Cold exposure modulates the use of carbohydrates (CHOs) and fat during exercise. This phenomenon has mostly been observed in controlled cycling studies, but not during walking and running when core temperature and oxygen consumption are controlled, as both may alter energy metabolism. This study aimed at examining energy substrate availability and utilization during walking and running in the cold when core temperature and oxygen consumption are maintained. Ten lightly clothed male subjects walked or ran for 60-min, at 50% and 70% of maximal oxygen consumption, respectively, in a climatic chamber set at 0°C or 22°C. Thermal, cardiovascular, and oxidative responses were measured every 15-min during exercise. Blood samples for serum non-esterified fatty acids (NEFAs), glycerol, glucose, beta-hydroxybutyrate (BHB), plasma catecholamines, and serum lipids were collected immediately prior, and at 30- and 60-min of exercise. Skin temperature strongly decreased while core temperature did not change during cold trials. Heart rate (HR) was also lower in cold trials. A rise in fat utilization in the cold was seen through lower respiratory quotient (RQ) (−0.03 ± 0.02), greater fat oxidation (+0.14 ± 0.13 g · min−1) and contribution of fat to total energy expenditure (+1.62 ± 1.99 kcal · min−1). No differences from cold exposure were observed in blood parameters. During submaximal walking and running, a greater reliance on derived fat sources occurs in the cold, despite the absence of concurrent alterations in NEFAs, glycerol, or catecholamine concentrations. This disparity may suggest a greater reliance on intra-muscular energy sources such as triglycerides during both walking and running.

The purpose of the study was to examine the effects of exercise on total leukocyte count and subsets, as well as hormone and cytokine responses in a thermoneutral and cold environment, with and without an individualized pre-cooling protocol inducing low-intensity shivering. Nine healthy young men participated in six experimental trials wearing shorts and t-shirts. Participants exercised for 60 min on a treadmill at low (LOW: 50% of peak VO2) and moderate (MOD: 70% VO2peak) exercise intensities in a climatic chamber set at 22°C (NT), and in 0°C (COLD) with and without a pre-exercise low-intensity shivering protocol (SHIV). Core and skin temperature, heart rate and oxygen consumption were collected continuously. Blood samples were collected before and at the end of exercise to assess endocrine and immunological changes. Core temperature in NT was greater than COLD and SHIV by 0.4±0.2°C whereas skin temperature in NT was also greater than COLD and SHIV by 8.5±1.4°C and 9.3±2.5°C respectively in MOD. Total testosterone, adenocorticotropin and cortisol were greater in NT vs. COLD and SHIV in MOD. Norepinephrine was greater in NT vs. other conditions across intensities. Interleukin-2, IL-5, IL-7, IL-10, IL-17, IFN-γ, Rantes, Eotaxin, IP-10, MIP-1β, MCP-1, VEGF, PDGF, and G-CSF were elevated in NT vs. COLD and/or SHIV. Furthermore, IFN-γ, MIP-1β, MCP-1, IL-10, VEGF, and PDGF demonstrate greater concentrations in SHIV vs. COLD, mainly in the MOD condition. This study demonstrated that exercising in the cold can diminish the exercise-induced systemic inflammatory response seen in a thermoneutral environment. Nonetheless, prolonged cooling inducing shivering thermogenesis prior to exercise, may induce an immuno-stimulatory response following moderate intensity exercise. Performing exercise in cold environments can be a useful strategy in partially inhibiting the acute systemic inflammatory response from exercise but oppositely, additional body cooling may reverse this benefit.

Exercise and shivering rely on different metabolic pathways and consequently, fuel selection. The present study examined the effects of a pre-exercise low-intensity shivering protocol on fuel selection during submaximal exercise in a cold environment. Nine male subjects exercised 4 times for 60 min at 50% (LOW) or 70% (MOD) of their peak oxygen consumption on a motorized treadmill in a climatic chamber set at 0 °C with (SHIV) and without (CON) a pre-exercise cooling protocol, inducing low-intensity shivering. Thermal, cardiorespiratory and metabolic responses were measured every 15 min whereas blood samples were collected every 30 min to assess serum nonesterified fatty acids (NEFA), glycerol, glucose, β-hydroxybutyrate (BHB) and plasma catecholamine concentrations. Rectal and skin temperatures were lower in the SHIV condition, within LOW and MOD conditions, during the first 45 min of exercise. Norepinephrine (NE) concentration was greater in SHIV vs. CON within LOW (1.39 ± 0.17 vs. 0.98 ± 0.17 ng·mL(-1)) and MOD (1.50 ± 0.20 vs. 1.01 ± 0.09 ng·mL(-1)), whereas NEFA, glycerol and BHB were greater in SHIV vs. CON (1060 ± 49 vs. 898 ± 78 μmol·L(-1); 0.27 ± 0.02 vs. 0.22 ± 0.03 mmol·L(-1); 0.39 ± 0.06 vs. 0.27 ± 0.04 mmol·L(-1), respectively) within MOD only. No changes were observed in fat or carbohydrate oxidation between SHIV and CON during exercise. Despite increases in NE, NEFA, glycerol and BHB from pre-exercise low-intensity shivering, fuel selection during short-term submaximal exercise in the cold was unaltered.

Early responses of stress-sensing proteins, muscle LIM protein (MLP), ankyrin repeat proteins (Ankrd1/CARP and Ankrd2/Arpp) and muscle-specific RING finger proteins (MuRF1 and MuRF2), along the titin molecule were investigated in the present experiment after submaximal exhaustive exercise. Ten healthy men performed continuous drop jumping unilaterally on a sledge apparatus with a submaximal height until complete exhaustion. Five stress-sensing proteins were analysed by mRNA measurements from biopsies obtained immediately and 3 h after the exercise from exercised vastus lateralis muscle while control biopsies were obtained from non-exercised legs before the exercise. Decreased maximal jump height and increased serum creatine kinase activities as indirect markers for muscle damage and HSP27 immunostainings on muscle biopsies as a direct marker for muscle damage indicated that the current exercised protocol caused muscle damage. mRNA levels for four (MLP, Ankrd1/CARP, MuRF1 and MuRF2) out of the five studied stress sensors significantly (p < 0.05) increased 3 h after fatiguing exercise. The magnitude of MLP and Ankrd2 responses was related to the proportion of type 1 myofibres. Our data showed that the submaximal exhaustive exercise with subject's own physical fitness level activates titin-based stretch-sensing proteins. These results suggest that both degenerative and regenerative pathways are activated in very early phase after the exercise or probably already during the exercise. Activation of these proteins represents an initial step forward adaptive remodelling of the exercised muscle and may also be involved in the initiation of myofibre repair.