This study examined the impact of heat acclimation on improving exercise performance in cool and hot environments. Twelve trained cyclists performed tests of maximal aerobic power (VO2max), time-trial performance, and lactate threshold, in both cool [13°C, 30% relative humidity (RH)] and hot (38°C, 30% RH) environments before and after a 10-day heat acclimation (∼50% VO2max in 40°C) program. The hot and cool condition VO2max and lactate threshold tests were both preceded by either warm (41°C) water or thermoneutral (34°C) water immersion to induce hyperthermia (0.8-1.0°C) or sustain normothermia, respectively. Eight matched control subjects completed the same exercise tests in the same environments before and after 10 days of identical exercise in a cool (13°C) environment. Heat acclimation increased VO2max by 5% in cool (66.8 ± 2.1 vs. 70.2 ± 2.3 ml·kg(-1)·min(-1), P = 0.004) and by 8% in hot (55.1 ± 2.5 vs. 59.6 ± 2.0 ml·kg(-1)·min(-1), P = 0.007) conditions. Heat acclimation improved time-trial performance by 6% in cool (879.8 ± 48.5 vs. 934.7 ± 50.9 kJ, P = 0.005) and by 8% in hot (718.7 ± 42.3 vs. 776.2 ± 50.9 kJ, P = 0.014) conditions. Heat acclimation increased power output at lactate threshold by 5% in cool (3.88 ± 0.82 vs. 4.09 ± 0.76 W/kg, P = 0.002) and by 5% in hot (3.45 ± 0.80 vs. 3.60 ± 0.79 W/kg, P < 0.001) conditions. Heat acclimation increased plasma volume (6.5 ± 1.5%) and maximal cardiac output in cool and hot conditions (9.1 ± 3.4% and 4.5 ± 4.6%, respectively). The control group had no changes in VO2max, time-trial performance, lactate threshold, or any physiological parameters. These data demonstrate that heat acclimation improves aerobic exercise performance in temperate-cool conditions and provide the scientific basis for employing heat acclimation to augment physical training programs.

Reactive hyperaemia is the increase in blood flow following arterial occlusion. The exact mechanisms mediating this response in skin are not fully understood. The purpose of this study was to investigate the individual and combined contributions of (1) sensory nerves and large-conductance calcium activated potassium (BK Ca ) channels, and (2) nitric oxide (NO) and prostanoids to cutaneous reactive hyperaemia. Laser-Doppler flowmetry was used to measure skin blood flow in a total of 18 subjects. Peak blood flow (BF) was defined as the highest blood flow value after release of the pressure cuff. Total hyperaemic response was calculated by taking the area under the curve (AUC) of the hyperaemic response minus baseline. Infusates were perfused through forearm skin using microdialysis in four sites. In the sensory nerve/BK Ca protocol:

The aim of this study was to explore heat acclimation effects on cutaneous vascular responses and sweating to local ACh infusions and local heating. We also sought to examine whether heat acclimation altered maximal skin blood flow. ACh (1, 10, and 100 mM) was infused in 20 highly trained cyclists via microdialysis before and after a 10-day heat acclimation program [two 45-min exercise bouts at 50% maximal O2 uptake (V̇o2max) in 40°C ( n = 12)] or control conditions [two 45-min exercise bouts at 50% V̇o2max in 13°C ( n = 8)]. Skin blood flow was monitored via laser-Doppler flowmetry (LDF), and cutaneous vascular conductance (CVC) was calculated as LDF ÷ mean arterial pressure. Sweat rate was measured by resistance hygrometry. Maximal brachial artery blood flow (forearm blood flow) was obtained by heating the contralateral forearm in a water spray device and measured by Doppler ultrasound. Heat acclimation increased %CVCmax responses to 1, 10, and 100 mM ACh (43.5 ± 3.4 vs. 52.6 ± 2.6% CVCmax, 67.7 ± 3.4 vs. 78.0 ± 3.0% CVCmax, and 81.0 ± 3.8 vs. 88.5 ± 1.1% CVCmax, respectively, all P < 0.05). Maximal forearm blood flow remained unchanged after heat acclimation (290.9 ± 12.7 vs. 269.9 ± 23.6 ml/min). The experimental group showed significant increases in sweating responses to 10 and 100 mM ACh (0.21 ± 0.03 vs. 0.31 ± 0.03 mg·cm−2·min−1 and 0.45 ± 0.05 vs. 0.67 ± 0.06 mg·cm−2·min−1, respectively, all P < 0.05), but not to 1 mM ACh (0.13 ± 0.02 vs. 0.18 ± 0.02 mg·cm−2·min−1, P = 0.147). No differences in any of the variables were found in the control group. Heat acclimation in highly trained subjects induced local adaptations within the skin microcirculation and sweat gland apparatus. Furthermore, maximal skin blood flow was not altered by heat acclimation, demonstrating that the observed changes were attributable to improvement in cutaneous vascular function and not to structural changes that limit maximal vasodilator capacity.

Obesity is a widespread and growing problem worldwide and is among the most important health challenges of the 21st century. 1 Exercise is an important component in the prevention and treatment of obesity and, thus, an accurate assessment of the patient's cardiorespiratory fitness (CRF) level to determine optimal workout intensities, exercise modes, and exercise routines is critical. 2 Moreover, a proper quantification and interpretation of CRF is important for assessing who has low CRF, underlying comorbidities, and increased disease risk.Peak oxygen uptake ( o 2 peak ) is routinely measured as a means of evaluating CRF by exercise physiologists, allied health-care providers, epidemiologists, Background: The quantifi cation and interpretation of cardiorespiratory fi tness (CRF) in obesity is important for adequately assessing cardiovascular conditioning , underlying comorbidities, and properly evaluating disease risk. We retrospectively compared peak oxygen uptake ( O 2 peak) (ie, CRF) in absolute terms, and relative terms (% predicted) using three currently suggested prediction equations (Equations R, W, and G). Methods: There were 19 nonobese and 66 obese participants. Subjects underwent hydrostatic weighing and incremental cycling to exhaustion. Subject characteristics were analyzed by independent t test, and % predicted O 2 peak by a two-way analysis of variance (group and equation) with repeated measures on one factor (equation). Results: O 2 peak (L/min) was not different between nonobese and obese adults (2.35 Ϯ 0.80 [SD] vs2.39 Ϯ 0.68 L/min). O 2 peak was higher ( P , .02) relative to body mass and lean body mass in the nonobese (34 Ϯ 8 mL/min/kg vs 22 Ϯ 5 mL/min/kg, 42 Ϯ 9 mL/min/lean body mass vs 37 Ϯ 6 mL/min/lean body mass). Cardiorespiratory fi tness assessed as % predicted was not different in the nonobese and obese (91% Ϯ 17% predicted vs 95% Ϯ 15% predicted) using Equation R, while using Equation W and G, CRF was lower ( P , .05) but within normal limits in the obese (94 Ϯ 15 vs 87 Ϯ 11; 101% Ϯ 17% predicted vs 90% Ϯ 12% predicted, respectively), depending somewhat on sex. Conclusions: Traditional methods of reporting O 2 peak do not allow adequate assessment and quantifi cation of CRF in obese adults. Predicted O 2 peak does allow a normalized evaluation of CRF in the obese, although care must be taken in selecting the most appropriate prediction equation, especially in women. In general, otherwise healthy obese are not grossly deconditioned as is commonly believed, although CRF may be slightly higher in nonobese subjects depending on the uniqueness of the prediction equation. CHEST 2012; 141(4):1031-1039Abbreviations: CRF 5 cardiorespiratory fi tness; LBM 5 lean body mass; MW 5 measured weight; PW 5 predicted weight; o 2 5 oxygen uptake; o 2 peak 5 peak oxygen uptake.