Substrate Utilization during Heavy Exercise after Different Diets

Maximal-intensity exercise does not fully restore muscle pyruvate dehydrogenase complex activation after 3 days of high-fat dietary intake

“…We previously demonstrated that muscle PDC activation increased with exercise intensity [7], resulting in nearly complete transformation of PDC to PDCa within 74 s of electrically evoked maximal intensity isometric contraction [9] or within 10 min of moderate exercise (75%VO2max) [8]. However, when moderate intensity exercise was preceded by several days of an HFD muscle PDCa was reduced at rest and further activation during exercise was reduced [1,12,25]. Since mitochondrial Ca 2+ uptake, the primary regulator of muscle PDC activation during exercise [10], is dictated by exercise intensity [26], we aimed to Furthermore, the slowing of muscle relaxation during contraction was increased after HFD intervention, possibly as a consequence of an HFD mediated increase in circulating concentrations of organic acids [27] and/or as demonstrated herein by the inability of muscle to maintain PDC flux during contraction, thus reducing mitochondrial ATP generation, and increasing muscle lactic acid accumulation.…”

“…The in vitro measurement of PDCa activity reflects the maximal possible flux through the PDC reaction for any given level of activation (dephosphorylated form), although this may not be the case in vivo since the availability of co-factors is likely to be lower than in the in [1,30], even at workloads as high as 100% VO2max [27]. However, this can be explained by pre-exercise muscle glycogen content being considerably less in previous studies (generally less than 200 mmol kg -1 dm vs 362-416 mmol kg -1 dm in the present study) and/or the intensity of exercise employed being considerably lower than that of the present study, which collectively would have reduced rates of glycogenolysis and glycolysis during exercise [31].…”

“…High-fat dietary intake (HFD) has been shown to reduce muscle PDC activation and carbohydrate (CHO) oxidation at rest and during moderate intensity exercise [1,11,12], and thereby has been suggested to play a causative role in the induction of dietary mediated skeletal muscle insulin resistance and, presumably under chronic conditions, the development of metabolic syndrome, i.e. central obesity, hypertriglyceridaemia, low HDL-cholesterol and hypertension [13].…”

Pre‐loading large volume oral electrolytes: tracing fluid and ion fluxes in horses during rest, exercise and recovery

“…In biopsies from human muscle, the onset of exercise is associated with increased extracellular and intracellular water content (Bergström & Hultman, 1966; Kowalchuk et al ., 1988). The increased muscle fluid content can be attributed to the osmotic movement of water resulting from increased intracellular [Na + ], [Cl – ], lactate], [inorganic phosphate] and [creatine] (Kowalchuk et al ., 1988; Putman et al ., 1994). Increased intracellular [Na + ] and [Cl – ] are normal with exercise (Kowalchuk et al ., 1988; Lindinger & Heigenhauser, 1988), with the increase in [Na + ] arising as a consequence of inward flux of Na + through Na + channels associated with action potentials (Lindinger & Cairns, 2021), and increased [Cl – ] as a requirement for maintaining charge balance (Stickland et al ., 2013) as well as membrane excitability (Cairns & Lindinger, 2008).…”