Effects of Cannabidiol Ingestion on Thermoregulatory and Inflammatory Responses to Treadmill Exercise in the Heat in Recreationally Active Males.

PURPOSE: Exertional heat stress can induce systemic endotoxin exposure and a pro-inflammatory cascade, likely impairing thermoregulation. Cannabidiol (CBD) is protective in pre-clinical models of tissue ischaemia and inflammation. Therefore, this study examined the effects of CBD ingestion on exercise-induced thermoregulatory and inflammatory responses. METHODS: In a randomised, double-blinded study, thirteen active males (age 25 ± 5 y; peak oxygen uptake [V̇O2peak] 50.4 ± 3.2 mL/kg/min) ingested 298 mg CBD or placebo 105 minutes before 1 h treadmill exercise (60-65% V̇O2peak) in 32 °C and 50% relative humidity. Core temperature, skin temperature, heart rate, subjective outcomes and sweat loss were assessed during/after exercise. Plasma osmolality, plasma volume changes and plasma markers of intestinal damage (I-FABP), monocyte activation (CD14) and inflammatory cytokine responses (IL-6, IL-8 and TNF-α) were assessed at baseline, pre-exercise, 20- and 90-min post-exercise. RESULTS: Core temperature (∆ 1.69 ± 0.48 °C [CBD] and 1.79 ± 0.53 °C [Placebo]) and I-FABP increased during exercise, with no differences between conditions (p > 0.050). Mean (95% CI) CD14 was 1776 (463 to 3090) pg/mL greater 90 min post-exercise in placebo (p = 0.049). Median (interquartile range) peak IL-6 concentration was -0.8 (-1.1, -0.3) pg/mL less in CBD (p = 0.050), whilst the between-conditions difference in IL-6 area under curve was -113 (-172, 27) pg/mL·270 min (p = 0.054). CONCLUSIONS: CBD did not affect thermoregulation during exertional heat stress but appeared to elicit minor immunosuppressive effects, reducing CD14 and IL-6 responses, warranting investigation in humans under more severe heat strain and other pro-inflammatory scenarios.

Fluid and electrolyte balance following consumption of skimmed milk and a plant-based soya beverage at rest in euhydrated males.

PURPOSE: Cow's milk is one of the most hydrating beverages, but many individuals choose not to consume dairy in their diet due to intolerance, allergy, or dietary preference. Milk is commonly replaced with plant-based beverages, including soya which has the most comparable protein content, but little is known about their hydration potential. This study compared fluid and electrolyte balance responses between a soya beverage and skimmed cow's milk. METHODS: Ten healthy males [age 27 (6) y; body mass index 24.6 (2.3) kg/m2] completed two randomised counterbalanced trials, involving consuming 1000 mL water from approximately isocaloric amounts of skimmed cow's milk (MILK) or a sweetened soya beverage (SOYA), in four aliquots over 30 min in a euhydrated fasted state. Volume, specific gravity, and electrolyte (sodium, potassium, chloride) concentrations were determined in total-void urine samples collected pre-/post-beverage ingestion, and hourly for 180 min thereafter. Hunger, thirst, nausea and stomach fullness were rated proximal to urine samples. RESULTS: Total urine mass (MILK, 986 ± 254 g; SOYA, 950 ± 248 g; P = 0.435) and urine specific gravity (P = 0.156) did not differ between trials. Potassium balance was greater in SOYA 0-180 min post-beverage (P ≤ 0.013), whilst chloride balance was greater in MILK 0-120 min post-beverage (P ≤ 0.036). Sodium balance (P = 0.258), total electrolyte balance (P = 0.258), and subjective measures (P ≥ 0.139) were not different between trials. CONCLUSION: Replacing cow's milk with a soya beverage did not negatively impact fluid balance in healthy young males, making it a viable option for those who choose not to consume dairy in their diet.

Skeletal muscle mitochondrial correlates of critical power and W' in healthy active individuals.

The asymptote (critical power; CP) and curvature constant (W') of the hyperbolic power-duration relationship can predict performance within the severe-intensity exercise domain. However, the extent to which these parameters relate to skeletal muscle mitochondrial content and respiratory function is not known. Fifteen males (peak O2 uptake, 52.2 ± 8.7 mL kg-1 min-1; peak work rate, 366 ± 40 W; and gas exchange threshold, 162 ± 41 W) performed three to five constant-load tests to task failure for the determination of CP (246 ± 44 W) and W' (18.6 ± 4.1 kJ). Skeletal muscle biopsies were obtained from the vastus lateralis to determine citrate synthase (CS) activity, as a marker of mitochondrial content, and the ADP-stimulated respiration (P) and maximal electron transfer (E) through mitochondrial complexes (C) I-IV. The CP was positively correlated with CS activity (absolute CP, r = 0.881, P < 0.001; relative CP, r = 0.751, P = 0.001). The W' was not correlated with CS activity (P > 0.05). Relative CP was positively correlated with mass-corrected CI + IIE (r = 0.659, P = 0.038), with absolute CP being inversely correlated with CS activity-corrected CIVE (r = -0.701, P = 0.024). Relative W' was positively correlated with CS activity-corrected CI + IIP (r = 0.713, P = 0.021) and the phosphorylation control ratio (r = 0.661, P = 0.038). There were no further correlations between CP or W' and mitochondrial respiratory variables. These findings support the assertion that skeletal muscle mitochondrial oxidative capacity is positively associated with CP and that this relationship is strongly determined by mitochondrial content.

Post-exercise rehydration: Comparing the efficacy of three commercial oral rehydration solutions.

Introduction: This study compared the efficacy of three commercial oral rehydration solutions (ORS) for restoring fluid and electrolyte balance, after exercise-induced dehydration. Method: Healthy, active participants (N = 20; ♀ = 3; age ∼27 y, V˙O2peak ∼52 ml/kg/min) completed three randomised, counterbalanced trials whereby intermittent exercise in the heat (∼36°C, ∼50% humidity) induced ∼2.5% dehydration. Subsequently, participants rehydrated (125% fluid loss in four equal aliquots at 0, 1, 2, 3 h) with a glucose-based (G-ORS), sugar-free (Z-ORS) or amino acid-based sugar-free (AA-ORS) ORS of varying electrolyte composition. Urine output was measured hourly and capillary blood samples collected pre-exercise, 0, 2 and 5 h post-exercise. Sodium, potassium, and chloride concentrations in urine, sweat, and blood were determined. Results: Net fluid balance peaked at 4 h and was greater in AA-ORS (141 ± 155 ml) and G-ORS (101 ± 195 ml) than Z-ORS (-47 ± 208 ml; P ≤ 0.010). Only AA-ORS achieved positive sodium and chloride balance post-exercise, which were greater for AA-ORS than G-ORS and Z-ORS (P ≤ 0.006), as well as for G-ORS than Z-ORS (P ≤ 0.007) from 1 to 5 h. Conclusion: when provided in a volume equivalent to 125% of exercise-induced fluid loss, AA-ORS produced comparable/superior fluid balance and superior sodium/chloride balance responses to popular glucose-based and sugar-free ORS.

Ischaemic preconditioning blunts exercise-induced mitochondrial dysfunction, speeds oxygen uptake kinetics but does not alter severe-intensity exercise capacity.

NEW FINDINGS: What is the central question of this study? Ischaemic preconditioning is a novel pre-exercise priming strategy. We asked whether ischaemic preconditioning would alter mitochondrial respiratory function and pulmonary oxygen uptake kinetics and improve severe-intensity exercise performance. What is the main finding and its importance? Ischaemic preconditioning expedited overall pulmonary oxygen uptake kinetics and appeared to prevent an increase in leak respiration, proportional to maximal electron transfer system and ADP-stimulated respiration, that was evoked by severe-intensity exercise in sham-control conditions. However, severe-intensity exercise performance was not improved. The results do not support ischaemic preconditioning as a pre-exercise strategy to improve exercise performance in recreationally active participants. ABSTRACT: We examined the effect of ischaemic preconditioning (IPC) on severe-intensity exercise performance, pulmonary oxygen uptake ( V ̇ O 2 ${\dot V_{{{\rm{O}}_{\rm{2}}}}}$ ) kinetics, skeletal muscle oxygenation (muscle tissue O2 saturation index) and mitochondrial respiration. Eight men underwent contralateral IPC (4 × 5 min at 220 mmHg) or sham-control (SHAM; 20 mmHg) before performing a cycling time-to-exhaustion test (92% maximum aerobic power). Muscle (vastus lateralis) biopsies were obtained before IPC or SHAM and ∼1.5 min postexercise. The time to exhaustion did not differ between SHAM and IPC (249 ± 37 vs. 240 ± 32 s; P = 0.62). Pre- and postexercise ADP-stimulated (P) and maximal (E) mitochondrial respiration through protein complexes (C) I, II and IV did not differ (P > 0.05). Complex I leak respiration was greater postexercise compared with baseline in SHAM, but not in IPC, when normalized to wet mass (P = 0.01 vs. P = 0.19), mitochondrial content (citrate synthase activity, P = 0.003 vs. P = 0.16; CI+IIP, P = 0.03 vs. P = 0.23) and expressed relative to P (P = 0.006 vs. P = 0.30) and E (P = 0.004 vs. P = 0.26). The V ̇ O 2 ${\dot V_{{{\rm{O}}_{\rm{2}}}}}$ mean response time was faster (51.3 ± 15.5 vs. 63.7 ± 14.5 s; P = 0.003), with a smaller slow component (270 ± 105 vs. 377 ± 188 ml min-1 ; P = 0.03), in IPC compared with SHAM. The muscle tissue O2 saturation index did not differ between trials (P > 0.05). Ischaemic preconditioning expedited V ̇ O 2 ${\dot V_{{{\rm{O}}_{\rm{2}}}}}$ kinetics and appeared to prevent an increase in leak respiration through CI, when expressed proportional to E and P evoked by severe-intensity exercise, but did not improve exercise performance.