Overtraining may be one frequent cause of stagnation or decrease in performance capacity of athletes. Israel (19) differentiates between addisonoid (parasympathetic) and basedowoid (sympathetic) overtraining, characterized by inhibition or excitation. We tried to induce an overtraining syndrome in 8 experienced middle- and long-distance runners, based on an increase in training volume from an average 85.9 km (week 1) to 115.1 km (week 2) and 143.1 km (week 3) to 174.6 km per week (week 4). The influence of this training on cardiovascular, metabolic and hormonal parameters was examined with special respect to plasma and urinary catecholamines. Laboratory testing including graded treadmill running was performed on the days 0, 14 and 28. Training was held six days each week, with nearly 30 km per day in the fourth week. A stagnation in endurance performance capacity (running velocity at the aerobic-anaerobic transition range) and a decrease in maximum working capacity were observed in 6 and a stagnation in 2 of the 8 sportsmen, indicated by a decrease in total running distance from 4719 + 912 m to 4361 + 788 m during incremental treadmill ergometry. The sportsmen could neither improve nor could they even approximately reach their personal records during the subsequent competitive season. Subjective complaints, classified on a four-point scale, increased from 1.2 (week 1) to 3.2 in week 4. Glucose, lactate, ammonia, glycerol, free fatty acids, albumin, LDL, VLDL cholesterol, hemoglobin level (transient), leukocytes, and heart rate (before and during exercise) decreased significantly. Urea, creatinine, uric acid, GOT, GPT, gamma-GT, serum electrolytes (except phosphate and calcium) remained constant at the measuring times, CPK was elevated.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of an increase in training volume (ITV; February 1989) vs intensity (ITI; February 1990) on performance, catecholamines, energy metabolism and serum lipids was examined in two studies on eight, and nine experienced middle- or long-distance runners; seven participated in both studies. During ITV, mean training volume was doubled from 85.9 km.week-1 (pretrial phase) to 174.6 km within 3 weeks. Some 96%-98% of the training was performed at 67 (SD 8)% of maximal performance. During ITI, speed-endurance, high-speed and interval runs increased within 3 weeks from 9 km.week-1 (pretrial phase) to 22.7 km.week-1 and the total training distance from 61.6 to 84.7 km.week-1. The ITV resulted in stagnation of running velocity at 4 mmol lactate concentration and a decrease in total running distance in the increment test. Heart rate, energy metabolic parameters, nocturnal urinary catecholamine excretion, low density, very low density lipoprotein-cholesterol and triglyceride concentrations decreased significantly; the exercise-related catecholamine plasma concentrations increased at an identical exercise intensity. The ITI produced an improvement in running velocity at 4 mmol lactate concentration and in total running distance in the increment test; heart rate, energy metabolic parameters, nocturnal catecholamine excretion, and serum lipids remained nearly constant, and the exercise-related plasma catecholamine concentrations decreased at an identical exercise intensity. The ITV-related changes in metabolism and catecholamines may have indicated an exhaustion syndrome in the majority of the athletes examined but this hypothesis has to be proven by future experimental studies.

We studied blood gases in ponies to assess the relationship of alveolar ventilation (VA) to pulmonary CO2 delivery during moderate treadmill exercise. In normal ponies for 1.8, 3, or 6 mph, respectively, partial pressure of CO2 in arterial blood (PaCO2) decreased maximally by 3.1, 4.4, and 5.7 Torr at 30-90 s of exercise and remained below rest by 1.4, 2.3, and 4.5 Torr during steady-state (4-8 min) exercise (P less than 0.01). Partial pressure of O2 in arterial blood (PaO2) and arterial pH, (pHa) also reflected hyperventilation. Mixed venus CO2 partial pressure (PVCO2) decreased 2.3 and 2.9 Torr by 30 s for 3 and 6 mph, respectively (P less than 0.05). In work transitions either from 1.8 to 6 mph or from 6 mph to 1.8 mph, respectively, PaCO2 either decreased 3.8 Torr or increased 3.3 Torr by 45 s of the second work load (P less than 0.01). During exercise in acute (2-4 wk) carotid body denervated (CBD) ponies at 1.8, 3, or 6 mph, respectively, PaCO2 decreased maximally below rest by 9.0, 7.6, and 13.2 Torr at 30-45 s of exercise and remained below rest by 1.3, 2.3, and 7.8 Torr during steady-state (4-8 min) exercise (P less than 0.1). In the chronic (1-2 yr) CBD ponies, the hypocapnia was generally greater than normal but less than in the acute CBD ponies. We conclude that in the pony 1) VA is not tightly matched to pulmonary CO2 delivery during exercise, particularly during transitional states, 2) the exercise hyperpnea is not mediated by PaCO2 or PVCO2, and 3) during transitional states in the normal pony, the carotid bodies attenuate VA drive thereby reducing arterial hypocapnia.

The objective was to determine the effect of moderate changes in ambient temperature (TA) on breathing and body temperature in ponies chronically exposed to a TA of 21 degrees C in the summer and 5 degrees C in the winter. Normal (n = 6) and chronic carotid body-denervated (n = 6, 1-2 yr) ponies were studied during 1) winter months over 3-4 days at 5 (control TA) and 23 degrees C and 2) summer months over 2-4 days at 21 (control TA), 30, and 12 degrees C. Neither rectal nor arterial temperature changed with any alteration of TA (P greater than 0.10). Skin temperature (Tsk) always changed by 2-4 degrees C in the same direction as changes in TA (P less than 0.01), and Tsk was the only variable that differed between summer and winter control TA. While breathing room air 24-48 h after TA was altered, pulmonary ventilation (VE) and breathing frequency (f) were approximately 100 and 300%, respectively, above control with elevated TA and approximately 25-50% below control with reduced TA (P less than 0.01). Changes in f were closely related to changes in Tsk. Tidal volume (VT) changed inversely with changes in TA. Generally, while breathing room air, arterial PCO2 (Paco2) did not change from control during the first 48 h of altered TA. In studies when inspired CO2 was elevated VT increased by the same amount at all TA; f increased at low and control TA but decreased at elevated TA; and VE and Paco2 both increased relatively less at elevated TA, but the VE-Paco2 slope was independent of TA.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the effect of changes in inspired [O2] on partial pressure of CO2 in arterial blood (PaCO2) during treadmill exercise (3 mph, 3% grade) in normal, acute (+2-4 wk), and chronic (+1-2 yr) carotid body-denervated (CBD) ponies. In all studies, PaCO2 decreased (P less than 0.01) from rest during exercise, reaching a nadir usually between 15 and 30 s of exercise. During normoxia [partial pressure of O2 in arterial blood (PaO2) approximately 95 Torr], the PaCO2 nadir was 2.3 +/- 0.6 Torr below resting level in normal ponies, but the nadir was greater (P less than -0.01) in acute (delta = 6.4 +/- 0.8 Torr) and chronic (delta = -4.7 +/- 1.1 Torr) CBD ponies. Hyperoxia (PaO2 approximately 180 Torr) accentuated (P less than 0.01) the hypocapnia only in the normal ponies (delta = -6.3 +/- 1.0 Torr). In contrast, hypoxia (PaO2 48 Torr) attenuated (P less than 0.01) the exercise-induced hypocapnia by 3-5 Torr in all ponies. Usually PaCO2 gradually increased after 30 s of exercise, reaching a stable level 1-3 Torr below rest by about 2 min (P less than 0.05). Tidal volume (VT) increased from rest during the first 15 s of exercise only when there was a large decrease in PaCO2. Recovery of PaCO2 after 30 s of exercise was associated with a decrease in VT toward rest. We concluded the following. 1) The accentuated hypocapnia caused by eliminating (CBD) or reducing (hyperoxia) carotid chemoreceptor activity suggests that the chemoreceptors normally dampen alveolar ventilation (VA) at the onset of exercise. 2) Attenuation of the hypocapnia at the onset of exercise by hypoxia in CBD ponies suggests that a direct CNS effect of hypoxia dampens VA. 3) Mechanisms tending to minimize the hypocapnia during exercise appear to adjust VA by modulating VT.