Kinesiology

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Cardiac autonomic control in elite juvenile cyclists
(Medicina Sportiva, 2011-03-02) Brown, S. J.; Raman, A.; Schlader, Z. J.; Stannard, S. R.
Introduction: Frequency domain analysis of heart rate variability (HRV) may potentially identify the dominance exhibited by different branches of the autonomic nervous system. Autonomic contribution to cardio-deceleration following exercise has been studied in adults; however, no data are available for endurance trained juvenile athletes. Aim: The aim of this study was to evaluate the association between the increase in heart rate following exercise and any change in HRV frequency components in trained juveniles. Methods: A 6 min resting ECG (lead 2) was recorded from trained juvenile cyclists (23 male, 7 female, mean age 14.7 years), before (Pre) and after (Post) incremental exercise to volitional exhaustion on a stationary cycle ergometer. Each subject performed a progressive ramp protocol where power increased by 20W min-1, with initial power set at 60 W for females and 100 W for males. Oxygen uptake (VO2) was measured using breath-by-breath techniques. ECG was analysed in both time and frequency domains using commercially available software. Results: Mean VO2 max was 75.5 ml Kg-1 min-1, and mean power at VO2 max was 440 W. The R-R interval SD was lower following exercise (Pre: 86ms vs. Post: 36ms, P<0.01). Normalised high frequency HRV was lower (Pre: 36.5 vs. Post: 18.7, P<0.01) and normalised low frequency HRV was higher (Pre: 58.5 vs. Post: 75.0, P<0.01) following exercise. Conclusions: In elite juvenile athletes there were no associations between exercise-induced changes in high frequency variability and heart rate (R2=0.073). This suggests that in elite juveniles, the heart may be less sensitive to vagal influences- a suggestion further supported by the relatively high pre-exercise resting heart rates with normal high frequency variability.
Adverse metabolic response to regular exercise: Is it a rare or common occurrence?
(Public Library of Science, 2012) Bouchard, C.; Blair, S.N.; Church, T.S.; Earnest, C.P.; Slentz, C.A.; Rankinen, T.
Background: Individuals differ in the response to regular exercise. Whether there are people who experience adverse changes in cardiovascular and diabetes risk factors has never been addressed. Methodology/Principal Findings: An adverse response is defined as an exercise-induced change that worsens a risk factor beyond measurement error and expected day-to-day variation. Sixty subjects were measured three times over a period of three weeks, and variation in resting systolic blood pressure (SBP) and in fasting plasma HDL-cholesterol (HDL-C), triglycerides (TG), and insulin (FI) was quantified. The technical error (TE) defined as the within-subject standard deviation derived from these measurements was computed. An adverse response for a given risk factor was defined as a change that was at least two TEs away from no change but in an adverse direction. Thus an adverse response was recorded if an increase reached 10 mm Hg or more for SBP, 0.42 mmol/L or more for TG, or 24 pmol/L or more for FI or if a decrease reached 0.12 mmol/L or more for HDL-C. Completers from six exercise studies were used in the present analysis: Whites (N = 473) and Blacks (N = 250) from the HERITAGE Family Study; Whites and Blacks from DREW (N = 326), from INFLAME (N = 70), and from STRRIDE (N = 303); and Whites from a University of Maryland cohort (N = 160) and from a University of Jyvaskyla study (N = 105), for a total of 1,687 men and women. Using the above definitions, 126 subjects (8.4%) had an adverse change in FI. Numbers of adverse responders reached 12.2% for SBP, 10.4% for TG, and 13.3% for HDL-C. About 7% of participants experienced adverse responses in two or more risk factors. Conclusions/Significance: Adverse responses to regular exercise in cardiovascular and diabetes risk factors occur. Identifying the predictors of such unwarranted responses and how to prevent them will provide the foundation for personalized exercise prescription.
One of these things is not like the other: the heterogeneity of the cerebral circulation
(The Journal of Physiology, 2013-01-14) Schlader, Z. J.; Lucas, R. A. I.; Pearson, J.; Crandall, C. G.
The human cerebral vasculature is highly sensitive to changes in arterial blood gases (i.e. arterial carbon dioxide and oxygen tensions), such that hypercapnia/hypoxia and hypocapnia/hyperoxia cause global increases and decreases in cerebral blood flow. It is generally accepted that all cerebral arter‐ioles – traditionally considered to be the regulators of brain blood flow – are equally sensitive to changes in arterial blood gases. However, this classic dogma may not be the case.
Acute volume expansion attenuates hyperthermia-induced reductions in cerebral perfusion during simulated hemorrhage
(Journal of Applied Physiology, 2013-06-15) Schlader, Z. J.; Seifert, T.; Wilson, T. E.; Bundgaard-Nielsen, M.; Secher, N. H.; Crandall, C. G.
Hyperthermia reduces the capacity to withstand a simulated hemorrhagic challenge, but volume loading preserves this capacity. This study tested the hypotheses that acute volume expansion during hyperthermia increases cerebral perfusion and attenuates reductions in cerebral perfusion during a simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Eight healthy young male subjects underwent a supine baseline period (pre-LBNP), followed by 15- and 30-mmHg LBNP while normothermic, hyperthermic (increased pulmonary artery blood temperature ∼1.1°C), and following acute volume infusion while hyperthermic. Primary dependent variables were mean middle cerebral artery blood velocity (MCAvmean), serving as an index of cerebral perfusion; mean arterial pressure (MAP); and cardiac output (thermodilution). During baseline, hyperthermia reduced MCAvmean (P = 0.001) by 12 ± 9% relative to normothermia. Volume infusion while hyperthermic increased cardiac output by 2.8 ± 1.4 l/min (P < 0.001), but did not alter MCAvmean (P = 0.99) or MAP (P = 0.39) compared with hyperthermia alone. Relative to hyperthermia, at 30-mmHg LBNP acute volume infusion attenuated reductions (P < 0.001) in cardiac output (by 2.5 ± 0.9 l/min; P < 0.001), MAP (by 5 ± 6 mmHg; P = 0.004), and MCAvmean (by 12 ± 13%; P = 0.002). These data indicate that acute volume expansion does not reverse hyperthermia-induced reductions in cerebral perfusion pre-LBNP, but that it does attenuate reductions in cerebral perfusion during simulated hemorrhage in hyperthermic humans.
Hyperthermia does not alter the capacity to increase cerebral perfusion during a cognitive task
(Experimental Physiology, 2013-07-17) Schlader, Z. J.; Lucas, R. A. I.; Pearson, J.; Crandall, C. G.
This study tested the hypothesis that hyperthermia attenuates the increase in cerebral perfusion during cognitive activation. Mean middle cerebral artery blood velocity (MCAVmean) served as an index of cerebral perfusion, while the nBack test (a test of working memory) was the cognitive task. Hyperthermia was characterized by elevations (P < 0.001) in skin (by 5.0 ± 0.8°C) and intestinal temperatures (by 1.3 ± 0.1°C) and reductions (P < 0.020) in mean arterial pressure (by 11 ± 10 mmHg), end‐tidal CO2 tension (by 3 ± 6 mmHg) and MCAVmean (by 10 ± 9 cm s−1). Hyperthermia had no influence on nBack test performance (mean difference from normothermia to hyperthermia, −1 ± 11%; P= 0.276) or, counter to the hypothesis, the increase in MCAVmean during nBack testing (mean difference from normothermia to hyperthermia: 0 ± 16 cm s−1; P= 0.608). These findings indicate that the capacity to increase cerebral perfusion during cognitive activation is unaffected by hyperthermia.
Hypercapnia-induced increases in cerebral blood flow do not improve lower body negative pressure tolerance during hyperthermia
(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2013-09-15) Lucas, R. A. I.; Pearson, J.; Schlader, Z. J.; Crandall, C. G.
Heat-related decreases in cerebral perfusion are partly the result of ventilatory-related reductions in arterial CO2 tension. Cerebral perfusion likely contributes to an individual's tolerance to a challenge like lower body negative pressure (LBNP). Thus increasing cerebral perfusion may prolong LBNP tolerance. This study tested the hypothesis that a hypercapnia-induced increase in cerebral perfusion improves LBNP tolerance in hyperthermic individuals. Eleven individuals (31 ± 7 yr; 75 ± 12 kg) underwent passive heat stress (increased intestinal temperature ∼1.3°C) followed by a progressive LBNP challenge to tolerance on two separate days (randomized). From 30 mmHg LBNP, subjects inhaled either (blinded) a hypercapnic gas mixture (5% CO2, 21% oxygen, balanced nitrogen) or room air (SHAM). LBNP tolerance was quantified via the cumulative stress index (CSI). Mean middle cerebral artery blood velocity (MCAvmean,) and end-tidal CO2 (PetCO2) were also measured. CO2 inhalation of 5% increased PetCO2 at ∼40 mmHg LBNP (by 16 ± 4 mmHg) and at LBNP tolerance (by 18 ± 5 mmHg) compared with SHAM (P < 0.01). Subsequently, MCAvmean was higher in the 5% CO2 trial during ∼40 mmHg LBNP (by 21 ± 12 cm/s, ∼31%) and at LBNP tolerance (by 18 ± 10 cm/s, ∼25%) relative to the SHAM (P < 0.01). However, hypercapnia-induced increases in MCAvmean did not alter LBNP tolerance (5% CO2 CSI: 339 ± 155 mmHg × min; SHAM CSI: 273 ± 158 mmHg × min; P = 0.26). These data indicate that inhaling a hypercapnic gas mixture increases cerebral perfusion during LBNP but does not improve LBNP tolerance when hyperthermic.
The relative overlooking of human behavioral temperature regulation – A paradox worth resolving
(Temperature, 2014-03-22) Schlader, Z. J.
It has long been appreciated that behavior is the most powerful and diverse thermoregulatory mechanism. In animal-based studies a behavioral assay is typically the first assessment when investigating the effect of a perturbation on thermoregulation, highlighting its importance. Oddly however, such an approach has been largely ignored in human research.
Normothermic central hypovolemia tolerance reflects hyperthermic tolerance
(Clinical Autonomic Research, 2014-04-04) Schlader, Z. J.; Crandall, C. G.
Purpose To test the hypothesis that those who are highly tolerant to lower body negative pressure (LBNP) while normothermic are also highly tolerant to this challenge while hyperthermic. Methods Sixty pairs of normothermic and hyperthermic LBNP tests to pre-syncope were evaluated. LBNP tolerance was quantified via the cumulative stress index (CSI), which is calculated as the sum of the product of the LBNP level and the duration of each level until test termination (i.e., 20 mmHg × 3 min + 30 mmHg × 3 min, etc.). CSI was compared between normothermic and hyperthermic trials. Internal and skin temperatures, heart rate, and arterial pressure were measured throughout. Results Hyperthermia reduced (P<0.001) CSI from 997 ± 437 to 303 ± 213 mmHg min. There was a positive correlation between normothermic and hyperthermic LBNP tolerance (R2 = 0.38; P<0.001). As a secondary analysis, the 20 trials with the highest LBNP tolerance while normothermic were identified (indicated as the HIGH group; CSI 1,467 ± 356 mmHg min), as were the 20 trials with the lowest normothermic tolerance (indicated as the LOW group; CSI 565 ± 166 mmHg min; P<0.001 between groups). While hyperthermia unanimously reduced CSI in both HIGH and LOW groups, in this hyperthermic condition CSI was ~threefold higher in the HIGH group (474 ± 226 mmHg min) relative to the LOW group (160 ± 115 mmHg min; P<0.001). Conclusions LBNP tolerance while hyperthermic is related to normothermic tolerance and, associated with this finding, those who have a high LBNP tolerance while normothermic remain relatively tolerant when hyperthermic.
Tissue oxygen saturation during hyperthermic progressive central hypovolemia
(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2014-09-15) Schlader, Z. J.; Rivas, E.; Soller, B. R.; Convertino, V. A.; Crandall, C. G.
During normothermia, a reduction in near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (So2) is an indicator of central hypovolemia. Hyperthermia increases skin blood flow and reduces tolerance to central hypovolemia, both of which may alter the interpretation of tissue So2 during central hypovolemia. This study tested the hypothesis that maximal reductions in tissue So2 would be similar throughout normothermic and hyperthermic central hypovolemia to presyncope. Ten healthy males (means ± SD; 32 ± 5 yr) underwent central hypovolemia via progressive lower-body negative pressure (LBNP) to presyncope during normothermia (skin temperature ≈34°C) and hyperthermia (+1.2 ± 0.1°C increase in internal temperature via a water-perfused suit, skin temperature ≈39°C). NIRS-derived forearm (flexor digitorum profundus) tissue So2 was measured throughout and analyzed as the absolute change from pre-LBNP. Hyperthermia reduced (P < 0.001) LBNP tolerance by 49 ± 33% (from 16.7 ± 7.9 to 7.2 ± 3.9 min). Pre-LBNP, tissue So2 was similar (P = 0.654) between normothermia (74 ± 5%) and hyperthermia (73 ± 7%). Tissue So2 decreased (P < 0.001) throughout LBNP, but the reduction from pre-LBNP to presyncope was greater during normothermia (−10 ± 6%) than during hyperthermia (−6 ± 5%; P = 0.041). Contrary to our hypothesis, these findings indicate that hyperthermia is associated with a smaller maximal reduction in tissue So2 during central hypovolemia to presyncope.
Active and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge
(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2014-10-01) Pearson, J.; Lucas, R. A. I.; Schlader, Z. J.; Zhao, J.; Gagnon, D.; Crandall, C. G.
Passive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage (lower body negative pressure; LBNP). We tested whether exercise-induced heat stress reduces LBNP tolerance to a greater extent relative to passive heat stress, when skin and core temperatures are similar. Eight participants (6 males, 32 ± 7 yr, 176 ± 8 cm, 77.0 ± 9.8 kg) underwent LBNP to presyncope on three separate and randomized occasions: 1) passive heat stress, 2) exercise in a hot environment (40°C) where skin temperature was moderate (36°C, active 36), and 3) exercise in a hot environment (40°C) where skin temperature was matched relative to that achieved during passive heat stress (∼38°C, active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Before LBNP, increases in core temperature from baseline were not different between trials (1.18 ± 0.20°C; P > 0.05). Also before LBNP, mean skin temperature was similar between passive heat stress (38.2 ± 0.5°C) and active 38 (38.2 ± 0.8°C; P = 0.90) trials, whereas it was reduced in the active 36 trial (36.6 ± 0.5°C; P ≤ 0.05 compared with passive heat stress and active 38). LBNP tolerance was not different between passive heat stress and active 38 trials (383 ± 223 and 322 ± 178 CSI, respectively; P = 0.12), but both were similarly reduced relative to active 36 (516 ± 147 CSI, both P ≤ 0.05). LBNP tolerance is not different between heat stresses induced either passively or by exercise in a hot environment when skin temperatures are similarly elevated. However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress.
The human thermoneutral and thermal comfort zones: Thermal comfort in your own skin blood flow
(Temperature, 2014-11-07) Schlader, Z. J.
Human thermoregulation is achieved via autonomic and behavioral responses. Autonomic responses involve 2 synchronous ‘components’. One counteracts large thermal perturbations, eliciting robust heat loss or gain (i.e., sweating or shivering). The other fends off smaller insults, relying solely on changes in sensible heat exchange (i.e., skin blood flow). This sensible component occurs within the thermoneutral zone [i.e., the ambient temperature range in which temperature regulation is achieved only by sensible heat transfer, without regulatory increases in metabolic heat production (e.g., shivering) or evaporative heat loss (e.g., sweating)].1 The combination of behavior and sensible heat exchange permits a range of conditions that are deemed thermally comfortable, which is defined as the thermal comfort zone.1 Notably, we spend the majority of our lives within the thermoneutral and thermal comfort zones. It is only when we are unable to stay within these zones that deleterious health and safety outcomes can occur (i.e., hypo- or hyperthermia). Oddly, although the thermoneutral zone and thermal preference (a concept similar to the thermal comfort zone) has been extensively studied in non-human animals, our understanding of human thermoregulation within the thermoneutral and thermal comfort zones remains rather crude.
Age-related changes to cardiac systolic and diastolic function during whole-body passive hyperthermia
(Experimental Physiology, 2015-01-15) Lucas, R. A. I.; Sarma, S.; Schlader, Z. J.; Pearson, J.; Crandall, C. G.
The effect of ageing on hyperthermia-induced changes in cardiac function is unknown. This study tested the hypothesis that hyperthermia-induced changes in left ventricular systolic and diastolic function are attenuated in older adults when compared with young adults. Eight older (71 ± 5 years old) and eight young adults (29 ± 5 years old), matched for sex, physical activity and body mass index, underwent whole-body passive hyperthermia. Mean arterial pressure (Finometer Pro), heart rate, forearm vascular conductance (venous occlusion plethysmography) and echocardiographic indices of diastolic and systolic function were measured during a normothermic supine period and again after an increase in internal temperature of ~1.0 °C. Hyperthermia decreased mean arterial pressure and left ventricular end-diastolic volumes and increased heart rate to a similar extent in both groups (P > 0.05). Ageing did not alter the magnitude of hyperthermia-induced changes in indices of systolic (lateral mitral annular S′ velocity) or diastolic function (lateral mitral annular E′ velocity, peak early diastolic filling and isovolumic relaxation time; P > 0.05). However, with hyperthermia the global longitudinal systolic strain increased in the older group, but was unchanged in the young group (P = 0.03). Also, older adults were unable to augment late diastolic ventricular filling [i.e. E/A ratio and A/(A + E) ratio] during hyperthermia, unlike the young (P <0.05). These findings indicate that older adults depend on a greater systolic contribution (global longitudinal systolic strain) to meet hyperthermic demand and that the atrial contribution to diastolic filling was not further augmented in older adults when compared with young adults.
Baroreceptor unloading does not limit forearm sweat rate during severe passive heat stress
(Journal of Applied Physiology, 2015-02-15) Schlader, Z. J.; Gagnon, D.; Lucas, R. A. I.; Pearson, J.; Crandall, C. G.
This study tested the hypothesis that sweat rate during passive heat stress is limited by baroreceptor unloading associated with heat stress. Two protocols were performed in which healthy subjects underwent passive heat stress that elicited an increase in intestinal temperature of ∼1.8°C. Upon attaining this level of hyperthermia, in protocol 1 (n = 10, 3 females) a bolus (19 ml/kg) of warm (∼38°C) isotonic saline was rapidly (5–10 min) infused intravenously to elevate central venous pressure (CVP), while in protocol 2 (n = 11, 5 females) phenylephrine was infused intravenously (60–120 μg/min) to return mean arterial pressure (MAP) to normothermic levels. In protocol 1, heat stress reduced CVP from 3.9 ± 1.9 mmHg (normothermia) to −0.6 ± 1.4 mmHg (P < 0.001), while saline infusion returned CVP to normothermic levels (5.1 ± 1.7 mmHg; P > 0.999). Sweat rate was elevated by heat stress (1.21 ± 0.44 mg·cm−2·min−1) but remained unchanged during rapid saline infusion (1.26 ± 0.47 mg·cm−2·min−1, P = 0.5), whereas cutaneous vascular conductance increased from 77 ± 10 to 101 ± 20% of local heating max (P = 0.029). In protocol 2, MAP was reduced with heat stress from 85 ± 7 mmHg to 76 ± 8 mmHg (P = 0.048). Although phenylephrine infusion returned MAP to normothermic levels (88 ± 7 mmHg; P > 0.999), sweat rate remained unchanged during phenylephrine infusion (1.39 ± 0.22 vs. 1.41 ± 0.24 mg·cm−2·min−1; P > 0.999). These data indicate that both cardiopulmonary and arterial baroreceptor unloading do not limit increases in sweat rate during passive heat stress.
Sympathetic activity during passive heat stress in healthy aged humans
(The Journal of Physiology, 2015-03-05) Gagnon, D.; Schlader, Z. J.; Crandall, C. G.
Cardiovascular adjustments during heat stress are generally attenuated in healthy aged humans, which could be due to lower increases in sympathetic activity compared to the young. We compared muscle sympathetic nerve activity (MSNA) between 11 young (Y: 28 ± 4 years) and 10 aged (A: 70 ± 5 years) subjects prior to and during passive heating. Furthermore, MSNA responses were compared when a cold pressor test (CPT) and lower body negative pressure (LBNP) were superimposed upon heating. Baseline MSNA burst frequency (Y: 15 ± 4 vs. A: 31 ± 3 bursts min−1, P ≤ 0.01) and burst incidence (Y: 26 ± 8 vs. A: 50 ± 7 bursts (100 cardiac cycles (CC))−1, P ≤ 0.01) were greater in the aged. Heat stress increased core temperature to a similar extent in both groups (Y: +1.2 ± 0.1 vs. A: +1.2 ± 0.0°C, P = 0.99). Absolute levels of MSNA remained greater in the aged during heat stress (burst frequency: Y: 47 ± 6 vs. A: 63 ± 11 bursts min−1, P ≤ 0.01; burst incidence: Y: 48 ± 8 vs. A: 67 ± 9 bursts (100 CC)−1, P ≤ 0.01); however, the increase in both variables was similar between groups (both P ≥ 0.1). The CPT and LBNP further increased MSNA burst frequency and burst incidence, although the magnitude of increase was similar between groups (both P ≥ 0.07). These results suggest that increases in sympathetic activity during heat stress are not attenuated in healthy aged humans.
Cognitive and perceptual responses during passive heat stress in younger and older adults
(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2015-05-15) Schlader, Z. J.; Gagnon, D.; Adams, A.; Rivas, E.; Cullum, C. M.; Crandall, C. G.
We tested the hypothesis that attention, memory, and executive function are impaired to a greater extent in passively heat-stressed older adults than in passively heat-stressed younger adults. In a randomized, crossover design, 15 older (age: 69 ± 5 yr) and 14 younger (age: 30 ± 4 yr) healthy subjects underwent passive heat stress and time control trials. Cognitive tests (outcomes: accuracy and reaction time) from the CANTAB battery evaluated attention [rapid visual processing (RVP), choice reaction time (CRT)], memory [spatial span (SSP), pattern recognition memory (PRM)], and executive function [one touch stockings of Cambridge (OTS)]. Testing was undertaken on two occasions during each trial, at baseline and after internal temperature had increased by 1.0 ± 0.2°C or after a time control period. For tests that measured attention, reaction time during RVP and CRT was slower (P ≤ 0.01) in the older group. During heat stress, RVP reaction time improved (P < 0.01) in both groups. Heat stress had no effect (P ≥ 0.09) on RVP or CRT accuracy in either group. For tests that measured memory, accuracy on SSP and PRM was lower (P < 0.01) in the older group, but there was no effect of heat stress (P ≥ 0.14). For tests that measured executive function, overall, accuracy on OTS was lower, and reaction time was slower in the older group (P ≤ 0.05). Reaction time generally improved during heat stress, but there was no effect of heat stress on accuracy in either group. These data indicate that moderate increases in body temperature during passive heat stress do not differentially compromise cognitive function in younger and older adults.
Heat acclimation improves heat exercise tolerance and heat dissipation in individuals with extensive skin grafts
(Journal of Applied Physiology, 2015-07-01) Schlader, Z. J.; Ganio, M. S.; Pearson, J.; Lucas, R. A. I.; Rivas, E.
Burn survivors with extensive skin grafts have impaired heat dissipation and thus heat tolerance. This study tested the hypothesis that heat acclimation (HA) improves these factors in this population. Thirty-four burn survivors were stratified into highly [>40% body surface area (BSA) grafted, n = 15] and moderately (17-40% BSA grafted, n = 19) grafted groups. Nine healthy nonburned subjects served as controls. Subjects underwent 7 days of HA involving 90 min of exercise at ∼50% peak oxygen uptake in 40°C, 30% relative humidity. On days 1 and 7, subjects exercised in the heat at a fixed rate of metabolic heat production. Pre-HA, all controls and 18/19 subjects in the 17–40% group completed 90 min of exercise. Conversely, heat exercise tolerance was lower (P < 0.01) in the >40% group, with 7/15 subjects not completing 90 min of exercise. Post-HA, heat exercise tolerance was similar between groups (P = 0.39) as all subjects, except one, completed 90 min of exercise. Pre-HA, the magnitude of the increase in internal temperature during exercise occurred sequentially (P ≤ 0.03) according to BSA grafted (>40%: 1.6 ± 0.5°C; 17–40%: 1.2 ± 0.3°C; control: 0.9 ± 0.2°C). HA attenuated (P < 0.01) increases in internal temperature in the control (by 0.2 ± 0.3°C), 17–40% (by 0.3 ± 0.3°C), and >40% (by 0.3 ± 0.4°C) groups, the magnitude of which was similar between groups (P = 0.42). These data indicate that HA improves heat tolerance and dissipation in burn survivors with grafted skin, and the magnitude of these improvements are not influenced by the extent of skin grafting.
Aerobic fitness is disproportionately low in adult burn survivors years after injury
(Journal of Burn Care and Research, 2015-07-01) Ganio, M. S.; Pearson, J.; Schlader, Z. J.; Brothers, R. M.; Lucas, R. A. I.; Rivas, E.; Kowalske, K. J.; Crandall, C. G.
Objective A maximal aerobic capacity below the 20th percentile is associated with an increased risk of all-cause mortality.1 Adult burn survivors have a lower aerobic capacity compared to non-burned adults when evaluated 38±23 days post-injury.2 However, it is unknown if burn survivors with well-healed skin grafts (i.e., multiple years post injury), also have low aerobic capacity. This project tested the hypothesis that aerobic fitness, as measured by maximal aerobic capacity (VO2max), is reduced in well-healed adult burn survivors when compared to normative values from non-burned individuals. Methods Twenty-five burn survivors (36 ± 12 years old; 13 females) with well-healed split thickness grafts (median: 16 years post-injury, range: 1 to 51 years) covering at least 17% of their body surface area (mean: 40±16%; range: 17 to 75%) performed a graded cycle ergometry exercise test to volitional fatigue. Expired gases and minute ventilation were measured via a metabolic cart for the determination of VO2max. Each subject’s VO2max was compared with sex- and age-matched normative values from population data published by the American College of Sports Medicine (ACSM), the American Heart Association (AHA), and recent epidemiological data.3 Results Subjects had a VO2max of 29.4 ± 10.1 ml O2/kg body mass/min (median: 27.5; range: 15.9 to 53.3). Using ACSM normative values, mean VO2max of the subjects was in the lower 24th percentile (median: 10th percentile). 88% of the subjects had a VO2max below AHA age-adjusted normative values. Similarly 20 of the 25 subjects had a VO2max in the lower 25% percentile of recent epidemiological data. Conclusions Relative to non-grafted subjects, 80–88% of the evaluated skin graft subjects had a very low aerobic capacity. Based upon these findings, adult burn survivors are disproportionally unfit relative to the general U.S. population, and this puts them at an increased risk of all-cause mortality.
Fluid restriction during exercise in the heat reduces tolerance to progressive central hypovolemia
(Experimental Physiology, 2015-08-06) Schlader, Z. J.; Gagnon, D.; Rivas, E.; Convertino, V. A.; Crandall, C. G.
This study tested the hypothesis that dehydration induced via exercise in the heat impairs tolerance to central hypovolaemia. Eleven male subjects (32 ± 7 years old, 81.5 ± 11.1 kg) walked (O2 uptake 1.7 ± 0.4 l min−1) in a 40°C, 30% relative humidity environment on three occasions, as follows: (i) subjects walked for 90 min, drinking water to offset sweat loss (Hydrated, n =11); (ii) water intake was restricted, and exercise was terminated when intestinal temperature increased to the same level as in the Hydrated trial (Isothermic Dehydrated, n = 11); and (iii) water intake was restricted, and exercise duration was 90 min (Time Match Dehydrated, n = 9). For each trial, tolerance to central hypovolaemia was determined following exercise via progressive lower body negative pressure and quantified as time to presyncope. Increases in intestinal temperature prior to lower body negative pressure were not different (P = 0.91) between Hydrated (1.1 ± 0.4°C) and Isothermic Dehydrated trials (1.1 ± 0.4°C), but both were lower than in the Time Match Dehydrated trial (1.7 ± 0.5°C, P < 0.01). Prior to lower body negative pressure, body weight was unchanged in the Hydrated trial (−0.1 ± 0.2%), but was reduced in Isothermic Dehydrated (−0.9 ± 0.4%) and further so in Time Match Dehydrated trial (−1.9 ± 0.6%, all P < 0.01). Time to presyncope was greater in Hydrated (14.7 ± 3.2 min) compared with Isothermic Dehydrated (11.9 ± 3.3 min, P < 0.01) and Time Match Dehydrated trials (10.2 ± 1.6 min, P = 0.03), which were not different (P = 0.19). These data indicate that inadequate fluid intake during exercise in the heat reduces tolerance to central hypovolaemia independent of increases in body temperature.
Cardiopulmonary and arterial baroreceptor unloading during passive hyperthermia does not contribute to hyperthermic-induced hyperventilation
(Experimental Physiology, 2015-08-24) Lucas, R. A. I.; Pearson, J.; Schlader, Z. J.; Crandall, C. G.
This study tested the hypothesis that baroreceptor unloading during passive hyperthermia contributes to increases in ventilation and decreases in end-tidal partial pressure of carbon dioxide (PET,CO2) during that exposure. Two protocols were performed, in which healthy subjects underwent passive hyperthermia (increasing intestinal temperature by ~1.8°C) to cause a sustained increase in ventilation and reduction in PET,CO2. Upon attaining hyperthermic hyperventilation, in protocol 1 (n = 10; three females) a bolus (19 ± 2 ml kg−1) of warm (~38°C) isotonic saline was rapidly (5–10 min) infused intravenously to restore reductions in central venous pressure, whereas in protocol 2 (n = 11; five females) phenylephrine was infused intravenously (60–120 μg min−1) to return mean arterial pressure to normothermic levels. In protocol 1, hyperthermia increased ventilation (by 2.2 ± 1.7 l min−1, P < 0.01), while reducing PET,CO2 (by 4 ± 3 mmHg, P = 0.04) and central venous pressure (by 5 ± 1 mmHg, P <0.01). Saline infusion increased central venous pressure by 5 ± 1 mmHg (P < 0.01), restoring it to normothermic values, but did not change ventilation or PET,CO2 (P > 0.05). In protocol 2, hyperthermia increased ventilation (by 5.0 ± 2.7l min−1, P <0.01) and reduced PET ,CO2 (by 5 ± 2 mmHg, P < 0.01) and mean arterial pressure (by 9 ± 7 mmHg, P <0.01). Phenylephrine infusion increased mean arterial pressure by 12 ± 3 mmHg (P < 0.01), restoring it to normothermic values, but did not change ventilation or PET,CO2 (P > 0.05). The absence of a reduction in ventilation upon reloading the cardiopulmonary and arterial baroreceptors to pre-hyperthermic levels indicates that baroreceptor unloading with hyperthermia is unlikely to contribute to hyperthermic hyperventilation in humans.
Non-grafted skin surface area best predicts exercise core temperature responses in burned individuals.
(Medicine and Science in Sports and Exercise, 2015-10-01) Ganio, M. S.; Schlader, Z. J.; Pearson, J.; Lucas, R. A. I.; Rivas, E.; Kowalske, K. J.; Crandall, C. G.
Abstract Grafted skin impairs heat dissipation, but it is unknown to what extent this impacts body temperature during exercise in the heat. PURPOSE We examined core body temperature responses during exercise in the heat in a group of individuals with a large range of grafts covering their body surface area (BSA; 0-75%). METHODS Forty-three individuals (19 females) were stratified into groups based upon BSA grafted: Control (0% grafted, n=9), 17-40% (n=19), and >40% (n=15). Subjects exercised at a fixed rate of metabolic heat production (339 ± 70 W; 4.3 ± 0.8 W/kg) in an environmental chamber set at 40°C, 30% RH for 90 min or until exhaustion (n=8). Whole-body sweat rate and core temperatures were measured. RESULTS Whole body sweat rates were similar between groups (Control: 14.7±3.4 ml/min, 17-40%: 12.6±4.0 ml/min, and >40%: 11.7±4.4 ml/min, P>0.05), but the increase in core temperature at the end of exercise in the >40% BSA grafted group (1.6±0.5°C) was greater than the 17-40% (1.2±0.3°C) and Control (0.9±0.2°C) groups (P<0.05). Absolute BSA of non-grafted skin (expressed in m2) was the strongest independent predictor of the core temperature increase (r2=0.41). When re-grouping all subjects, individuals with the lowest BSA of non-grafted skin (<1.0 m2) had greater increases in core temperature (1.6±0.5°C) than those with >1.5 m2 non-grafted skin (1.0±0.3°C, P<0.05). CONCLUSIONS These data imply that individuals with grafted skin have greater increases in core temperature when exercising in the heat and that the magnitude of this increase is best explained by the amount of non-grafted skin available for heat dissipation.

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