Adaptations in Capillarization and Citrate Synthase Activity in Response to Endurance Training in Older and Young Men
The time-course of adaptation in cardiorespiratory fitness, measures of capillarization, and citrate synthase (CS) activity were examined in seven older (O; 69 ± 7 years) and seven young (Y; 22 ± 1 years) men pre-, mid-, and posttraining during a 12-week endurance training program. Training was performed on a cycle ergometer three times per week for 45 minutes at ~70% of maximal VO(2) (VO(2max)). VO(2max) and maximal cardiac output increased similarly from pre- to posttraining in O and Y (p < .05), and maximal a-vO(2diff) was greater (p < .05) posttraining in O and Y. CS was elevated at mid- and posttraining compared with pretraining in both O and Y (p < .05). Indices of capillarization increased 30%-40% in O and 20%-30% in Y and were elevated at posttraining compared with pre- and midtraining in both groups (p < .05). This study showed that both O and Y undertaking similar endurance training displayed capillary angiogenesis and improved mitochondrial respiratory capacity.
Available from: Carlo Capelli
- "For instance, in addition to increasing maximal aerobic power, ˙ V O 2 kinetics becomes faster after short training periods (Fukuoka et al. 2002; Grassi 2000). Several peripheral muscular modifications underpin these functional adaptations, including (a) an increase in citrate synthase activity (Murias et al. 2011b), as well as mitochondrial size and number (Holloszy and Coyle 1984); (b) a shift from fast to slow switch fibers (Holloszy and Coyle 1984); and (c) as recently suggested (Zoladz et al. 2006), improved metabolic stability of skeletal muscle due to intensification of " the parallel activation " of oxidative phosphorylation, which may even precede any apparent mitochondrial biogenesis (Zoladz et al. 2013) and be the primary cause of the acceleration of ˙ V O 2 kinetics. On these theoretical grounds, we measured (a) maximal oxygen uptake; (b) ˙ "
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We investigated the effects of moderate-intensity training at low and high altitude on V˙O2 and Q˙aO2 kinetics and on myosin heavy-chain expression (MyHC) in seven women (36.3 yy ± 7.1; 65.8 kg ± 11.7; 165 cm ± 8) who participated in two 12- to 14-day trekking expeditions at low (598 m) and high altitude (4132 m) separated by 4 months of recovery.
Breath-by-breath V˙O2 and beat-by-beat Q˙aO2 at the onset of moderate-intensity cycling exercise and energy cost of walking (C w) were assessed before and after trekking. MyHC expression of vastus lateralis was evaluated before and after low-altitude and after high-altitude trekking; muscle fiber high-resolution respirography was performed at the beginning of the study and after high-altitude trekking.
Mean response time of V˙O2 kinetics was faster (P = 0.002 and P = 0.001) and oxygen deficit was smaller (P = 0.001 and P = 0.0004) after low- and high-altitude trekking, whereas Q˙aO2 kinetics and C w did not change. Percentages of slow and fast isoforms of MyHC and mitochondrial mass were not affected by low- and high-altitude training. After training altitude, muscle fiber ADP-stimulated mitochondrial respiration was decreased as compared with the control condition (P = 0.016), whereas leak respiration was increased (P = 0.031), leading to a significant increase in the respiratory control ratio (P = 0.016).
Although training did not significantly modify muscle phenotype, it induced beneficial adaptations of the oxygen transport–utilization systems witnessed by faster V˙O2 kinetics at exercise onset.
European Journal of Applied Physiology and Occupational Physiology 09/2015; DOI:10.1007/s00421-015-3256-z
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ABSTRACT: BACKGROUND: Older heart failure patients with preserved ejection fraction (HFpEF) have severely reduced exercise capacity and quality of life. Both brachial artery flow-mediated dilation (FMD) and peak exercise oxygen uptake (peak VO(2)) decline with normal aging. However, uncertainty remains regarding whether FMD is reduced beyond the degree associated with normal aging and if this contributes to reduced peak VO(2) in elderly HFpEF patients. METHODS: Sixty-six older (70 ± 7 years) HFpEF patients and 47 healthy participants (16 young, 25 ± 3 years, and 31 older, 70 ± 6 years) were studied. Brachial artery diameter was measured before and after cuff occlusion using high-resolution ultrasound. Peak VO(2) was measured using expired gas analysis during upright cycle exercise. RESULTS: Peak VO(2) was severely reduced in older HFpEF patients compared with age-matched healthy participants (15.2 ± 0.5 vs 19.6 ± 0.6 mL/kg/min, p < .0001), and in both groups, peak VO(2) was reduced compared with young healthy controls (28.5 ± 0.8 mL/kg/min; both p < .0001). Compared with healthy young participants, brachial artery FMD (healthy young, 6.13% ± 0.53%) was significantly reduced in healthy older participants (4.0 ± 0.38; p < .0002) and in HFpEF patients (3.64% ± 0.28%; p < .0001). However, FMD was not different in HFpEF patients compared with healthy older participants (p = .86). Although brachial artery FMD was modestly related to peak VO(2) in univariate analyses (r = .19; p = .048), it was not related in multivariate analyses that accounted for age, gender, and body size. CONCLUSION: These results suggest that endothelial dysfunction may not be a significant independent contributor to the severely reduced exercise capacity in elderly HFpEF patients.
The Journals of Gerontology Series A Biological Sciences and Medical Sciences 04/2012; 68(2). DOI:10.1093/gerona/gls099 · 5.42 Impact Factor
Available from: Rozalyn M Anderson
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ABSTRACT: Moderate caloric restriction (CR) without malnutrition increases healthspan in virtually every species studied, including nonhuman primates. In mice, CR exerts significant microvascular protective effects resulting in increased microvascular density in the heart and the brain, which likely contribute to enhanced tolerance to ischemia and improved cardiac performance and cognitive function. Yet, the underlying mechanisms by which CR confer microvascular protection remain elusive. To test the hypothesis that circulating factors triggered by CR regulate endothelial angiogenic capacity, we treated cultured human endothelial cells with sera derived from Macaca mulatta on long-term (over 10 years) CR. Cells treated with sera derived from ad-libitum-fed control monkeys served as controls. We found that factors present in CR sera upregulate vascular endothelial growth factor (VEGF) signaling and stimulate angiogenic processes, including endothelial cell proliferation and formation of capillary-like structures. Treatment with CR sera also tended to increase cellular migration (measured by a wound-healing assay using electric cell-substrate impedance sensing [ECIS] technology) and adhesion to collagen. Collectively, we find that circulating factors induced by CR promote endothelial angiogenic processes, suggesting that increased angiogenesis may be a potential mechanism by which CR improves cardiac function and prevents vascular cognitive impairment.
The Journals of Gerontology Series A Biological Sciences and Medical Sciences 08/2012; 68(3). DOI:10.1093/gerona/gls158 · 5.42 Impact Factor
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