A primary focus of the management of type 1 diabetes has been on matching prandial insulin therapy with carbohydrate amount consumed. However, even with the introduction of more flexible intensive insulin regimes, people with type 1 diabetes still struggle to achieve optimal glycaemic control. More recently, dietary fat and protein have been recognised as having a significant impact on postprandial blood glucose levels. Fat and protein independently increase the postprandial glucose excursions and together their effect is additive. This article reviews how the fat and protein in a meal impact the postprandial glycaemic response and discusses practical approaches to managing this in clinical practice. These insights have significant implications for patient education, mealtime insulin dose calculations and dosing strategies.

The high forces undergone during repetitive eccentric, or lengthening, contractions place skeletal muscle under considerable stress, in particular if unaccustomed. Although muscle is highly adaptive, the responses to stress may not be optimally regulated by the body. Reactive oxygen species (ROS) are one component of the stress response that may contribute to muscle damage after eccentric exercise. Antioxidants may in turn scavenge ROS, thereby preventing or attenuating muscle damage. The antioxidant vitamins C (ascorbic acid) and E (tocopherol) are among the most commonly used sport supplements, and are often taken in large doses by athletes and other sportspersons because of their potential protective effect against muscle damage. This review assesses studies that have investigated the effects of these two antioxidants, alone or in combination, on muscle damage and oxidative stress. Studies have used a variety of supplementation strategies, with variations in dosage, timing and duration of supplementation. Although there is some evidence to show that both antioxidants can reduce indices of oxidative stress, there is little evidence to support a role for vitamin C and/or vitamin E in protecting against muscle damage. Indeed, antioxidant supplementation may actually interfere with the cellular signalling functions of ROS, thereby adversely affecting muscle performance. Furthermore, recent studies have cast doubt on the benign effects of long-term, high-dosage antioxidant supplementation. High doses of vitamin E, in particular, may increase all-cause mortality. Although some equivocation remains in the extant literature regarding the beneficial effects of antioxidant vitamin supplementation on muscle damage, there is little evidence to support such a role. Since the potential for long-term harm does exist, the casual use of high doses of antioxidants by athletes and others should perhaps be curtailed.

Postprandial lipaemia may lead to an increase in oxidative stress, inducing endothelial dysfunction. Exercise can slow gastric emptying rates, moderating postprandial lipaemia. The purpose of this study was to determine if moderate exercise, prior to fat ingestion, influences gastrointestinal transit, lipaemia, oxidative stress and arterial wall function. Eight apparently healthy males (age 23.6 ± 2.8 yrs; height 181.4 ± 8.1 cm; weight 83.4 ± 16.2 kg; all data mean ± SD) participated in the randomised, crossover design, where (i) subjects ingested a high-fat meal alone (control), and (ii) ingested a high-fat meal, preceded by 1 h of moderate exercise. Pulse Wave Velocity (PWV) was examined at baseline, post-exercise, and in the postprandial period. Gastric emptying was measured using the 13C-octanoic acid breath test. Measures of venous blood were obtained prior to and following exercise and at 2, 4 and 6 hours post-ingestion. PWV increased (6.5 ± 1.9 m/sec) at 2 (8.9 ± 1.7 m/sec) and 4 hrs (9.0 ± 1.6 m/sec) post-ingestion in the control group (time × group interaction, P < 0.05). PWV was increased at 2 hrs post-ingestion in the control compared to the exercise trial; 8.9 ± 1.7 vs. 6.2 ± 1.5 m/sec (time × group interaction, P < 0.05). Lipid hydroperoxides increased over time (pooled exercise and control data, P < 0.05). Serum triacylglycerols were elevated postprandially (pooled exercise and control data, P < 0.05). There were no changes in gastric emptying, cholesterol, or C-reactive protein levels. These data suggest that acute exercise prior to the consumption of a high-fat meal has the potential to reduce vascular impairments.

Reactive oxygen species may contribute to exercise-induced skeletal muscle damage, and antioxidants may protect against such damage. This study examined the effectiveness of prophylactic supplementation with vitamins C and E on symptoms of muscle damage in a single blind, two-group study design. Twelve male volunteers were randomly assigned to either treatment or control groups. The treatment group received 500 mg of vitamin C and 1,200 IU of alpha-tocopherol daily and the control group received glucose placebo for 37 days. After 30 days of treatment, volunteers performed 300 maximal eccentric contractions of the knee extensor muscles of one leg. Maximal voluntary isometric contraction force and electrically evoked force at a frequency of 20 Hz and 50 Hz were recorded before and after exercise, and on days 1, 2 and 7 after exercise. Muscle soreness questionnaires were completed and muscle girth recorded at the same time points. Eccentric contractile torque and work during the bout declined significantly in both groups ( P<0.001), but this decline was smaller in the vitamin-supplemented group ( P<0.05). Maximal voluntary isometric contraction force and 20:50 Hz force ratio declined significantly after exercise in both groups ( P<0.01), but the decline was smaller in the treatment group on days 1 and 2 post-exercise ( P<0.05). Both groups experienced similar significant muscle soreness and swelling after exercise. These data suggest that prior supplementation with dietary antioxidants ameliorates muscle functional decrements subsequent to eccentric muscle contraction.

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