Ventilatory changes in heat-stressed humans with spinal-cord injury

Wilsmore, Bradley; Cotter, James D.; Bashford, Guy; Taylor, Nigel A.S.

doi:10.1038/sj.sc.3101823

Cited by 14 publications

(12 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The hypothesis that hyperthermic ventilatory response is augmented for compensating for low heat dissipating ability might be supported by previous studies. Previous studies reported that the individuals with congenital anhidrotic ectodermal dysplasia or with spinal-cord injury, who have an impaired sweating response, showed greater increase in their breathing than able-bodied subjects during hyperthermia (Totel 1974;Wilsmore et al 2006). Further studies are needed to clarify this relationship and to confirm whether ventilation increases to compensate for weak thermoregulatory responses (e.g., cutaneous vasodilation and sweating).…”

Section: Discussionmentioning

confidence: 86%

The cross-sectional relationships among hyperthermia-induced hyperventilation, peak oxygen consumption, and the cutaneous vasodilatory response during exercise

et al. 2009

View full text Add to dashboard Cite

To test the hypothesis that the hyperthermia-induced ventilatory response relates to aerobic power and/or the cutaneous vasodilatory response during exercise, we asked 18 subjects to perform 3 kinds of exercise: an incremental exercise to determine peak oxygen consumption (V(O)(2peak)), a steady state exercise at 50% of V(O)(2peak) to determine the ventilatory response to increasing body temperature, and a steady state exercise at 60% of V(O)(2peak) to determine the cutaneous vasodilatory response to increasing body temperature. The ventilatory and cutaneous vasodilatory responses were evaluated by plotting the increase in minute ventilation or in forearm vascular conductance against the increase in oesophageal temperature. Regression analysis revealed that: (1) there was a negative relationship between the hyperthermic ventilatory response and cutaneous vasodilatory response, (2) there was a negative relationship between the hyperthermic ventilatory response and V(O)(2peak), and (3) there was a positive relationship between the cutaneous vasodilatory response and V(O)(2peak). These results support our hypothesis and suggest that exercise training suppresses the hyperthermic ventilatory response and improves the thermoregulatory response.

show abstract

Section: Discussionmentioning

confidence: 86%

The cross-sectional relationships among hyperthermia-induced hyperventilation, peak oxygen consumption, and the cutaneous vasodilatory response during exercise

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Previous studies showed that individuals whose sweating response is impaired due to quadriplegia, ectodermal dysplasia, or spinal-cord injury show greater increases in ventilation than able-bodied subjects during passive heating at rest (Totel 1974;Wilsmore et al 2006). We therefore suggest that hyperthermia-induced hyperventilation is augmented when thermoregulatory responses are impaired during passive heating at rest (hyperthermia-induced hyperventilation is linked to thermoregulatory responses).…”

Section: Introductionmentioning

confidence: 73%

Short-term exercise-heat acclimation enhances skin vasodilation but not hyperthermic hyperpnea in humans exercising in a hot environment

et al. 2011

View full text Add to dashboard Cite

We tested the hypothesis that short-term exercise-heat acclimation (EHA) attenuates hyperthermia-induced hyperventilation in humans exercising in a hot environment. Twenty-one male subjects were divided into the two groups: control (C, n = 11) and EHA (n = 10). Subjects in C performed exercise-heat tests [cycle exercise for ~75 min at 58% [Formula: see text] (37°C, 50% relative humidity)] before and after a 6-day interval with no training, while subjects in EHA performed the tests before and after exercise training in a hot environment (37°C). The training entailed four 20-min bouts of exercise at 50% [Formula: see text] separated by 10 min of rest daily for 6 days. In C, comparison of the variables recorded before and after the no-training period revealed no changes. In EHA, the training increased resting plasma volume, while it reduced esophageal temperature (T (es)), heart rate at rest and during exercise, and arterial blood pressure and oxygen uptake ([Formula: see text]) during exercise. The training lowered the T (es) threshold for increasing forearm vascular conductance (FVC), while it increased the slope relating FVC to T (es) and the peak FVC during exercise. It also lowered minute ventilation ([Formula: see text]) during exercise, but this effect disappeared after removing the influence of [Formula: see text] on [Formula: see text]. The training did not change the slope relating ventilatory variables to T (es). We conclude that short-term EHA lowers ventilation largely by reducing metabolism, but it does not affect the sensitivity of hyperthermia-induced hyperventilation during submaximal, moderate-intensity exercise in humans.

show abstract

“…It has been reported, for example, that ventilatory sensitivity to increasing body temperature (slope of the regression line relating V ・ E to Tes) has a negative linear relationship with the sensitivity of cutaneous vasodilation in heated exercising humans 23) . It has also been reported that subjects with congenital anhidrotic ectodermal dysplasia and those with spinal-cord injuries, leading to reduced sweating responses, show greater increases in ventilation during hyperthermia at rest than healthy subjects 24,25) . It is thus possible that hyperthermia-induced hyperventilation has some relationship to thermoregulatory responses, though the physiological mechanism remains unclear.…”

Section: Characteristics Of Hyperthermia-induced Hyperventilationmentioning

confidence: 99%

Effect of hyperthermia-induced hyperventilation on central fatigue during exercise in heat

Hayashi

2012

JPFSM

View full text Add to dashboard Cite

Exercise endurance is reduced by heat. Among several factors that influence exercise performance is central fatigue, which appears to be caused by an increase in brain temperature. During prolonged exercise in heat, the core body temperature rises, and there is a corresponding and proportional increase in minute ventilation. It has been suggested that this hyperthermia-induced hyperventilation is related to central fatigue. Although hyperthermiainduced hyperventilation may have some relationship to heat-dissipating responses, it differs in several ways. For example, hyperthermia-induced hyperventilation causes a reduction in arterial CO 2 pressure, which makes it different from thermal panting in animals. In fact, it has been suggested that hyperthermia-induced hyperventilation causes a reduction in cerebral perfusion, which reinforces the increase in brain temperature during exercise. This short review presents an overview of the characteristics of hyperthermia-induced hyperventilation and its effect on central fatigue.

show abstract

Ventilatory changes in heat-stressed humans with spinal-cord injury

Cited by 14 publications

References 27 publications

The cross-sectional relationships among hyperthermia-induced hyperventilation, peak oxygen consumption, and the cutaneous vasodilatory response during exercise

The cross-sectional relationships among hyperthermia-induced hyperventilation, peak oxygen consumption, and the cutaneous vasodilatory response during exercise

Short-term exercise-heat acclimation enhances skin vasodilation but not hyperthermic hyperpnea in humans exercising in a hot environment

Effect of hyperthermia-induced hyperventilation on central fatigue during exercise in heat

Contact Info

Product

Resources

About