The model for human physical activity patterns was established not in gymnasia, athletic fields, or exercise physiology laboratories, but by natural selection acting over eons of evolutionary experience. This paper examines how evolution has determined the potential for contemporary human performance, and advances the experience of recently-studied hunter-gatherers as the best available (although admittedly imperfect) indicator of the physical activity patterns for which our genetically determined biology was originally selected. From the emergence of the genus Homo, over 2 million years ago (MYA), until the agricultural revolution of roughly 10000 years ago our ancestors were hunter-gatherers, so the adaptive pressures inherent in that environmental niche have exerted defining influence on human genetic makeup. The portion of our genome that determines basic anatomy and physiology has remained relatively unchanged over the past 40 000 years. Thus, the complex interrelationship between energy intake, energy expenditure and specific physical activity requirements for current humans remains very similar to that originally selected for Stone Age men and women who lived by gathering and hunting. Research investigating optimal physical activity for human health and performance can be guided by understanding the evolution of physical activity patterns in our species.
Studies of the cardiovascular response to lower body negative pressure (LBNP) in men and women have suggested that women may have less tolerance to LBNP than men, although tolerance per se was not determined. To investigate the effect of gender on tolerance to LBNP, 10 men 10 women were subjected to increasing levels of LBNP until presyncopal symptoms developed. The cumulative stress index (CSI) score was determined, as were cardiovascular variables. Women had 62% less tolerance to LBNP with a CSI of 412 +/- 43 mmHg/min compared with a CSI of 1,070 +/- 149 mmHg/min for men. Cardiovascular changes associated with LBNP were similar for men and women when expressed relative to the occurrence of presyncope, but women had a higher heart rate response when the data were expressed at absolute levels of LBNP (-30 and -50 mmHg LBNP). Thus men and women had similar cardiovascular adjustments to the LBNP, with the changes in women occurring lower levels of LBNP. These data are important in a consideration of the development of antigravitational countermeasures for women. These data raise questions as to the manner in which blood pools within the lower body in men and women under LBNP.
Exercise-induced asthma, or more appropriately, exercise-induced bronchoconstriction (EIB), occurs in 80 to 90% of individuals with asthma and in approximately 11% of the general population without asthma. EIB is characterised by post-exercise airways obstruction resulting in reductions in forced expiratory volume in 1 second (FEV(1)) of greater than 10% compared with pre-exercise values. The mechanism of EIB remains elusive, although both cooling and drying of airways play prominent roles. Cold, dry inhaled air during exercise or voluntary hyperventilation is the most potent stimulus for EIB. Inflammatory mediators play central roles in causing the post-exercise airways obstruction. Diagnosis of EIB requires the use of an exercise test. The exercise can be a field or laboratory based test, but should be of relatively high intensity (80 to 90% of maximal heart rate) and duration (at least 5 to 8 minutes). Pre- and post-exercise pulmonary function should be compared, and post exercise pulmonary function determined over 20 to 30 minutes for characterisation of EIB. A pre- to post-exercise drop in FEV(1) of greater than 10% is abnormal. Approaches to treatment of EIB include both nonpharmacological and pharmacological strategies. A light exercise warm up prior to moderate to heavy exercise reduces the severity of EIB. More recently, studies have supported a role for dietary salt as a modifier of the severity of EIB, suggesting that salt restrictive diets should reduce symptoms of EIB. Short acting, inhaled beta(2)-agonists constitute the most used prophylactic treatment for EIB. However, antileukotriene agents are emerging as effective, well tolerated, long-term treatments for EIB.
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