positive pressure

Lower body positive pressure (LBPP) has been used in the treatment of haemorrhagic shock and in offsetting g‐force induced fluid shifts. However, the middle cerebral artery blood flow velocity (MCAv) response to supine LBPP is unknown. Fifteen healthy volunteers (mean ± SD: age, 26 ± 5 year; body mass, 79 ± 10 kg; height, 174 ± 9 cm) completed 5 minutes of 20 and 40 mm Hg LBPP, in a randomized order, separated by 5 minutes rest (baseline). Beat‐to‐beat MCAv and blood pressure, partial pressure of end‐tidal carbon dioxide (P_ETCO₂) and heart rate were recorded and presented as the change from the preceding baseline. All measures were similar between baseline periods (all P>0·30). Mean arterial pressure (MAP) increased by 7 ± 6 (8 ± 7%) and 13 ± 7 mm Hg (19 ± 11%) from baseline during 20 and 40 mm Hg (P<0·01), respectively. The greater MAP increase at 40 mm Hg (P<0·01 versus 20 mm Hg) was mediated via a greater increase in total peripheral resistance (P<0·01), with heart rate, cardiac output (Model flow) and P_ETCO₂ remaining unchanged (all P>0·05) throughout. MCAv increased from baseline by 3 ± 4 cm s^?1 (5 ± 5%) during 20 mm Hg (P = 0·003), whilst no change (P = 0·18) was observed during 40 mm Hg. Our results indicate a divergent response, in that 20 mm Hg LBPP‐induced modest increases in both MCAv and MAP, yet no change in MCAv was observed at the higher LBPP of 40 mm Hg despite a further increase in MAP.     

Changes after arterial reconstruction in the forefoot local vasoconstrictor response to increased venous transmural pressure

Local blood flow regulation on the forefoot was studied by the 133Xe wash-out technique in twenty-seven patients before and after arterial reconstruction for occlusive arterial disease. In thirteen limbs with severe symptoms the local vasoconstrictor response to increased venous pressure was absent preoperatively, as blood flow in the foot increased in median by 47% when the foot was lowered 40 cm below the heart. Three months postoperatively the vasoconstrictor response had returned as blood flow decreased 28% during lowering. Fourteen limbs with milder symptoms had a vasoconstrictor response before operation. In nine limbs of this group treated with aortoiliac reconstruction the vasoconstrictor response was absent at the early postoperative examination, but the response returned till the late examination. It is concluded that the local vasoconstrictor response is normalized after arterial reconstruction. Disturbances may, however, occur in the postoperative period, possibly due to operative stress.     

Influence of arterial wave reflection on carotid blood pressure and intima‐media thickness in older endurance trained men and women with pre‐hypertension

Increased carotid intima‐media thickness (IMT) with aging is a significant predictor of mortality. Older endurance trained (ET) individuals have lower carotid artery stiffness but similar carotid IMT when compared to sedentary (SED) age‐matched peers. The purpose of this study was to examine the contribution of arterial wave reflections to carotid hemodynamics and IMT in older ET and SED with pre‐hypertension. Subjects consisted of endurance‐trained master athletes and age‐matched sedentary controls (mean age 67 years). Carotid artery Beta‐stiffness index and IMT was assessed with ultrasonography. Carotid pressure and augmented pressure from wave reflections (obtained from pulse contour analysis) was measured with applanation tonometry. Carotid systolic blood pressure (SBP) and IMT were not different between groups (P>0·05). Carotid stiffness was significantly lower in ET versus SED (7·3 ± 0·8 versus 9·9 ± 0·6, P<0·05). Augmented pressure was significantly greater in ET versus SED (17·7 ± 1·6 versus 13·3 ± 1·5 mmHg, P<0·05). When adjusting for differences in resting heart rate, there were no group differences in augmented pressure. In conclusion, older ET persons with pre‐hypertension have reduced carotid artery stiffness, but similar carotid SBP and carotid IMT when compared to SED. The lack of change in carotid SBP and IMT in older ET may be related to the inability of chronic exercise training to reduce bradycardia‐related augmented pressure from wave reflections with aging.     

Systemic and Renal Haemodynamics, Body Fluids and Renin in Benign Essential Hypertension with Special Reference to Natural History

Abstract. Forty patients with uncomplicated essential hypertension were investigated with respect to diurnal variability of arterial pressure (indirect recordings), intra-arterial pressure, cardiac output, plasma volume, renal plasma flow and glomerular filtration rate. Extracellular volume was estimated in 17, plasma renin concentration in 33 and vector-cardiograms were recorded in 27 patients. Treatment was discontinued at least a fortnight before and sodium intake was standardized.—Blood pressure varied across a wide range. Variability (lability) of blood pressure was quantified by expressing the difference between highest and lowest automatic blood pressure readings as a percentage of the highest reading. Cardiac output correlated with variability of blood pressure, blood volume and renal blood flow.—Plasma renin concentration was correlated with renal vascular resistance and filtration fraction.— QRS magnitude appeared to be related with the level of arterial pressure.—Haemodynamic variables exhibited a definite relationship with age, deviating in part from distribution according to age in normal populations.