Decrease in peak heart rate with acute hypoxia in relation to sea level V?O2max

Benoît, H.; Busso, Thierry; Castells, J.; Geyssant, A.; Denis, Christian

doi:10.1007/s00421-003-0899-y

Cited by 38 publications

(52 citation statements)

References 28 publications

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“…V O2 peak and maximum heart rate (HRmax) were both significantly lower for the hypoxia V O2 peak test (V O2 peak 2.34 Ϯ 0.16 l/min, HRmax 181 Ϯ 3 beats/min) compared with the normoxia V O2 peak test (V O2 peak 3.56 Ϯ 0.30 l/min, HRmax 189 Ϯ 2 beats/min), in accord with previous findings (1,31).…”

Section: Preliminary Testingsupporting

confidence: 79%

Effect of exercise intensity and hypoxia on skeletal muscle AMPK signaling and substrate metabolism in humans

Wadley¹,

Lee²,

Canny³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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221 phosphorylation, free AMP content, and glucose clearance were more influenced by the absolute than by the relative exercise intensity, being greatest in 73% Normoxia with no difference between 51% Normoxia and 72% Hypoxia. In contrast to this, increases in muscle glycogen use, muscle lactate content, and plasma catecholamine concentration were more influenced by the relative than by the absolute exercise intensity, being similar in 72% Hypoxia and 73% Normoxia, with both trials higher than in 51% Normoxia. In conclusion, increases in muscle AMPK signaling, free AMP content, and glucose disposal during exercise are largely determined by the absolute exercise intensity, whereas increases in plasma catecholamine levels, muscle glycogen use, and muscle lactate levels are more closely associated with the relative exercise intensity. metabolic regulation; glucose kinetics; contraction AMP-ACTIVATED PROTEIN KINASE (AMPK) is a serine/threonine protein kinase that responds to cellular energy status by inhibiting ATP-consuming pathways and activating ATP-producing pathways (27). The catalytic ␣-subunits of AMPK (␣1 and ␣2) are expressed in skeletal muscle and are activated allosterically by increased AMP levels following phosphorylation of the upstream kinase LKB1 (17,27,48,53,58). Skeletal muscle AMPK activity is increased during contractions and exercise in rodents (18, 19, 38, 50) and humans (8, 9, 14, 57).It has been suggested that skeletal muscle glucose uptake during exercise is regulated by AMPK (53). This is largely based on studies using the nucleoside intermediate 5Ј-aminoimidazole-4-carboxamide ribonucleoside (AICAR). AICAR activates AMPK in rat skeletal muscle and increases glucose uptake (2, 19, 54) and GLUT4 translocation (32). Further support for AMPK in the regulation of glucose uptake during exercise is the finding that AICAR and contraction stimulation of glucose uptake are not additive (2, 19). However, in some circumstances, AMPK activation and glucose uptake during exercise are not tightly coupled. For example, during lowintensity exercise (9, 56) and during moderate-intensity exercise following short-term exercise training (35), skeletal muscle AMPK␣2 activity does not increase despite large increases in glucose disposal during exercise. In addition, AMPK dominant negative mice and AMPK␣2 null mice have partially reduced and normal contraction-stimulated glucose uptake, respectively (24, 37).Hypoxic exercise may be a useful experimental model to tease out the role of AMPK in skeletal muscle glucose uptake during exercise, as some studies suggest that hypoxia and contractions involve the same pathway to activate skeletal muscle glucose uptake (6). Indeed, both hypoxia and muscle contraction increase glucose uptake in isolated rat muscle, alter muscle energy status, and activate AMPK (18). However, others find that hypoxia has an additive effect on glucose uptake during contractions in perfused rat hindlimbs (12, 13). In addition, hypoxia-stimulated glucose uptake is absent in mice expressing a dom...

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Section: Preliminary Testingsupporting

confidence: 79%

Effect of exercise intensity and hypoxia on skeletal muscle AMPK signaling and substrate metabolism in humans

Wadley¹,

Lee²,

Canny³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…Some previous authors (Benoit et al 2003;Martin and O'Kroy 1993) observed a decrement in peak HR during maximal exercise in hypoxia (10.4% and 13% O 2 , respectively). However, Lawler et al (1988) reported no change in peak HR in hypoxia (14% O 2 ).…”

Section: Discussionmentioning

confidence: 92%

“…We observed a lower peak HR in H than in N in both of the running tests. In a recent study, Benoit et al (2003) reported that the decrease in peak HR in severe hypoxia (10.4% O 2 ) was larger in trained than in untrained subjects. Thus, the lower peak HR in H than in N observed in the present study could be associated with the relatively high fitness level of our subjects.…”

Section: Discussionmentioning

confidence: 96%

Intermittent short-term graded running performance in middle-distance runners in hypobaric hypoxia

Ogawa

Ohba²,

Nabekura

et al. 2005

Eur J Appl Physiol

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This study investigated whether in trained middle-distance runners, intermittent short-term graded running performance is affected by a hypobaric hypoxic environment (simulated 2,500 m) (H). Seven male middle-distance runners performed an aerobic performance test and an intermittent short-term graded anaerobic running-performance test (MART) both in H and in a normobaric normoxic environment (N). VO(2max) and OBLA were markedly lower (by 18.1% and 8.7%, respectively) in H than in N. In MART, neither maximal running velocity (V(max)) nor exhaustion-time was different between N and H (454 (7) m min(-1) vs. 451 (6) m min(-1), respectively, and 208.7 (5.2) s vs. 205.7 (4.2) s, respectively). The blood lactate concentration at sub-maximal running speed (425 m min(-1)) was significantly greater in H than in N (paired t-test: P<0.05). These results suggest that, in trained middle-distance runners, intermittent short-term graded running performance is not affected by H, despite a considerable decrease in aerobic power in H during the aerobic performance test.

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“…Also during hypoxia, EIH subjects present a lower SaO 2 at exhaustion associated with a higher decrease in _ V O 2 max when compared to non-EIH subjects (Lawler et al 1988;Gore et al 1996;Chapman et al 1999;Benoit et al 2003). The increase in O 2 supply (due to the CaO 2 improvement) is not sufficient to account for the entire rise in _ V O 2 max observed among the EIH group (Peltonen et al 2001;Prieur et al 2002).…”

Section: Validity Of Measurementsmentioning

confidence: 83%

“…A decrease in SaO 2 (induced by lowered O 2 gas mixture among EIH subjects) can reduce peak HR (Benoit et al 2003). Also aerobic training, especially in EIH athletes, could lower peak HR (Zavorsky 2000) .…”

Section: Validity Of Measurementsmentioning

confidence: 99%

Effect of hyperoxia on maximal O2 uptake in exercise-induced arterial hypoxaemic subjects

et al. 2005

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This study focuses on the effect of hyperoxia on maximal oxygen uptake VO2max and maximal power (Pmax) in subjects exhibiting exercise-induced arterial hypoxemia (EIH) at sea level. Sixteen competing male cyclists VO2max > 60 ml.min(-1).kg(-1)) performed exhaustive ramp exercise (cycle-ergometer) under normoxia and moderate hyperoxia (FIO2 = 30%). After the normoxic trial, the subjects were divided into those demonstrating EIH during exercise [arterial O2 desaturation (delta SaO2) >5%; n = 9] and those who did not (n = 7). Under hyperoxia, SaO2 raised and the increase was greater for the EIH than for the non-EIH group (P<0.001). VO2max improved for both groups and to a greater extent for EIH (12.8 +/- 5.7% vs. 4.2 +/- 4.6%, P<0.01; mean+/-SD) and the increase was correlated to the gain in SaO2 for all subjects (r = 0.71, P<0.01). Pmax improved by 3.3 +/- 3.3% (P<0.01) regardless of the group. These data suggest that pulmonary gas exchange contributes to a limitation in VO2max and power for especially EIH subjects.

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Decrease in peak heart rate with acute hypoxia in relation to sea level V?O2max

Cited by 38 publications

References 28 publications

Effect of exercise intensity and hypoxia on skeletal muscle AMPK signaling and substrate metabolism in humans

Effect of exercise intensity and hypoxia on skeletal muscle AMPK signaling and substrate metabolism in humans

Intermittent short-term graded running performance in middle-distance runners in hypobaric hypoxia

Effect of hyperoxia on maximal O2 uptake in exercise-induced arterial hypoxaemic subjects

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