Alan Hayes

Effect of whey protein isolate on strength, body composition and muscle hypertrophy during resistance training.

Purpose of reviewSarcopenia (skeletal muscle wasting with aging) is thought to underlie a number of serious age-related health issues. While it may be seen as inevitable, decreasing this gradual loss of muscle is vital for healthy aging. Thus, it is imperative to investigate exercise and nutrition-based strategies designed to build a reservoir of muscle mass as early as possible. Recent findingsElderly individuals are still able to respond to both resistance training and the anabolic signals provided by protein ingestion, provided specific amino acids, such as leucine, are present. Whey proteins are a rich source of these essential amino acids and rapidly elevate plasma amino acids, thus providing the foundations for preservation of muscle mass. Several studies involving supplementation with whey protein have been shown to be effective in augmenting the effects of resistance exercise, particularly when supplementation occurs in the hours surrounding the exercise training. SummaryWhile further work is required, particularly in elderly people, simple dietary and exercise strategies that may improve the maintenance of skeletal muscle mass will likely result in a decrease in the overall burden of a number of diseases and improve the quality of life as we age.

The Effects of Endurance Exercise on Dystrophic mdx Mice. I. Contractile and Histochemical Properties of Intact Muscles

Genetically normal (C57BL/10) and dystrophic (mdx) mice underwent a 15 week endurance swimming programme (2 hours per day, 5 days per week) where animals were weighted (5% body weight) during most sessions. No significant changes were seen in the contractile properties or morphology of muscles from control mice following the exercise protocol. In contrast, the soleus muscles of exercised mdx mice displayed higher normalized tensions, and the extensor digitorum longus (EDL) exhibited longer half-relaxation times compared with sedentary mdx mice. Both the EDL and soleus muscles of mdx mice exhibited increased resistance to fatigue after endurance exercise. Sedentary mdx mice exhibited increased proportions of type I (slow oxidative) fibres in the soleus and type IIA (fast, oxidative glycolytic) fibres in the EDL compared with animals of the normal strain. In both the EDL and soleus muscles of mdx mice an even greater proportion of type I fibres was apparent following the training programme. The endurance exercise was beneficial to the mdx mice, enhancing the regeneration of function of their muscles by increasing the proportion of oxidative fibres and reducing muscle fatiguability.

Creatine supplementation enhances muscle force recovery after eccentrically-induced muscle damage in healthy individuals

BackgroundEccentric exercise-induced damage leads to reductions in muscle force, increased soreness, and impaired muscle function. Creatine monohydrates (Cr) ergogenic potential is well established; however few studies have directly examined the effects of Cr supplementation on recovery after damage. We examined the effects of Cr supplementation on muscle proteins and force recovery after eccentrically-induced muscle damage in healthy individuals.MethodsFourteen untrained male participants (22.1 ± 2.3 yrs, 173 ± 7.7 cm, 76.2 ± 9.3 kg) were randomly separated into 2 supplement groups: i) Cr and carbohydrate (Cr-CHO; n = 7); or ii) carbohydrate (CHO; n = 7). Participants consumed their supplement for a period of 5 days prior to, and 14 days following a resistance exercise session. Participants performed 4 sets of 10 eccentric-only repetitions at 120% of their maximum concentric 1-RM on the leg press, leg extension and leg flexion exercise machine. Plasma creatine kinase (CK) and lactate dehydrogenase (LDH) activity were assessed as relevant blood markers of muscle damage. Muscle strength was examined by voluntary isokinetic knee extension using a Cybex dynamometer. Data were analyzed using repeated measures ANOVA with an alpha of 0.05.ResultsThe Cr-supplemented group had significantly greater isokinetic (10% higher) and isometric (21% higher) knee extension strength during recovery from exercise-induced muscle damage. Furthermore, plasma CK activity was significantly lower (by an average of 84%) after 48 hrs (P < 0.01), 72 hrs (P < 0.001), 96 hrs (P < 0.0001), and 7 days (P < 0.001) recovery in the Cr-supplemented group.ConclusionThe major finding of this investigation was a significant improvement in the rate of recovery of knee extensor muscle function after Cr supplementation following injury.

Taurine supplementation increases skeletal muscle force production and protects muscle function during and after high-frequency in vitro stimulation

Recent studies report that depletion and repletion of muscle taurine (Tau) to endogenous levels affects skeletal muscle contractility in vitro. In this study, muscle Tau content was raised above endogenous levels by supplementing male Sprague-Dawley rats with 2.5% (wt/vol) Tau in drinking water for 2 wk, after which extensor digitorum longus (EDL) muscles were examined for in vitro contractile properties, fatigue resistance, and recovery from fatigue after two different high-frequency stimulation bouts. Tau supplementation increased muscle Tau content by approximately 40% and isometric twitch force by 19%, shifted the force-frequency relationship upward and to the left, increased specific force by 4.2%, and increased muscle calsequestrin protein content by 49%. Force at the end of a 10-s (100 Hz) continuous tetanic stimulation was 6% greater than controls, while force at the end of the 3-min intermittent high-frequency stimulation bout was significantly higher than controls, with a 12% greater area under the force curve. For 1 h after the 10-s continuous stimulation, tetanic force in Tau-supplemented muscles remained relatively stable while control muscle force gradually deteriorated. After the 3-min intermittent bout, tetanic force continued to slowly recover over the next 1 h, while control muscle force again began to decline. Tau supplementation attenuated F(2)-isoprostane production (a sensitive indicator of reactive oxygen species-induced lipid peroxidation) during the 3-min intermittent stimulation bout. Finally, Tau transporter protein expression was not altered by the Tau supplementation. Our results demonstrate that raising Tau content above endogenous levels increases twitch and subtetanic and specific force in rat fast-twitch skeletal muscle. Also, we demonstrate that raising Tau protects muscle function during high-frequency in vitro stimulation and the ensuing recovery period and helps reduce oxidative stress during prolonged stimulation.

Contractile function and low-intensity exercise effects of old dystrophic (mdx) mice

Old mdx mice display a severe myopathy almost identical to Duchennes muscular dystrophy. This study examined the contractile properties of old mdxmuscles and investigated any effects of low-intensity exercise. Isometric contractile properties of the extensor digitorum longus (EDL) and soleus muscles were tested in adult (8-10 mo) and old (24 mo, split into sedentary and exercised groups) mdx mice. The EDL and soleus from old mdx mice exhibited decreased absolute twitch and tetanic forces, and the soleus exhibited a >50% decrease in relative forces (13.4 ± 0.4 vs. 6.0 ± 0.9 N/cm2) compared with adult mice. Old mdx muscles also showed longer contraction times and a higher percentage of type I fibers. Normal and mdx mice completed 10 wk of swimming, but mdx mice spent significantly less time swimming than normal animals (7.8 ± 0.4 vs. 15.8 ± 1.1 min, respectively). However, despite their severe dystrophy, mdx muscles responded positively to the low-intensity exercise. Relative tetanic tensions were increased (∼25% and ∼45% for the EDL and soleus, respectively) after the swimming, although absolute forces were unaffected. Thus these results indicate that, even with a dystrophin-deficient myopathy, mdx muscles can still respond to low-intensity exercise. This study shows that the contractile function of muscles of old mdx mice displays many similarities to that of human dystrophic patients and provides further evidence that the use of non-weight-bearing, low-intensity exercises, such as swimming, has no detrimental effect on dystrophic muscle and could be a useful therapeutic aid for sufferers of muscular dystrophy.Old mdx mice display a severe myopathy almost identical to Duchennes muscular dystrophy. This study examined the contractile properties of old mdx muscles and investigated any effects of low-intensity exercise. Isometric contractile properties of the extensor digitorum longus (EDL) and soleus muscles were tested in adult (8-10 mo) and old (24 mo, split into sedentary and exercised groups) mdx mice. The EDL and soleus from old mdx mice exhibited decreased absolute twitch and tetanic forces, and the soleus exhibited a > 50% decrease in relative forces (13.4 +/- 0.4 vs. 6.0 +/- 0.9 N/cm2) compared with adult mice. Old mdx muscles also showed longer contraction times and a higher percentage of type I fibers. Normal and mdx mice completed 10 wk of swimming, but mdx mice spent significantly less time swimming than normal animals (7.8 +/- 0.4 vs. 15.8 +/- 1.1 min, respectively). However, despite their severe dystrophy, mdx muscles responded positively to the low-intensity exercise. Relative tetanic tensions were increased (approximately 25% and approximately 45% for the EDL and soleus, respectively) after the swimming, although absolute forces were unaffected. Thus these results indicate that, even with a dystrophin-deficient myopathy, mdx muscles can still respond to low-intensity exercise. This study shows that the contractile function of muscles of old mdx mice displays many similarities to that of human dystrophic patients and provides further evidence that the use of non-weight-bearing, low-intensity exercises, such as swimming, has no detrimental effect on dystrophic muscle and could be a useful therapeutic aid for sufferers of muscular dystrophy.

Whey protein isolate attenuates strength decline after eccentrically-induced muscle damage in healthy individuals

BackgroundWe examined the effects of short-term consumption of whey protein isolate on muscle proteins and force recovery after eccentrically-induced muscle damage in healthy individuals.MethodsSeventeen untrained male participants (23 ± 5 yr, 180 ± 6 cm, 80 ± 11 kg) were randomly separated into two supplement groups: i) whey protein isolate (WPH; n = 9); or ii) carbohydrate (CHO; n = 8). Participants consumed 1.5 g/kg.bw/day supplement (~30 g consumed immediately, and then once with breakfast, lunch, in the afternoon and after the evening meal) for a period of 14 days following a unilateral eccentric contraction-based resistance exercise session, consisting of 4 sets of 10 repetitions at 120% of maximum voluntary contraction on the leg press, leg extension and leg flexion exercise machine. Plasma creatine kinase and lactate dehydrogenase (LDH) levels were assessed as blood markers of muscle damage. Muscle strength was examined by voluntary isokinetic knee extension using a Cybex dynamometer. Data were analyzed using repeated measures ANOVA with an alpha of 0.05.ResultsIsometric knee extension strength was significantly higher following WPH supplementation 3 (P < 0.05) and 7 (P < 0.01) days into recovery from exercise-induced muscle damage compared to CHO supplementation. In addition, strong tendencies for higher isokinetic forces (extension and flexion) were observed during the recovery period following WPH supplementation, with knee extension strength being significantly greater (P < 0.05) after 7 days recovery. Plasma LDH levels tended to be lower (P = 0.06) in the WPH supplemented group during recovery.ConclusionsThe major finding of this investigation was that whey protein isolate supplementation attenuated the impairment in isometric and isokinetic muscle forces during recovery from exercise-induced muscle injury.

Sarcopenic obesity and dynapenic obesity: 5‐year associations with falls risk in middle‐aged and older adults

To determine whether obesity concurrent with sarcopenia (low muscle mass) or dynapenia (low muscle strength) is associated with increased falls risk in middle‐aged and older adults.

Examining potential drug therapies for muscular dystrophy utilising the dy/dy mouse: I. Clenbuterol

As a potent promoter of muscle growth, clenbuterol has been proposed as a treatment for muscle wasting diseases. Thus, the effects of clenbuterol on dystrophic skeletal muscle was examined. Male dystrophic (dy/dy) mice aged 4-5 weeks were treated with clenbuterol for 3 weeks, and the isometric contractile, fatigue and histochemical properties of the slow-twitch soleus and fast-twitch plantaris muscles measured. Muscles of dystrophic animals produced lower forces, contracted more slowly and exhibited greater fatigue resistance than age-matched normal animals. Dystrophic soleus muscles also had higher proportions of type I fibres than normal mice. Clenbuterol significantly reduced the natural death rate of dystrophic mice, as 3 of 11 untreated animals died prior to completion of the 3-week experimental period, whereas none of the 9 clenbuterol-treated animals died. Clenbuterol treatment significantly increased the relative mass (P<0.001) and relative tetanic force production (P<0.01) of the soleus of dystrophic animals, most likely due to increases in protein accretion and improved regeneration. The plantaris of clenbuterol-treated dystrophic animals also exhibited higher mass (P<0.05) and higher absolute forces than untreated mice. The results from this study show that clenbuterol could be a valuable adjunct to treatments of muscle wasting diseases such as muscular dystrophy.

Contractile properties and temperature sensitivity of the extraocular muscles, the levator and superior rectus, of the rabbit.

1. Contractile and fatigue‐resistance characteristics, temperature sensitivity (10‐37 degrees C) of contraction, and histochemical fibre types were determined for two of the extraocular muscles, the superior rectus and levator palpebrae superioris (levator), of the rabbit. 2. The levator displayed similar contractile characteristics (time to peak, half‐relaxation time of twitch response, and twitch‐tetanus force ratio) to mammalian fast‐twitch limb muscle at room temperature (20 degrees C). However, normalized twitch and tetanic force levels were significantly less than those found in limb muscle. The superior rectus displayed the characteristics of even faster contraction than the levator at 20 degrees C, but generated lower maximum force levels than the levator. 3. The twitch response of the superior rectus showed a biphasic relaxation phase. This response was not due to non‐twitch (tonic) fibres present in the superior rectus as it was unaffected by propranolol application during muscle stimulation. 4. The superior rectus and levator displayed significantly less fatigue in the tetanic force response than fast‐twitch limb muscles did in response to a fatiguing electrical stimulation protocol. The levator was significantly more fatigue resistant than the superior rectus. 5. The force responses of both extraocular muscles displayed a similar dependence on temperature (10‐37 degrees C) to limb skeletal muscles. 6. The superior rectus and levator exhibited a high proportion of fast‐twitch muscle fibres (type II) as shown by myosin ATPase staining. Succinate dehydrogenase activity indicated that these muscles showed a high oxidative capacity, with a staining intensity typical of type I or type II A fibres of limb muscles. 7. The results emphasize the morphological and functional complexity of mammalian extraocular muscles. The combination of very fast contractile properties with high oxidative capacity make these muscles well suited to their role in eye/eyelid movement.

Defects in Mitochondrial ATP Synthesis in Dystrophin-Deficient Mdx Skeletal Muscles May Be Caused by Complex I Insufficiency

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.