Cardiovascular responses to military antishock trouser inflation during standing arm exercise

Military antishock trousers (MAST) inflated to 50 mmHg were used with 12 healthy males (mean age 28 +/- 1 yr) to determine the effects of lower-body positive pressure on cardiac output (Q), stroke volume (SV), heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MABP), total peripheral resistance (TPR), and O2 uptake (VO2) during graded arm-cranking exercise. Subjects were studied while standing at rest and at 25, 50, and 75% of maximal arm-cranking VO2. At each level, rest or work was continued for 6 min with MAST inflated and for 6 min with MAST deflated. Order of inflation and deflation was alternated at each experimental rest or exercise level. Measurements were obtained during the last 2 min at each level. Repeated-measures analysis of variance revealed significant increases (P less than 0.001) in Q, SV, and MABP and a consistent decrease in HR with MAST inflation. There was no apparent change in Q/VO2 between inflated and control conditions. There was no effect of MAST inflation on VO2 or TPR. MAST inflation counteracts the gravitational effect of venous return in upright exercise, restoring central blood volume and thereby increasing Q and MABP from control. HR is decreased consequent to increased MABP through arterial baroreflexes. The associated decrease in TPR is not observed, being offset by the mechanical compression of leg vasculature with MAST inflation.     

Chronic exercise and its hemodynamic influences on resting blood pressure of hypertensive rats.

Studies with male spontaneously hypertensive rats (SHR) were initiated to determine the hemodynamic relationships associated with the lower resting caudal artery systolic blood pressure (SBP) of endurance-trained SHR populations. After assignment into nontrained (NT, n = 38) and trained (T, n = 38) groups, the T animals were exercised 5 times/wk on a motor-driven treadmill for 12-16 wk at a moderate intensity that ranged from 40 to 70% of their maximum O2 consumption capacity (VO2max). SBP, VO2max, and treadmill run time were determined before the experimental period began and before the animals were instrumented for hemodynamic measurements. At the end of the study, the T rats exhibited significantly lower SBP (NT = 210 +/- 3, T = 200 +/- 3 mmHg) and significantly higher VO2max (NT = 75 +/- 2, T = 83 +/- 2 ml.min-1.kg-1) and run durations (NT = 11.4 +/- 0.4, T = 14.5 +/- 0.3 min). When the animals were anesthetized for insertion of catheters and microprobes for blood pressure and cardiac output (thermodilution) measurements, the T rats had lower values for body mass, heart rate, mean blood pressure, cardiac output, and cardiac index than the NT rats; however, only the body mass and heart rate differences were statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Frequency-dependent baroreflex modulation of blood pressure and heart rate variability in conscious mice

The goal of this study was to determine the baroreflex influence on systolic arterial pressure (SAP) and pulse interval (PI) variability in conscious mice. SAP and PI were measured in C57Bl/6J mice subjected to sinoaortic deafferentation (SAD, n = 21) or sham surgery (n = 20). Average SAP and PI did not differ in SAD or control mice. In contrast, SAP variance was enhanced (21 +/- 4 vs. 9.5 +/- 1 mmHg2) and PI variance reduced (8.8 +/- 2 vs. 26 +/- 6 ms2) in SAD vs. control mice. High-frequency (HF: 1-5 Hz) SAP variability quantified by spectral analysis was greater in SAD (8.5 +/- 2.0 mmHg2) compared with control (2.5 +/- 0.2 mmHg2) mice, whereas low-frequency (LF: 0.1-1 Hz) SAP variability did not differ between the groups. Conversely, LF PI variability was markedly reduced in SAD mice (0.5 +/- 0.1 vs. 10.8 +/- 3.4 ms2). LF oscillations in SAP and PI were coherent in control mice (coherence = 0.68 +/- 0.05), with changes in SAP leading changes in PI (phase = -1.41 +/- 0.06 radians), but were not coherent in SAD mice (coherence = 0.08 +/- 0.03). Blockade of parasympathetic drive with atropine decreased average PI, PI variance, and LF and HF PI variability in control (n = 10) but had no effect in SAD (n = 6) mice. In control mice, blockade of sympathetic cardiac receptors with propranolol increased average PI and decreased PI variance and LF PI variability (n = 6). In SAD mice, propranolol increased average PI (n = 6). In conclusion, baroreflex modulation of PI contributes to LF, but not HF PI variability, and is mediated by both sympathetic and parasympathetic drives in conscious mice.     

Living and training in moderate hypoxia does not improve VO2 max more than living and training in normoxia.

The objective of these experiments was to determine whether living and training in moderate hypoxia (MHx) confers an advantage on maximal normoxic exercise capacity compared with living and training in normoxia. Rats were acclimatized to and trained in MHx [inspired PO2 (PI(O2)) = 110 Torr] for 10 wk (HTH). Rats living in normoxia trained under normoxic conditions (NTN) at the same absolute work rate: 30 m/min on a 10 degrees incline, 1 h/day, 5 days/wk. At the end of training, rats exercised maximally in normoxia. Training increased maximal O2 consumption (VO2 max) in NTN and HTH above normoxic (NS) and hypoxic (HS) sedentary controls. However, VO2 max and O2 transport variables were not significantly different between NTN and HTH: VO2 max 86.6 +/- 1.5 vs. 86.8 +/- 1.1 ml x min(-1) x kg(-1); maximal cardiac output 456 +/- 7 vs. 443 +/- 12 ml x min(-1) x kg(-1); tissue blood O2 delivery (cardiac output x arterial O2 content) 95 +/- 2 vs. 96 +/- 2 ml x min(-1) x kg(-1); and O2 extraction ratio (arteriovenous O2 content difference/arterial O2 content) 0.91 +/- 0.01 vs. 0.90 +/- 0.01. Mean pulmonary arterial pressure (Ppa, mmHg) was significantly higher in HS vs. NS (P < 0.05) at rest (24.5 +/- 0.8 vs. 18.1 +/- 0.8) and during maximal exercise (32.0 +/- 0.9 vs. 23.8 +/- 0.6). Training in MHx significantly attenuated the degree of pulmonary hypertension, with Ppa being significantly lower at rest (19.3 +/- 0.8) and during maximal exercise (29.2 +/- 0.5) in HTH vs. HS. These data indicate that, despite maintaining equal absolute training intensity levels, acclimatization to and training in MHx does not confer significant advantages over normoxic training. On the other hand, the pulmonary hypertension associated with acclimatization to hypoxia is reduced with hypoxic exercise training.     

原发性高血压患者红细胞抗高血压因子对高血压...

The effects of antihypertensive factor (AHF) from erythrocytes of essential hypertensive human subjects on the systolic blood pressure (SBP) and diastolic blood pressure (DBP) in spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR), Wistar-Kyoto rats (WKY) and Wistar rats were examined. Single intraperitoneal injection of AHF (1.6 mg/kg body weight) resulted in a significant decrease in SBP of SHR and RHR. At 10 min postinjection, AHF lowered the SBP in SHR by 34.0 mmHg. SBP recovered to the original level at 3 h. The maximal decrease of SBP in RHR by 92.5 mmHg was at 24h postadministration and the SBP did not recover until the 9th day. When AHF was administered via femoral vein (0.8 mg/kg body weight), the maximal decrease values of the SBP and the DBP were 42.8 and 48.2 mmHg in SHR at 12 min and 38.3 and 42.5 mmHg in RHR at 25 min postinjection respectively. The DBP in Wistar rats decreased considerably (from 96.7 +/- 12.9 to 83.3 +/- 11.7 mmHg) at 5 min postadministration of AHF, but no effect on DBP in WKY rats was observed. The depressor effect of AHF on SBP in RHR was dose-dependent. AHF could also antagonize the pressor effect of norepinephrine in Wistar rats.     

Voluntary exercise and its effects on young SHR and stroke-prone hypertensive rats

To determine whether voluntary exercise would lower resting blood pressure in spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SP-SHR), two separate but interrelated investigations were undertaken. The studies were initiated when the animals were 28-35 days of age and after they were assigned to either activity or sedentary cages. The activity cages were connected to transducers and recorders that allowed the monitoring and calculation of frequency, duration, and running speed. The SHR group ran 3-7 km/day intermittently for 12 wk at high speeds (48-68 m/min), which resulted in heart rates in excess of 500 beats/min. When the SHR exercised, they seldom exceeded 33 revolutions/bout (37 m) with the majority being less than 22 revolutions/bout. This type of exercise training significantly lowered, but did not normalize, resting blood pressure by approximately 20 mmHg [nontrained (NT) = 185 +/- 5; trained (T) = 163 +/- 5 mmHg] while increasing maximum O2 consumption (VO2max) (NT = 78 +/- 2.6; T = 95 +/- 2.2 ml X min-1 X kg-1) and endurance run time (NT = 62 +/- 9.0; T = 286 +/- 15.0 min), respectively. Although SP-SHR exhibited comparable patterns of voluntary activity, the effects were not similar. First, after approximately 5 wk of consuming a special Japanese rat chow and a 1% NaCl drinking solution, cerebrovascular lesions occurred and deaths ultimately resulted in both exercising and sedentary groups. Second, although there was statistical evidence for a training effect (higher VO2max, longer VO2 test run times), voluntary exercise had no advantage in either male or female runners in lowering resting blood pressures or in improving their life-spans. Whereas voluntary activity wheel exercise or moderate forced treadmill exercise will lower resting blood pressures in young SHR populations, similar generalizations cannot be made with young SP-SHR rats.     

Exercise training and its effects with renal hypertensive rats

The influence of endurance training on functional capacity [maximal O2 consumption (VO2 max)], caudal arterial blood pressure, and myocardial capillary density were investigated in normotensive rats and rats made hypertensive using the two-kidney one-clip approach (Goldblatt's hypertension). Male Sprague-Dawley rats were assigned to sham (N: 120-140 mmHg), moderately hypertensive (MH = 0.30-mm clips, 150-170 mmHg), or severely hypertensive (SH = 0.25-mm clips, 190-230 mmHg) groups. Rats designated to be runners (T) were exercised on a motor-driven treadmill equal to 50-70% of their VO2 max values for 8-12 wk. Compared with their nontrained (NT) controls, training was associated with significantly higher VO2 max values (12-15%) and muscle cytochrome-c oxidase activities (33-78%). Resting systolic blood pressure was not significantly changed in the N-and MH-T subgroups; however, it was 20-30 mmHg higher in the SH-T subgroup. Mean absolute heart weight for only the N-T group was significantly heavier than their NT controls. However, the mean predicted heart weights (heart wt = 0.639 X body wt of N-NT + 0.001 g) of the two SH groups were significantly higher than expected. The SH-T group had a lower (11%) subepicardial capillary density mean than its NT control and significantly fewer capillaries in the subendocardial region than the other five subgroups. It was concluded that moderate exercise training appeared to be detrimental to rats with severe hypertension because it increased resting blood pressure and decreased myocardial capillary density, even though it improved their functioning capacity.     

Influence of exercise training on resting blood pressures of Dahl rats

To determine whether female Dahl salt-sensitive (SS) hypertensive rats would adapt to chronic treadmill exercise by exhibiting lower resting systolic blood pressures (RSBP), a 12-wk training program was undertaken. Female Dahl salt-resistant (SR) rats were also trained for the same time period a a similar intensity [40-70% maximal O2 consumption (VO2max)] and duration (55 min). Postexperimental treadmill run times and VO2max values [SR: nontrained (NT) 87 +/- 1, trained (T) 97 +/- 2; SS: NT 82 +/- 2, T 92 +/- 3 ml.min-1 X min-1 X kg-1] indicated that the prescribed program had produced a trained state. However, the training program caused no group differences between the SR or the SS and their nontrained controls in measurements associated with sodium chloride intake, fluid consumption, urine production, 24-h sodium excretion, plasma volumes, plasma insulin, or blood volumes. Chronic exercise did significantly lower RSBP in the SR subgroup after 6 wk (NT 123 +/- 4, T 110 +/- 3 mmHg) and 8 wk (NT 120 +/- 4, T 106 +/- 2 mmHg) and remained lower throughout the remaining weeks of the experiment. On the other hand, the RSBP results of the trained SS rats were significantly higher than the nontrained SS rats after 6 wk (NT 155 +/- 8, T 191 +/- 7 mmHg) and were never significantly different than the controls for the remainder of the study.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vagal cardiac function and arterial blood pressure stability

This study was designed to investigate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability before and after glycopyrrolate or atropine treatment. Changes in R-R interval (RRI) and ABP were assessed in 10 healthy young (age, 22 +/- 1.8 yr) volunteers during graded lower body negative pressure (LBNP) before and after muscarinic cholinergic (MC) blockade. Transient hypertension was induced by phenylephrine (1 microg/kg body wt), whereas systemic hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. Power spectral densities of systolic [systolic blood pressure (SBP)] and diastolic ABP variability were examined. Both antimuscarinic agents elicited tachycardia similarly without significantly affecting baseline ABP. The increase in SBP after phenylephrine injection (+14 +/- 2 mmHg) was significantly augmented with atropine (+26 +/- 2 mmHg) or glycopyrrolate (+27 +/- 3 mmHg) and associated with a diminished reflex bradycardia. The decrease in SBP after cuff deflation (-9.2 +/- 1.2 mmHg) was significantly greater after atropine (-15 +/- 1 mmHg) or glycopyrrolate (-14 +/- 1 mmHg), with abolished reflex tachycardia. LBNP significantly decreased both SBP and RRI. However, after antimuscarinic agents, the reduction in SBP was greater (P < 0.05) and was associated with less tachycardia. Antimuscarinic agents reduced (P < 0.05) the low-frequency (LF; 0.04-0.12 Hz) power of ABP variability at rest. The LF SBP oscillation was significantly augmented during LBNP, which was accentuated (P < 0.05) after antimuscarinic agents and was correlated (r = -0.79) with the decrease in SBP. We conclude that antimuscarinic agents compromised ABP stability by diminishing baroreflex sensitivity, reflecting the importance of vagal cardiac function in hemodynamic homeostasis. The difference between atropine and glycopyrrolate was not significant.     

Circadian relations among cardiovascular variables of young adults.

Every 4 hours for 24 hours, 14 clinically healthy young individuals (6 women and 8 men), 26 +/- 4 years of age, measured systolic (S) and diastolic (D) blood pressure (BP) by sphygmomanometer and heart rate by ECG and did impedance cardiography under usual living conditions. Stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were calculated. Time series of SBP, DBP, HR, SV, CO and TPR were analyzed by single and population-mean cosinor. A circadian cardiovascular rhythm is demonstrated by rejection of the zero amplitude assumption in the population-mean cosinor test for SBP, DBP, HR, SV, CO and TPR (P < 0.01). TPR peaks around 0400 (-61 degrees from local midnight), in antiphase with all other variables, their acrophase occurring around 1600 (-240 degrees). A circadian rhythm of statistical significance or of borderline statistical significance is found for all variables except TPR in women. Circadian rhythm characteristics were otherwise mostly similar in men and women with a statistically significant gender difference found by parameter tests only for the MESOR and amplitude of SBP.     

Vascular and metabolic response to cycle exercise in sedentary humans: effect of age

We measured leg blood flow (LBF), drew arterial-venous (A-V) blood samples, and calculated muscle O(2) consumption (VO(2)) during incremental cycle ergometry exercise [15, 30, and 99 W and maximal effort (maximal work rate, WR(max))] in nine sedentary young (20 +/- 1 yr) and nine sedentary old (70 +/- 2 yr) males. LBF was preserved in the old subjects at 15 and 30 W. However, at 99 W and at WR(max), leg vascular conductance was attenuated because of a reduced LBF (young: 4.1 +/- 0.2 l/min and old: 3.1 +/- 0.3 l/min) and an elevated mean arterial blood pressure (young: 112 +/- 3 mmHg and old: 132 +/- 3 mmHg) in the old subjects. Leg A-V O(2) difference changed little with increasing WR in the old group but was elevated compared with the young subjects. Muscle maximal VO(2) and cycle WR(max) were significantly lower in the old subjects (young: 0.8 +/- 0.05 l/min and 193 +/- 7 W; old: 0.5 +/- 0.03 l/min and 117 +/- 10 W). The submaximally unchanged and maximally reduced cardiac output associated with aging coupled with its potential maldistribution are candidates for the limited LBF during moderate to heavy exercise in older sedentary subjects.     

Effects of detraining on cardiovascular responses to exercise: role of blood volume

In this study we determined whether the decline in exercise stroke volume (SV) observed when endurance-trained men stop training for a few weeks is associated with a reduced blood volume. Additionally, we determined the extent to which cardiovascular function could be restored in detrained individuals by expanding blood volume to a similar level as when trained. Maximal O2 uptake (VO2max) was determined, and cardiac output (CO2 rebreathing) was measured during upright cycling at 50-60% VO2max in eight endurance-trained men before and after 2-4 wk of inactivity. Detraining produced a 9% decline in blood volume (5,177 to 4,692 ml; P less than 0.01) during upright exercise, due primarily to a 12% lowering (P less than 0.01) of plasma volume (PV; Evans blue dye technique). SV was reduced by 12% (P less than 0.05) and VO2max declined 6% (P less than 0.01), whereas heart rate (HR) and total peripheral resistance (TPR) during submaximal exercise were increased 11% (P less than 0.01) and 8% (P less than 0.05), respectively. When blood volume was expanded to a similar absolute level in the trained and detrained state (approximately 5,500 +/- 200 ml) by infusing a 6% dextran solution in saline, the effects of detraining on cardiovascular response were reversed. SV and VO2max were increased (P less than 0.05) by PV expansion in the detrained state to within 2-4% of trained values. Additionally, HR and TPR during submaximal exercise were lowered to near trained values. These findings indicate that the decline in cardiovascular function following a few weeks of detraining is largely due to a reduction in blood volume, which appears to limit ventricular filling during upright exercise.     

Cardiovascular responses to lower body negative pressure in trained and untrained older men.

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59-73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.     

Left ventricular hypertrophy: physiopathological signs using a hemodynamic and cardio-autonomic approach]

The presence of left ventricular hypertrophy (LVH) in either hypertensives -H- or in normotensives -N-, suggests that not only blood pressure is determining this anatomic change, but various factors, as neural or endocrine ones, could be involved in its genesis. In order to evaluate the role of sympathetic dys-reactivity on LVH, we studied three groups of subjects: a) 12 -H- (SBP 159+/-9; DBP 99.6+/-7; FC 80+/-7) with LVH, diagnosed by echocardiogram. b) 12 -N- (SBP 138.2+/-8; DBP 83+/-2; FC 75.6+/-4) with LVH. c) 12 -N- (SBP 136.6+/-11; DBP 81.8+/-5; FC 76.3+/-5) without LVH. Using computer interfaced equipment, we measured beat to beat, hemodynamic and extra-cardiovascular autonomic functions, during a session of stressors (Mental Arithmetic, Color Word Stroop, Cold Pressure and Handgrip Tests), preceded and followed by 10' of observation. Among the various considered indexes, we evaluated the Percentual Total Activity Index (PTAI), as percentual total activity change + percentual total recovery change. Our findings point out that the PTAI of N with LVH is significantly higher for SCL, PHT, HR, SV, CO, TPR than either in H with LVH or N without LVH. These data seem to demonstrate a prolonged reactivity in N without LVH and are according to the hypothesis that LVH could also be supported by a hyper-adrenergic state with sympathetic dys-reactivity, independently from high blood pressure values.     

Comparison of incremental and steady state tests of endurance training

To compare the results obtained by incremental or constant work load exercises in the evaluation of endurance conditioning, a 20-week training programme was performed by 9 healthy human subjects on the bicycle ergometer for 1 h a day, 4 days a week, at 70-80% VO2max. Before and at the end of the training programme, (1) the blood lactate response to a progressive incremental exercise (18 W increments every 2nd min until exhaustion) was used to determine the aerobic and anaerobic thresholds (AeT and AnT respectively). On a different day, (2) blood lactate concentrations were measured during two sessions of constant work load exercises of 20 min duration corresponding to the relative intensities of AeT (1st session) and AnT (2nd session) levels obtained before training. A muscle biopsy was obtained from vastus lateralis at the end of these sessions to determine muscle lactate. AeT and AnT, when expressed as % VO2max, increased with training by 17% (p less than 0.01) and 9% (p less than 0.05) respectively. Constant workload exercise performed at AeT intensity was linked before training (60% VO2max) to a blood lactate steady state (4.8 +/- 1.4 mmol.l-1) whereas, after training, AeT intensity (73% VO2max) led to a blood lactate accumulation of up to 6.6 +/- 1.7 mmol.l-1 without significant modification of muscle lactate (7.6 +/- 3.1 and 8.2 +/- 2.8 mmol.kg-1 wet weight respectively). It is concluded that increase in AeT with training may reflect transient changes linked to lower early blood lactate accumulation during incremental exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determinants of endurance in well-trained cyclists

Fourteen competitive cyclists who possessed a similar maximum O2 consumption (VO2 max; range, 4.6-5.0 l/min) were compared regarding blood lactate responses, glycogen usage, and endurance during submaximal exercise. Seven subjects reached their blood lactate threshold (LT) during exercise of a relatively low intensity (group L) (i.e., 65.8 +/- 1.7% VO2 max), whereas exercise of a relatively high intensity was required to elicit LT in the other seven men (group H) (i.e., 81.5 +/- 1.8% VO2 max; P less than 0.001). Time to fatigue during exercise at 88% of VO2 max was more than twofold longer in group H compared with group L (60.8 +/- 3.1 vs. 29.1 +/- 5.0 min; P less than 0.001). Over 92% of the variance in performance was related to the % VO2 max at LT and muscle capillary density. The vastus lateralis muscle of group L was stressed more than that of group H during submaximal cycling (i.e., 79% VO2 max), as reflected by more than a twofold greater (P less than 0.001) rate of glycogen utilization and blood lactate concentration. The quality of the vastus lateralis in groups H and L was similar regarding mitochondrial enzyme activity, whereas group H possessed a greater percentage of type I muscle fibers (66.7 +/- 5.2 vs. 46.9 +/- 3.8; P less than 0.01). The differing metabolic responses to submaximal exercise observed between the two groups appeared to be specific to the leg extension phase of cycling, since the blood lactate responses of the two groups were comparable during uphill running. These data indicate that endurance can vary greatly among individuals with an equal VO2 max.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

Diminished baroreflex control of forearm vascular resistance in physically fit humans

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR) were studied in five unfit [UF, maximal O2 consumption (VO2 max) = 38.5 ml X min-1 X kg-1] and six fit (F, VO2 max = 57.0 ml X min-1 X kg-1) subjects. We assessed the relationship between reflex stimulus, i.e., changes in central venous pressure (CVP) and response, i.e., FVR, during selective unloading of the cardiopulmonary mechanoreceptors with lower body negative pressure (0 to -20 mmHg). The linear relationship between FVR and CVP, the gain of this baroreflex, was significantly diminished in the F subjects, -2.42 +/- 0.57 U/mmHg, compared with the UF, -5.15 +/- 0.58 U/mmHg. Both groups, F and UF, had similar resting values for CVP and FVR; thus the diminished gain in F subjects was not simply an artifact resulting from a shift of the set point along the baroreflex stimulus-response curve. We also found a linear relationship between baroreflex gain and total blood volume (r = 0.59, P less than 0.05). We conclude that the gain of this vascular reflex is attenuated in trained individuals and is related to cardiovascular adaptations, such as an increased blood volume, associated with exercise training.     

Effects of one-year swimming training on blood pressure and insulin sensitivity in mild hypertensive young patients

Swimming is a lifestyle intervention recommended by many clinicians in the prevention and treatment of hypertension. Yet, not all studies have agreed that swimming training can reduce blood pressure (BP). Inclusion of normotensive subjects could be a confounder for discrepancies among studies. In this one-year longitudinal study, long-term effects of swimming training on BP were investigated in 7 mild hypertensive patients (systolic BP (SBP) > 140 mmHg) and 16 normotensive controls. At baseline, these subjects (aged 21.5 +/- 0.1 years) did not participate in any form of sport training activity for the previous 3 months before enrollment into the training program. The training distance progressed from 0 (baseline) to 7 kilometers per week. BP and the homeostasis model assessment for insulin resistance (HOMA-IR) were determined under fasted condition at baseline and 48 h after the last swimming bout. The hypertensive patients displayed significantly greater HOMA-IR than age-matched normotensive controls. When data of all subjects were pooled, plasma glucose concentration was only slightly lowered after training, but weight, height, body mass index, SBP, diastolic BP (DBP) and HOMA-IR values were not significantly altered. However, when observation was restricted to the hypertensive patients, swimming training significantly lowered SBP by approximately 17 mmHg, concurrent with 41% reduction in HOMA-IR. Intriguingly, SBP in the normotensive subjects was elevated by approximately 6 mmHg after training. CONCLUSIONS: The present study found normalization rather than universal reduction effect of swimming training on BP. Furthermore, the BP-lowering effect of training in hypertensive patients appears to be associated with improvement in insulin sensitivity.     

An evaluation of the concept of living at moderate altitude and training at sea level

Despite equivocal findings about the benefit of altitude training, current theory dictates that the best approach is to spend several weeks living at > or =2500 m but training near sea level. This paper summarizes six studies in which we used simulated altitude (normobaric hypoxia) to examine: (i) the assumption that moderate hypoxia compromises training intensity (two studies); and (ii) the nature of physiological adaptations to sleeping in moderate hypoxia (four studies). When submaximal exercise was >55% of sea level maximum oxygen uptake (VO2max), 1800 m simulated altitude significantly increased heart rate, blood lactate and perceived exertion of skiers. In addition, cyclists self-selected lower workloads during high-intensity exercise in hypoxia (2100 m) than in normoxia. Consequently, our findings partially confirm the rationale for 'living high, training low'. In the remaining four studies, serum erythropoietin increased 80% in the early stages of hypoxic exposure, but the reticulocyte response did not significantly exceed that of control subjects. There was no significant increase in haemoglobin mass (Hb(mass)) and VO2max tended to decrease. Performance in exercise tasks lasting approximately 4 min showed a non-significant trend toward improvement (1.0+/-0.4% vs. 0.1+/-0.4% for a control group; P=0.13 for group x time interaction). We conclude that sleeping in moderate hypoxia (2650-3000 m) for up to 23 days may offer practical benefit to elite athletes, but that any effect is not likely due to increased Hb(mass) or VO2max.