14 research outputs found

    The Effect of the Stretch-Shortening Cycle in the Force–Velocity Relationship and Its Association With Physical Function in Older Adults With COPD

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    This study aimed to evaluate the effect of the stretch-shortening cycle (SSC) on different portions of the force–velocity (F–V) relationship in older adults with and without chronic obstructive pulmonary disease (COPD), and to assess its association with physical function. The participants were 26 older adults with COPD (79 ± 7 years old; FEV1 = 53 ± 36% of predicted) and 10 physically active non-COPD (77 ± 4 years old) older adults. The F–V relationship was evaluated in the leg press exercise during a purely concentric muscle action and compared with that following an eccentric muscle action at 10% intervals of maximal unloaded shortening velocity (V0). Vastus lateralis (VL) muscle thickness, pennation angle (PA), and fascicle length (FL) were assessed by ultrasound. Habitual gait speed was measured over a 4-m distance. COPD subjects exhibited lower physical function and concentric maximal muscle power (Pmax) values compared with the non-COPD group (both p < 0.05). The SSC increased force and power values among COPD participants at 0–100 and 1–100% of V0, respectively, while the same was observed among non-COPD participants only at 40–90 and 30–90% of V0, respectively (all p < 0.05). The SSC induced greater improvements in force, but not power, among COPD compared with non-COPD subjects between 50 and 70% of V0 (all p < 0.05). Thus, between-group differences in muscle power were not statistically significant after the inclusion of the SSC (p > 0.05). The SSC-induced potentiation at 50–100% of V0 was negatively associated with physical function (r = -0.40–0.50), while that observed at 80–100% of V0 was negatively associated with VL muscle thickness and PA (r = -0.43–0.52) (all p < 0.05). In conclusion, older adults with COPD showed a higher SSC-induced potentiation compared with non-COPD subjects, which eliminated between-group differences in muscle power when performing SSC muscle actions. The SSC-induced potentiation was associated with lower physical function, VL muscle thickness, and VL PA values. The SSC-induced potentiation may help as a compensatory mechanism in those older subjects with a decreased ability to produce force/power during purely concentric muscle actions

    Which one came first: movement behavior or frailty? A cross-lagged panel model in the Toledo Study for Healthy Aging

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    Background There has been limited longitudinal assessment of the relationship between moderate-to-vigorous physical activity (MVPA) and sedentary behaviour (SB) with frailty, and no studies have explored the possibility of reverse causality. This study aimed to determine the potential bidirectionality of the relationship between accelerometer-assessed MVPA, SB, and frailty over time in older adults. Methods Participants were from the Toledo Study for Healthy Aging. We analysed 186 older people aged 67 to 90 (76.7 ± 3.9; 52.7% female participants) over a 4-year period. Time spent in SB and MVPA was assessed by accelerometry. Frailty Trait Scale was used to determine frailty levels. A cross-lagged panel model design was used to test the reciprocal relationships between MVPA/SB and frailty. Results Frailty Trait Scale score changed from 35.4 to 43.8 points between the two times (P < 0.05). We also found a reduction of 7 min/day in the time spent on MVPA (P < 0.05), and participants tended to spend more time on SB (P = 0.076). Our analyses revealed that lower levels of initial MVPA predicted higher levels of later frailty [std. ÎČ = 0.126; confidence interval (CI) = 0.231, 0.021; P < 0.05], whereas initial spent time on SB did not predict later frailty (std. ÎČ = 0.049; CI = 0.185, 0.087; P = 0.48). Conversely, an initial increased frailty status predicted higher levels of later SB (std. ÎČ = 0.167; CI = 0.026, 0.307; P < 0.05) but not those of MVPA (std. ÎČ = 0.071; CI = 0.033, 0.175; P = 0.18). Conclusions Our observations suggest that the relationship between MVPA/SB and frailty is unidirectional: individuals who spent less time on MVPA at baseline are more likely to increase their frailty score, and individuals who are more frail are more likely to spent more time on SB at follow-up. Interventions and policies should aim to increase MVPA levels from earlier stages to promote successful aging

    Relationship between physical performance and frailty syndrome in older adults: the mediating role of physical activity, sedentary time and body composition

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    The objectives were to clarify whether the relationship between physical performance and frailty was independently and jointly mediated by movement behaviors and body composition. We analyzed 871 older adults (476 women) from The Toledo Study for Healthy Aging. Skeletal muscle index (SMI) and fat index (FI) were determined using bone densitometry. Sedentary time (ST) and moderate-to-vigorous physical activity (MVPA) were assessed using accelerometry. The Frailty Trait Scale and The Short Physical Performance Battery (SPPB) were used to evaluate frailty and physical performance, respectively. Simple and multiple mediation analyses were carried out to determine the role of movement behaviors and body composition, adjusted for potential confounders. ST and MVPA acted independently as mediators in the relationship between SPPB and frailty (0.06% for ST and 16.89% for MVPA). FI also acted as an independent mediator in the same relationship (36.47%), while the mediation role of SMI was not significant. MVPA and FI both acted jointly as mediators in this previous relationship explaining 58.15% of the model. Our data support the fact that interventions should simultaneously encourage the promotion of MVPA and strategies to decrease the FI in order to prevent or treat frailty through physical performance improvement

    Relative sit-to-stand power cut-off points and their association with negatives outcomes in older adults

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    The purposes of this study were: (i) to evaluate the association of sit-to-stand (STS) power and body composition parameters [body mass index (BMI) and legs skeletal muscle index (SMI)] with age; (ii) to provide cut-off points for low relative STS power (STSrel), (iii) to provide normative data for well-functioning older adults and (iv) to assess the association of low STSrel with negative outcomes. Cross-sectional design (1369 older adults). STS power parameters assessed by validated equations, BMI and Legs SMI assessed by dual-energy X-ray absorptiometry were recorded. Sex- and age-adjusted segmented and logistic regression analyses and receiver operator characteristic curves were used. Among men, STSrel showed a negative association with age up to the age of 85 years (− 1.2 to − 1.4%year−1; p < 0.05). In women, a negative association with age was observed throughout the old adult life (− 1.2 to − 2.0%year−1; p < 0.001). Cut-off values for low STSrel were 2.5 W kg−1 in men and 1.9 W kg−1 in women. Low STSrel was associated with frailty (OR [95% CI] = 5.6 [3.1, 10.1]) and low habitual gait speed (HGS) (OR [95% CI] = 2.7 [1.8, 3.9]) in men while low STSrel was associated with frailty (OR [95% CI] = 6.9 [4.5, 10.5]) low HGS (OR [95% CI] = 2.9 [2.0, 4.1]), disability in activities of daily living (OR [95% CI] = 2.1 [1.4, 3.2]), and low quality of life (OR [95%CI] = 1.7 [1.2, 2.4]) in women. STSrel declined with increasing age in both men and women. Due to the adverse outcomes related to STSrel, the reported cut-off points can be used as a clinical tool to identify low STSrel among older adults

    Relative sit‑to‑stand power cut‑of points and their association with negatives outcomes in older adults

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    The purposes of this study were: (i) to evaluate the association of sit-to-stand (STS) power and body composition parameters [body mass index (BMI) and legs skeletal muscle index (SMI)] with age; (ii) to provide cut-of points for low relative STS power (STSrel), (iii) to provide normative data for well functioning older adults and (iv) to assess the association of low STSrel with negative outcomes. Cross-sectional design (1369 older adults). STS power parameters assessed by validated equations, BMI and Legs SMI assessed by dual-energy X-ray absorptiometry were recorded. Sex- and age adjusted segmented and logistic regression analyses and receiver operator characteristic curves were used. Among men, STSrel showed a negative association with age up to the age of 85 years (− 1.2 to − 1.4%year−1; p < 0.05). In women, a negative association with age was observed throughout the old adult life (− 1.2 to − 2.0%year−1; p < 0.001). Cut-of values for low STSrel were 2.5W ­kg−1 in men and 1.9W ­kg−1 in women. Low STSrel was associated with frailty (OR [95% CI] = 5.6 [3.1, 10.1]) and low habitual gait speed (HGS) (OR [95% CI] = 2.7 [1.8, 3.9]) in men while low STSrel was associated with frailty (OR [95% CI] = 6.9 [4.5, 10.5]) low HGS (OR [95% CI] = 2.9 [2.0, 4.1]), disability in activities of daily living (OR [95% CI] = 2.1 [1.4, 3.2]), and low quality of life (OR [95%CI] = 1.7 [1.2, 2.4]) in women. STSrel declined with increasing age in both men and women. Due to the adverse outcomes related to STSrel, the reported cut-of points can be used as a clinical tool to identify low STSrel among older adults

    KCNMA1 Encoded Cardiac BK Channels Afford Protection against Ischemia-Reperfusion Injury

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    Mitochondrial potassium channels have been implicated in myocardial protection mediated through pre-/postconditioning. Compounds that open the Ca2+-and voltage-activated potassium channel of big-conductance (BK) have a pre-conditioninglike effect on survival of cardiomyocytes after ischemia/reperfusion injury. Recently, mitochondrial BK channels (mitoBKs) in cardiomyocytes were implicated as infarct-limiting factors that derive directly from the KCNMA1 gene encoding for canonical BKs usually present at the plasma membrane of cells. However, some studies challenged these cardio-protective roles of mitoBKs. Herein, we present electrophysiological evidence for paxilline- and NS11021-sensitive BK-mediated currents of 190 pS conductance in mitoplasts from wild-type but not BK-/- cardiomyocytes. Transmission electron microscopy of BK-/- ventricular muscles fibres showed normal ultra-structures and matrix dimension, but oxidative phosphorylation capacities at normoxia and upon re-oxygenation after anoxia were significantly attenuated in BK-/- permeabilized cardiomyocytes. In the absence of BK, post-anoxic reactive oxygen species (ROS) production from cardiomyocyte mitochondria was elevated indicating that mitoBK fine-tune the oxidative state at hypoxia and reoxygenation. Because ROS and the capacity of the myocardium for oxidative metabolism are important determinants of cellular survival, we tested BK-/- hearts for their response in an ex-vivo model of ischemia/reperfusion (I/R) injury. Infarct areas, coronary flow and heart rates were not different between wild-type and BK-/- hearts upon I/R injury in the absence of ischemic pre-conditioning (IP),but differed upon IP. While the area of infarction comprised 28 +/- 3% of the area at risk in wild-type, it was increased to 58 +/- 5% in BK-/- hearts suggesting that BK mediates the beneficial effects of IP. These findings suggest that cardiac BK channels are important for proper oxidative energy supply of cardiomyocytes at normoxia and upon re-oxygenation after prolonged anoxia and that IP might indeed favor survival of the myocardium upon I/R injury in a BK-dependent mode stemming from both mitochondrial post-anoxic ROS modulation and non-mitochondrial localizations

    Severe energy deficit upregulates leptin receptors, leptin signaling, and PTP1B in human skeletal muscle

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    In obesity, leptin receptors (OBR) and leptin signaling in skeletal muscle are downregulated. To determine whether OBR and leptin signaling are upregulated with a severe energy deficit, 15 overweight men were assessed before the intervention (PRE), after 4 days of caloric restriction (3.2 kcal·kg body wt-1·day-1) in combination with prolonged exercise (CRE; 8 h walking + 45 min single-arm cranking/day) to induce an energy deficit of ~5,500 kcal/day, and following 3 days of control diet (isoenergetic) and reduced exercise (CD). During CRE, the diet consisted solely of whey protein (n = 8) or sucrose (n = 7; 0.8 g·kg body wt-1·day-1). Muscle biopsies were obtained from the exercised and the nonexercised deltoid muscles and from the vastus lateralis. From PRE to CRE, serum glucose, insulin, and leptin were reduced. OBR expression was augmented in all examined muscles associated with increased maximal fat oxidation. Compared with PRE, after CD, phospho-Tyr1141, phospho-Tyr985OBR, JAK2, and phospho- Tyr1007/1008JKK2protein expression were increased in all muscles, whereas STAT3 and phospho-Tyr705STAT3 were increased only in the arms. The expression of protein tyrosine phosphatase 1B (PTP1B) in skeletal muscle was increased by 18 and 45% after CRE and CD, respectively (P &amp;lt; 0.05). Suppressor of cytokine signaling 3 (SOCS3) tended to increase in the legs and decrease in the arm muscles (ANOVA interaction: P &amp;lt; 0.05). Myosin heavy chain I isoform was associated with OBR protein expression (r-=0.75), phospho- Tyr985OBR (r = 0.88), and phospho-Tyr705STAT3/STAT3 (r = 0.74). In summary, despite increased PTP1B expression, skeletal muscle OBR and signaling are upregulated by a severe energy deficit with greater response in the arm than in the legs likely due to SOCS3 upregulation in the leg muscles NEW &amp;amp; NOTEWORTHY This study shows that the skeletal muscle leptin receptors and their corresponding signaling cascade are upregulated in response to a severe energy deficit, contributing to increase maximal fat oxidation. The responses are more prominent in the arm muscles than in the legs but partly blunted by whey protein ingestion and high volume of exercise. This occurs despite an increase of protein tyrosine phosphatase 1B protein expression, a known inhibitor of insulin and leptin signaling

    Impact of data averaging strategies on V̇O2max assessment: Mathematical modeling and reliability

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    Background: No consensus exists on how to average data to optimize VO2max assessment. Although the VO2max value is reduced with larger averaging blocks, no mathematical procedure is available to account for the effect of the length of the averaging block on VO2max. Aims: To determine the effect that the number of breaths or seconds included in the averaging block has on the VO2max value and its reproducibility and to develop correction equations to standardize VO2max values obtained with different averaging strategies. Methods: Eighty‐four subjects performed duplicate incremental tests to exhaustion (IE) in the cycle ergometer and/or treadmill using two metabolic carts (Vyntus and Vmax N29). Rolling breath averages and fixed time averages were calculated from breath‐by‐breath data from 6 to 60 breaths or seconds. Results: VO2max decayed from 6 to 60 breath averages by 10% in low fit (VO2max 0.97). There was a linear‐log relationship between the number of breaths or seconds in the averaging block and VO2max (R2 > 0.99, P < 0.001), and specific equations were developed to standardize VO2max values to a fixed number of breaths or seconds. Reproducibility was higher in trained than low‐fit subjects and not influenced by the averaging strategy, exercise mode, maximal respiratory rate, or IE protocol. Conclusions: The VO2max decreases following a linear‐log function with the number of breaths or seconds included in the averaging block and can be corrected with specific equations as those developed here

    Antioxidant enzymes and Nrf2/Keap1 in human skeletal muscle: Influence of age, sex, adiposity and aerobic fitness

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    Whether a higher aerobic fitness is associated with increased expression of antioxidant enzymes and their regulatory factors in skeletal muscle remains unknown. Although oestrogens could promote a higher antioxidant capacity in females, it remains unknown whether a sex dimorphism exists in humans regarding the antioxidant capacity of skeletal muscle. Thus, the aim was to determine the protein expression levels of the antioxidant enzymes SOD1, SOD2, catalase and glutathione reductase (GR) and their regulatory factors Nrf2 and Keap1 in 189 volunteers (120 males and 69 females) to establish whether sex differences exist and how age, VO2max and adiposity influence these. For this purpose, vastus lateralis muscle biopsies were obtained in all participants under resting and unstressed conditions. No significant sex differences in Nrf2, Keap1, SOD1, SOD2, catalase and GR protein expression levels were observed after accounting for VO2max, age and adiposity differences. Multiple regression analysis indicates that the VO2max in mL.kg LLM−1.min−1can be predicted from the levels of SOD2, Total Nrf2 and Keap1 (R = 0.58, P &lt; 0.001), with SOD2 being the main predictor explaining 28 % of variance in VO2max, while Nrf2 and Keap1 explained each around 3 % of the variance. SOD1 protein expression increased with ageing in the whole group after accounting for differences in VO2max and body fat percentage. Overweight and obesity were associated with increased pSer40-Nrf2, pSer40-Nrf2/Total Nrf2 ratio and SOD1 protein expression levels after accounting for differences in age and VO2max. Overall, at the population level, higher aerobic fitness is associated with increased basal expression of muscle antioxidant enzymes, which may explain some of the benefits of regular exercise.Validerad;2023;NivĂ„ 2;2023-11-13 (joosat);Funder: Consejo Superior de Deportes (EXP_75097); Swedish Olympic Committee (070–4058960); Ministerio de EconomĂ­a y Competitividad (DEP2015-71171-R, DEP2017-86409-C2-1-P, PI14/01509, PID2021-125354OB-C21); University of Las Palmas de Gran Canaria (ULPAPD-08/01–4); Agencia Canaria de InvestigaciĂłn, InnovaciĂłn y Sociedad de la InfomaciĂłn (ProID2017010106); Cabildo de Gran Canaria (12/22);License fulltext: CC BY</p
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