Becoming a World Champion Powerlifter at 71 Years of Age: It Is Never Too Late to Start Exercising.

This case study assessed body composition, muscle strength, cardiorespiratory fitness, and metabolic health of the present female world champion powerlifter in the 70+ age category who started resistance exercise training at 63 years of age with no prior experience with structured exercise training. Measures of body composition (magnetic resonance imaging, computed tomography, and dual-energy X-ray absorptiometry scanning, leg volume); strength (one-repetition maximum leg press and extension, maximum voluntary contraction, and handgrip strength); physical function (short physical performance battery); cardiorespiratory fitness (peak oxygen consumption); and metabolic health (oral glucose tolerance test) were assessed. In addition, a muscle biopsy was collected to assess muscle fiber type distribution and cross-sectional area (CSA). Where possible, data were compared with previously (un)published sex- and age-matched data using z scores. Skeletal muscle mass index was calculated by dividing limb muscle mass by height squared. Data from the control groups are expressed as mean ± 95% confidence interval. Our participant (age: 71 years; body mass: 64.5 kg; body mass index: 27.6 kg/m2) reported a good bone mineral density of 1.09 g/cm2 (T score between -1 and +1) and very low values of abdominal and organ body fat (i.e., between 20% and 70% lower compared with a reference group of postmenopausal women). In addition, she showed a 33% greater skeletal muscle mass index when compared with healthy, older female control subjects (7.9 vs. 5.9 [5.7-6.2] kg/m2; n = 61) as well as 37% greater muscle quadriceps CSA (63.8 vs. 46.6 [44.5-48.7] cm2; n = 48) and 46% greater Type II muscle fiber CSA (4,536 vs. 3,097 [2,707-3,488] µm2; n = 19). Absolute leg press muscle strength was 36% greater (190 vs. 140 [132-147] kg; n = 30) and handgrip strength was 33% greater (33 vs. 25 [23-26] kg; n = 48) when compared with healthy, age-matched controls. In conclusion, even for resistance exercise naïve individuals, starting exercise at an advanced age can lead to improvements in body composition and muscle strength allowing older adults to reduce the risk for developing metabolic syndrome, live independently, and even compete at a world class level.

Energy Expenditure, Body Composition, and Skeletal Muscle Oxidative Capacity in Patients with Myotonic Dystrophy Type 1.

BACKGROUND: Myotonic dystrophy type 1 (DM1) patients are at risk for metabolic abnormalities and commonly experience overweight and obesity. Possibly, weight issues result from lowered resting energy expenditure (EE) and impaired muscle oxidative metabolism. OBJECTIVES: This study aims to assess EE, body composition, and muscle oxidative capacity in patients with DM1 compared to age-, sex- and BMI-matched controls. METHODS: A prospective case control study was conducted including 15 DM1 patients and 15 matched controls. Participants underwent state-of-the-art methodologies including 24 h whole room calorimetry, doubly labeled water and accelerometer analysis under 15-days of free-living conditions, muscle biopsy, full body magnetic resonance imaging (MRI), dual-energy x-ray absorptiometry (DEXA), computed tomography (CT) upper leg, and cardiopulmonary exercise testing. RESULTS: Fat ratio determined by full body MRI was significantly higher in DM1 patients (56 [49-62] %) compared to healthy controls (44 [37-52] % ; p = 0.027). Resting EE did not differ between groups (1948 [1742-2146] vs (2001 [1853-2425>] kcal/24 h, respectively; p = 0.466). In contrast, total EE was 23% lower in DM1 patients (2162 [1794-2494] vs 2814 [2424-3310] kcal/24 h; p = 0.027). Also, DM1 patients had 63% less steps (3090 [2263-5063] vs 8283 [6855-11485] steps/24 h; p = 0.003) and a significantly lower VO2 peak (22 [17-24] vs 33 [26-39] mL/min/kg; p = 0.003) compared to the healthy controls. Muscle biopsy citrate synthase activity did not differ between groups (15.4 [13.3-20.0] vs 20.1 [16.6-25.8] µM/g/min, respectively; p = 0.449). CONCLUSIONS: Resting EE does not differ between DM1 patients and healthy, matched controls when assessed under standardized circumstances. However, under free living conditions, total EE is substantially reduced in DM1 patients due to a lower physical activity level. The sedentary lifestyle of DM1 patients seems responsible for the undesirable changes in body composition and aerobic capacity.

Collagen Protein Ingestion during Recovery from Exercise Does Not Increase Muscle Connective Protein Synthesis Rates.

INTRODUCTION: Protein ingestion during recovery from exercise has been reported to augment myofibrillar protein synthesis rates, without increasing muscle connective protein synthesis rates. It has been suggested that collagen protein may be effective in stimulating muscle connective protein synthesis. The present study assessed the capacity of both whey and collagen protein ingestion to stimulate postexercise myofibrillar and muscle connective protein synthesis rates. METHODS: In a randomized, double-blind, parallel design, 45 young male ( n = 30) and female ( n = 15) recreational athletes (age, 25 ± 4 yr; body mass index, 24.1 ± 2.0 kg·m -2 ) were selected to receive primed continuous intravenous infusions with l -[ring- 13 C 6 ]-phenylalanine and l -[3,5- 2 H 2 ]-tyrosine. After a single session of resistance type exercise, subjects were randomly allocated to one of three groups ingesting either 30 g whey protein (WHEY, n = 15), 30 g collagen protein (COLL, n = 15) or a noncaloric placebo (PLA, n = 15). Blood and muscle biopsy samples were collected over a subsequent 5-h recovery period to assess both myofibrillar and muscle connective protein synthesis rates. RESULTS: Protein ingestion increased circulating plasma amino acid concentrations ( P < 0.05). The postprandial rise in plasma leucine and essential amino acid concentrations was greater in WHEY compared with COLL, whereas plasma glycine and proline concentrations increased more in COLL compared with WHEY ( P < 0.05). Myofibrillar protein synthesis rates averaged 0.041 ± 0.010, 0.036 ± 0.010, and 0.032 ± 0.007%·h -1 in WHEY, COLL and PLA, respectively, with only WHEY resulting in higher rates when compared with PLA ( P < 0.05). Muscle connective protein synthesis rates averaged 0.072 ± 0.019, 0.068 ± 0.017, and 0.058 ± 0.018%·h -1 in WHEY, COLL, and PLA, respectively, with no significant differences between groups ( P = 0.09). CONCLUSIONS: Ingestion of whey protein during recovery from exercise increases myofibrillar protein synthesis rates. Neither collagen nor whey protein ingestion further increased muscle connective protein synthesis rates during the early stages of postexercise recovery in both male and female recreational athletes.

Primary, Secondary, and Tertiary Effects of Carbohydrate Ingestion During Exercise.

The purpose of this current opinion paper is to describe the journey of ingested carbohydrate from 'mouth to mitochondria' culminating in energy production in skeletal muscles during exercise. This journey is conveniently described as primary, secondary, and tertiary events. The primary stage is detection of ingested carbohydrate by receptors in the oral cavity and on the tongue that activate reward and other centers in the brain leading to insulin secretion. After digestion, the secondary stage is the transport of monosaccharides from the small intestine into the systemic circulation. The passage of these monosaccharides is facilitated by the presence of various transport proteins. The intestinal mucosa has carbohydrate sensors that stimulate the release of two 'incretin' hormones (GIP and GLP-1) whose actions range from the secretion of insulin to appetite regulation. Most of the ingested carbohydrate is taken up by the liver resulting in a transient inhibition of hepatic glucose release in a dose-dependent manner. Nonetheless, the subsequent increased hepatic glucose (and lactate) output can increase exogenous carbohydrate oxidation rates by 40-50%. The recognition and successful distribution of carbohydrate to the brain and skeletal muscles to maintain carbohydrate oxidation as well as prevent hypoglycaemia underpins the mechanisms to improve exercise performance.