Critical Environmental Core Temperature Limits and Heart Rate Thresholds across the Adult Age Span (PSU HEAT Project).

The frequency, duration, and severity of extreme heat events have increased and are projected to continue to increase throughout the next century. As a result, there is an increased risk of excessive heat- and cardiovascular-related morbidity and mortality during these extreme heat events. Therefore, the purposes of this investigation were to establish (1) critical environmental core temperature (Tc) limits for middle-aged adults (MA), (2) environmental thresholds that cause heart rate (HR) to progressively rise in MA and older (O) adults, and (3) examine critical environmental Tc limits and HR environmental thresholds across the adult age span. Thirty-three young (Y) (15 F; 23±3 yrs), 28 MA (17F; 51±6 yrs), and 31 O (16F; 70±3 yrs) subjects were exposed to progressive heat stress in an environmental chamber in a warm-humid (WH, 34-36°C, 50-90% rh) and a hot-dry (HD, 38°C-52°C, <30% rh) environment while exercising at a low metabolic rate reflecting activities of daily living (~1.8 METS). In both environments, there was a main effect of age on the critical environmental Tc limit and environmental HR thresholds (main effect of age all p < 0.001). Across the life span, critical environmental Tc and HR thresholds decline linearly with age in HD environments (R2 ≥ 0.3), and curvilinearly in WH environments (R2 ≥ 0.4). These data support an age-associated shift in critical environmental Tc limits and HR thresholds toward lower environmental conditions, and can be used to develop evidence-based safety guidelines to minimize future heat-related morbidity and mortality across the adult age span.

The vascular response to acute sauna heating is similar in young and middle-aged adults.

Sauna has been linked to a reduction of cardiovascular disease risk and is a promising nonpharmacological treatment for populations at risk of cardiovascular disease. This study examined the vascular response to an acute bout of sauna heating in young and middle-aged individuals. Ten young (25 ± 4 yr, 6 males and 4 females) and eight middle-aged adults (56 ± 4 yr, 4 males and 4 females) underwent 40 min of sauna exposure at 80°C. Esophageal and intramuscular temperatures, brachial and superficial femoral artery blood flow, artery diameter, and shear rates were recorded at baseline and following heat exposure. Brachial artery flow-mediated dilation (FMD) was measured at baseline and following 90 min of recovery. Esophageal and muscle temperatures increased similarly in the young and middle-aged adults by 1.5 ± 0.53 and 1.95 ± 0.70°C, respectively (P < 0.05). The shear rate increased by 170-200% (P < 0.001), while blood flow increased by 180-390% (P < 0.001) in the superficial femoral and brachial arteries, respectively, and did not differ between age groups (P = 0.190-0.899). Systolic blood pressure was reduced from 135 ± 17 to 122 ± 20 mmHg (P = 0.017) in middle-aged participants. These data indicate that young and middle-aged adults have similar vascular responses to acute sauna heating.NEW & NOTEWORTHY Sauna therapy has been shown to improve cardiovascular health and function in older adults and individuals with cardiovascular disease risk factors. Specifically, improvements in vascular function have been reported and have been attributed to the increased hemodynamic stimuli on the vasculature associated with thermal stress. The present study quantified this hemodynamic response to a sauna protocol associated with improved cardiovascular health across the lifespan. Our data show that middle-aged adults have the same shear rate and blood flow response to sauna as young adults.

Vascular dysfunction and the age-related decline in critical power.

Ageing results in lower exercise tolerance, manifested as decreased critical power (CP). We examined whether the age-related decrease in CP occurs independently of changes in muscle mass and whether it is related to impaired vascular function. Ten older (63.1 ± 2.5 years) and 10 younger (24.4 ± 4.0 years) physically active volunteers participated. Physical activity was measured with accelerometry. Leg muscle mass was quantified with dual X-ray absorptiometry. The CP and maximum power during a graded exercise test (PGXT ) of single-leg knee-extension exercise were determined over the course of four visits. During a fifth visit, vascular function of the leg was assessed with passive leg movement (PLM) hyperaemia and leg blood flow and vascular conductance during knee-extension exercise at 10 W, 20 W, slightly below CP (90% CP) and PGXT . Despite not differing in leg lean mass (P = 0.901) and physical activity (e.g., steps per day, P = 0.735), older subjects had ∼30% lower mass-specific CP (old = 3.20 ± 0.94 W kg-1 vs. young = 4.60 ± 0.87 W kg-1 ; P < 0.001). The PLM-induced hyperaemia and leg blood flow and/or conductance were blunted in the old at 20 W, 90% CP and PGXT (P < 0.05). When normalized for leg muscle mass, CP was strongly correlated with PLM-induced hyperaemia (R2  = 0.52; P < 0.001) and vascular conductance during knee-extension exercise at 20 W (R2  = 0.34; P = 0.014) and 90% CP (R2  = 0.39; P = 0.004). In conclusion, the age-related decline in CP is not only an issue of muscle quantity, but also of impaired muscle quality that corresponds to impaired vascular function.

Rapid onset vasodilation during baroreceptor loading and unloading.

The purpose of these experiments was to determine if the increase in vascular conductance following a single muscle contraction (50% of maximal voluntary contraction) (6 male and 6 female subjects) was altered during baroceptor loading and unloading. Rapid onset vasodilation (ROV) was determined by measuring brachial artery blood flow (Doppler ultrasound) and blood pressure (Finapress monitor). Brachial artery vascular conductance was calculated by dividing blood flow by mean arterial pressure. ROV was described by the area under the Δvascular conductance (VC)-time curve during the 30 s following muscle contraction. ROV was determined using chamber pressures of +20, +10, 0, -10, -20, and -40 mmHg (lower body positive and negative pressure, LBPP, and LBNP). We tested the hypothesis that the impact of baroreceptor loading and unloading produces a proportion change in ROV. The level of ROV following each contraction was proportional to the peak force (r2 = 0.393, P = 0.0001). Peak force was therefore used as a covariate in further analysis. ROV during application of -40 mmHg LBNP (0.345 ± 0.229 mL·mmHg-1) was lower than that observed at Control (0.532 ± 0.284 mL·mmHg-1, P = 0.034) and +20 mmHg LBPP (0.658 ± 0.364 mL·mmHg-1, P = 0.0008). ROV was linearly related to chamber pressure from -40 to +20 mmHg chamber pressure (r2 = 0.512, P = 0.022, n = 69) and from -20 to +10 mmHg chamber pressure (r2= 0.973, P < 0.0425, n = 45), Overall, vasoconstrictor tone altered with physiologically relevant baroreceptor loading and unloading resulted in a proportion change in ROV.NEW & NOTEWORTHY Rapid onset vasodilation (ROV) was linearly related to the peak force of each single 1-s muscle contraction. In addition, ROV is reduced by baroreceptor unloading (LBNP: -10, -120, and -40 mmHg) and increased by baroreceptor loading (LBPP: +10 and +20 mmHg). Without accounting for peak force and the level of baroreceptor engagement makes comparison of ROV in subjects of differing muscle size or strength untenable.

The exercise power-duration relationship is equally reproducible in eumenorrheic female and male humans.

This study aims to investigate the effect of the menstrual cycle (MC) on exercise performance across the power-duration relationship (PDR). We hypothesized females would exhibit greater variability in the PDR across the MC than males across a similar timespan, with critical power (CP) and work-prime (W') being lower during the early follicular phase than the late follicular and midluteal phases. Seven eumenorrheic, endurance-trained female adults performed multiple constant-load-to-task-failure and maximum-power tests at three timepoints across the MC (early follicular, late follicular, and midluteal phases). Ten endurance-trained male adults performed the same tests approximately 10 days apart. No differences across the PDR were observed between MC phases (CP: 186.74 ± 31.00 W, P = 0.955, CV = 0.81 ± 0.65%) (W': 7,961.81 ± 2,537.68 J, P = 0.476, CV = 10.48 ± 3.06%). CP was similar for male and female subjects (11.82 ± 1.42 W·kg-1 vs. 11.56 ± 1.51 W·kg-1, respectively) when controlling for leg lean mass. However, W' was larger (P = 0.047) for male subjects (617.28 ± 130.10 J·kg-1) than female subjects (490.03 ± 136.70 J·kg-1) when controlling for leg lean mass. MC phase does not need to be controlled when conducting aerobic endurance performance research on eumenorrheic female subjects without menstrual dysfunction. Nevertheless, several sex differences in the power-duration relationship exist, even after normalizing for body composition. Therefore, previous studies describing the physiology of exercise performance in male subjects may not perfectly describe that of female subjects.NEW & NOTEWORTHY Females are often excluded from exercise performance research due to experimental challenges in controlling for the menstrual cycle (MC), causing uncertainty regarding how the MC impacts female performance. The present study examined the influences that biological sex and the MC have on the power-duration relationship (PDR) by comparing critical power (CP), Work-prime (W'), and maximum power output (PMAX) in males and females. Our data provide evidence that the MC does not influence the PDR and that females exhibit similar reproducibility as males. Thus, when conducting aerobic endurance exercise research on eumenorrheic females without menstrual dysfunction, the phase of the MC does not need to be controlled. Although differences in body composition account for some differences between the sexes, sex differences in W' and PMAX persisted even after normalizing for different metrics of body composition. These data highlight the necessity and feasibility of examining sex differences in performance, as previously generated male-only data within the literature may not apply to female subjects.

Localized Heat Therapy Improves Mitochondrial Respiratory Capacity but Not Fatty Acid Oxidation.

AIM: Mild heat stress can improve mitochondrial respiratory capacity in skeletal muscle. However, long-term heat interventions are scarce, and the effects of heat therapy need to be understood in the context of the adaptations which follow the more complex combination of stimuli from exercise training. The purpose of this work was to compare the effects of 6 weeks of localized heat therapy on human skeletal muscle mitochondria to single-leg interval training. METHODS: Thirty-five subjects were assigned to receive sham therapy, short-wave diathermy heat therapy, or single-leg interval exercise training, localized to the quadriceps muscles of the right leg. All interventions took place 3 times per week. Muscle biopsies were performed at baseline, and after 3 and 6 weeks of intervention. Mitochondrial respiratory capacity was assessed on permeabilized muscle fibers via high-resolution respirometry. RESULTS: The primary finding of this work was that heat therapy and exercise training significantly improved mitochondrial respiratory capacity by 24.8 ± 6.2% and 27.9 ± 8.7%, respectively (p < 0.05). Fatty acid oxidation and citrate synthase activity were also increased following exercise training by 29.5 ± 6.8% and 19.0 ± 7.4%, respectively (p < 0.05). However, contrary to our hypothesis, heat therapy did not increase fatty acid oxidation or citrate synthase activity. CONCLUSION: Six weeks of muscle-localized heat therapy significantly improves mitochondrial respiratory capacity, comparable to exercise training. However, unlike exercise, heat does not improve fatty acid oxidation capacity.