Many mammals have the ability to autotransfuse a large quantity of red blood cells from the spleen into the active circulation during times of stress. This enhancement of the oxygen transport system has benefited the athletic mammal, that is, the thoroughbred horse, fox and greyhound in an improved aerobic performance. The role of the spleen in sequestering 50% of the total red cell volume in seals and horses, during times of inactivity, dramatically reduces the viscosity of the blood and therefore the work of the heart. In comparison, the human spleen contains only a small percentage of red blood cells, and has been primarily thought of as a lymphoid organ. The aim of this review is to emphasise the similarities between the human spleen and that of several athletic mammalian species during acute physiological stress. In the athletic mammalian model the expulsion of blood from the spleen is facilitated via the sympathetic nervous system resulting in contraction of smooth muscle within the splenic capsule. In comparison, the lack of smooth muscle contained within the human splenic capsule has meant that active contraction of the spleen has historically been viewed as unlikely, although evidence of contractile proteins within the red pulp have suggested otherwise. Exercise results in haemoconcentration, which has been attributed solely to a reduction in plasma volume. Indirect calculation of plasma volume changes utilise haemoglobin and haematocrit and assume that the circulating red cell volume remains constant. However, several studies have suggested that the human spleen could account for 30% of the increase in haematocrit. This would result in a substantial overestimation of the reduction in plasma volume, indicating that the expulsion of red blood cells from the spleen must not be overlooked when utilising these equations.

No abstract

Explosive ordnance disposal (EOD) technicians are required to wear protective clothing to protect themselves from the threat of overpressure, fragmentation, impact and heat. The engineering requirements to minimise these threats results in an extremely heavy and cumbersome clothing ensemble that increases the internal heat generation of the wearer, while the clothing’s thermal properties reduce heat dissipation. This study aimed to evaluate the heat strain encountered wearing EOD protective clothing in simulated environmental extremes across a range of differing work intensities. Eight healthy males [age 25±6 years (mean ± sd), height 180±7 cm, body mass 79±9 kg, V˙O2max 57±6 ml.kg−1.min−1] undertook nine trials while wearing an EOD9 suit (weighing 33.4 kg). The trials involved walking on a treadmill at 2.5, 4 and 5.5 km⋅h−1 at each of the following environmental conditions, 21, 30 and 37°C wet bulb globe temperature (WBGT) in a randomised controlled crossover design. The trials were ceased if the participants’ core temperature reached 39°C, if heart rate exceeded 90% of maximum, if walking time reached 60 minutes or due to fatigue/nausea. Tolerance times ranged from 10–60 minutes and were significantly reduced in the higher walking speeds and environmental conditions. In a total of 15 trials (21%) participants completed 60 minutes of walking; however, this was predominantly at the slower walking speeds in the 21°C WBGT environment. Of the remaining 57 trials, 50 were ceased, due to attainment of 90% maximal heart rate. These near maximal heart rates resulted in moderate-high levels of physiological strain in all trials, despite core temperature only reaching 39°C in one of the 72 trials.

No abstract

Neurodegenerative diseases involve the progressive deterioration of structures within the central nervous system responsible for motor control, cognition, and autonomic function. Alzheimer's disease and Parkinson's disease are among the most common neurodegenerative disease and have an increasing prevalence over the age of 50. Central in the pathophysiology of these neurodegenerative diseases is the loss of protein homeostasis, resulting in misfolding and aggregation of damaged proteins. An element of the protein homeostasis network that prevents the dysregulation associated with neurodegeneration is the role of molecular chaperones. Heat shock proteins (HSPs) are chaperones that regulate the aggregation and disaggregation of proteins in intracellular and extracellular spaces, and evidence supports their protective effect against protein aggregation common to neurodegenerative diseases. Consequently, upregulation of HSPs, such as HSP70, may be a target for therapeutic intervention for protection against neurodegeneration. A novel therapeutic intervention to increase the expression of HSP may be found in heat therapy and/or heat acclimation. In healthy populations, these interventions have been shown to increase HSP expression. Elevated HSP may have central therapeutic effects, preventing or reducing the toxicity of protein aggregation, and/or peripherally by enhancing neuromuscular function. Broader physiological responses to heat therapy have also been identified and include improvements in muscle function, cerebral blood flow, and markers of metabolic health. These outcomes may also have a significant benefit for people with neurodegenerative disease. While there is limited research into body warming in patient populations, regular passive heating (sauna bathing) has been associated with a reduced risk of developing neurodegenerative disease. Therefore, the emerging evidence is compelling and warrants further investigation of the potential benefits of heat acclimation and passive heat therapy for sufferers of neurodegenerative diseases.