Temperature of Ingested Water and Thermoregulation During Moderate-Intensity Exercise

1997 ◽  
Vol 22 (5) ◽  
pp. 479-493 ◽  
Author(s):  
Gregory S. Wimer ◽  
David R. Lamb ◽  
William M. Sherman ◽  
Scott C. Swanson

The effect of the temperature of ingested water on the rise in core temperature (TCO) during exercise is not clear. Seven trained subjects were recruited to complete 2 hr of recumbent cycling at 51% VO2 peak in a temperate environment (Ta = 26 °C, relative humidity = 40%) on four occasions, while ingesting either no fluid (trial NF26), cold water (0.5 °C; trial CD26), cool water (19 °C; trial CL26), or warm water (38 °C; trial WA26) during the second hour of exercise. A fifth trial was conducted during which convective and radiative heat loss were reduced by raising Ta to 31 °C. During this trial, subjects ingested cold water (0.5 °C; trial CD31). When compared to WA26, over the second hour of exercise, CD26 attenuated the time-averaged changes in (TCO) and forearm blood flow and decreased whole-body sweat rate and forearm sweat rate (p < .05). Similarly, relative to WA26, the CL26 trial attenuated the time-averaged changes in TCO and reduced whole-body sweat rate (p < .05) during the second hour of exercise, but CL26 had no significant effect on forearm sweat rate or blood flow. Finally, regardless of beverage temperature, water ingestion (vs. NF26) reduced the time-averaged changes in TCO and in heat storage during the second hour of exercise (p < .05). Key words: exertion, temperature regulation, skin blood flow, body temperatures, fluid replacement

Aging Cell ◽  
2021 ◽  
Vol 20 (2) ◽  
Author(s):  
Carolyn Chee ◽  
Chris E. Shannon ◽  
Aisling Burns ◽  
Anna L. Selby ◽  
Daniel Wilkinson ◽  
...  

2019 ◽  
Vol 30 (2) ◽  
pp. 525-533 ◽  
Author(s):  
J J Steventon ◽  
C Foster ◽  
H Furby ◽  
D Helme ◽  
R G Wise ◽  
...  

Abstract Long-term exercise interventions have been shown to be a potent trigger for both neurogenesis and vascular plasticity. However, little is known about the underlying temporal dynamics and specifically when exercise-induced vascular adaptations first occur, which is vital for therapeutic applications. In this study, we investigated whether a single session of moderate-intensity exercise was sufficient to induce changes in the cerebral vasculature. We employed arterial spin labeling magnetic resonance imaging to measure global and regional cerebral blood flow (CBF) before and after 20 min of cycling. The blood vessels’ ability to dilate, measured by cerebrovascular reactivity (CVR) to CO2 inhalation, was measured at baseline and 25-min postexercise. Our data showed that CBF was selectively increased by 10–12% in the hippocampus 15, 40, and 60 min after exercise cessation, whereas CVR to CO2 was unchanged in all regions. The absence of a corresponding change in hippocampal CVR suggests that the immediate and transient hippocampal adaptations observed after exercise are not driven by a mechanical vascular change and more likely represents an adaptive metabolic change, providing a framework for exploring the therapeutic potential of exercise-induced plasticity (neural, vascular, or both) in clinical and aged populations.


2017 ◽  
Vol 122 (5) ◽  
pp. 1125-1133 ◽  
Author(s):  
Sandra A. Billinger ◽  
Jesse C. Craig ◽  
Sarah J. Kwapiszeski ◽  
Jason-Flor V. Sisante ◽  
Eric D. Vidoni ◽  
...  

The dynamic response to a stimulus such as exercise can reveal valuable insights into systems control in health and disease that are not evident from the steady-state perturbation. However, the dynamic response profile and kinetics of cerebrovascular function have not been determined to date. We tested the hypotheses that bilateral middle cerebral artery blood flow mean velocity (MCAV) increases exponentially following the onset of moderate-intensity exercise in 10 healthy young subjects. The MCAV response profiles were well fit to a delay (TD) + exponential (time constant, τ) model with substantial agreement for baseline [left (L): 69, right (R): 64 cm/s, coefficient of variation (CV) 11%], response amplitude (L: 16, R: 13 cm/s, CV 23%), TD (L: 54, R: 52 s, CV 9%), τ (L: 30, R: 30 s, CV 22%), and mean response time (MRT) (L: 83, R: 82 s, CV 8%) between left and right MCAV as supported by the high correlations (e.g., MRT r = 0.82, P < 0.05) and low CVs. Test-retest reliability was high with CVs for the baseline, amplitude, and MRT of 3, 14, and 12%, respectively. These responses contrasted markedly with those of three healthy older subjects in whom the MCAV baseline and exercise response amplitude were far lower and the kinetics slowed. A single older stroke patient showed baseline ipsilateral MCAV that was lower still and devoid of any exercise response whatsoever. We conclude that kinetics analysis of MCAV during exercise has significant potential to unveil novel aspects of cerebrovascular function in health and disease. NEW & NOTEWORTHY Resolution of the dynamic stimulus-response profile provides a greater understanding of the underlying the physiological control processes than steady-state measurements alone. We report a novel method of measuring cerebrovascular blood velocity (MCAv) kinetics under ecologically valid conditions from rest to moderate-intensity exercise. This technique reveals that brain blood flow increases exponentially following the onset of exercise with 1) a strong bilateral coherence in young healthy individuals, and 2) a potential for unique age- and disease-specific profiles.


1995 ◽  
Vol 79 (4) ◽  
pp. 1112-1119 ◽  
Author(s):  
W. L. Kenney ◽  
C. W. Ho

During dynamic exercise in warm environments, requisite increases in skin and active muscle blood flows are supported by increasing cardiac output (Qc) and redistributing flow away from splanchnic and renal circulations. To examine the effect of age on these responses, six young (Y; 26 +/- 2 yr) and six older (O; 64 +/- 2 yr) men performed upright cycle exercise at 35 and 60% of peak O2 consumption (VO2peak) in 22 and 36 degrees C environments. To further isolate age, the two age groups were closely matched for VO2peak, weight, surface area, and body composition. Measurements included heart rate, Qc (CO2 rebreathing), skin blood flow (from increases in forearm blood flow (venous occlusion plethysmography), splanchnic blood flow (indocyanine green dilution), renal blood flow (p-amino-hippurate clearance), and plasma norepinephrine concentration. There were no significant age differences in Qc; however, in both environments the O group maintained Qc at a higher stroke volume and lower heart rate. At 60% VO2peak, forearm blood flow was significantly lower in the O subjects in each environment. Splanchnic blood flow fell (by 12–14% in both groups) at the lower intensity, then decreased to a greater extent at 60% VO2peak in Y than in O subjects (e.g., -45 +/- 2 vs. -33 +/- 3% for the hot environment, P < 0.01). Renal blood flow was lower at rest in the O group, remained relatively constant at 35% VO2peak, then decreased by 20–25% in both groups at 60% VO2peak. At 60% VO2peak, 27 and 37% more total blood flow was redistributed away from these two circulations in the Y than in the O group at 22 and 36 degrees, respectively. It was concluded that the greater increase in skin blood flow in Y subjects is partially supported by a greater redistribution of blood flow away from splanchnic and renal vascular beds.


2011 ◽  
Vol 21 (6) ◽  
pp. 492-500 ◽  
Author(s):  
Matthew J.E. Lott ◽  
Stuart D.R. Galloway

This study assessed fluid balance, sodium losses, and effort intensity during indoor tennis match play (17 ± 2 °C, 42% ± 9% relative humidity) over a mean match duration of 68.1 ± 12.8 min in 16 male tennis players. Ad libitum fluid intake was recorded throughout the match. Sweat loss from change in nude body mass; sweat electrolyte content from patches applied to the forearm, calf, and thigh, and back of each player; and electrolyte balance derived from sweat, urine, and daily food-intake analysis were measured. Effort intensity was assessed from on-court heart rate compared with data obtained during a maximal treadmill test. Sweat rate (M ± SD) was 1.1 ± 0.4 L/hr, and fluid-ingestion rate was 1.0 ± 0.6 L/hr (replacing 93% ± 47% of fluid lost), resulting in only a small mean loss in body mass of 0.15% ± 0.74%. Large interindividual variabilities in sweat rate (range 0.3–2.0 L/hr) and fluid intake (range 0.31–2.52 L/hr) were noted. Whole-body sweat sodium concentration was 38 ± 12 mmol/L, and total sodium losses during match play were 1.1 ± 0.4 g (range 0.5–1.8 g). Daily sodium intake was 2.8 ± 1.1 g. Indoor match play largely consisted of low-intensity exercise below ventilatory threshold (mean match heart rate was 138 ± 24 beats/min). This study shows that in moderate indoor temperature conditions players ingest sufficient fluid to replace sweat losses. However, the wide range in data obtained highlights the need for individualized fluid-replacement guidance.


2012 ◽  
Vol 97 (11) ◽  
pp. 4193-4200 ◽  
Author(s):  
A. J. Fahey ◽  
N. Paramalingam ◽  
R. J. Davey ◽  
E. A. Davis ◽  
T. W. Jones ◽  
...  

Context: Recently we showed that a 10-sec maximal sprint effort performed before or after moderate intensity exercise can prevent early hypoglycemia during recovery in individuals with type 1 diabetes mellitus (T1DM). However, the mechanisms underlying this protective effect of sprinting are still unknown. Objective: The objective of the study was to test the hypothesis that short duration sprinting increases blood glucose levels via a disproportionate increase in glucose rate of appearance (Ra) relative to glucose rate of disappearance (Rd). Subjects and Experimental Design: Eight T1DM participants were subjected to a euglycemic-euinsulinemic clamp and, together with nondiabetic participants, were infused with [6,6-2H]glucose before sprinting for 10 sec and allowed to recover for 2 h. Results: In response to sprinting, blood glucose levels increased by 1.2 ± 0.2 mmol/liter (P &lt; 0.05) within 30 min of recovery in T1DM participants and remained stable afterward, whereas glycemia rose by only 0.40 ± 0.05 mmol/liter in the nondiabetic group. During recovery, glucose Ra did not change in both groups (P &gt; 0.05), but glucose Rd in the nondiabetic and diabetic participants fell rapidly after exercise before returning within 30 min to preexercise levels. After sprinting, the levels of plasma epinephrine, norepinephrine, and GH rose transiently in both experimental groups (P &lt; 0.05). Conclusion: A sprint as short as 10 sec can increase plasma glucose levels in nondiabetic and T1DM individuals, with this rise resulting from a transient decline in glucose Rd rather than from a disproportionate rise in glucose Ra relative to glucose Rd as reported with intense aerobic exercise.


Medicine ◽  
2021 ◽  
Vol 100 (31) ◽  
pp. e25368
Author(s):  
Robson F. Borges ◽  
Gaspar R. Chiappa ◽  
Paulo T. Muller ◽  
Alexandra Correa Gervazoni Balbuena de Lima ◽  
Lawrence Patrick Cahalin ◽  
...  

Author(s):  
Ed A. Maunder ◽  
Helen E. Bradley ◽  
Colleen S. Deane ◽  
Adrian B. Hodgson ◽  
Michael Jones ◽  
...  

Altering dietary carbohydrate (CHO) intake modulates fuel utilization during exercise. However, there has been no systematic evaluation of metabolic responses to graded changes in short-term (< 1 week) dietary CHO intake. Thirteen active men performed interval running exercise combined with isocaloric diets over 3 days before evaluation of metabolic responses to 60-min running at 65% V̇O2max on three occasions. Diets contained lower (LOW, 2.40 ± 0.66 g CHO.kg-1.d-1, 21.3 ± 0.5% of energy intake [EI]), moderate (MOD, 4.98 ± 1.31 g CHO.kg-1.d-1, 46.3 ± 0.7% EI), or higher (HIGH, 6.48 ± 1.56 g CHO.kg-1.d-1, 60.5 ± 1.6% EI) CHO. Pre-exercise muscle glycogen content was lower in LOW (54.3 ± 26.4 mmol.kg-1 wet weight [ww]) compared to MOD (82.6 ± 18.8 mmol.kg-1 ww) and HIGH (80.4 ± 26.0 mmol.kg-1 ww, P<0.001; MOD vs. HIGH, P=0.85). Whole-body substrate oxidation, systemic responses, and muscle substrate utilization during exercise indicated increased fat and decreased CHO metabolism in LOW (RER: 0.81 ± 0.01) compared to MOD (RER 0.86 ± 0.01, P = 0.0005) and HIGH (RER: 0.88 ± 0.01, P < 0.0001; MOD vs. HIGH, P=0.14). Higher basal muscle expression of genes encoding proteins implicated in fat utilization was observed in LOW. In conclusion, muscle glycogen availability and subsequent metabolic responses to exercise were resistant to increases in dietary CHO intake from ~5.0 to ~6.5 g CHO.kg-1.d-1 (46% to 61% EI), while muscle glycogen, gene expression and metabolic responses were sensitive to more marked reductions in CHO intake (~2.4 g CHO.kg-1.d-1, ~21% EI).


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