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This study tested the hypothesis that exercise elicits monocytic cytokine expression and that prolonged cold exposure modulates such responses. Nine men (age, 24.6 +/- 3.8 y; VO(2 peak), 56.8 +/- 5.6 ml. kg(-1). min(-1)) completed 7 days of exhausting exercise (aerobic, anaerobic, resistive) and underwent three cold, wet exposures (CW). CW trials comprised

The contribution of hyperthermia to the differential leukocytosis of exercise remains obscure. This study examined changes in circulating sympathoadrenal hormone concentrations and patterns of leukocyte and lymphocyte subset (CD3(+), CD4(+), CD8(+), CD19(+), CD3(-)16(+)/56(+)) redistribution during exercise, with and without a significant rise of rectal temperature (T(re)). Ten healthy men [age 26.9 +/- 5.7 (SD) yr, body mass 76.0 +/- 10.9 kg, body fat 13.9 +/- 4.6%, peak O(2) consumption: 48.0 +/- 12.4 ml x kg(-1) x min(-1)] exercised for 40 min (65% peak O(2) consumption) during water immersion at 39 or 18 degrees C. T(re) increased from 37.2 to 39.3 degrees C (P < 0.0001) after 40 min of exercise in 39 degrees C water but was held constant to an increment of 0.5 degrees C during exercise in 18 degrees C water. Application of this thermal clamp reduced exercise-associated increments of plasma epinephrine (Epi) and norepinephrine (NE) by >50% (P < 0.05) and abolished the postexercise increase in cortisol. Thermal clamping also reduced the exercise-induced leukocytosis and lymphocytosis. Multiple regression demonstrated that T(re) had no direct association with lymphocyte subset mobilization but was significantly (P < 0.0001) correlated with hormone levels. Epi was an important determinant of total leukocytes, lymphocytes, and CD3(+), CD4(+), CD8(+), and CD3(-)CD16(+)/56(+) subset redistribution. The relationship between NE and lymphocyte subsets was weaker than that with Epi, with the exception of CD3(-)CD16(+)/56(+) counts, which were positively (P < 0.0001) related to NE. Cortisol was negatively associated with leukocytes, CD14(+) monocytes, and CD19(+) B- and CD4(+) T-cell subsets but was positively related to granulocytes. We conclude that hyperthermia mediates exercise-induced immune cell redistribution to the extent that it causes sympathoadrenal activation, with alterations in circulating Epi, NE, and cortisol.

Purpose: This study examined the effects of advancing gestational age and maternal aerobic conditioning (stationary cycling) on fetal heart rate (FHR) responses to strenuous non-steady-state maternal exercise., Methods: Subjects chose to participate in either an exercise group (EG) or control group (CG). Fourteen healthy, previously sedentary pregnant women participated in the exercise group, and six pregnant controls remained sedentary. Stationary cycling (heart rate target: 145 beats x min(-1)) was performed 3 d x wk(-1) by the exercised group. Exercise duration was increased from 14 to 25 min x session(-1) during the second trimester and was maintained at 25 min x session(-1) throughout the third trimester. FHR was monitored before, during, and after a progressive submaximal cycle ergometer test (peak heart rate = 170 beats x min(-1)) performed at approximately 27 and 37 wk gestation., Results: Mean FHR increased significantly (P < 0.05) during exercise, followed by a modest suppression and then a delayed rise during the recovery period at both observation times. Fetal bradycardia was not observed in any of the exercise tests. Effects of advancing gestational age included a lower FHR baseline both at rest and in response to maternal exercise and a lower incidence of exercise-induced tachycardia. Maternal physical conditioning did not significantly alter FHR response to maternal exercise., Conclusion: Our results support the hypothesis that FHR responses to strenuous exercise are altered by advancing gestational age and a brief progressive exercise test terminated at a maternal heart rate of 170 beats x min(-1) does not induce fetal distress during a healthy pregnancy.

Minimal information is available on the autonomic response to exercise under adverse environmental conditions. Traditionally, pharmacological blockade has been used to study autonomic responsiveness but, owing to its invasive nature, such studies have been limited in their scope. Recent advances in electrocardiographic tape recording, telemetry and associated computing systems have provided investigators with noninvasive methods for assessing the autonomic response to various physiological stressors. This article describes methods for the analysis of heart rate variability (HRV) and discusses the reports of those who have used HRV analysis to evaluate autonomic regulation during exercise, heat exposure and the combination of these 2 stressors. Spectral analysis of HRV reduces variations in the R-R interval into component sine waves of differing amplitude and frequency. Amplitude (variance) is displayed as a function of frequency, and power (cumulative variance) is calculated for specified frequency ranges (< 0.03 Hz, 0.03 to 0.15 Hz and 0.15 to 0.5 Hz). Parasympathetic nervous system activity can be inferred from the several indices of high frequency power; however, the estimation of sympathetic nervous system activity from low frequency power is more problematic. Data on HRV have shown that sympathovagal regulation during exercise is dependent on the intensity of the activity and the environmental conditions. At the onset of exercise, heart rate is increased by a reduction in vagal tone and a temporary increase in sympathetic tone. A continuation of physical activity is associated with a continued withdrawal of vagal activity and an attenuation of sympathetic nervous system tone. However, with the additional stimulus of a heated environment, sympathetic activity remains increased throughout exercise.

Coaches and athletic team physicians have provided anecdotal information and case studies to support their beliefs that athletes may be unusually prone to illness during strenuous training or competition. Many athletes, in contrast, believe that physical activity improves their resistance to infectious disease. However, it is generally agreed that the stress of competition may make athletes temporarily more susceptible to infectious illness. A review of the literature shows that upper respiratory tract infections and skin infections are more prevalent in top level athletes than in the general population, particularly during periods of intensive training. Exercise induced changes occur in both the innate and adaptive components of the immune system; however, the relative importance of each component is unknown. Strenuous exertion and contact sports may compromise host defence both by reducing physical protection and by impairing immunosurveillance. Skin lacerations, vigorous sweating and maceration of the dermis impair the defence normally provided by the skin surface. In addition, adverse changes in soluble and cellular components of the immune system can increase susceptibility to infection. Persistence with strenuous training during an infectious illness can have deleterious effects; not only is athletic performance impaired, but the severity of the disease process can be augmented.