Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise

Engelen, Marielle, Janos Porszasz, Marshall Riley, KarlmanWasserman, Kazuhira Maehara, and Thomas J. Barstow. Effects ofhypoxic hypoxia on O₂ uptake andheart rate kinetics during heavy exercise. J. Appl.Physiol. 81(6): 2500-2508, 1996.It is unclearwhether hypoxia alters the kinetics ofO₂ uptake(O₂) during heavy exercise[above the lactic acidosis threshold (LAT)] and how thesealterations might be linked to the rise in blood lactate. Eight healthyvolunteers performed transitions from unloaded cycling to the sameabsolute heavy work rate for 8 min while breathing one of threeinspired O₂ concentrations: 21%(room air), 15% (mild hypoxia), and 12% (moderate hypoxia). Breathing12% O₂ slowed the time constantbut did not affect the amplitude of the primary rise inO₂ (period of first2-3 min of exercise) and had no significant effect on either thetime constant or the amplitude of the slowO₂ component (beginning2-3 min into exercise). Baseline heart rate was elevated inproportion to the severity of the hypoxia, but the amplitude andkinetics of increase during exercise and in recovery were unaffected bylevel of inspired O₂.We conclude that the predominant effect of hypoxia during heavyexercise is on the early energetics as a slowed time constant forO₂ and an additionalanaerobic contribution. However, the sum total of the processesrepresenting the slow component of O₂ is unaffected.

     

Oxygen uptake as related to work rate increment during cycle ergometer exercise

We postulated that the commonly observed constant linear relationship between VO2 and work rate during cycle ergometry to exhaustion is fortuitous and not due to an unchanging cost of external work. Therefore we measured VO2 continuously in 10 healthy men during such exercise while varying the rate of work incrementation and analyzed by linear regression techniques the relationship between VO2 and work rate (delta VO2/delta wr). After excluding the first and last portions of each test we found the mean +/- SD of the delta VO2/delta wr in ml.min-1.W-1 to be 11.2 +/- 0.15, 10.2 +/- 0.16, and 8.8 +/- 0.15 for the 15, 30, and 60 W.min-1 tests, respectively, expressed as ml.J-1 the values were 0.187 +/- 0.0025, 0.170 +/- 0.0027 and 0.147 +/- 0.0025. The slopes of the lower halves of the 15 and 30 W.min-1 tests were 9.9 +/- 0.2 ml.min-1.W-1 similar to the values for aerobic work reported by others. However the upper halves of the 15, 30, and 60 W.min-1 tests demonstrated significant differences: 12.4 +/- 0.36 vs 10.5 +/- 0.31 vs 8.7 +/- 0.23 ml.min-1.W-1 respectively. We postulate that these systematic differences are due to two opposing influences: 1) the fraction of energy from anaerobic sources is larger in the brief 60 W.min-1 tests and 2) the increased energy requirement per W of heavy work is evident especially in the long 15 W.min-1 tests.     

Muscle fiber recruitment and the slow component of O2 uptake: constant work rate vs. all-out sprint exercise

The slow component of pulmonary O(2) uptake (Vo(2)) during constant work rate (CWR) high-intensity exercise has been attributed to the progressive recruitment of (type II) muscle fibers. We tested the following hypotheses: 1) the Vo(2) slow component gain would be greater in a 3-min all-out cycle test than in a work-matched CWR test, and 2) the all-out test would be associated with a progressive decline, and the CWR test with a progressive increase, in muscle activation, as estimated from the electromyogram (EMG) of the vastus lateralis muscle. Eight men (aged 21-39 yr) completed a ramp incremental test, a 3-min all-out test, and a work- and time-matched CWR test to exhaustion. The maximum Vo(2) attained in an initial ramp incremental test (3.97 ± 0.83 l/min) was reached in both experimental tests (3.99 ± 0.84 and 4.03 ± 0.76 l/min for all-out and CWR, respectively). The Vo(2) slow component was greater (P < 0.05) in the all-out test (1.21 ± 0.31 l/min, 4.2 ± 2.2 ml·min(-1)·W(-1)) than in the CWR test (0.59 ± 0.22 l/min, 1.70 ± 0.5 ml·min(-1)·W(-1)). The integrated EMG declined by 26% (P < 0.001) during the all-out test and increased by 60% (P < 0.05) during the CWR test from the first 30 s to the last 30 s of exercise. The considerable reduction in muscle efficiency in the all-out test in the face of a progressively falling integrated EMG indicates that progressive fiber recruitment is not requisite for development of the Vo(2) slow component during voluntary exercise in humans.     

Native soil and fresh fertilizer phosphorus uptake as affected by rate of application and P fertilizers

³²P labelled fertilizers were used to measure native soil and fresh fertilizer phosphorus uptake byLolium perenne L. in greenhouse experiments. The P source evaluation was carried out for multiple rates of application for a standard P fertilizer (DAP) on low and medium soil P levels and for North Carolina rock phosphate (RP) at the medium soil P level only. At the low soil P level, the native P uptake increase was independent of P-DAP applied, and represented 19% of the nil P uptake. At the medium soil P level, the variability of the native soil as a nutrient P source depended on the phosphate fertilizer applied, and the rate of application. Consequently the amount of total P uptake could conceal differences in P fertilizer evaluations as the nutrient P source. Fresh P uptake increased linearly with the rates of P applied as standard or tested P fertilizer. The comparison of various P sources by means of fresh P uptake ratio (i.e. fresh P uptake from tested phosphate divided by fresh P uptake from standard phosphate) was independent of the rate of application. It was therefore suggested that various phosphorus sources be evaluated by measuring the fresh P uptake for a single rate of application.     

Kinetics of oxygen uptake and heart rate at onset of exercise in children

Requirements for cellular homeostasis appear to be unchanged between childhood and maturity. We hypothesized, therefore, that the kinetics of O2 uptake (VO2) in the transition from rest to exercise would be the same in young children as in teenagers. To test this, VO2 and heart rate kinetics from rest to constant work rate (75% of the subject's anaerobic threshold) in 10 children (5 boys and 5 girls) aged 7-10 yr were compared with values found in 10 teenagers (5 boys and 5 girls) aged 15-18 yr. Gas exchange was measured breath to breath, and phases I and II of the transition and phase III (steady-state exercise) were evaluated from multiple transitions in each child. Phase I (the VO2 at 20 s of exercise expressed as percent rest-to-steady-state exercise VO2) was not significantly correlated with age or weight [mean value 42.5 +/- 8.9% (SD)] nor was the phase II time constant for VO2 [mean 27.3 +/- 4.7 (SD) s]. The older girls had significantly slower kinetics than the other children but were also found to be less fit. When the teenagers exercised at work rates well below 75% of their anaerobic threshold, phase I VO2 represented a higher proportion of the overall response, but the phase II kinetics were unchanged. The temporal coupling between the cellular production of mechanical work at the onset of exercise and the uptake of environmental O2 appears to be controlled throughout growth in children.     

Pulmonary O2 uptake kinetics as a determinant of high-intensity exercise tolerance in humans

Tolerance to high-intensity constant-power (P) exercise is well described by a hyperbola with two parameters: a curvature constant (W') and power asymptote termed "critical power" (CP). Since the ability to sustain exercise is closely related to the ability to meet the ATP demand in a steady state, we reasoned that pulmonary O(2) uptake (Vo(2)) kinetics would relate to the P-tolerable duration (t(lim)) parameters. We hypothesized that 1) the fundamental time constant (τVo(2)) would relate inversely to CP; and 2) the slow-component magnitude (ΔVo(2sc)) would relate directly to W'. Fourteen healthy men performed cycle ergometry protocols to the limit of tolerance: 1) an incremental ramp test; 2) a series of constant-P tests to determine Vo(2max), CP, and W'; and 3) repeated constant-P tests (WR(6)) normalized to a 6 min t(lim) for τVo(2) and ΔVo(2sc) estimation. The WR(6) t(lim) averaged 365 ± 16 s, and Vo(2max) (4.18 ± 0.49 l/min) was achieved in every case. CP (range: 171-294 W) was inversely correlated with τVo(2) (18-38 s; R(2) = 0.90), and W' (12.8-29.9 kJ) was directly correlated with ΔVo(2sc) (0.42-0.96 l/min; R(2) = 0.76). These findings support the notions that 1) rapid Vo(2) adaptation at exercise onset allows a steady state to be achieved at higher work rates compared with when Vo(2) kinetics are slower; and 2) exercise exceeding this limit initiates a "fatigue cascade" linking W' to a progressive increase in the O(2) cost of power production (Vo(2sc)), which, if continued, results in attainment of Vo(2max) and exercise intolerance. Collectively, these data implicate Vo(2) kinetics as a key determinant of high-intensity exercise tolerance in humans.     

Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise

We used anexercise paradigm with repeated bouts of heavy forearm exercise to testthe hypothesis that alterations in local acid-base environment thatremain after the first exercise result in greater blood flow andO₂ delivery at the onset of the second bout of exercise.Two bouts of handgrip exercise at 75% peak workload were performed for5 min, separated by 5 min of recovery. We continuously measured bloodflow using Doppler ultrasound and sampled venous blood forO₂ content, PCO₂, pH, and lactateand potassium concentrations, and we calculated muscle O₂uptake (O₂). Forearm blood flow waselevated before the second exercise compared with the first andremained higher during the first 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min, P < 0.05). Flow was notdifferent at 5 min. Arteriovenous O₂ content difference waslower before the second bout (4.6 ± 0.9 vs. 7.2 ± 0.7 mlO₂/dl) and higher by 30 s of exercise(11.2 ± 0.7 vs. 10.8 ± 0.7 ml O₂/dl,P < 0.05). Muscle O₂was unchanged before the start of exercise but was elevated during thefirst 30 s of the transition to the second exercise bout(26.0 ± 2.1 vs. 20.0 ± 0.9 ml/min, P < 0.05). Changes in venous blood PCO₂, pH, andlactate concentration were consistent with reduced reliance onanaerobic glycolysis at the onset of the second exercise bout. Thesedata show that limitations of muscle blood flow can restrict theadaptation of oxidative metabolism at the onset of heavy muscular exertion.

     

Prior exercise speeds pulmonary O2 uptake kinetics by increases in both local muscle O2 availability and O2 utilization.

The effect of prior exercise on pulmonary O(2) uptake (Vo(2)(p)), leg blood flow (LBF), and muscle deoxygenation at the onset of heavy-intensity alternate-leg knee-extension (KE) exercise was examined. Seven subjects [27 (5) yr; mean (SD)] performed step transitions (n = 3; 8 min) from passive KE following no warm-up (HVY 1) and heavy-intensity (Delta50%, 8 min; HVY 2) KE exercise. Vo(2)(p) was measured breath-by-breath; LBF was measured by Doppler ultrasound at the femoral artery; and oxy (O(2)Hb)-, deoxy (HHb)-, and total (Hb(tot)) hemoglobin/myoglobin of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). Phase 2 Vo(2)(p), LBF, and HHb data were fit with a monoexponential model. The time delay (TD) from exercise onset to an increase in HHb was also determined and an HHb effective time constant (HHb - MRT = TD + tau) was calculated. Prior heavy-intensity exercise resulted in a speeding (P < 0.05) of phase 2 Vo(2)(p) kinetics [HVY 1: 42 s (6); HVY 2: 37 s (8)], with no change in the phase 2 amplitude [HVY 1: 1.43 l/min (0.21); HVY 2: 1.48 l/min (0.21)] or amplitude of the Vo(2)(p) slow component [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)]. O(2)Hb and Hb(tot) were elevated throughout the on-transient following prior heavy-intensity exercise. The tauLBF [HVY 1: 39 s (7); HVY 2: 47 s (21); P = 0.48] and HHb-MRT [HVY 1: 23 s (4); HVY 2: 21 s (7); P = 0.63] were unaffected by prior exercise. However, the increase in HHb [HVY 1: 21 microM (10); HVY 2: 25 microM (10); P < 0.001] and the HHb-to-Vo(2)(p) ratio [(HHb/Vo(2)(p)) HVY 1: 14 microM x l(-1) x min(-1) (6); HVY 2: 17 microM x l(-1) x min(-1) (5); P < 0.05] were greater following prior heavy-intensity exercise. These results suggest that the speeding of phase 2 tauVo(2)(p) was the result of both elevated local O(2) availability and greater O(2) extraction evidenced by the greater HHb amplitude and HHb/Vo(2)(p) ratio following prior heavy-intensity exercise.     

Increasing maximal heart rate increases maximal O2 uptake in rats acclimatized to simulated altitude

Gonzalez, Norberto C., Richard L. Clancy, Yoshihiro Moue,and Jean-Paul Richalet. Increasing maximal heart rate increases maximal O₂ uptake in ratsacclimatized to simulated altitude. J. Appl.Physiol. 84(1): 164-168, 1998.Maximal exerciseheart rate (HR_max) is reducedafter acclimatization to hypobaric hypoxia. The lowHR_max contributes to reducemaximal cardiac output(_max) andmay limit maximal O₂ uptake(O_{2 max}). Theobjective of these experiments was to test the hypothesisthat the reduction in_max afteracclimatization to hypoxia, due, in part, to the lowHR_max, limitsO_{2 max}. Ifthis hypothesis is correct, an increase in _max wouldresult in a proportionate increase inO_{2 max}. Rats acclimatized to hypobaric hypoxia [inspiredPO₂(PI_O2) = 69.8 ± 3 Torr for 3 wk] exercised on a treadmill in hypoxic (PI_O2 = 71.7 ± 1.1 Torr) or normoxic conditions(PI_O2 = 142.1 ± 1.1 Torr). Each rat ran twice: in one bout the rat was allowed to reach itsspontaneous HR_max, which was 505 ± 7 and 501 ± 5 beats/min in hypoxic and normoxic exercise,respectively; in the other exercise bout,HR_max was increased by 20% to the preacclimatization value of 600 beats/min by atrial pacing. This resulted in an ~10% increase in_max, since theincrease in HR_max was offset by a10% decrease in stroke volume, probably due to shortening of diastolicfilling time. The increase in_max was accompanied by a proportionate increase in maximal rate of convective O₂ delivery(_max × arterial O₂ content), maximal workrate, and O_{2 max} inhypoxic and normoxic exercise. The data show that increasingHR_max topreacclimatization levels increasesO_{2 max}, supportingthe hypothesis that the lowHR_max tends to limitO_{2 max} after acclimatization to hypoxia.

     

Zinc uptake by corn as affected by vesicular-arbuscular mycorrhizae

Pot-grown mycorrhizal and non-mycorrhizal sweet corn were grown in a low Zn soil. All treatments received a complete nutrient solution with or without Zn. Treatments were harvested sequentially to detemine temporal mycorrhizal effects on: (a) tissue and water soluble Zn and (b) differential uptake of P and Zn. Plants grown with supplemental Zn had greater growth and Zn tissue concentration than those not receiving Zn. With no supplemental Zn, mycorrhizal treatments had greater growth and Zn concentration than non-mycorrhizal treatments. There was no indication of nutrient interaction between Zn and P. Over the range of tissue Zn found, there appeared to be no advantage to water soluble Zn analysis over total Zn in assessing plant Zn status.     

Fractal scaling properties of heart rate dynamics following resistance exercise training.

With aging and disease, there is a breakdown of the natural fractal-like organization of heart rate (HR). Fractal-like correlation properties of HR can be assessed with detrended fluctuation analysis (DFA). A short-time scaling exponent (alpha(s)) value of 1 is associated with healthy HR dynamics, whereas values that deviate away from 1, in either direction, indicate fractal collapse. The purpose of this study was to examine the effect of resistance exercise training (RT) on fractal correlation properties of HR dynamics. Resting ECG was collected at baseline, following a 4-wk time control period and 6 wk of RT (3 days per wk) in 34 men (23 +/- 1 years of age). Fractal properties of HR were assessed with DFA. There was no change in alpha(s) following either the time control period or RT (1.01 +/- 0.06 to 0.98 +/- 0.06 to 0.93 +/- 0.04, P > 0.05). Given the potential bidirectional nature of fractal collapse, subjects were retrospectively separated into two groups (higher alpha(s) and lower alpha(s)) on the basis of the initial alpha(s) by using cluster analysis. An interaction was detected for alpha(s) following RT (P < 0.05). There was no change in alpha(s) in either group following the time control, but alpha(s) increased following RT in the lower alpha(s) group (n = 18; 0.73 +/- 0.04 to 0.69 +/- 0.04 to 0.88 +/- 0.04) and alpha(s) decreased following RT in the higher alpha(s) group (n = 16; 1.20 +/- 0.04 to 1.24 +/- 0.04 to 0.98 +/- 0.04). In conclusion, RT improves fractal properties of HR dynamics.     

Plasma norepinephrine and heart rate dynamics during recovery from submaximal exercise in man

The time course of heart rate (HR) and venous blood norepinephrine concentration [NE], as an expression of the sympathetic nervous activity (SNA), was studied in six sedentary young men during recovery from three periods of cycle ergometer exercise at 21% +/- 2.8%, 43% +/- 2.1% and 65% +/- 2.3% of VO2max respectively (mean +/- SE). The HR decreased mono-exponentially with tau values of 13.6 +/- 1.6 s, 32.7 +/- 5.6 s and 55.8 +/- 8.1 s respectively in the three periods of exercise. At the low exercise level no change in [NE] was found. At medium and high exercise intensity: (a) [NE] increased significantly at the 5th min of exercise (delta [NE] = 207.7 +/- 22.5 pg.ml-1 and 521.3 +/- 58.3 pg.ml-1 respectively); (b) after a time lag of 1 min [NE] decreased exponentially (tau = 87 s and 101 s respectively); (c) in the 1st min HR decreased about 35 beats.min-1; (d) from the 2nd to 5th min of recovery HR and [NE] were linearly related (100 pg.ml-1 delta [NE] congruent to 5 beats.min-1). In the 1st min of recovery, independent of the exercise intensity, the adjustment of HR appears to have been due mainly to the prompt restoration of vagal tone. The further decrease in HR toward the resting value could then be attributed to the return of SNA to the pre-exercise level.