No abstract

Cold water submersion can induce a high incidence of cardiac arrhythmias in healthy volunteers. Submersion and the release of breath holding can activate two powerful and antagonistic responses: the 'cold shock response' and the 'diving response' . The former involves the activation of a sympathetically driven tachycardia while the latter promotes a parasympathetically mediated bradycardia. We propose that the strong and simultaneous activation of the two limbs of the autonomic nervous system ('autonomic conflict') may account for these arrhythmias and may, in some vulnerable individuals, be responsible for deaths that have previously wrongly been ascribed to drowning or hypothermia. In this review, we consider the evidence supporting this claim and also hypothesise that other environmental triggers may induce autonomic conflict and this may be more widely responsible for sudden death in individuals with other predisposing conditions.

Many stressors cause an increase in ventilation in humans. This is predominantly reported as an increase in minute ventilation (V̇E). But, the same V̇E can be achieved by a wide variety of changes in the depth (tidal volume, V ) and number of breaths (respiratory frequency, ƒ ). This review investigates the impact of stressors including: cold, heat, hypoxia, pain and panic on the contributions of ƒ and V to V̇E to see if they differ with different stressors. Where possible we also consider the potential mechanisms that underpin the responses identified, and propose mechanisms by which differences in ƒ and V are mediated. Our aim being to consider if there is an overall differential control of ƒ and V that applies in a wide range of conditions. We consider moderating factors, including exercise, sex, intensity and duration of stimuli. For the stressors reviewed, as the stress becomes extreme V̇E generally becomes increased more by ƒ than V . We also present some tentative evidence that the pattern of ƒ and V could provide some useful diagnostic information for a variety of clinical conditions. In The Physiological Society's year of 'Making Sense of Stress', this review has wide-ranging implications that are not limited to one discipline, but are integrative and relevant for physiology, psychophysiology, neuroscience and pathophysiology.

We examined the effect of short-term heat acclimation with permissive dehydration (STHADe) on heat acclimation (HA) and cycling performance in a temperate environment.

Cold weather can have deleterious effects on health, tolerance, and performance. This paper will review the physiological responses and external factors that impact cold tolerance and physical performance. Tolerance is defined as the ability to withstand cold stress with minimal changes in physiological strain. Physiological and pathophysiological responses to short-term (cold shock) and long-term cold water and air exposure are presented. Factors (habituation, anthropometry, sex, race, and fitness) that influence cold tolerance are also reviewed. The impact of cold exposure on physical performance, especially aerobic performance, has not been thoroughly studied. The few studies that have been done suggest that aerobic performance is degraded in cold environments. Potential physiological mechanisms (decreases in deep body and muscle temperature, cardiovascular, and metabolism) are discussed. Likewise, strength and power are also degraded during cold exposure, primarily through a decline in muscle temperature. The review also discusses the concept of thermoregulatory fatigue, a reduction in the thermal effector responses of shivering and vasoconstriction, as a result of multistressor factors, including exhaustive exercise.