The present study investigated the effects of hyperthermia on the contributions of central and peripheral factors to the development of neuromuscular fatigue. Fourteen men exercised at 60% maximal oxygen consumption on a cycle ergometer in hot (40 degrees C; hyperthermia) and thermoneutral (18 degrees C; control) environments. In hyperthermia, the core temperature increased throughout the exercise period and reached a peak value of 40.0 +/- 0.1 degrees C (mean +/- SE) at exhaustion after 50 +/- 3 min of exercise. In control, core temperature stabilized at approximately 38.0 +/- 0.1 degrees C, and exercise was maintained for 1 h without exhausting the subjects. Immediately after the cycle trials, subjects performed 2 min of sustained maximal voluntary contraction (MVC) either with the exercised legs (knee extension) or with a "nonexercised" muscle group (handgrip). The degree of voluntary activation during sustained maximal knee extensions was assessed by superimposing electrical stimulation (EL) to nervus femoralis. Voluntary knee extensor force was similar during the first 5 s of contraction in hyperthermia and control. Thereafter, force declined in both trials, but the reduction in maximal voluntary force was more pronounced in the hyperthermic trial, and, from 30 to 120 s, the force was significantly lower in hyperthermia compared with control. Calculation of the voluntary activation percentage (MVC/MVC + EL) revealed that the degree of central activation was significantly lower in hyperthermia (54 +/- 7%) compared with control (82 +/- 6%). In contrast, total force of the knee extensors (MVC + force from EL) was not different in the two trials. Force development during handgrip contraction followed the same pattern of response as was observed for the knee extensors. In conclusion, these data demonstrate that the ability to generate force during a prolonged MVC is attenuated with hyperthermia, and the impaired performance is associated with a reduction in the voluntary activation percentage.

P Krustrup, J J Nielsen, B R Krustrup, et al. health-promoting activity for untrained menRecreational soccer is an effective http://bjsm.bmj.com/content/43/11/825.full.html Updated information and services can be found at: ABSTRACTTo examine the effects of regular participation in recreational soccer on health profile, 36 healthy untrained Danish men aged 20-43 years were randomised into a soccer group (SO; n = 13), a running group (RU; n = 12) and a control group (CO; n = 11). Training was performed for 1 h two or three times per week for 12 weeks; at an average heart rate of 82% (SEM 2%) and 82% (1%) of HR max for SO and RU, respectively. During the 12 week period, maximal oxygen uptake increased (p,0.05) by 13% (3%) and 8% (3%) in SO and RU, respectively. In SO, systolic and diastolic blood pressure were reduced (p,0.05) from 130 (2) to 122 (2) mm Hg and from 77 (2) to 72 (2) mm Hg, respectively, after 12 weeks, with similar decreases observed for RU. After the 12 weeks of training, fat mass was 3.0% (2.7 (0.6) kg) and 1.8% (1.8 (0.4) kg) lower (p,0.05) for SO and RU, respectively. Only SO had an increase in lean body mass (1.7 (0.4) kg, p,0.05), an increase in lower extremity bone mass (41 (8) g, p,0.05), a decrease in LDL-cholesterol (2.7 (0.2) to 2.3 (0.2) mmol/l; p,0.05) and an increase (p,0.05) in fat oxidation during running at 9.5 km/h. The number of capillaries per muscle fibre was 23% (4%) and 16% (7%) higher (p,0.05) in SO and RU, respectively, after 12 weeks. No changes in any of the measured variables were observed for CO. In conclusion, participation in regular recreational soccer training, organised as smallsided drills, has significant beneficial effects on health profile and physical capacity for untrained men, and in some aspects it is superior to frequent moderate-intensity running.

This study demonstrates that the Yo-Yo IR2 test is reproducible and can be used to evaluate an athlete's ability to perform intense intermittent exercise with a high rate of aerobic and anaerobic energy turnover. Specifically, the Yo-Yo IR2 test was shown to be a sensitive tool to differentiate between intermittent exercise performance of soccer players in different seasonal periods and at different competitive levels and playing positions.

The relationship between quadriceps muscle temperature (T(m)) and sprint performance was evaluated during soccer matches in 25 competitive players. In one game, T(m) was determined frequently (n=9). In another game, eight players performed low-intensity activities at half-time (re-warm-up, (RW), whereas another eight players recovered passively (CON). T(m) was 36.0+/-0.2 degrees C at rest and increased (P<0.05) to 39.4+/-0.2 degrees C before the game and remained unaltered during the first half. At half-time, T(m) decreased (P<0.05) to 37.4+/-0.2 degrees C, but increased (P<0.05) to 39.2+/- degrees C during the second half. In CON and RW, T(m) and core temperature (T(c)) were similar before and after the first half, but 2.1+/-0.1 and 0.9+/-0.1 degrees C higher (P<0.05), respectively, in RW prior to the second half. At the onset of the second half, the sprint performance was reduced (P<0.05) by 2.4% in CON, but unchanged in RW. The decrease in T(m) was correlated to the decrease in performance (r=0.60, P<0.05, n=16). This study demonstrates that in soccer, the decline in T(m) and T(c) during half-time is associated with a lowered sprint capacity at the onset of the second half, whereas sprint performance is maintained when low-intensity activities preserve muscle temperature.

Hot ambient conditions and associated heat stress can increase mortality and morbidity, as well as increase adverse pregnancy outcomes and negatively affect mental health. High heat stress can also reduce physical work capacity and motor-cognitive performances, with consequences for productivity, and increase the risk of occupational health problems. Almost half of the global population and more than 1 billion workers are exposed to high heat episodes and about a third of all exposed workers have negative health effects. However, excess deaths and many heat-related health risks are preventable, with appropriate heat action plans involving behavioural strategies and biophysical solutions. Extreme heat events are becoming permanent features of summer seasons worldwide, causing many excess deaths. Heat-related morbidity and mortality are projected to increase further as climate change progresses, with greater risk associated with higher degrees of global warming. Particularly in tropical regions, increased warming might mean that physiological limits related to heat tolerance (survival) will be reached regularly and more often in coming decades. Climate change is interacting with other trends, such as population growth and ageing, urbanisation, and socioeconomic development, that can either exacerbate or ameliorate heat-related hazards. Urban temperatures are further enhanced by anthropogenic heat from vehicular transport and heat waste from buildings. Although there is some evidence of adaptation to increasing temperatures in high-income countries, projections of a hotter future suggest that without investment in research and risk management actions, heat-related morbidity and mortality are likely to increase.

INT for 12 wk is an effective training stimulus for improvement of cardiorespiratory fitness and glucose tolerance, but in relation to the treatment of hyperlipidemia and obesity, it is less effective than prolonged training. Furthermore and in contrast to strength training, 12 wk of INT had no impact on muscle mass or indices of skeletal health.

Brain temperature appears to be an important factor affecting motor activity, but it is not known to what extent brain temperature increases during prolonged exercise in humans. Cerebral heat exchange was therefore evaluated in seven males during exercise with and without hyperthermia. Middle cerebral artery mean blood velocity (MCA V(mean)) was continuously monitored while global cerebral blood flow (CBF) and cerebral energy turnover were determined at the end of the two exercise trials in three subjects. The arterial to venous temperature difference across the brain (v-aD(temp)) was determined via thermocouples placed in the internal jugular vein and in the aorta. The jugular venous blood temperature was always higher than that of the arterial blood, demonstrating that heat was released via the CBF during the normothermic as well as the hyperthermic exercise condition. However, heat removal via the jugular venous blood was 30 +/- 6 % lower during hyperthermia compared to the control trial. The reduced heat removal from the brain was mainly a result of a 20 +/- 6 % lower CBF (22 +/- 9 % reduction in MCA V(mean)), because the v-aD(temp) was not significantly different in the hyperthermic (0.20 +/- 0.05 degrees C) compared to the control trial (0.22 +/- 0.05 degrees C). During hyperthermia, the impaired heat removal via the blood was combined with a 7 +/- 2 % higher heat production in the brain and heat was consequently stored in the brain at a rate of 0.20 +/- 0.06 J g(-1) min(-1). The present results indicate that the average brain temperature is at least 0.2 degrees C higher than that of the body core during exercise with or without hyperthermia.

This article presents a historical overview and an up-to-date review of hyperthermia-induced fatigue during exercise in the heat. Exercise in the heat is associated with a thermoregulatory burden which mediates cardiovascular challenges and influence the cerebral function, increase the pulmonary ventilation, and alter muscle metabolism; which all potentially may contribute to fatigue and impair the ability to sustain power output during aerobic exercise. For maximal intensity exercise, the performance impairment is clearly influenced by cardiovascular limitations to simultaneously support thermoregulation and oxygen delivery to the active skeletal muscle. In contrast, during submaximal intensity exercise at a fixed intensity, muscle blood flow and oxygen consumption remain unchanged and the potential influence from cardiovascular stressing and/or high skin temperature is not related to decreased oxygen delivery to the skeletal muscles. Regardless, performance is markedly deteriorated and exercise-induced hyperthermia is associated with central fatigue as indicated by impaired ability to sustain maximal muscle activation during sustained contractions. The central fatigue appears to be influenced by neurotransmitter activity of the dopaminergic system, but inhibitory signals from thermoreceptors arising secondary to the elevated core, muscle and skin temperatures and augmented afferent feedback from the increased ventilation and the cardiovascular stressing (perhaps baroreceptor sensing of blood pressure stability) and metabolic alterations within the skeletal muscles are likely all factors of importance for afferent feedback to mediate hyperthermia-induced fatigue during submaximal intensity exercise. Taking all the potential factors into account, we propose an integrative model that may help understanding the interplay among factors, but also acknowledging that the influence from a given factor depends on the exercise hyperthermia situation.