Improvements in vascular function in response to acute lower limb heating in young healthy males and females.

Regular exposure to passive heat stress improves vascular function, but the optimal heating prescription remains undefined. Local limb heating is more feasible than whole body heating, but the evidence demonstrating its efficacy is lacking. The purpose of this study was to determine whether acute improvements in vascular function can be achieved with lower limb heating in 16 young healthy individuals (8 female, 8 male). In separate visits, participants underwent 45 min of ankle- and knee-level hot water immersion (45°C). A subset of seven participants also participated in a time-control visit. Endothelial function was assessed through simultaneous brachial and superficial femoral artery flow-mediated dilation (FMD) tests. Macrovascular function was quantified by %FMD, whereas microvascular function was quantified by vascular conductance during reactive hyperemia. Arterial stiffness was assessed through carotid-femoral and femoral-foot pulse wave velocity (PWV). Plasma concentrations of interleukin-6 and extracellular heat shock protein-72 (eHSP72) were used as indicators of inflammation. Our findings showed that 45 min of lower limb heating-regardless of condition-acutely improved upper limb macrovascular endothelial function (i.e., brachial %FMD; Pre: 4.6 ± 1.7 vs. Post: 5.4 ± 2.0%; P = 0.004) and lower limb arterial stiffness (i.e., femoral-foot PWV; Pre: 8.4 ± 1.2 vs. Post: 7.7 ± 1.1 m/s; P = 0.011). However, only knee-level heating increased upper limb microvascular function (i.e., brachial peak vascular conductance; Pre: 6.3 ± 2.7 vs. Post: 7.8 ± 3.5 mL/min â‹… mmHg; P ≤ 0.050) and plasma eHSP72 concentration (Pre: 12.4 ± 9.4 vs. Post: 14.8 ± 9.8 ng/mL; P ≤ 0.050). These findings show that local lower limb heating acutely improves vascular function in younger individuals, with knee-level heating improving more outcome measures.NEW & NOTEWORTHY This study demonstrates that lower limb hot water immersion is an effective strategy for acutely improving vascular function in young, healthy males and females, thereby encouraging the development of accessible modes of heat therapy for vascular health.

Effect of heat stress on vascular outcomes in humans.

In addition to its role as an environmental stressor, scientists have recently demonstrated the potential for heat to be a therapy for improving or mitigating declines in arterial health. Many studies at both ends of the scientific controls spectrum (tightly controlled, experimental vs. practical) have demonstrated the beneficial effects of heating on microvascular function (e.g., reactive hyperemia, cutaneous vascular conductance); endothelial function (e.g., flow-mediated dilation); and arterial stiffness (e.g., pulse-wave velocity, compliance, ß-stiffness index). It is important to note that findings of beneficial effects are not unanimous, likely owing to the varied methodology in both heating protocols and assessments of outcome measures. Mechanisms of action for the effects of both acute and chronic heating are also understudied. Heat science is a very promising area of human physiology research, as it has the potential to contribute to approaches addressing the global cardiovascular disease burden, particularly in aging and at risk populations, and those for whom exercise is not feasible or recommended.

Influences of nutrition and adiposity on bone mineral density in individuals with chronic spinal cord injury: A cross-sectional, observational study.

BACKGROUND: Dietary inadequacy and adiposity, both prevalent in the chronic spinal cord injury (SCI) population, are known to influence bone turnover and may be potential modifiable risk factors for the development of sublesional osteoporosis following SCI. This pilot study in an SCI cohort aimed to assess measures of nutrition and obesity, to determine if these measures were associated with bone mineral density (BMD), and to compare these measures to a non-SCI control cohort. METHODS: In a cross-sectional observational study, volunteers with chronic SCI (> 1 year post-injury, lesions from C1 to T12 and severity category A-D by the American Spinal Injury Association Impairment Scale) were assessed, and 8 non-SCI individuals were recruited as a comparison group. BMD at the femoral neck (FN) and lumbar spine (LS), and an estimate of visceral adipose tissue (VAT) from lumbar vertebrae 1 through 4 were measured using dual energy X-ray absorptiometry (DXA); nutrient intake of calcium, vitamins D & K, and protein were estimated using a food frequency questionnaire; plasma 25-hydroxyvitamin D (25(OH)D) was analyzed using ultra-high performance liquid chromatography/tandem mass spectroscopy; and serum leptin, adiponectin and insulin were analyzed using a multiplex assay. RESULTS: A total of 34 individuals with SCI (n = 22 tetraplegic; n = 12 paraplegic; 94% male) who averaged 12.7 (9.0) years post-injury, age 40.0 (10.9) years and % body fat of 28.4 (7.3) were assessed. Multiple linear regression analyses in the SCI cohort showed significant associations between BMD at the FN and LS with leptin (FN: r = 0.529, p = 0.005; LS: r = 0.392, p = 0.05), insulin (FN: r = 0.544, p = 0.003; LS: r = 0.388, p = 0.05), and VAT percent (FN: r = 0.444, p = 0.02; LS: r = 0.381, p = 0.05). Adiponectin was only correlated with LS BMD (r = 0.429, p = 0.03). No significant relationships were found between BMD and serum 25(OH)D, or intakes of calcium, vitamins D & K, and protein. Intake of vitamin D was adequate in 69% of participants with SCI, where 91% of those persons consumed either vitamin D and/or multivitamin supplements. Vitamin D status was similar between SCI and non-SCI groups as was sub-optimal status (25(OH)D < 75 nmol/L) (60% of SCI compared to 50% of non-SCI). Participants with SCI had significantly lower FN BMD in comparison to non-SCI controls (p = 0.001). CONCLUSIONS: Compromised BMD among individuals with SCI was not associated with a deficiency of vitamin D or other bone nutrients. The observed positive associations between BMD and leptin, insulin, adiponectin and VAT provide a framework to evaluate links between adiposity and bone health in a larger SCI cohort.

Bolus arginine supplementation affects neither muscle blood flow nor muscle protein synthesis in young men at rest or after resistance exercise.

The aim of this study was to investigate the ergogenic potential of arginine on NO synthesis, muscle blood flow, and skeletal muscle protein synthesis (MPS). Eight healthy young men (22.1 ± 2.6 y, 1.79 ± 0.06 m, 76.6 ± 6.2 kg; mean ± SD) participated in 2 trials where they performed a bout of unilateral leg resistance exercise and ingested a drink containing either 10 g essential amino acids with 10 g l-arginine (ARG) or an isonitrogenous control (CON). Femoral artery blood flow of both the nonexercised and exercised leg was measured continuously using pulsed-wave Doppler ultrasound, while rates of mixed and myofibrillar MPS were determined using a primed continuous infusion of L-[ring-(13)C(6)] or L-[ring-(2)H(5)]phenylalanine. The plasma arginine concentration increased 300% during the ARG trial but not during the CON trial (P < 0.001). Plasma nitrate, nitrite, and endothelin-1, all markers of NO synthesis, did not change during either the ARG or CON trial. Plasma growth hormone increased to a greater degree after exercise in the ARG trial than CON trial (P < 0.05). Femoral artery blood flow increased 270% above basal in the exercised leg (P < 0.001) but not in the nonexercised leg, with no differences between the ARG and CON trials. Mixed and myofibrillar MPS were both greater in the exercised leg compared with the nonexercised leg (P < 0.001), but did not differ between the ARG and CON treatments. We conclude that an oral bolus (10 g) of arginine does not increase NO synthesis or muscle blood flow. Furthermore, arginine does not enhance mixed or myofibrillar MPS either at rest or after resistance exercise beyond that achieved by feeding alone.