Heat and Dehydration Additively Enhance Cardiovascular Outcomes following Orthostatically-Stressful Calisthenics Exercise

Abstract

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 (TCORE) rose 0.7°C more in HEAT than CON (95% CL: [0.5, 0.9]; p < 0.001), and another 0.4°C in HEAT+DEHY ([0.2, 0.5]; p < 0.001, vs. HEAT). Skin temperature also rose 1.2°C more in HEAT than CON ([0.6, 1.8]; p < 0.001), and similarly to HEAT+DEHY (p = 0.922 vs. HEAT). Peak heart rate was 40 b·min−1 higher in HEAT than in CON ([28, 51]; p < 0.001), and another 15 b·min−1 higher in HEAT+DEHY ([3, 27]; p = 0.011, vs. HEAT). Mean arterial pressure at 24-h recovery was not consistently below baseline after CON or HEAT (p ≥ 0.452), but was reduced 4 ± 1 mm Hg after HEAT+DEHY ([0, 8]; p = 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%; p = 0.335), but was an additional 4% larger after HEAT+DEHY ([1, 8]; p = 0.005 vs. HEAT). Pooled-trial correlational analysis showed the rise in TCORE predicted the hypotension (r = −0.4) and plasma volume expansion (r = 0.6) at 24 h, with more hypotension reflecting more plasma expansion (r = −0.5). In conclusion, transient dehydration with heat potentiates short-term (24-h) hematological (hypervolemic) and cardiovascular (hypotensive) outcomes following calisthenics.

Five weeks of heat training increases haemoglobin mass in elite cyclists

“…Accordingly, Nielsen et al (1993) found PV to increase by 13% following 9-12 days with exhausting exercise training conducted at 40 • C. Similarly, Lorenzo and co-workers (2010) found PV to increase by 6.5% following 10 days with light exercise training conducted at 40 • C. In a similar manner, we have previously found PV to be elevated by 6% following 10 days of similar heat training as in the present study (Keiser et al, 2015). The magnitude of acute increase in PV has been suggested to be related to the magnitude of fluid loss during heat exercise (Akerman, Lucas, Katare, & Cotter, 2017). Despite the increase in PV being a robust observation following heat training, we have recently conducted a 5-…”

“…In a similar manner, we have previously found PV to be elevated by 6% following 10 days of similar heat training as in the present study (Keiser et al., 2015). The magnitude of acute increase in PV has been suggested to be related to the magnitude of fluid loss during heat exercise (Akerman, Lucas, Katare, & Cotter, 2017). Despite the increase in PV being a robust observation following heat training, we have recently conducted a 5‐week heat training study (i.e.…”

Influence of Sodium Citrate Supplementation after Dehydrating Exercise on Responses of Stress Hormones to Subsequent Endurance Cycling Time-Trial in the Heat

“…Our observation of blunted ALDO response to TT together with lower ALDO concentrations before and after exercise in CIT compared to PLC trial is in good agreement with previous data that were collected in a temperate environment [10]. The novel aspect of the current study is that it demonstrates the capacity of CIT to reduce blood ALDO levels during exercise-heat stress that is strong stimulus for ALDO secretion [34]. Similarly, after CIT ingestion, significantly lower blood CORT levels occurred prior to and immediately after completing the TT.…”

“…Simultaneous influence of various stressors may provide a larger physiological stress to the body and induce larger neuroendocrine responses than exposure to a single stressor [27]. Indeed, prolonged exercise in the heat compared to the same exercise performed in a temperate environment induces greater increases in blood PRL [28,29], GH [30,31], CORT [32,33] and ALDO [34] levels, but to the best of our knowledge, it is unknown whether CIT or NaHCO 3 ingestion alleviates responses of stress hormones to prolonged endurance exercise in warm environments.…”

Maximizing Cellular Adaptation to Endurance Exercise in Skeletal Muscle

“…Long-term passive heat acclimation increased HIF1-a protein levels and thus induced larger upregulation of gene activation for Vegf, HO1, epo, and epo receptor in response to a single bout of heat stress (Maloyan et al, 2005). Heat stress increases circulating epo concentration in humans, although this finding is not universal despite substantive heat stress (Akerman et al, 2017), perhaps reflecting the important potentiating effect gained from long-term heat acclimation. The success of runners from Kenya and Ethiopia in endurance-based events in the context of thermal adaptation warrants consideration.…”