Akerman Ashley P, Lucas Samuel J E, Katare Rajesh, Cotter James D
School of Physical Education, Sport and Exercise Sciences, Division of Sciences, University of Otago, Dunedin, New Zealand.
Department of Physiology, Division of Health Sciences, University of Otago, Dunedin, New Zealand.
Front Physiol. 2017 Oct 9;8:756. doi: 10.3389/fphys.2017.00756. eCollection 2017.
Exercise and exogenous heat each stimulate multiple adaptations, but their roles are not well delineated, and that of the related stressor, dehydration, is largely unknown. While severe and prolonged hypohydration potentially "silences" the long-term heat acclimated phenotype, mild and transient dehydration may enhance cardiovascular and fluid-regulatory adaptations. We tested the hypothesis that exogenous heat stress and dehydration additively potentiate acute (24 h) cardiovascular and hematological outcomes following exercise. In a randomized crossover study, 10 physically-active volunteers (mean ± SD: 173 ± 11 cm; 72.1 ± 11.5 kg; 24 ± 3 year; 6 females) completed three trials of 90-min orthostatically-stressful calisthenics, in: (i) temperate conditions (22°C, 50% rh, no airflow; CON); (ii) heat (40°C, 60% rh) whilst euhydrated (HEAT), and (iii) heat with dehydration (no fluid ~16 h before and during exercise; HEAT+DEHY). Using linear mixed effects model analyses, core temperature (T) rose 0.7°C more in HEAT than CON (95% CL: [0.5, 0.9]; < 0.001), and another 0.4°C in HEAT+DEHY ([0.2, 0.5]; < 0.001, vs. HEAT). Skin temperature also rose 1.2°C more in HEAT than CON ([0.6, 1.8]; < 0.001), and similarly to HEAT+DEHY ( = 0.922 vs. HEAT). Peak heart rate was 40 b·min higher in HEAT than in CON ([28, 51]; < 0.001), and another 15 b·min higher in HEAT+DEHY ([3, 27]; = 0.011, vs. HEAT). Mean arterial pressure at 24-h recovery was not consistently below baseline after CON or HEAT ( ≥ 0.452), but was reduced 4 ± 1 mm Hg after HEAT+DEHY ([0, 8]; = 0.020 vs. baseline). Plasma volume at 24 h after exercise increased in all trials; the 7% increase in HEAT was not reliably more than in CON (5%; = 0.335), but was an additional 4% larger after HEAT+DEHY ([1, 8]; = 0.005 vs. HEAT). Pooled-trial correlational analysis showed the rise in T predicted the hypotension ( = -0.4) and plasma volume expansion ( = 0.6) at 24 h, with more hypotension reflecting more plasma expansion ( = -0.5). In conclusion, transient dehydration with heat potentiates short-term (24-h) hematological (hypervolemic) and cardiovascular (hypotensive) outcomes following calisthenics.
运动和外源性热刺激均可引发多种适应性变化,但其作用尚未明确界定,而相关应激因素脱水的作用在很大程度上仍不清楚。虽然严重且持续的低水合状态可能会“消除”长期热适应表型,但轻度和短暂的脱水可能会增强心血管和液体调节适应性。我们检验了这样一种假设,即外源性热应激和脱水会在运动后相加增强急性(24小时)心血管和血液学指标。在一项随机交叉研究中,10名身体活跃的志愿者(平均±标准差:身高173±11厘米;体重72.1±11.5千克;年龄24±3岁;6名女性)完成了三项90分钟的体位性应激健身操试验,分别在:(i)常温条件下(22°C,相对湿度50%,无气流;CON);(ii)热环境(40°C,相对湿度60%)且水合正常(HEAT),以及(iii)热环境且伴有脱水(运动前及运动期间约16小时无液体摄入;HEAT+DEHY)。使用线性混合效应模型分析,核心温度(T)在HEAT组比CON组升高了0.7°C(95%置信区间:[0.5, 0.9];P<0.001),在HEAT+DEHY组比HEAT组又升高了0.4°C([0.2, 0.5];P<0.001,与HEAT组相比)。皮肤温度在HEAT组比CON组也升高了1.2°C([0.6, 1.8];P<0.001),与HEAT+DEHY组相似(与HEAT组相比P = 0.922)。峰值心率在HEAT组比CON组高40次·分钟([28, 51];P<0.001),在HEAT+DEHY组比HEAT组又高15次·分钟([3, 27];P = 0.011,与HEAT组相比)。运动后24小时恢复时的平均动脉压在CON组或HEAT组后并非始终低于基线(P≥0.452),但在HEAT+DEHY组后降低了4±1毫米汞柱([0, 8];与基线相比P = 0.020)。运动后24小时的血浆量在所有试验中均增加;HEAT组增加7%并不比CON组增加5%更显著(P = 0.335),但在HEAT+DEHY组后比HEAT组又额外增加了4%([1, 8];与HEAT组相比P = 0.005)。合并试验的相关性分析表明,T的升高可预测24小时时的低血压(P = -0.4)和血浆量扩张(P = 0.6),低血压越明显反映血浆扩张越显著(P = -0.5)。总之,热环境下的短暂脱水会增强健身操后短期(24小时)的血液学(血容量过多)和心血管(低血压)指标。