| 1. |
- Ciuha, Urša, et al.
(author)
-
Heat acclimation enhances the cold-induced vasodilation response.
- 2021
-
In: European Journal of Applied Physiology. - : Springer Nature. - 1439-6319 .- 1439-6327. ; 121:11, s. 3005-3015
-
Journal article (peer-reviewed)abstract
- PURPOSE: It has been reported that the cold-induced vasodilation (CIVD) response can be trained using either regular local cold stimulation or exercise training. The present study investigated whether repeated exposure to environmental stressors, known to improve aerobic performance (heat and/or hypoxia), could also provide benefit to the CIVD response.METHODS: Forty male participants undertook three 10-day acclimation protocols including daily exercise training: heat acclimation (HeA; daily exercise training at an ambient temperature, Ta = 35 °C), combined heat and hypoxic acclimation (HeA/HypA; daily exercise training at Ta = 35 °C, while confined to a simulated altitude of ~ 4000 m) and exercise training in normoxic thermoneutral conditions (NorEx; no environmental stressors). To observe potential effects of the local acclimation on the CIVD response, participants additionally immersed their hand in warm water (35 °C) daily during the HeA/HypA and NorEx. Before and after the acclimation protocols, participants completed hand immersions in cold water (8 °C) for 30 min, followed by 15-min recovery phases. The temperature was measured in each finger.RESULTS: Following the HeA protocol, the average temperature of all five fingers was higher during immersion (from 13.9 ± 2.4 to 15.5 ± 2.5 °C; p = 0.04) and recovery (from 22.2 ± 4.0 to 25.9 ± 4.9 °C; p = 0.02). The HeA/HypA and NorEx protocols did not enhance the CIVD response.CONCLUSION: Whole-body heat acclimation increased the finger vasodilatory response during cold-water immersion, and enhanced the rewarming rate of the hand, thus potentially contributing to improved local cold tolerance. Daily hand immersion in warm water for 10 days during HeA/Hyp and NorEx, did not contribute to any changes in the CIVD response.
|
|
| 2. |
- Sotiridis, Alexandros, et al.
(author)
-
Exercise cardiorespiratory and thermoregulatory responses in normoxic, hypoxic and hot environment following 10-day continuous hypoxic exposure
- 2018
-
In: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 125:4, s. 1284-1295
-
Journal article (peer-reviewed)abstract
- We examined the effects of acclimatization to normobaric hypoxia on aerobic performance and exercise thermoregulatory responses under normoxic, hypoxic and hot conditions. Twelve males performed tests of maximal oxygen uptake (V̇O2max) in normoxic (NOR), hypoxic (13.5% FiO2; HYP) and hot (35℃, 50% RH; HE) conditions in a randomized manner before and after a 10-day continuous normobaric hypoxic exposure (FiO2 = 13.65(0.35)%, PiO2 = 87(3) mmHg). The acclimatization protocol included daily exercise (60min @ 50% hypoxia-specific peak power output, Wpeak). All maximal tests were preceded by a steady-state exercise (30 min at 40% Wpeak) to assess the sweating response. Hematological data were assessed from venous blood samples obtained before and after acclimatization. V̇O2max increased by 10.7% (P = 0.002) and 7.9% (P = 0.03) from pre- to post-acclimatization in NOR and HE, respectively, whereas no differences were found in HYP (pre: 39.9(3.8) vs post: 39.4(5.1) mL.kg-1.min-1, P = 1.0). However, the increase in V̇O2max did not translate into increased Wpeak in either NOR or HE. Maximal heart rate and ventilation remained unchanged following acclimatization. Νo differences were noted in the sweating gain and thresholds independent of the acclimatization or environmental conditions. Hypoxic acclimatization markedly increased hemoglobin (P < 0.001), hematocrit (P < 0.001) and extracellular HSP72 (P = 0.01). These data suggest that 10 days of normobaric hypoxic acclimatization combined with moderate-intensity exercise training improves V̇O2max in NOR and HE, but does not seem to affect exercise performance or thermoregulatory responses in any of the tested environmental conditions.
|
|
| 3. |
- Sotiridis, Alexandros, et al.
(author)
-
Heat acclimation does not affect maximal aerobic power in thermoneutral normoxic or hypoxic conditions
- 2019
-
In: Experimental Physiology. - 0958-0670 .- 1469-445X. ; 104, s. 1250-1261
-
Journal article (peer-reviewed)abstract
- What is the central question of this study? Controlled-hyperthermia heat acclimation protocols induce an array of thermoregulatory and cardiovascular adaptations that facilitate exercise in hot conditions. We investigated whether this ergogenic potential can be transferred to thermoneutral normoxic or hypoxic exercising conditions. What is the main finding and its importance? We show that heat acclimation did not affect maximal cardiac output or maximal aerobic power in thermoneutral normoxic/hypoxic conditions. Heat acclimation augmented the sweating response in thermoneutral normoxic conditions. The cross-adaptation theory according to which heat acclimation could facilitate hypoxic exercise capacity is not supported by our data. ABSTRACT: Heat acclimation (HA) mitigates heat-induced decrements in maximal aerobic power (V̇O2peak ) and augments exercise thermoregulatory responses in the heat. Whether this beneficial effect of HA is observed in hypoxic or thermoneutral conditions remains unresolved. We explored the effects of HA on exercise cardiorespiratory and thermoregulatory responses in normoxic, hypoxic, and hot conditions. Twelve males (V̇O2peak 54.7(5.7) mL·kg-1 ·min-1 ) participated in a HA protocol comprising 10 daily 90-min controlled-hyperthermia (target rectal temperature, Tre = 38.5 °C) exercise sessions. Before and after HA, we determined V̇O2peak in thermoneutral normoxic (NOR), thermoneutral hypoxic (13.5% Fi O2 ; HYP) and hot (35 °C, 50% RH; HE) conditions in a randomized and counterbalanced order. Preceding each maximal cycling test, a 30-min steady-state exercise at 40% of the NOR peak power output (Wpeak ) was employed to evaluate thermoregulatory responses. HA induced the expected adaptations in HE: reduced Tre and submaximal heart rate (HR), enhanced sweating response and expanded plasma volume. However, HA did not affect V̇O2peak or maximal cardiac output (COmax ) (P = 0.61). Wpeak was increased post-HA in NOR (P < 0.001) and HE (P < 0.001) by 41 ± 21 and 26 ± 22 W, respectively but not in HYP (P = 0.14). Gross mechanical efficiency was higher (P = 0.004) whereas resting Tre and sweating thresholds were lower (P < 0.01) post-HA across environments. Nevertheless, the gain of the sweating response decreased (P = 0.05) in HYP. In conclusion, our data do not support a beneficial cross-over effect of HA on V̇O2peak in normoxic or hypoxic conditions. This article is protected by copyright.
|
|
