The application of maximal heart rate predictive equations in hypoxic conditions.

PURPOSE: Peak heart rate (HRpeak) is a common tool used in exercise prescription for groups in which maximal exercise intensity is contraindicated; however, the application of this method in normobaric hypoxia is unknown. Therefore, this study investigated the response of HRpeak and the application of predictive HRpeak equations to prescribe exercise intensity in acute normobaric hypoxia. Results were used to examine whether age-derived HRpeak predictive equations are valid in hypoxic conditions. METHODS: Fifteen untrained (eight men) volunteers (age 22 ± 2 years; peak rate of oxygen consumption 46.3 ± 7.0 ml kg(-1) min(-1)) completed incremental cycle ergometer tests (randomised order) to measure HRpeak at sea-level (SL (ambient inspiratory oxygen fraction (FIO2) 0.209)) and four normobaric hypoxic conditions FIO2: 0.185, 0.165, 0.142, 0.125 (≈1,000-4,000 m). RESULTS: HRpeak was similar across all conditions (SL, 182 ± 13; 0.185, 178 ± 11; 0.165, 177 ± 9; 0.142, 178 ± 9; 0.125, 175 ± 10 b min(-1)) despite a reduction in oxygen saturation with increasing hypoxia (SL, 95 ± 5; 0.185, 95 ± 2; 0.165, 92 ± 2; 0.142, 88 ± 3; 0.125, 82 ± 4 %; P ≤ 0.05). The HRpeak was overestimated by all equations compared to the measured value (P < 0.05). Four equations overestimated HRpeak in all conditions (P < 0.01); two in four conditions (0.185, 0.165, 0.142, 0.125; P < 0.01); and two in three conditions (0.165, 0.142, 0.125; P < 0.01). CONCLUSION: The overestimation of HRpeak by commonly used age-derived predictive equations in normobaric hypoxic conditions suggests that despite possible contraindications researchers should directly measure HRpeak whenever possible if it is to be used to prescribe exercise intensities.

High-intensity intermittent exercise increases pulmonary interstitial edema at altitude but not at simulated altitude.

OBJECTIVE: Ascent to high altitude leads to a reduction in ambient pressure and a subsequent fall in available oxygen. The resulting hypoxia can lead to elevated pulmonary artery (PA) pressure, capillary stress, and an increase in interstitial fluid. This fluid can be assessed on lung ultrasound (LUS) by the presence of B-lines. We undertook a chamber and field study to assess the impact of high-intensity exercise in hypoxia on the development of pulmonary interstitial edema in healthy lowlanders. METHODS: Thirteen volunteers completed a high-intensity intermittent exercise (HIIE) test at sea level, in acute normobaric hypoxia (12% O2, approximately 4090 m equivalent altitude), and in hypobaric hypoxia during a field study at 4090 m after 6 days of acclimatization. Pulmonary interstitial edema was assessed by the evaluation of LUS B-lines. RESULTS: After HIIE, no increase in B-lines was seen in normoxia, and a small increase was seen in acute normobaric hypoxia (2 ± 2; P < .05). During the field study at 4090 m, 12 participants (92%) demonstrated 7 ± 4 B-lines at rest, which increased to 17 ± 5 immediately after the exercise test (P < .001). An increase was evident in all participants. There was a reciprocal fall in peripheral arterial oxygen saturations (Spo2) after exercise from 88% ± 4% to 80% ± 8% (P < .01). B-lines and Spo2 in all participants returned to baseline levels within 4 hours. CONCLUSIONS: HIIE led to an increase in B-lines at altitude after subacute exposure but not during acute exposure at equivalent simulated altitude. This may indicate pulmonary interstitial edema.

Effect of acute normobaric hypoxia on the ventilatory threshold.

PURPOSE: This study investigated the response of the ventilatory threshold (VT) to acute normobaric hypoxia and compared the agreement between software-based algorithms which use automatic detection to identify the VT. Results were used to examine whether the VT can be used as a physiological parameter to prescribe and monitor exercise intensity in hypoxic exercise training programs. METHODS: Fourteen untrained individuals (7 women, 7 men; age 22 ± 2 years, [Formula: see text]O2peak 46 ± 7 mL kg(-1) min(-1)) completed five identical graded exercise tests (randomized order) on a cycle ergometer to measure VT at sea-level (SL) and in response to four normobaric hypoxic conditions (FIO2: 0.185, 0.165, 0.142, 0.125) equivalent to 1,000, 2,000, 3,000 and 4,000 m. Data were analyzed using a one-way analysis of variance (ANOVA) with repeated measures. RESULTS: The VT was similar across all conditions (SL = 1.98 ± 0.46, 1,000 m = 2.03 ± 0.61, 2,000 m = 2.27 ± 0.62, 3,000 m = 1.84 ± 0.50, 4,000 m = 2.29 ± 0.58 L min(-1)) for all algorithms used despite a reduction in arterial oxygen saturation at 3,000 (P ≤ 0.01) and 4,000 m (P ≤ 0.01) compared with SL values. CONCLUSION: The VT appears to be a suitable physiological parameter for exercise prescription in normobaric hypoxia up to an altitude of 4,000 m.

High altitude impairs in vivo immunity in humans.

The aim was to assess the effect of high altitude on the development of new immune memory (induction) using a contact sensitization model of in vivo immunity. We hypothesized that high-altitude exposure would impair induction of the in vivo immune response to a novel antigen, diphenylcyclopropenone (DPCP). DPCP was applied (sensitization) to the lower back of 27 rested controls at sea level and to ten rested mountaineers 28 hours after passive ascent to 3777 m. After sensitization, mountaineers avoided strenuous exercise for a further 24 hours, after which they completed alpine activities for 11-18 days. Exactly 4 weeks after sensitization, the strength of immune memory induction was quantified in rested mountaineers and controls at sea level, by measuring the response to a low, dose-series DPCP challenge, read at 48 hours as skin measures of edema (skinfold thickness) and redness (erythema). Compared with control responses, skinfold thickness and erythema were reduced in the mountaineers (skinfold thickness,-52%, p=0.01, d=0.86; erythema, -36%, p=0.02, d=0.77). These changes in skinfold thickness and erythema were related to arterial oxygen saturation (r=0.7, p=0.04), but not cortisol (r<0.1, p>0.79), at sensitization. In conclusion, this is the first study to show, using a contact sensitization model of in vivo immunity, that high altitude exposure impairs the development of new immunity in humans.