Intramuscular adipose tissue, muscle area, and power as predictors of performance in breast cancer survivors.

PURPOSE: The decline in physical performance, assessed by physical tests such as the timed up and go (TUG) test, is a consequence of reduced physiological reserves at higher levels of a hierarchical process. This occurs due to changes in muscle architecture, including atrophy and fat infiltration into the muscles, which in turn lead to changes in muscle function, resulting in reduced muscle strength and power and, consequently, affecting physical performance. This study investigated predictive factors for physical performance in breast cancer survivor (BCS), focusing on intramuscular adipose tissue (IMAT), quadríceps muscle area (QMA), and muscular power. METHODS: This observational, analytical, and cross-sectional study included 23 women without a history of cancer (age, 58.5 ± 8.3 years; BMI, 27.2 ± 5.1 kg/m2) and 56 BCS (age, 58.5 ± 8.3 years; BMI, 27.2 ± 5.1 kg/m2). QMA and IMAT were assessed using computed tomography images. Muscular power and physical performance were measured using the 5-repetition sit-to-stand and TUG tests, respectively. RESULTS: IMAT (r = 0.4, P < 0.01) and muscular power (r = - 0.4, P < 0.01) were associated with TUG performance in BCS, whereas QMA (r = - 0.22, P = 0.10) showed no significant association. QMA (r = 0.55, P < 0.01) was associated with muscular power, while no significant association was found between IMAT and muscular power (r = - 0.05, P = 0.73). Age explained 19% (P < 0.01) of TUG performance variability. Adding muscular power increased explanatory power by 12% (P < 0.01), and including IMAT further increased it by 7% (P = 0.02) for TUG performance. Collectively, age, muscular power, and IMAT accounted for 38% of the performance variance in the TUG test (age, B = 0.06, P = 0.043; muscular power, B = - 0.01, P = 0.002; IMAT, B = - 0.05, P = 0.020). CONCLUSIONS: Our findings suggest that IMAT and muscular power predict the physical performance of BCS, while QMA does not have the same predictive capability.

Acute resistance exercise reduces increased gene expression in muscle atrophy of ovariectomised arthritic rats.

OBJECTIVE: We studied the effect of resistance exercise (RE) on mRNA levels of atrogin-1, MuRF-1, and myostatin in the gastrocnemius muscle of arthritic rats after loss of ovarian function (LOF). MATERIAL AND METHODS: Thirty female Wistar rats (nine weeks old, 195.3 ±17.4 grams) were randomly allocated into five groups: control group (CT-Sham; n = 6); group with rheumatoid arthritis (RA; n = 6); group with rheumatoid arthritis subjected to RE (RAEX; n = 6); ovariectomy group with rheumatoid arthritis (RAOV; n = 6); and an ovariectomy group with rheumatoid arthritis subjected to RE (RAOVEX; n = 6). After 15 days of intra-articular injections with Met-BSA the animals were subjected to RE and six hours after workout were euthanised. RESULTS: The rheumatoid arthritis provoked reduction in the cross-sectional area (CSA) of muscle fibres, but the CSA was lower in the RAOV when compared to the RA groups. Skeletal muscle atrogin-1 mRNA level was increased in arthritic rats (RA and RAOV), but the atrogin-1 level was higher in RAOV group when compared to other arthritic groups. The Muscle MuRF-1 mRNA level was also increased in the RAOV group. The increased atrogin-1 and MuRF-1 mRNA levels were lower in the RAOVEX group than in the RAOV group. The myostatin mRNA level was similar in all groups, except for the RAOVEX group, in which it was lower than the other groups. CONCLUSIONS: LOF results in increased loss of skeletal muscle-related ubiquitin ligases (atrogin-1 and MuRF-1). However, the RE reduces the atrogin-1, MuRF-1, and myostatin mRNA levels in muscle of arthritic rats affected by LOF.

Low-load resistance training promotes muscular adaptation regardless of vascular occlusion, load, or volume.

PURPOSE: This study investigates the impact of two different intensities and different volumes of low-load resistance training (LLRT) with and without blood flow restriction on the adaptation of muscle strength and size. METHODS: The sample was divided into five groups: one set of 20 % of one repetition maximum (1RM), three sets of 20 % of 1RM, one set of 50 % of 1RM, three sets of 50 % of 1RM, or control. LLRT was performed with (OC) or without (NOC) vascular occlusion, which was selected randomly for each subject. The maximal muscle strength (leg extension; 1RM) and the cross-sectional area (quadriceps; CSA) were assessed at baseline and after 8 weeks of LLRT. RESULTS: 1RM performance was increased in both groups after 8 weeks of training: OC (1 × 50 % = 20.6 %; 3 × 50 % = 20.9 %; 1 × 20 % = 26.6 %; 3 × 20 % = 21.6 %) and NOC (1 × 50 % = 18.6 %; 3 × 50 % = 26.8 %; 1 × 20 % = 18.5 %; 3 × 20 % = 21.6 %; 3 × 20 % = 24.7 %) compared with the control group (-1.7 %). Additionally, the CSA was increased in both groups: OC (1 × 50 % = 2.4 %; 3 × 50 % = 3.8 %; 1 × 20 % = 4.6 %; 3 × 20 % = 4.8 %) and NOC (1 × 50 % = 2.4 %; 3 × 50 % = 1.5 %; 1 × 20 % = 4.3 %; 3 × 20 % = 3.8 %) compared with the control group (-0.7 %). There were no significant differences between the OC and NOC groups. CONCLUSION: We conclude that 8 weeks of LLRT until failure in novice young lifters, regardless of occlusion, load or volume, produces similar magnitudes of muscular hypertrophy and strength.