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Long-term excessive positive energy balance results in overweight and obesity, which is caused by adipose tissue deposition. This increases the occurrence of cardiovascular diseases and type 2 diabetes. Adipose tissue plays an active role in the development of these diseases and so it is important to understand how this tissue responds to relevant stimuli such as feeding, fasting and physical activity. The study in Chapter 4 examined the impact of fasting and feeding, on adipose tissue responsiveness to prolonged moderate intensity exercise. Ten healthy overweight men aged 26 ± 5 years (mean ± SD) with a waist circumference of 105 ± 10 cm walked at 60% of maximum oxygen uptake under either fasted (12 h overnight fasting) or fed (70% carbohydrate breakfast) conditions in a randomised, counterbalanced design. Feeding comprised 648 ± 115 kcal 2 h before exercise. The expression of several metabolism-related adipose tissue genes was acutely regulated whilst participants undertook fasted exercise, including up-regulation of lipolytic lipase and transporter (adipose triglyceride lipase, hormone sensitive lipase & fatty acid translocase/CD36), glycolytic inhibitor (pyruvate dehydrogenase 4), insulin singling molecules (glucose transporter type 4 & insulin receptor substrate 2) as well as adipose insulin receptor substrate 2 protein contents (all p ≤ 0.05), compared to exercise in the fed state. The results indicate that adipose tissue responsiveness to prolonged exercise is affected by the dietary conditions. The study in Chapter 5 examined whether adipose tissue would be influenced by more modest changes in accumulated physical activity. Eleven overweight participants (7 men and 4 post-menopausal women) aged 50 ± 5 years (means ± SD) completed two identical mixed meal (~1,700 ± 360 kcal in total) feeding trials (prolonged sitting versus breaking sitting) in a randomised, counterbalanced design. The breaking sitting intervention comprised walking for 2 min every 20 min over 5 h. The results demonstrated that postprandial insulin and glucose concentrations were attenuated (all p ≤ 0.05) while participating in regular small bouts of walking but this did not affect adipose tissue metabolic- and insulin-associated pathways in adipose tissue. The study in Chapter 6 examined the responsiveness to aforementioned different forms of physical activity (a single bout of prolonged exercise versus accumulation of small bout of physical activity) on a challenge imposed by 50% overfeeding. Twenty-four lean, active and healthy men aged 21 ± 3 years were recruited. Participants were randomised to either an overfeeding with restricted physical activity (≤ 4,000 steps per day) group (OVER, n = 8), overfeeding with restricted physical activity (≤ 4,000 steps per day) plus daily 45 min endurance moderate intensity walking group (50% V̇O2max) (OVER + EN, n = 8) or overfeeding with restricted physical activity (≤ 4,000 steps per day) plus intermittent breaking sitting group (OVER + BREAKS, n = 8). All groups achieved the same overfeeding (50% of overfeeding based on their habitual diet). Notably, despite the impairment of insulin sensitivity as a result of the energy surplus, the accumulation of small bouts of physical activity blunted overfeeding induced up-regulation of adipose lipogenetic activity (i.e. the down-regulation of sterol regulatory element binding protein 1c and fatty acid synthase) and circulating inflammation (i.e. no change of white blood cell count) compared to energy surplus with sedentary lifestyle and/or overfeeding plus a single bout of moderate intensity exercise. This could mean that the form of physical activity undertaken could play a key role in lipogenesis activation. Based on the results from this thesis, it appears that energy consumption and physical activity are both capable of acutely and chronically influencing adipose tissue metabolic signalling and regulation.