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Biomedical subjects

Michael I Trenell

Publications and source records attributed to Michael I Trenell.

6 recordsLinked to original sources
PubMed2007

Supplemental oxygen and muscle metabolism in mitochondrial myopathy patients.

Patients with mitochondrial myopathy (MM) have a reduced capacity to perform exercise due to a reduced oxidative capacity. We undertook this study to determine whether skeletal muscle metabolism could be improved with oxygen therapy in patients with MM. Six patients with MM and six controls, matched for age, gender and physical activity, underwent (31)P-magnetic resonance spectroscopy ((31)P-MRS) examination. (31)P-MR spectra were collected at rest and in series during exercise and recovery whilst breathing normoxic (0.21 O(2)) or hyperoxic (1.0 O(2)) air. At rest, MM showed an elevated [ADP] (18 +/- 3 micromol/l) and pH (7.03 +/- 0.01) in comparison to the control group (12 +/- 1 micromol/l, 7.01 +/- 0.01) (P < 0.05) consistent with mitochondrial dysfunction. Oxygen supplementation did not change resting metabolites in either MM or the control group (P > 0.05). Inferred maximal ATP synthesis rate improved by 33% with oxygen in MM (21 +/- 3 vs. 28 +/- 5 mmol/(l min), P < 0.05) but only improved by 5% in controls (40 +/- 3 vs. 42 +/- 3 mmol/(l min), P > 0.05). We conclude that oxygen therapy is associated with significant improvements in muscle metabolism in patients with MM. These data suggest that patients with MM could benefit from therapies which improve the provision of oxygen.

Adenosine Diphosphate↗
PubMed2006

Exercise capacity and quadriceps muscle metabolism following training in subjects with COPD.

The aim of the study was to determine whether 16 sessions of exercise training, completed twice weekly, alters exercise capacity, quadriceps muscle metabolism, cross-sectional area (CSA) and strength in subjects with chronic obstructive pulmonary disease (COPD). We studied (a) 10 COPD subjects (mean age+/-sem = 71+/-2 years; FEV1 = 0.99+/-0.1 L) before and after 16 sessions of exercise training, and (b) 10 healthy subjects (age = 68+/-3 years). The COPD subjects underwent an incremental peak exercise test using a cycle ergometer and a 6-min walk test: both improved following exercise training (P < 0.05). Magnetic resonance spectroscopy measurements, in quadriceps muscle, of post-exercise phosphocreatinine (PCr) recovery kinetics were used to assess mitochondrial function in vivo: in the COPD subjects pre-training this was 19+/-8% lower than in healthy subjects (P = 0.03), but a 38+/-12% increase was seen in the COPD subjects following training (P = 0.003). Magnetic resonance imaging was used to assess quadriceps CSA: after training in the COPD subjects this showed a 7+/-2% increase (P = 0.03). Quadriceps strength, measured by the best of five maximum voluntary contractions, also showed a 32+/-11% increase in the COPD subjects (P = 0.007). Sixteen sessions of exercise training, performed twice weekly, increased exercise capacity as well as quadriceps mitochondrial capacity, CSA and strength in the subjects with COPD.

Aged↗
PubMed2006

Aerobic exercise and muscle metabolism in patients with mitochondrial myopathy.

Exercise therapy improves mitochondrial function in patients with mitochondrial myopathy (MM). We undertook this study to determine the metabolic abnormalities that are improved by exercise therapy. This study identified metabolic pathology using (31)P-magnetic resonance spectroscopy and magnetic resonance imaging (MRI) in a group of patients with MM compared to a control group matched for age, gender, and physical activity. We also observed the effect of exercise therapy for 12 weeks on muscle metabolism and physical function in the MM group. During muscle activity, there was impaired responsiveness of the mitochondria to changes in cytosolic adenosine diphosphate concentration, increased dependence on anaerobic energy pathways, and an adaptive increase in proton efflux in patients with MM. Following exercise therapy, mitochondrial function and muscle mass improved without any change in proton efflux rate. These metabolic findings were accompanied by improvements in functional ability. We conclude that there are significant metabolic differences between patients with MM and a control population, independent of age, gender, and physical activity. Exercise therapy can assist in improving mitochondrial function in MM patients.

Adult↗
PubMed2002

The effect of phosphate loading on erythrocyte 2,3-bisphosphoglycerate levels.

BACKGROUND: Phosphate supplementation has been used in an effort to enhance athletic performance by increasing erythrocyte 2,3-bisphosphoglycerate levels ([2,3-BPG]) and hence improve oxygen offloading from haemoglobin. Claimed effects of phosphate loading upon both exercise performance and erythrocyte [2,3-BPG] are inconsistent, and the basis of any change in [2,3-BPG] is unknown. METHODS: We analysed plasma inorganic phosphate concentration ([P(i)]) and erythrocyte [P(i)] and [2,3-BPG] in venous blood samples from 12 healthy subjects. We re-examined a subset of five of these subjects after 7 days of phosphate loading. RESULTS: There were significant positive correlations between plasma [P(i)] and erythrocyte [P(i)] (r(2)=0.51, p=0.009) and between erythrocyte [P(i)] and [2,3-BPG] (r(2)=0.68, p<0.001). Following phosphate loading, there was a 30% increase in plasma [P(i)] (1.02+/-0.22 to 1.29+/-0.15 mmol/l (mean+/-S.D.), p=0.03) and a 25% increase in erythrocyte [2,3-BPG] (6.77+/-1.12 to 9.11+/-1.87 mmol/l cells, p=0.03). There is no relation between [2,3-BPG] and plasma [P(i)]. CONCLUSIONS: Phosphate loading increases both plasma and erythrocyte phosphate pools and the rise in [2,3-BPG] is probably a consequence of the rise in cell [P(i)].

2,3-Diphosphoglycerate↗
PubMedDate not supplied

Sleep and metabolic control: waking to a problem?

1. The aim of the present review is to outline: (i) the association between sleep and metabolism; (ii) how sleep duration influences the development of disease; and (iii) how sex differences, ageing and obesity may potentially influence the relationship between sleep, metabolic control and subsequent disease. 2. Sleep is associated with a number of endocrine changes, including a change in insulin action in healthy young individuals. Sleep duration shows a prospective U-shaped relationship with all-cause mortality, cardiovascular disease and Type 2 diabetes. 3. Chronic sleep restriction is becoming more common. Experimental sleep restriction impedes daytime glucose control and increases appetite. 4. The sex hormones oestrogen and testosterone influence sleep duration and quality and may account for sex differences in the prevalence of sleep-related disorders. 5. Ageing is associated with a decreased sleep duration, decreased muscle mass and impaired insulin action. 6. Obesity impairs insulin action and is associated with the incidence and severity of obstructive sleep apnoea. 7. Sleep plays an integral role in metabolic control. Consequently, insufficient sleep may represent a modifiable risk factor for the development of Type 2 diabetes. The challenge ahead is to identify how sex differences, ageing and obesity could potentially influence the relationship between sleep and metabolism.

Aging↗