In 10 women, external cold and heat exposures were performed both in the middle of luteal phase (L) and in the early follicular phase (F) of the menstrual cycle. Serum progesterone concentrations in L and F averaged 46.0 and 0.9 nmol X l-1, respectively. The experiments took place between 3:00 and 4:30 A.M., when the L-F core temperature difference is maximal. At neutral ambient temperature, esophageal (Tes), tympanic (Tty), rectal (Tre), and mean skin (Tsk) temperatures averaged 0.59 degrees C higher in L than in F. The thresholds for shivering, chest sweating, and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were increased in L by an average of 0.47 degrees C, related to mean body temperature [Tb(es) = 0.87Tes + 0.13 Tsk] and to Tes, Tty, Tre, or Tsk. The above-threshold chest sweat rate and cutaneous heat clearances at the thumb and forearm were also enhanced in L, when related to Tb(es) or time. The metabolic rate, arm blood flow, and heart rate at thermoneutral conditions were increased in L by 5.0%, 1.1 ml X 100 ml-1 X min-1, and 4.6 beats X min-1, respectively. The concomitant increase in threshold temperatures for all autonomic thermoregulatory responses in L supports the concept of a resetting of the set point underlying the basal body temperature elevation in L. The effects of the increased threshold temperatures are counteracted by enhanced heat loss responses.

Ten women [mean maximal O2 uptake (VO2max), 2.81 l X min-1] exercised for 15 min on a cycle ergometer in the middle of the luteal phase (L) and in the early follicular phase (F) of the menstrual cycle at the same constant work rates (mean 122 W) and an ambient temperature of 18 degrees C. Serum progesterone averaged 44.7 nmol X l-1 in L and 0.7 nmol X l-1 in F. After a 4-h resting period, exercise was performed between 3 and 4 A.M., when the L-F core temperature difference is maximal. Preexercise esophageal (Tes), tympanic (Tty), and rectal (Tre) temperatures averaged 0.6 degrees C higher in L. During exercise Tes, Tty, and Tre averaged 0.5 degrees C higher. The thresholds for chest sweating and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were elevated in L by an average of 0.47 degrees C, related to mean body temperature (Tb(es) = 0.87Tes + 0.13Tskin), Tes, Tty, or Tre. The above-threshold chest sweat rate and cutaneous heat clearances were also increased in L. The mean exercise heart rate was 170.0 beats X min-1 in L and 163.8 beats X min-1 in F. The mean exercise VO2 in L (2.21 l X min-1) was 5.2% higher than in F (2.10 l X min-1), the metabolic rate was increased in L by 5.6%, but the net efficiency was 5.3% lower. No significant L-F differences in the respiratory exchange ratio and postexercise plasma lactate were demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Eight well-trained male rowers exercised as hard as possible on a bicycle ergometer for 60 min at an ambient temperature of 18 degrees C. On 1 day (precooling test, PRET) exercise was preceded by a double cold exposure that caused starting body temperatures to be approximately 4.5, 1.0, 0.8, and 0.4 degrees C (mean skin, mean body, tympanic, and esophageal temperatures, respectively) lower than in the control test (CONT). In PRET the mean 1-h work rate (172 W) was 6.8% larger than in CONT (161 W), O2 uptake (Vo2) was 9.6% higher (2.86 vs. 2.61 1 X min-1), and O2 pulse was increased by 5.6% (18.8 vs. 17.8 ml), whereas the sweat rate was 20.3% lower in PRET (1.06 vs. 1.33 mg X cm-2.min-1). No differences in heart rate, efficiency, postexercise blood values of lactate, or acid-base status were demonstrated. It appears that the improved performance in PRET was related to an increased O2 supply to the working muscles. Although plasma levels of total beta H-endorphin immunoreactivity were in the same range under both test conditions, different components of beta H-endorphin immunoreactivity were indicated to exist in PRET and CONT.

Two series of experiments were performed in physically untrained subjects. In series A (heat adaptation, HA), seven male subjects were adapted to dry heat (five consecutive days at 55 degrees C ambient air temperature (Ta) for 1 h X day-1) under resting conditions. Before and after HA, the subjects' shivering responses were determined in a cold test (Ta + 10 to 0 degrees C). In series B, eight male subjects underwent mild exercise training (five consecutive days at a heart rate, HR, of 120 b X min-1) under Ta conditions individually adjusted (Ta + 15 to +5 degrees C) to prevent both sweating and cold sensations. Before and after "sweatless training", the subjects were subjected to a combined cold and heat test. During HA the thresholds for shivering, cutaneous vasodilatation (thumb and forearm) and sweating were shifted significantly (p less than 0.05) towards lower mean body temperatures (Tb). The mean decrease in threshold Tb was 0.36 degrees C. "Sweatless training" resulted in a mean increase in work rate (at HR 120 b X min-1) and oxygen pulse of 13 and 8%, respectively. However, "sweatless training" did not change the threshold Tb for shivering or sweating. Neither HA nor "sweatless training" changed the slopes of the relationships of shivering and sweating to Tb. It is concluded that the previously reported lowering of shivering and sweating threshold Tb in long-distance runners is not due to an increased fitness level, but is essentially identical with HA. The decreased shivering threshold following HA is interpreted as "cross adaptation" produced by the stressors cold and heat.

Methods: OPA, using the Langham Ocular Blood Flow (OBF) System, applanation intraocular pressure (lOP), systemic blood pressure and heart rate were measured and vasospasm was determined by a fingernail capillary blood flow test.Results: OPA (mmHg) in the LTG patients with a vasospastic reaction (LTG-V, 1.4 ± 0.1, n = 17) was not significantly (p>0.09) different when compared with non-vasospastic LTG patients (LTG-NV, 1.5 ± 0.2, n = 15) but was significantly (p0.05) different when compared with each other, but was significantly (p<0.05) lower when compared with matched coutrol subgroups (15.0 ± 0.3 and 15.2 ± 0.4, respectively). Haemodyuamic para meters were not significautly different from controls. Conclusion:The abnormality in choroidal perfusion indicated by a rednction in OPA in all LTG patients is unrelated to the presence or absence of vasospasm. Quigley et al. 5 did not find a reduction in the number of blood vessels in the optic nerve head region whereas Schwartz6 using fluorescein angiogra phy showed filling defects in this area in glaucoma tous subjects. These findings suggest a connection between LTG and vascular abnormalities.The present study was designed to evaluate a parameter of choroidal perfusion, the ocular pulse amplitude (OPA), in LTG patients with respect to vasospasm.