V’O2 kinetics are slowed when exercise transitions begin from an elevated work and/or metabolic rate. Slower O2 provision, recruitment of fast fibres, reduced muscle energy status and phosphocreatine concentration ([PCr]) have been the proposed mechanisms. Incomplete recovery is associated with an elevated baseline V’O2 and with a reduced [PCr], with little effect on recruitment and O2 delivery. PURPOSE: We tested the hypothesis that pre-transition metabolic rate and/or [PCr] set the time course of the adjustment of oxidative metabolism: the lower the recovery time, the slower the VO2 kinetics. METHODS: In 7 young active males (24±2 yrs, 48±11 ml·kg-1·min-1), we measured breath by breath alveolar V’O2 kinetics during a sequence of 6 moderate intensity step transitions, each lasting 6 min. Pre-transition V’O2 and intramuscular [PCr] were manipulated by progressively reducing the recovery time, in random order, at 30 s, 60 s, 90 s, 120 s and 300 s. V’O2 data from the 6 repetitions of the same transition were combined and fitted with a monoexponential model (excluding the initial 20s of data) to calculate phase 2 time constant (τ2) of V’O2 kinetics. [PCr] changes, from a baseline value of 25 mmol·Kg-1 of muscle, were estimated based on oxygen deficit. recovery time (s) baseline VO2 (ml·min-1) steady state VO2 (ml·min-1) baseline [PCr] (mmol·kg-1) τ2 (s) 300 507±83 1943±136 23.6±2.3 21.4±7.3 120 580±95* 1970±129 26.2±3.5 19.6 ± 4.4 90 660±120* 1976±133 23.5±3.4 18.6 ± 4.9 60 892±134* 1981±136 19.7±4.5* 21.4 ± 5.5 30 1323±134* 1977±119 18.1±4.5* 28.7 ± 8.0* * indicates a significant difference (repeated measures ANOVA) form complete recovery (i.e. 300s) RESULTS: Steady state V’O2 was unaffected by recovery time. Pre-transition V’O2 decreased and [PCr] increased linearly with recovery time up to 120s (r2=0.91 and 0.98, respectively). τ2 linearly increased with baseline metabolic rate and decreased with baseline [PCr] (r2 = 0.77 and 0.63 respectively). CONCLUSION: Our data favor the hypothesis that baseline metabolic rate and [PCr] affect the time course of the adjustment of oxidative metabolism. A lower energy status and altered PCr splitting kinetics could be responsible for a slower activation of oxidative phosphorylation and in turn, slower the V’O2 kinetics.
Effect of incomplete recovery on V’O2-on-kinetics during moderate-intensity exercise transitions in healthy humans
POGLIAGHI, Silvia;TAM, Enrico;CAPELLI, Carlo
2014-01-01
Abstract
V’O2 kinetics are slowed when exercise transitions begin from an elevated work and/or metabolic rate. Slower O2 provision, recruitment of fast fibres, reduced muscle energy status and phosphocreatine concentration ([PCr]) have been the proposed mechanisms. Incomplete recovery is associated with an elevated baseline V’O2 and with a reduced [PCr], with little effect on recruitment and O2 delivery. PURPOSE: We tested the hypothesis that pre-transition metabolic rate and/or [PCr] set the time course of the adjustment of oxidative metabolism: the lower the recovery time, the slower the VO2 kinetics. METHODS: In 7 young active males (24±2 yrs, 48±11 ml·kg-1·min-1), we measured breath by breath alveolar V’O2 kinetics during a sequence of 6 moderate intensity step transitions, each lasting 6 min. Pre-transition V’O2 and intramuscular [PCr] were manipulated by progressively reducing the recovery time, in random order, at 30 s, 60 s, 90 s, 120 s and 300 s. V’O2 data from the 6 repetitions of the same transition were combined and fitted with a monoexponential model (excluding the initial 20s of data) to calculate phase 2 time constant (τ2) of V’O2 kinetics. [PCr] changes, from a baseline value of 25 mmol·Kg-1 of muscle, were estimated based on oxygen deficit. recovery time (s) baseline VO2 (ml·min-1) steady state VO2 (ml·min-1) baseline [PCr] (mmol·kg-1) τ2 (s) 300 507±83 1943±136 23.6±2.3 21.4±7.3 120 580±95* 1970±129 26.2±3.5 19.6 ± 4.4 90 660±120* 1976±133 23.5±3.4 18.6 ± 4.9 60 892±134* 1981±136 19.7±4.5* 21.4 ± 5.5 30 1323±134* 1977±119 18.1±4.5* 28.7 ± 8.0* * indicates a significant difference (repeated measures ANOVA) form complete recovery (i.e. 300s) RESULTS: Steady state V’O2 was unaffected by recovery time. Pre-transition V’O2 decreased and [PCr] increased linearly with recovery time up to 120s (r2=0.91 and 0.98, respectively). τ2 linearly increased with baseline metabolic rate and decreased with baseline [PCr] (r2 = 0.77 and 0.63 respectively). CONCLUSION: Our data favor the hypothesis that baseline metabolic rate and [PCr] affect the time course of the adjustment of oxidative metabolism. A lower energy status and altered PCr splitting kinetics could be responsible for a slower activation of oxidative phosphorylation and in turn, slower the V’O2 kinetics.
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