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Exhaustive dynamic exercise with large muscle groups in chronic hypobaric hypoxia may be limited by central (nervous) rather than peripheral (metabolic) fatigue. Six males [32 +/- 4 (SD) yr] at sea level (SL) and after 1-mo acclimatization at 5,050 m (HA) performed exhaustive dynamic forearm exercise at a constant absolute load, requiring regional maximum aerobic power at SL, and exhaustive cycle exercise at prevailing maximal O2 uptake (HA approximately equal to 80% SL). Exhaustion time (t(ex)), blood O2 saturation (SaO2), and heart rate (HR) were measured during each exercise bout. Before and after both arm and leg exercise, lactate concentration ([La]), PO2, PCO2, and pH were measured in arterialized blood samples. Integrated electromyogram activity (IEMG) and mean (MPF) and centroid (CPF) power frequencies of the EMG power spectrum during exercise were calculated for forearm flexors and vastus lateralis muscle. t(ex) for forearm exercise at the same absolute load was the same at SL and HA. Similar increases of IEMG (+214% at SL vs. +172% at HA) and decreases of CPF (-13% at SL vs. -16% at HA) and MPF (-22% at SL vs. -21% at HA) were observed. By contrast, at HA, for similar t(ex), leg exercise had to be performed at the same relative (i.e., prevailing maximal O2 uptake) but lower absolute load (approximately equal to 80% of SL).(ABSTRACT TRUNCATED AT 250 WORDS)

To investigate possible changes in autonomic regulation of heart rate as a result of acclimatization to high altitude, indexes of autonomic nervous activity were obtained non invasively by spectrum analysis of heart rate variability on five healthy male subjects [age, 31 (SEM 2) years] during a postural change from supine to seated, both at sea level and after 1 month of exposure to an altitude of 5050 m. Heart rate fluctuations at the respiratory frequency (high frequency, HF) are mediated by the parasympathetic system whereas fluctuations at about 0.1 Hz (low frequency, LF) are due to both sympathetic and parasympathetic nervous systems. Maximal heart rate, as measured during an incremental exercise test, decreased from 184 (SEM 5) beats.min-1 at sea level to 152 (SEM 2) beats.min-1 at 5050 m. At sea level, the change in posture from supine to seated induced an increase in LF amplitude accompanied by an increase or a decrease in HF amplitude, whereas after 1 month at altitude the HF amplitude decreased in all subjects, with little or no change in LF amplitude. These results indicate a changed strategy of heart rate regulation after acclimatization to high altitude. At sea level, the postural change induced an increase in sympathetic activity in all subjects with different individual vagal responses, whereas at altitude the postural change induced a net decrease in vagal tone in all subjects, with little or no change in sympathetic activity. These results corroborate the reported reduced sensitivity of the heart to adrenergic drive in chronic hypoxia, which may, at least in part, explain the decreased maximal heart rate in altitude-acclimatized human subjects.

The aim of the present study was to test the hypothesis that the net maximal blood lactate accumulation ([La]max) during heavy exercise in lowlanders acclimatized to chronic hypoxia may be limited by the reduced bicarbonate stores. Six men [age 32 +/- 4 (SD) yr] performed supramaximal exercise until voluntary exhaustion at sea level (204 +/- 54 W) and after sojourning for 1 mo at 5,050 m (175 +/- 23 W), without (C) and with (B) oral sodium-bicarbonate loading (0.3 g/kg body wt). Exhaustion time, arterial blood lactate concentration, arterial pH (pHa), arterial PCO2, and intramuscular pH were measured at rest and after exercise. At sea level, exhaustion time increased from 6.5 +/- 2.8 min in C to 7.5 +/- 2.7 min in B (P < 0.05). At altitude, exhaustion times were similar to the sea level C values and the same in C and B. At sea level, resting pHa increased from 7.41 +/- 0.02 in C to 7.46 +/- 0.03 in B (P < 0.001); the corresponding values at altitude were 7.46 +/- 0.04 and 7.55 +/- 0.03 (P < 0.001). Postexercise pHa at sea level was 7.22 +/- 0.02 in C and 7.25 +/- 0.08 in B (NS). After exercise at altitude, pHa was 7.32 +/- 0.04 and 7.44 +/- 0.03 in C and B, respectively (P < 0.001). [La]max increased from 12.86 +/- 1.45 mM in C to 16.63 +/- 1.76 mM in B (P < 0.01) at sea level and from 6.85 +/- 1.40 mM in C to 7.95 +/- 1.74 mM in B (NS) at altitude.(ABSTRACT TRUNCATED AT 250 WORDS)

It has been hypothesized that chronic hypobaric hypoxia could lead to inhibition of the alpha-motoneuron pool, thus limiting the maximal activation of working skeletal muscles. To test this hypothesis six subjects [32 (SEM 2) years] were evaluated in resting conditions, at sea level and after acclimatization at 5,050 m. The recruitment curves of the Hofmann-reflex (H-) and the direct muscle-response. (M-) of the right soleus muscle were obtained by stimulating the posterior tibial nerve with different intensities while recording the electromyogram of the soleus muscle. From the recorded data the net alpha-motoneuron excitability (ratio of maximal H-reflex to M-response Hmax:Mmax ratio), the threshold and gain for both responses, obtained from linear regressions through the rising phase of the recruitment curves of both responses, as well as the latency times of both responses were determined. The latency times and the Hmax:Mmax ratio were unchanged at altitude. The thresholds of both responses and the gain of the M-response were unaltered. The gain of the H-response was significantly higher at altitude when compared to sea level.(ABSTRACT TRUNCATED AT 250 WORDS)

The O2 equivalent of lactic acid accumulation in blood was estimated from data on ten subjects acclimatized to altitudes up to 6500 m in the course of a Mt. Everest expedition. The calculated value of the O2 equivalent of La by standard least squares regression was 2.07 +/- 0.4 l O2 for a rise of blood lactic acid concentration [Lab] of 1 g per liter of blood (2.92 ml O2 per kg of body weight per 1 mM increase in blood lactate). This value, as well as the value obtained by the regression procedure suggested by Brace (2.84 +/- 0.5 l), was not significantly different from the previously reported value of 2.38 +/- 0.22 (14) for sea-level conditions. This finding indicated that, after La equilibrium is achieved, the redistribution of La among extra- and intracellular body compartments, as reflected by [Lab], appears not to be substantially affected by chronic hypoxia. The calculated maximum lactic O2 debt values at the Mt. Everest base camp (5350 m) were 1.26 and 1.42 liters for acclimatized Caucasians and for Sherpas, respectively. The amount of the measured maximum O2 debt at altitude was somewhat increased by pure O2 breathing (1.53 vs 1.26 l).