Some studies report greater muscle hypertrophy during resistance exercise (RE) training from supplement timing (i.e., the strategic consumption of protein and carbohydrate before and/or after each workout). However, no studies have examined whether this strategy provides greater muscle hypertrophy or strength development compared with supplementation at other times during the day. The purpose of this study was to examine the effects of supplement timing compared with supplementation in the hours not close to the workout on muscle-fiber hypertrophy, strength, and body composition during a 10-wk RE program. In a single-blind, randomized protocol, resistance-trained males were matched for strength and placed into one of two groups; the PRE-POST group consumed a supplement (1 g x kg(-1) body weight) containing protein/creatine/glucose immediately before and after RE. The MOR-EVE group consumed the same dose of the same supplement in the morning and late evening. All assessments were completed the week before and after 10 wk of structured, supervised RE training. Assessments included strength (1RM, three exercises), body composition (DEXA), and vastus lateralis muscle biopsies for determination of muscle fiber type (I, IIa, IIx), cross-sectional area (CSA), contractile protein, creatine (Cr), and glycogen content. PRE-POST demonstrated a greater (P < 0.05) increase in lean body mass and 1RM strength in two of three assessments. The changes in body composition were supported by a greater (P < 0.05) increase in CSA of the type II fibers and contractile protein content. PRE-POST supplementation also resulted in higher muscle Cr and glycogen values after the training program (P < 0.05). Supplement timing represents a simple but effective strategy that enhances the adaptations desired from RE-training.

Background: Sarcopenia is an age‐associated skeletal muscle condition characterized by low muscle mass, strength, and physical performance. There is no international consensus on a sarcopenia definition and no contemporaneous clinical and research guidelines specific to Australia and New Zealand. The Australian and New Zealand Society for Sarcopenia and Frailty Research (ANZSSFR) Sarcopenia Diagnosis and Management Task Force aimed to develop consensus guidelines for sarcopenia prevention, assessment, management and research, informed by evidence, consumer opinion, and expert consensus, for use by health professionals and researchers in Australia and New Zealand.Methods: A four‐phase modified Delphi process involving topic experts and informed by consumers, was undertaken between July 2020 and August 2021. Phase 1 involved a structured meeting of 29 Task Force members and a systematic literature search from which the Phase 2 online survey was developed (Qualtrics). Topic experts responded to 18 statements, using 11‐point Likert scales with agreement threshold set a priori at >80%, and five multiple‐choice questions. Statements with moderate agreement (70%–80%) were revised and re‐introduced in Phase 3, and statements with low agreement (80%) were confirmed by the Task Force in Phase 4.Conclusions: The ANZSSFR Task Force present 17 sarcopenia management and research recommendations for use by health professionals and researchers which includes the recommendation to adopt the EWGSOP2 sarcopenia definition in Australia and New Zealand. This rigorous Delphi process that combined evidence, consumer expert opinion and topic expert consensus can inform similar initiatives in countries/regions lacking consensus on sarcopenia.

Duchenne Muscular Dystrophy is a chronic, progressive and ultimately fatal skeletal muscle wasting disease characterised by sarcolemmal fragility and intracellular Ca²⁺ dysregulation secondary to the absence of dystrophin. Mounting literature also suggests that the dysfunction of key energy systems within the muscle may contribute to pathological muscle wasting by reducing ATP availability to Ca²⁺ regulation and fibre regeneration. No study to date has biochemically quantified and contrasted mitochondrial ATP production capacity by dystrophic mitochondria isolated from their pathophysiological environment such to determine whether mitochondria are indeed capable of meeting this heightened cellular ATP demand, or examined the effects of an increasing extramitochondrial Ca²⁺ environment. Using isolated mitochondria from the diaphragm and tibialis anterior of 12 week-old dystrophin-deficient mdx and healthy control mice (C57BL10/ScSn) we have demonstrated severely depressed Complex I-mediated mitochondrial ATP production rate in mdx mitochondria that occurs irrespective of the macronutrient-derivative substrate combination fed into the Kreb’s cycle, and, which is partially, but significantly, ameliorated by inhibition of Complex I with rotenone and stimulation of Complex II-mediated ATP-production with succinate. There was no difference in the MAPR response of mdx mitochondria to increasing extramitochondrial Ca²⁺ load in comparison to controls, and 400 nM extramitochondrial Ca²⁺ was generally shown to be inhibitory to MAPR in both groups. Our data suggests that DMD pathology is exacerbated by a Complex I deficiency, which may contribute in part to the severe reductions in ATP production previously observed in dystrophic skeletal muscle.