The purpose of this study was to determine whether the trajectory and magnitude of physiological adaptation to controlled work rate heat acclimation (HEAT) differ between male and female highly trained endurance runners, while comparing adaptations with work rate matched temperate exercise training (TEMP). Eighteen highly trained endurance runners (8 males, 10 females) completed two seven-session interventions consisting of HEAT (40°C, 35% relative humidity [RH]) and TEMP (22°C, 35% RH) in a randomized, counterbalanced crossover design. Each session consisted of 60 min of running at 50% of velocity at maximal oxygen uptake. Physiological adaptation was quantified as the change (Δ) relative to session 1 for core temperature (T c ), skin temperature, heart rate (HR), whole-body sweat rate (WBSR), and plasma volume (PV). No intervention × sex × session interactions were observed for T c , HR, or WBSR (p > 0.05), indicating that the trajectory of adaptation did not differ between sexes or interventions. Likewise, no sex differences in the overall magnitude of adaptation were observed for any HEAT outcome. Significant main effects of intervention demonstrated greater reductions in mean and peak T c ; baseline, mean, and peak HR; as well as greater increases in WBSR during HEAT compared with TEMP (p < 0.05). PV did not change following either intervention. Male and female highly trained endurance runners exhibited comparable thermoregulatory and cardiovascular adaptation to controlled work rate heat acclimation. Although work rate matched temperate exercise induced partial physiological adaptation, environmental heat stress enhanced the overall adaptation magnitude without altering the adaptation trajectory between sexes.
This reanalysis challenges the original interpretation that maximal oxygen uptake increased linearly during the 10-wk strenuous endurance program investigated by Hickson et al. (1977). Using mixed-effects modeling of weekly individual data, adaptations were better described by curvilinear trajectories with diminishing returns. Systematic interindividual variability in response magnitude remained despite a normalized, “maximal” training stimulus. These findings demonstrate the value of revisiting legacy datasets to refine understanding of human adaptability and inform individualized exercise prescription.
We compared peripheral mechanisms of exercise intolerance in heart failure with preserved ejection fraction (HFpEF) patients and healthy older adults. HFpEF patients exhibited significantly greater intermuscular steatosis and impaired whole body and quadriceps oxidative capacity [i.e., peak O 2 uptake (V̇o 2peak ) and phosphocreatine recovery time constant (τPCr), respectively], all of which were associated with impaired exercise tolerance. However, increased intermuscular steatosis was not associated with impaired V̇o 2peak and τPCr, suggesting that steatosis and impaired oxidative capacity affect exercise tolerance through different physiological mechanisms.
This study examined whether hormonal and body composition responses to 10-weeks of U.S. Army Basic Combat Training (BCT) differ by baseline testosterone and sex. Methods: Male (n=97) and female (n=105) trainees were stratified at baseline as having LOW (men <10.4 nmol/L; women <0.82 nmol/L) or NORMAL baseline testosterone. We measured serum total and free testosterone, sex hormone binding globulin (SHBG), luteinizing hormone (LH) and estradiol (E2) at weeks 0, 2, 4, 6, 8, and 9 and cortisol weekly; dual-energy X-ray absorptiometry (DXA) assessed body composition at week 0 and 9. Linear mixed models tested time and group effects; generalized linear models related baseline testosterone status and testosterone area under the curve with changes in body composition. Results: In LOW women, testosterone increased at each timepoint (all p<0.01), reaching concentrations 53% higher at week 9 compared to week 0 (30.2± 7.8 vs 19.7± 3.2 ng/dl). In men, testosterone increased (LOW: +76%; NORMAL: +23%) across BCT (all p<0.05), except at week 2. Among LOW men, concentrations stabilized by week 4 (344.8± 81.4 ng/dl) and remained normal. Cortisol was highest at baseline and declined in all men and in NORMAL women. LH and E2 remained stable in both sexes, while SHBG declined only in women, independent of baseline testosterone. Neither baseline testosterone nor cumulative exposure were associated with changes in lean or fat mass. Conclusions: SHBG and cortisol trajectories differed by sex and baseline testosterone status. Testosterone changes were sex specific, reflecting an anabolic training environment in men and modest increased androgen availability in LOW women.
Pulsatile Perfusion Therapy (PPT), a method we developed to induce 0.1 Hz hemodynamic oscillations (10-second cycles), protects blood oxygen saturation during ischemia. PPT via oscillatory lower body negative pressure (LBNP) protected cerebrovascular blood oxygen saturation (ScO 2 ) during simulated hemorrhage in humans (induced via LBNP). Thigh cuff compressions are a new approach to achieve similar 0.1 Hz hemodynamic oscillations. We hypothesized that PPT via thigh cuff compressions would attenuate reductions in cerebral blood flow and cerebrovascular blood oxygen saturation during LBNP in humans. Fifteen healthy humans (6F/9M; age, 25.8 ± 4.5 y) completed two protocols of -60 mmHg LBNP. In the PPT condition, thigh cuffs intermittently inflated and deflated in 10-s cycles during the LBNP protocol. In the control condition (CON), the thigh cuffs remained deflated. Internal carotid artery (ICA) blood flow and ScO 2 were measured continuously. PPT attenuated reductions in ICA blood flow (PPT: -17.6 ± 11.3% vs. CON: -31.0 ± 11.8%; P=0.02) and ScO 2 (PPT: -5.2 ± 2.4% vs. CON: -7.1 ± 3.6%; P=0.07) compared to CON. These data provide evidence for PPT as a potential intervention for the treatment of cerebral hypoperfusion during hemorrhage.
