Difference between revisions of "Boushel 2014 Pro Can Soc Exercise Physiol"
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{{Publication | {{Publication | ||
|title=Boushel | |title=Boushel RC, Hattel H, Saltin B (2014) Lifelong endurance training keeps mitochondria young. Pro Can Soc Exercise Physiol S6. | ||
|info=[http://www.nrcresearchpress.com/doi/pdf/10.1139/apnm-2014-0270 Abstracts] | |info=[http://www.nrcresearchpress.com/doi/pdf/10.1139/apnm-2014-0270 Abstracts] | ||
|authors=Boushel | |authors=Boushel RC, Hattel H, Saltin B | ||
|year=2014 | |year=2014 | ||
|journal=Pro Can Soc Exercise Physiol | |journal=Pro Can Soc Exercise Physiol | ||
|abstract=Aging is associated with diminished cardiovascular function and sarcopenia, and loss of muscle oxidative capacity is considered a salient feature of aging. While moderate-to-high intensity training evokes mitochondrial biogenesis in skeletal muscle, it remains unclear to what extent aging in itself or rather a lower training stimulus that accompanies aging contributes to loss of skeletal muscle mitochondrial function. To address this question leg muscle mitochondrial respiratory capacity in 8 older men (65±2 yrs) who had maintained road cycling training 200 km/week for 50 years was compared to that of 8 age-matched sedentary (UT) controls (67±1 yrs).V˙ O2 max was measured on a bicycle ergometer and a biopsy obtained from vastus lateralis muscle was permeabilized and prepared for high resolution respirometry (Oxygraph, Oroboros, AT). V˙ O2 max was substantially higher (p<0.05) in lifelong trained (45±2 ml/kg/min) compared to UT (27±2 ml/kg/min). Mitochondrial LEAK respiration was higher in ET, and Vmax of mitochondrial respiration (OXPHOS) with mixed substrates was 2-fold higher in the ET (132±6 pmol/sec/mg) compared to UT (72±4 pmol/sec/mg, p<0.01). Higher fatty acid oxidation and substrate control ratios in ET indicate regulatory changes in mitochondria in addition to a larger mitochondrial volume. The findings indicate that skeletal muscle mitochondrial respiratory capacity of ‘lifelong trained’ older males is retained at a level comparable to young athletic individuals, and suggest that decrements in aerobic performance with age are primarily attributed to diminished cardiovascular function. | |abstract=Aging is associated with diminished cardiovascular function and sarcopenia, and loss of muscle oxidative capacity is considered a salient feature of aging. While moderate-to-high intensity training evokes mitochondrial biogenesis in skeletal muscle, it remains unclear to what extent aging in itself or rather a lower training stimulus that accompanies aging contributes to loss of skeletal muscle mitochondrial function. To address this question leg muscle mitochondrial respiratory capacity in 8 older men (65±2 yrs) who had maintained road cycling training 200 km/week for 50 years was compared to that of 8 age-matched sedentary (UT) controls (67±1 yrs).V˙ O2 max was measured on a bicycle ergometer and a biopsy obtained from vastus lateralis muscle was permeabilized and prepared for high resolution respirometry (Oxygraph, Oroboros, AT). V˙ O2 max was substantially higher (p<0.05) in lifelong trained (45±2 ml/kg/min) compared to UT (27±2 ml/kg/min). Mitochondrial LEAK respiration was higher in ET, and Vmax of mitochondrial respiration (OXPHOS) with mixed substrates was 2-fold higher in the ET (132±6 pmol/sec/mg) compared to UT (72±4 pmol/sec/mg, p<0.01). Higher fatty acid oxidation and substrate control ratios in ET indicate regulatory changes in mitochondria in addition to a larger mitochondrial volume. The findings indicate that skeletal muscle mitochondrial respiratory capacity of ‘lifelong trained’ older males is retained at a level comparable to young athletic individuals, and suggest that decrements in aerobic performance with age are primarily attributed to diminished cardiovascular function. | ||
|mipnetlab=SE Stockholm Boushel RC | |mipnetlab=CA Vancouver Boushel RC, SE Stockholm Boushel RC | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
| Line 14: | Line 14: | ||
|preparations=Permeabilized tissue | |preparations=Permeabilized tissue | ||
|couplingstates=LEAK, OXPHOS | |couplingstates=LEAK, OXPHOS | ||
| | |pathways=NS | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 12:22, 8 November 2016
| Boushel RC, Hattel H, Saltin B (2014) Lifelong endurance training keeps mitochondria young. Pro Can Soc Exercise Physiol S6. |
Boushel RC, Hattel H, Saltin B (2014) Pro Can Soc Exercise Physiol
Abstract: Aging is associated with diminished cardiovascular function and sarcopenia, and loss of muscle oxidative capacity is considered a salient feature of aging. While moderate-to-high intensity training evokes mitochondrial biogenesis in skeletal muscle, it remains unclear to what extent aging in itself or rather a lower training stimulus that accompanies aging contributes to loss of skeletal muscle mitochondrial function. To address this question leg muscle mitochondrial respiratory capacity in 8 older men (65±2 yrs) who had maintained road cycling training 200 km/week for 50 years was compared to that of 8 age-matched sedentary (UT) controls (67±1 yrs).V˙ O2 max was measured on a bicycle ergometer and a biopsy obtained from vastus lateralis muscle was permeabilized and prepared for high resolution respirometry (Oxygraph, Oroboros, AT). V˙ O2 max was substantially higher (p<0.05) in lifelong trained (45±2 ml/kg/min) compared to UT (27±2 ml/kg/min). Mitochondrial LEAK respiration was higher in ET, and Vmax of mitochondrial respiration (OXPHOS) with mixed substrates was 2-fold higher in the ET (132±6 pmol/sec/mg) compared to UT (72±4 pmol/sec/mg, p<0.01). Higher fatty acid oxidation and substrate control ratios in ET indicate regulatory changes in mitochondria in addition to a larger mitochondrial volume. The findings indicate that skeletal muscle mitochondrial respiratory capacity of ‘lifelong trained’ older males is retained at a level comparable to young athletic individuals, and suggest that decrements in aerobic performance with age are primarily attributed to diminished cardiovascular function.
• O2k-Network Lab: CA Vancouver Boushel RC, SE Stockholm Boushel RC
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS
Pathway: NS
HRR: Oxygraph-2k
