Handgrip and sex-specific cardiometabolic risk factors in Hispanic/Latino migrant farmworkers.

Studies have suggested that handgrip strength might be a marker for cardiometabolic risk (CMR), but it has not been studied in Hispanic/Latino farmworker population. This study aimed to characterize absolute and relative handgrip strength in Hispanic/Latino farmworkers, and investigate the sex-specific association between handgrip strength and CMR factors. CMR factors and seated isometric absolute (the sum of both hands) and relative (absolute handgrip strength divided by body mass index) handgrip strengths were collected in 173 Hispanic/Latino farmworkers (mean age 35.1 ± 0.7 years; 49% female). The absolute and the relative handgrip strengths were 89.2 ± 1.8 kg, 3.3 ± 0.1 kg among males, and 56.5 ± 1.9 kg, 1.9 ± 0.1 kg among females, respectively. Age was correlated with absolute (r = - 0.17, p = 0.03) and relative handgrip strengths (r = - 0.28, p < 0.01). In males, absolute handgrip was related to triglycerides (r = - 0.25, p < 0.05), whereas relative handgrip was related to waist circumference (r = - 0.32, p < 0.01), waist/hip circumference ratio (r = - 0.36, p < 0.01), high-density lipoprotein (r = 0.24, p < 0.05), and triglycerides (r = - 0.35, p < 0.01). In females, absolute handgrip was related to fasting plasma glucose (r = - 0.28, p = 0.03), whereas relative handgrip was related to waist circumference (r = - 0.38, p < 0.01) and fasting plasma glucose (r = - 0.22, p < 0.05). Males had lower absolute handgrip strength when their triglycerides levels were at risk (p = 0.021), and lower relative handgrip strength when their plasma glucose (p = 0.034) and triglycerides (p = 0.002) levels were at risk. Females had lower relative handgrip strength when their plasma glucose (p = 0.001) and blood pressure (p = 0.004) were at risk. This study suggests that handgrip strength may be associated with sex-specific CMR factors in a Hispanic/Latino farmworker population.

Can α-lipoic acid mitigate progression of aging-related decline caused by oxidative stress?

Aging is progressively deteriorating physiological function that leads to increasing risks of illness and death. Increases in life expectancy and the aging of a large segment of the population have made age-related disability and morbidity increasingly important issues. Supplements such as α-lipoic acid may have antiaging effects by positively affecting oxidative stress, cognitive function, and cardiovascular function.

Leptin regulates CD16 expression on human monocytes in a sex-specific manner.

Fat mass is linked mechanistically to the cardiovascular system through leptin, a 16 kDa protein produced primarily by adipocytes. In addition to increasing blood pressure via hypothalamic-sympathetic pathways, leptin stimulates monocyte migration, cytokine secretion, and other functions that contribute to atherosclerotic plaque development. These functions are also characteristics of CD16-positive monocytes that have been implicated in the clinical progression of atherosclerosis. This investigation sought to determine if leptin promoted the development of such CD16-positive monocytes. Cells from 45 healthy men and women with age ranging from 20 to 59 years were analyzed. Circulating numbers of CD14(++)16(++) monocytes, which are primary producers of TNFα, were positively related to plasma leptin concentrations (P < 0.0001), with a stronger correlation in men (P < 0.05 for leptin × sex interaction). In vitro, recombinant human leptin induced CD16 expression in a dose-related manner (P = 0.02), with a stronger influence on monocytes from men (P = 0.03 for leptin × sex interaction). There were no sex-related differences in total leptin receptor expression on any monocyte subtypes, relative expression of long versus short isoforms of the receptor, or soluble leptin receptor concentrations in the plasma. The number of circulating CD14(+)16(++) monocytes, which preferentially migrate into nascent plaques, was positively related to systolic blood pressure (R = 0.56, P = 0.0008) and intima-media thickness (R = 0.37, P = 0.03), and negatively related to carotid compliance (R = -0.39, P = 0.02). These observations indicate that leptin promotes the development of CD16-positive monocyte populations in a sex-specific manner and that these subpopulations are associated with diminished vascular function.

Soluble TNF and IL-6 receptors: indicators of vascular health in women without cardiovascular disease.

Cytokine receptor subunits are released from cells in a regulated manner and circulate in soluble forms at concentrations that are orders of magnitude greater than the concentrations of the cytokines themselves. The purpose of this study was to determine if the circulating concentrations of soluble receptor subunits for interleukin-1 beta (IL-1ß), tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6) might serve as early indicators of vascular dysfunction independent of the traditional cardiovascular disease (CVD) risk factors in women. Healthy women, aged 20-50 years (n = 36), were assessed for circulating concentrations of the cytokines IL-1ß, IL-6 and TNFα and the soluble cytokine receptor subunits interleukin-1 receptor type I (sIL-1RI), sIL-1RII, sIL-6Rα, glycoprotein 130 (s-gp130), soluble TNF receptor type 1 (sTNFR1), and sTNFR2, along with traditional CVD risk factors. Cytokine receptor subunit expression on mononuclear cells and the release of these subunits in vitro were also determined. Brachial artery flow-mediated dilation (FMD), carotid intima-media thickness (cIMT) and carotid-femoral pulse wave velocity (cfPWV) were assessed by ultrasonography and Doppler probes. Circulating sIL-6Rα correlated negatively with FMD (r = -0.56, p = 0.007) independent of age and other CVD risk factors. Circulating sTNFR1 correlated positively with cfPWV (r = 0.60, p = 0.002). TNFR1 receptor expression on monocytes correlated positively with cIMT (r = 0.51, p = 0.004). Plasma concentrations of IL-1ß, IL-6 and TNFα were not significantly associated with FMD, cIMT or cfPWV. These data suggest that the receptors for IL-6 and TNFα, rather than the cytokines themselves, may be better indicators of early vascular changes that are associated with CVD.

Follicle-stimulating hormone, interleukin-1, and bone density in adult women.

Recent studies have indicated that follicle-stimulating hormone (FSH) promotes bone loss. The present study tested the hypothesis that FSH enhances the activity of bone-resorbing cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and IL-6], either by inducing their secretion or by altering their receptor expression. Thirty-six women between the ages of 20 and 50 were assessed for bone mineral density (BMD), reproductive hormone, cytokine ligand and soluble receptor concentrations, and surface expression of cytokine receptors on monocytes. In addition, isolated mononuclear cells were incubated in vitro with exogenous FSH. Univariate regression analyses indicated that BMD was inversely related to serum FSH (r = -0.29 to -0.51, P = 0.03-0.001, depending upon the skeletal site). Physical activity and body composition were also identified as significant factors by multiple regressions. Exogenous FSH induced isolated cells to secrete IL-1beta, TNF-alpha, and IL-6 in proportion to the surface expression of FSH receptors on the monocytes. Endogenous (serum) FSH concentrations correlated with the circulating concentrations of these cytokines. None of these individual cytokines was related to BMD, but the IL-1beta to IL-1 receptor antagonist (IL-1Ra) ratio was inversely related to BMD (r = -0.53, P = 0.002) in all but the most physically active women, who had significantly lower expression of IL-1 type I receptors relative to type II (decoy receptors, P = 0.01). Physical activity also correlated positively with secretion of inhibitory soluble IL-1 receptors (r = 0.53, P = 0.003). Moreover, IL-1Ra correlated strongly with percent body fat (r = 0.66, P < 0.0001). These results indicate that BMD is related to FSH concentration, physical activity, and body composition. Although each of these factors likely has direct effects on bone, the present study suggests that each may also influence BMD by modulating the activity of the osteoresorptive cytokine IL-1beta.

Femoral artery diameter and arteriogenic cytokines in healthy women.

Animal studies have identified monocyte chemoattractive protein-1 (MCP-1) and vascular endothelial growth factor (VEGF) as critical mediators of arterial diameter enlargement in response to chronic increases in blood flow (arteriogenesis). Furthermore, cellular studies have shown that the shear stresses resulting from increased blood flow stimulate synthesis of MCP-1, which in turn stimulates synthesis of VEGF. The purpose of this study was to determine if these mechanisms are evident in healthy women. Resting femoral artery diameter and blood flow, lean leg mass, MCP-1 and VEGF concentrations, and aerobic capacity were measured in 34 healthy women along with plasma concentrations of lipids associated with cardiovascular disease risk. Femoral artery diameter was independently related to metabolically active (lean) leg mass (b=0.41, P=0.008) and aerobic capacity (b=0.45, P=0.004). Plasma MCP-1 correlated negatively with the ratio of femoral artery diameter to lean leg mass (b=-0.42, P=0.009) and positively with serum triglycerides (b=0.46, P=0.005). Plasma VEGF exhibited similar correlations and strongly correlated with MCP-1 (R=0.92, P<0.0001). The results indicate that circulating MCP-1 and VEGF concentrations are associated with both arteriogenic and atherogenic stimuli in healthy women.

Leptin, blood pressure, and aerobic capacity in women.

BACKGROUND: In animals, the adipocyte-derived hormone leptin induces increased blood pressure centrally via the hypothalamus, and one study has reported that exercise training decreases hypothalamic leptin receptor expression. In humans, high circulating leptin concentrations are associated with high blood pressure, but the possible influence of physical activity or aerobic capacity on this association is unknown. METHODS: Forty-two healthy women, 25-40 years of age, with diverse ranges of body fatness and aerobic capacities, were studied under basal resting conditions. Blood pressure (sphygmomanometry), arterial stiffness (pulse wave velocity (PWV)), percent body fat (dual energy X-ray absorptiometry), circulating concentrations of leptin, soluble leptin receptor (sLR) (enzyme-linked immunoassay), and nitric oxide (Griess reaction) were measured. RESULTS: Serum leptin correlated with percent body fat (R(2) = 0.74, P < 0.0001) but was not significantly associated with aerobic capacity. Blood pressure correlated positively with serum leptin concentrations and had a negative interaction with aerobic capacity for both systolic (overall model: R(2) = 0.33, P = 0.002) and diastolic (R(2) = 0.48, P < 0.0001) pressure. The relation between leptin and blood pressure was attributable solely to women with below-median aerobic capacity even though their body fat percentages and leptin concentrations were similar to those of women above the median. The results could not be attributed to differences in peripheral factors such as sLR or nitric oxide concentrations or to differences in arterial stiffness determined by aortic PWV. CONCLUSIONS: Circulating leptin concentrations are related to body fatness, but the hypertensive influence of leptin is modified by physical fitness.

The effects of strength training on central arterial compliance in middle-aged and older adults.

BACKGROUND: Contrary to aerobic exercise, strength training (ST) is associated with decreased central arterial compliance in young men. It is unknown whether ST, with or without concurrent endurance training, would have a similar effect in older adults with reduced baseline arterial compliance. OBJECTIVE: The primary aim of this study was to determine the effect of a ST program on central arterial compliance in middle-aged and older adults. DESIGN: Randomized, controlled intervention study in which 37 healthy, sedentary men and women (52+/-2 years) performed 13 weeks of ST (n=13), ST+aerobic exercise (n=12) or stretching exercises as a control group (n=12). METHODS: Participants were rigorously screened for cardiovascular disease and underwent pre-post testing for carotid arterial compliance (via simultaneous ultrasound and applanation tonometry), carotid-femoral pulse wave velocity, plasma endothelin-1 and angiotensin II concentrations and carotid artery vasoreactivity (cold pressor test). RESULTS: ST performed alone, or in conjunction with aerobic exercise, improved maximal muscle strength and increased total lean body mass (both P<0.01). No significant changes were observed in carotid artery compliance or carotid-femoral pulse wave velocity following ST or ST+aerobic exercise. Carotid artery compliance increased significantly (23%) following stretching which may be attributed to a reduction in carotid pulse pressure. No significant changes were observed in plasma vasoconstrictor hormones or carotid artery vasoreactivity following the interventions. CONCLUSION: Thirteen weeks of moderate ST two or three times per week does not reduce central arterial compliance in middle-aged and older adults.

Resistance training increases basal limb blood flow and vascular conductance in aging humans.

Age-related reductions in basal limb blood flow and vascular conductance are associated with the metabolic syndrome, functional impairments, and osteoporosis. We tested the hypothesis that a strength training program would increase basal femoral blood flow in aging adults. Twenty-six sedentary but healthy middle-aged and older subjects were randomly assigned to either a whole body strength training intervention group (52 +/- 2 yr, 3 men, 10 women) who underwent three supervised resistance training sessions per week for 13 wk or a control group (53 +/- 2 yr, 4 men, 9 women) who participated in a supervised stretching program. At baseline, there were no significant differences in blood pressure, cardiac output, basal femoral blood flow (via Doppler ultrasound), vascular conductance, and vascular resistance between the two groups. The strength training group increased maximal strength in all the major muscle groups tested (P < 0.05). Whole body lean body mass increased (P < 0.05) with strength training, but leg fat-free mass did not. Basal femoral blood flow and vascular conductance increased by 55-60% after strength training (both P < 0.05). No such changes were observed in the control group. In both groups, there were no significant changes in brachial blood pressure, plasma endothelin-1 and angiotensin II concentrations, femoral artery wall thickness, cardiac output, and systemic vascular resistance. Our results indicate that short-term strength training increases basal femoral blood flow and vascular conductance in healthy middle-aged and older adults.

Cigarette smoking, regular exercise, and peripheral blood flow.

Acute and chronic smoking reduces peripheral blood flow and shear stress, contributing to the increased incidence of peripheral arterial disease in smokers. Currently, it is not known whether physical activity status influences peripheral blood flow among chronic smokers. Blood flow was measured using Doppler ultrasound on the common femoral artery in nine young otherwise healthy sedentary smokers (eight males/one female) and nine physically-active smokers (six males/three females). Physically-active smokers performed strenuous exercise 4.4 times/week for 8 h/week. No significant differences in body fat, blood pressure, and total cholesterol were observed between groups. Basal femoral artery blood flow was approximately 50% higher in physically-active smokers compared with sedentary smokers (259+/-108 ml min(-1) versus 173+/-47 ml min(-1), P<0.05). The higher basal femoral artery blood flow in physically-active smokers compared with sedentary smokers was associated with a 47% higher femoral artery vascular conductance (2.99+/-1.2 U versus 2.03+/-0.5 U, P<0.05) and a 39% lower vascular resistance (0.38+/-0.13 U versus 0.53+/-0.15 U, P<0.05). Cardiac output, systemic vascular resistance, femoral intima-media thickness, and plasma norepinephrine concentration were not different between the groups. We concluded that smokers who habitually perform physical activity demonstrate greater levels of peripheral blood flow and peripheral vascular conductance. The findings from the present cross-sectional study suggest that chronic smokers may be able to negate, at least in part, the adverse effects of chronic smoking on the peripheral vasculature by performing regular physical activity.

Arterial compliance of rowers: implications for combined aerobic and strength training on arterial elasticity.

Regular endurance exercise increases central arterial compliance, whereas resistance training decreases it. It is not known how the vasculature adapts to a combination of endurance and resistance training. Rowing is unique, because its training encompasses endurance- and strength-training components. We used a cross-sectional study design to determine arterial compliance of 15 healthy, habitual rowers [50 +/- 9 (SD) yr, 11 men and 4 women] and 15 sedentary controls (52 +/- 8 yr, 10 men and 5 women). Rowers had been training 5.4 +/- 1.2 days/wk for 5.7 +/- 4.0 yr. The two groups were matched for age, body composition, blood pressure, and metabolic risk factors. Central arterial compliance (simultaneous ultrasound and applanation tonometry on the common carotid artery) was higher (P < 0.001) and carotid beta-stiffness index was lower (P < 0.001) in rowers than in sedentary controls. There were no group differences for measures of peripheral (femoral) arterial stiffness. The higher central arterial compliance in rowers was associated with a greater cardiovagal baroreflex sensitivity, as estimated during a Valsalva maneuver (r = 0.54, P < 0.005). In conclusion, regular rowing exercise in middle-aged and older adults is associated with a favorable effect on the elastic properties of the central arteries. Our results suggest that simultaneously performed endurance training may negate the stiffening effects of strength training.

Effects of high intensity resistance training on arterial stiffness and wave reflection in women.

BACKGROUND: Cross-sectional studies reported that chronic resistance training is associated with arterial stiffening in men. These findings are in marked contrast to those found with aerobic exercise and may have important clinical relevance with regard to cardiovascular disease risk. However, the effect of resistance training on arterial stiffness has not been confirmed by interventional studies nor has this relation been investigated in women. METHODS: To determine whether a strength training program increases regional and central arterial stiffness in women, 23 healthy young women (29+/-1 years; mean+/-SD) participated in a high-intensity strength and power training program for 11 weeks. Ten other women (27+/-2 years) served as time controls. RESULTS: In the intervention group, one repetition maximal strength increased 12% to 17% (P<.0001), and leg fat-free mass (via DEXA) increased significantly. Brachial blood pressure (BP) and fasting plasma lipid and lipoprotein concentrations did not change across the 11 weeks. Carotid augmentation index, a measure of arterial wave reflection and arterial stiffness, increased from -8%+/-13% to 1%+/-18% (P<.05), and carotid-femoral pulse wave velocity increased (791+/-88 v 833+/-96 cm/sec; P<.05). There were no changes in femoral-ankle pulse wave velocity, a segmental measure of peripheral arterial stiffness. CONCLUSIONS: We concluded that a high-intensity resistance training program increases arterial stiffness and wave reflection in young healthy women. Our present interventional results are consistent with the previous cross-sectional studies in men in which high-intensity strength training is associated with arterial stiffening.

Post-exercise palpation of pulse rates: its applicability to habitual exercisers.

Despite the increased popularity of heart rate (HR) monitors, endurance-trained adults as well as habitual exercisers often use pulse rate palpation to periodically monitor exercise intensity. However, due to the rapid recovery of HR following exercise bouts, post-exercise palpation of pulse rates may underestimate exercise HR. To test this hypothesis, we studied 20 young physically active adults performing two sets of exercise for 5 min at 70% and 85% of maximal HR on the treadmill; one with carotid and another with radial pulse count. Post-exercise palpation of pulse rate was lower (P < 0.01) than the actual HR during exercise, underestimating exercise HR by 20-27 bpm (beats per min). Even when ECG tracings of HR were analyzed immediately after exercise (0-15 s), a significant underestimation of exercise HR (7-9 bpm) still persisted (P < 0.05). Following exercise, pulse rate obtained by carotid palpation at both intensities and radial palpation at the lower intensity was no different from the corresponding HR measured with ECG. In the radial artery trial at the higher exercise intensity, pulse rate following exercise was lower (10 bpm; P < 0.05) than ECG-derived HR. Arterial stiffness, which is closely associated with arterial baroreflex sensitivity, was not significantly related to the changes in HR with carotid palpation. We concluded that post-exercise pulse palpations may not be appropriate as an indicator of exercise intensity in habitual exercisers.

Acute effects of resistance exercise on arterial compliance.

Decreased central arterial compliance is an emerging risk factor for cardiovascular disease. Resistance training is associated with reductions in the elastic properties of central arteries. Currently, it is not known whether this reduction is from one bout of resistance exercise or from an adaptation to multiple bouts of resistance training. Sixteen healthy sedentary or recreationally active adults (11 men and 5 women, age 27 +/- 1 yr) were studied under parallel experimental conditions on 2 separate days. The order of experiments was randomized between resistance exercise (9 resistance exercises at 75% of 1 repetition maximum) and sham control (seated rest in the exercise room). Baseline hemodynamic values were not different between the two experimental conditions. Carotid arterial compliance (via simultaneous B-mode ultrasound and applanation tonometry) decreased and beta-stiffness index increased (P < 0.01) immediately and 30 min after resistance exercise. Immediately after resistance exercise, carotid systolic blood pressure increased (P < 0.01), although no changes were observed in brachial systolic blood pressure at any time points. These measures returned to baseline values within 60 min after the completion of resistance exercise. No significant changes in these variables were observed during the sham control condition. These results indicate that one bout of resistance exercise acutely decreases central arterial compliance, but this effect is sustained for <60 min after the completion of resistance exercise.